A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures.
Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.
An antineoplastic agent. It has significant activity against melanomas. (from Martindale, The Extra Pharmacopoeia, 31st ed, p564)
Benign and malignant central nervous system neoplasms derived from glial cells (i.e., astrocytes, oligodendrocytes, and ependymocytes). Astrocytes may give rise to astrocytomas (ASTROCYTOMA) or glioblastoma multiforme (see GLIOBLASTOMA). Oligodendrocytes give rise to oligodendrogliomas (OLIGODENDROGLIOMA) and ependymocytes may undergo transformation to become EPENDYMOMA; CHOROID PLEXUS NEOPLASMS; or colloid cysts of the third ventricle. (From Escourolle et al., Manual of Basic Neuropathology, 2nd ed, p21)
A cell line derived from cultured tumor cells.
Neoplasms of the brain and spinal cord derived from glial cells which vary from histologically benign forms to highly anaplastic and malignant tumors. Fibrillary astrocytomas are the most common type and may be classified in order of increasing malignancy (grades I through IV). In the first two decades of life, astrocytomas tend to originate in the cerebellar hemispheres; in adults, they most frequently arise in the cerebrum and frequently undergo malignant transformation. (From Devita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2013-7; Holland et al., Cancer Medicine, 3d ed, p1082)
A class of drugs that differs from other alkylating agents used clinically in that they are monofunctional and thus unable to cross-link cellular macromolecules. Among their common properties are a requirement for metabolic activation to intermediates with antitumor efficacy and the presence in their chemical structures of N-methyl groups, that after metabolism, can covalently modify cellular DNA. The precise mechanisms by which each of these drugs acts to kill tumor cells are not completely understood. (From AMA, Drug Evaluations Annual, 1994, p2026)
Enzymes that are part of the restriction-modification systems. They are responsible for producing a species-characteristic methylation pattern, on either adenine or cytosine residues, in a specific short base sequence in the host cell's own DNA. This methylated sequence will occur many times in the host-cell DNA and remain intact for the lifetime of the cell. Any DNA from another species which gains entry into a living cell and lacks the characteristic methylation pattern will be recognized by the restriction endonucleases of similar specificity and destroyed by cleavage. Most have been studied in bacterial systems, but a few have been found in eukaryotic organisms.
Highly proliferative, self-renewing, and colony-forming stem cells which give rise to NEOPLASMS.
Mutant mice homozygous for the recessive gene "nude" which fail to develop a thymus. They are useful in tumor studies and studies on immune responses.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
In vivo methods of screening investigative anticancer drugs, biologic response modifiers or radiotherapies. Human tumor tissue or cells are transplanted into mice or rats followed by tumor treatment regimens. A variety of outcomes are monitored to assess antitumor effectiveness.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
Ability of neoplasms to infiltrate and actively destroy surrounding tissue.
Primary and metastatic (secondary) tumors of the brain located above the tentorium cerebelli, a fold of dura mater separating the CEREBELLUM and BRAIN STEM from the cerebral hemispheres and DIENCEPHALON (i.e., THALAMUS and HYPOTHALAMUS and related structures). In adults, primary neoplasms tend to arise in the supratentorial compartment, whereas in children they occur more frequently in the infratentorial space. Clinical manifestations vary with the location of the lesion, but SEIZURES; APHASIA; HEMIANOPSIA; hemiparesis; and sensory deficits are relatively common features. Metastatic supratentorial neoplasms are frequently multiple at the time of presentation.
Benign and malignant neoplastic processes that arise from or secondarily involve the brain, spinal cord, or meninges.
Transplantation between animals of different species.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Experimental transplantation of neoplasms in laboratory animals for research purposes.
A performance measure for rating the ability of a person to perform usual activities, evaluating a patient's progress after a therapeutic procedure, and determining a patient's suitability for therapy. It is used most commonly in the prognosis of cancer therapy, usually after chemotherapy and customarily administered before and after therapy. It was named for Dr. David A. Karnofsky, an American specialist in cancer chemotherapy.
Enzymes that are involved in the reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule, which contained damaged regions.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
A cell surface receptor involved in regulation of cell growth and differentiation. It is specific for EPIDERMAL GROWTH FACTOR and EGF-related peptides including TRANSFORMING GROWTH FACTOR ALPHA; AMPHIREGULIN; and HEPARIN-BINDING EGF-LIKE GROWTH FACTOR. The binding of ligand to the receptor causes activation of its intrinsic tyrosine kinase activity and rapid internalization of the receptor-ligand complex into the cell.
A lipid phosphatase that acts on phosphatidylinositol-3,4,5-trisphosphate to regulate various SIGNAL TRANSDUCTION PATHWAYS. It modulates CELL GROWTH PROCESSES; CELL MIGRATION; and APOPTOSIS. Mutations in PTEN are associated with COWDEN DISEASE and PROTEUS SYNDROME as well as NEOPLASTIC CELL TRANSFORMATION.
The treatment of a disease or condition by several different means simultaneously or sequentially. Chemoimmunotherapy, RADIOIMMUNOTHERAPY, chemoradiotherapy, cryochemotherapy, and SALVAGE THERAPY are seen most frequently, but their combinations with each other and surgery are also used.
Antineoplastic agent especially effective against malignant brain tumors. The resistance which brain tumor cells acquire to the initial effectiveness of this drug can be partially overcome by the simultaneous use of membrane-modifying agents such as reserpine, calcium antagonists such as nicardipine or verapamil, or the calmodulin inhibitor, trifluoperazine. The drug has also been used in combination with other antineoplastic agents or with radiotherapy for the treatment of various neoplasms.
Rare mixed tumors of the brain and rarely the spinal cord which contain malignant neuroectodermal (glial) and mesenchymal components, including spindle-shaped fibrosarcoma cells. These tumors are highly aggressive and present primarily in adults as rapidly expanding mass lesions. They may arise in tissue that has been previously irradiated. (From Br J Neurosurg 1995 Apr;9(2):171-8)
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
A pathologic process consisting of the proliferation of blood vessels in abnormal tissues or in abnormal positions.
A relatively slow-growing glioma that is derived from oligodendrocytes and tends to occur in the cerebral hemispheres, thalamus, or lateral ventricle. They may present at any age, but are most frequent in the third to fifth decades, with an earlier incidence peak in the first decade. Histologically, these tumors are encapsulated, relatively avascular, and tend to form cysts and microcalcifications. Neoplastic cells tend to have small round nuclei surrounded by unstained nuclei. The tumors may vary from well-differentiated to highly anaplastic forms. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, p2052; Adams et al., Principles of Neurology, 6th ed, p655)
The local recurrence of a neoplasm following treatment. It arises from microscopic cells of the original neoplasm that have escaped therapeutic intervention and later become clinically visible at the original site.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
Spherical, heterogeneous aggregates of proliferating, quiescent, and necrotic cells in culture that retain three-dimensional architecture and tissue-specific functions. The ability to form spheroids is a characteristic trait of CULTURED TUMOR CELLS derived from solid TUMORS. Cells from normal tissues can also form spheroids. They represent an in-vitro model for studies of the biology of both normal and malignant cells. (From Bjerkvig, Spheroid Culture in Cancer Research, 1992, p4)
A mutant strain of Rattus norvegicus without a thymus and with depressed or absent T-cell function. This strain of rats may have a small amount of hair at times, but then lose it.
An enzyme of the oxidoreductase class that catalyzes the conversion of isocitrate and NAD+ to yield 2-ketoglutarate, carbon dioxide, and NADH. It occurs in cell mitochondria. The enzyme requires Mg2+, Mn2+; it is activated by ADP, citrate, and Ca2+, and inhibited by NADH, NADPH, and ATP. The reaction is the key rate-limiting step of the citric acid (tricarboxylic) cycle. (From Dorland, 27th ed) (The NADP+ enzyme is EC 1.1.1.42.) EC 1.1.1.41.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Proteins that are normally involved in holding cellular growth in check. Deficiencies or abnormalities in these proteins may lead to unregulated cell growth and tumor development.
A cell-cycle phase nonspecific alkylating antineoplastic agent. It is used in the treatment of brain tumors and various other malignant neoplasms. (From Martindale, The Extra Pharmacopoeia, 30th ed, p462) This substance may reasonably be anticipated to be a carcinogen according to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (From Merck Index, 11th ed)
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.
An enzyme that transfers methyl groups from O(6)-methylguanine, and other methylated moieties of DNA, to a cysteine residue in itself, thus repairing alkylated DNA in a single-step reaction. EC 2.1.1.63.
A prediction of the probable outcome of a disease based on a individual's condition and the usual course of the disease as seen in similar situations.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
Mice homozygous for the mutant autosomal recessive gene "scid" which is located on the centromeric end of chromosome 16. These mice lack mature, functional lymphocytes and are thus highly susceptible to lethal opportunistic infections if not chronically treated with antibiotics. The lack of B- and T-cell immunity resembles severe combined immunodeficiency (SCID) syndrome in human infants. SCID mice are useful as animal models since they are receptive to implantation of a human immune system producing SCID-human (SCID-hu) hematochimeric mice.
The artificial induction of GENE SILENCING by the use of RNA INTERFERENCE to reduce the expression of a specific gene. It includes the use of DOUBLE-STRANDED RNA, such as SMALL INTERFERING RNA and RNA containing HAIRPIN LOOP SEQUENCE, and ANTI-SENSE OLIGONUCLEOTIDES.
Agents and endogenous substances that antagonize or inhibit the development of new blood vessels.
An interleukin-13 receptor subunit that is closely-related to the INTERLEUKIN-13 RECEPTOR ALPHA1 SUBUNIT. The receptor is found as a monomeric protein and has been considered to be a decoy receptor for interleukin-13 due the fact that it lacks cytoplasmic signaling domains.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
A nonparametric method of compiling LIFE TABLES or survival tables. It combines calculated probabilities of survival and estimates to allow for observations occurring beyond a measurement threshold, which are assumed to occur randomly. Time intervals are defined as ending each time an event occurs and are therefore unequal. (From Last, A Dictionary of Epidemiology, 1995)
The proto-oncogene c-erbB-1 codes for the epidermal growth factor receptor. Its name originates from the viral homolog v-erbB which was isolated from an avian erythroblastosis virus (AEV) where it was contained as a fragment of the chicken c-ErbB-1 gene lacking the amino-terminal ligand-binding domain. Overexpression of erbB-1 genes occurs in a wide range of tumors, commonly squamous carcinomas of various sites and less commonly adenocarcinomas. The human c-erbB-1 gene is located in the chromosomal region 7p14 and 7p12.
Molecular products metabolized and secreted by neoplastic tissue and characterized biochemically in cells or body fluids. They are indicators of tumor stage and grade as well as useful for monitoring responses to treatment and predicting recurrence. Many chemical groups are represented including hormones, antigens, amino and nucleic acids, enzymes, polyamines, and specific cell membrane proteins and lipids.
A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.
A class of statistical procedures for estimating the survival function (function of time, starting with a population 100% well at a given time and providing the percentage of the population still well at later times). The survival analysis is then used for making inferences about the effects of treatments, prognostic factors, exposures, and other covariates on the function.
The ability of some cells or tissues to survive lethal doses of IONIZING RADIATION. Tolerance depends on the species, cell type, and physical and chemical variables, including RADIATION-PROTECTIVE AGENTS and RADIATION-SENSITIZING AGENTS.
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
Processes required for CELL ENLARGEMENT and CELL PROLIFERATION.
Drugs used to potentiate the effectiveness of radiation therapy in destroying unwanted cells.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.

Comparative molecular genetic profiles of anaplastic astrocytomas/glioblastomas multiforme and their subsequent recurrences. (1/4101)

Malignant glial tumors (anaplastic astrocytomas and glioblastomas multiforme) arise mostly either from the progression of low grade precursor lesions or rapidly in a de novo fashion and contain distinct genetic alterations. There is, however, a third subset of malignant gliomas in which genetic lesions remain to be identified. Following surgical resection, all gliomas appear to have an inherent tendency to recur. Comparative molecular analysis of ten primary malignant gliomas (three anaplastic astrocytomas and seven glioblastomas multiforme) with their recurrences identified two distinct subgroups of recurrent tumors. In one group, primary tumors harbored genetic aberrations frequently associated with linear progression or de novo formation pathways of glial tumorigenesis and maintained their genetic profiles upon recurrence. In the other subset with no detectable known genetic mutations at first presentation, the recurrent tumors sustained specific abnormalities associated with pathways of linear progression or de novo formation. These included loss of genes on chromosomes 17 and 10, mutations in the p53 gene, homozygous deletion of the DMBTA1 and p16 and/ or p15 genes and amplification and/or overexpression of CDK4 and alpha form of the PDGF receptor. Recurrent tumors from both groups also displayed an abnormal expression profile of the metalloproteinase, gel A, and its inhibitor, TIMP-2, consistent with their highly invasive behavior. Delineation of the molecular differences between malignant glioblastomas and their subsequent recurrences may have important implications for the development of rational clinical approaches for this neoplasm that remains refractory to existing therapeutic modalities.  (+info)

Expression and tissue localization of membrane-type 1, 2, and 3 matrix metalloproteinases in human astrocytic tumors. (2/4101)

Three different membrane-type matrix metalloproteinases (MT1-, MT2-, and MT3-MMPs) are known to activate in vitro the zymogen of MMP-2 (pro-MMP-2, progelatinase A), which is one of the key MMPs in invasion and metastasis of various cancers. In the present study, we have examined production and activation of pro-MMP-2, expression of MT1-, MT2-, and MT3-MMPs and their correlation with pro-MMP-2 activation, and localization of MMP-2, MT1-MMP, and MT2-MMP in human astrocytic tumors. The sandwich enzyme immunoassay demonstrates that the production levels of pro-MMP-2 in the anaplastic astrocytomas and glioblastomas are significantly higher than that in the low-grade astrocytomas (P<0.05 and P<0.01, respectively), metastatic brain tumors (P<0.05), or normal brains (P<0.01). Gelatin zymography indicates that the pro-MMP-2 activation ratio is significantly higher in the glioblastomas than in other astrocytic tumors (P<0.01), metastatic brain tumors (P<0.01), and normal brains (P<0.01). The quantitative reverse transcription polymerase chain reaction analyses demonstrate that MT1-MMP and MT2-MMP are expressed predominantly in glioblastoma tissues (17/17 and 12/17 cases, respectively), and their expression levels increase significantly as tumor grade increases. MT3-MMP is detectable in both astrocytic tumor and normal brain tissues, but the mean expression level is approximately 50-fold lower compared with that of MT1-MMP and MT2-MMP in the glioblastomas. The activation ratio of pro-MMP-2 correlates directly with the expression levels of MT1-MMP and MT2-MMP but not MT3-MMP. In situ hybridization indicates that neoplastic astrocytes express MT1-MMP and MT2-MMP in the glioblastoma tissues (5/5 cases and 5/5 cases, respectively). Immunohistochemically, MT1-MMP and MT2-MMP are localized to the neoplastic astrocytes in glioblastoma samples (17/17 cases and 12/17 cases, respectively), which are also positive for MMP-2. In situ zymography shows gelatinolytic activity in the glioblastoma tissues but not in the normal brain tissues. These results suggest that both MT1-MMP and MT2-MMP play a key role in the activation of pro-MMP-2 in the human malignant astrocytic tumors and that the gelatinolytic activity is involved in the astrocytic tumor invasion.  (+info)

Novel regions of allelic deletion on chromosome 18p in tumors of the lung, brain and breast. (3/4101)

Lung cancer is now the number one cause of cancer death for both men and women. An age-adjusted analysis over the past 25 years shows that in women specifically, lung cancer incidence is on the rise. It is estimated that 10-20 genetic events including the alteration of oncogenes and tumor suppressor genes will have occurred by the time a lung tumor becomes clinically evident. In an effort to identify regions containing novel cancer genes, chromosome 18p11, a band not previously implicated in disease, was examined for loss of heterozygosity (LOH). In this study, 50 matched normal and NSCLC tumor samples were examined using six 18p11 and one 18q12.3 PCR-based polymorphic markers. In addition, LOH was examined in 29 glioblastoma pairs and 14 paired breast carcinomas. This analysis has revealed potentially two regions of LOH in 18p11 in up to 38% of the tumor samples examined. The regions of LOH identified included a 2 cm area between markers D18S59 and D18S476, and a more proximal, 25 cm region of intermediate frequency between D18S452 and D18S453. These results provide evidence for the presence of one or more potential tumor suppressor genes on the short arm of chromosome 18 which may be involved in NSCLC, brain tumors and possibly breast carcinomas as well.  (+info)

Regulation of interleukin-8 expression by reduced oxygen pressure in human glioblastoma. (4/4101)

Oxygen deprivation is an important biological feature of tumor growth. We previously showed that in glioma, anoxia increases expression of IL-8, a chemokine and angiogenic factor. Here, we analysed for the first time the biochemical mechanisms inducing the IL-8 gene upon anoxia in glioma cells, and showed that they differ from those inducing the VEGF gene. Both genes are induced in biologically and genetically heterogenous glioblastoma cell lines (LN-229, LN-Z308, U87MG, T98G), whereas, in gliosarcoma cells (D247MG), only the VEGF gene is induced. The kinetics of IL-8 and VEGF mRNA inductions differ in these cells and reoxygenation experiments showed that the induction is due to the anoxic stress per se. Furthermore, in LN-229 and LN-Z308 cell lines actinomycin D, DRB and nuclear run-on experiments showed that anoxia stimulates increased transcription of both genes. Electromobility shift assays show increased protein binding to the AP-1 site on the IL-8 promoter following anoxia treatment. Finally, in situ hybridization on glioblastoma sections shows that the in vivo expression patterns of IL-8 and VEGF genes overlap, but are not identical. Since intratumoral augmentation of IL-8 and VEGF secretion, following microenvironmental decreases in oxygen pressure, may promote angiogenesis, further definition of these pathways is essential to appropriately target them for antitumoral therapy.  (+info)

Clinical importance of c-Met protein expression in high grade astrocytic tumors. (5/4101)

The clinical importance of the expression of c-Met protein, the receptor of hepatocyte growth factor/scatter factor, was evaluated in neuroepithelial tissue tumors. c-Met immunohistochemistry was performed using the streptavidin-biotin-peroxidase complex method with anti-c-Met polyclonal antibody. Specimens were classified as c-Met negative (< 30%) or c-Met positive (> or = 30%) according to the proportion of immunopositive cells under microscopic examination. All c-Met-positive cases occurred in high grade astrocytic tumors, not in other neuroepithelial tissue tumors. Most c-Met-positive astrocytic tumors were classified histologically as high grade tumors. Epidermal growth factor-receptor (EGFR) and MIB-1 immunohistochemistry were also performed for high grade astrocytic tumors. Survival analysis was performed for patients with these tumors with variables including c-Met positivity, EGFR positivity, and MIB-1 labeling index. Positivity of c-Met was independent from EGFR positivity and MIB-1 labeling index, and the c-Met-positive group showed a significant shorter survival (p < 0.05). c-Met immunopositivity may be a parameter of biological aggressiveness in high grade astrocytic tumors. Examination of c-Met expression in astrocytic tumors provides significant clinical information, especially as a prognostic factor.  (+info)

Secondary glioblastoma remarkably reduced by steroid administration after anaplastic transformation from gliomatosis cerebri--case report. (6/4101)

A 45-year-old female presented with gliomatosis cerebri manifesting as hemiballismus-like involuntary movement in the arm, motor weakness in the leg, and hypesthesia in her left side. Computed tomography showed only diffuse swelling of the right cerebral hemisphere, but T2-weighted magnetic resonance imaging revealed a diffuse lesion spreading from the right thalamus to the temporal, parietal, and occipital lobes on the same side. No abnormal enhancement was recognized. Cerebral angiography showed no specific finding. A right occipital lobectomy was performed to confirm the diagnosis of gliomatosis cerebri. Anaplastic transformation was recognized 5 months later. The disease did not resolve with radiation or interferon administration, but steroid therapy achieved remarkably effective tumor regression. The patient died due to pneumonia. Autopsy showed the features of diffuse glioblastoma. Steroid therapy may be an effective treatment for gliomatosis cerebri before the terminal stage.  (+info)

Genetic aberrations in glioblastoma multiforme: translocation of chromosome 10 in an O-2A-like cell line. (7/4101)

We have examined the genetic aberrations in two near-diploid glioblastoma multiforme cell lines that appear to have arisen from different glial lineages. One cell line, Hu-O-2A/Gb1, expresses antigens and metabolic profiles characteristic of the oligodendrocyte-type-2 astrocyte (0-2A) lineage of the rat central nervous system. This line generates, in vitro, cells with characteristics of 0-2A progenitor cells, oligodendrocytes and astrocytes. The second cell line, IN1434, is derived from an astrocyte or a precursor cell restricted to astrocytic differentiation. In Hu-O-2A/Gb1 the sole homologue of chromosome 10 is disrupted at band 10p11-12.1 by translocation with chromosomes X and 15. The translocation breakpoint is localized between genetic markers D10S2103 and [D10S637, D10S1962, D10S355]. Other aberrations include a 5;14 translocation, deletion of the long and short arms of chromosome 16 and loss of one copy of the CDKN2 gene. IN1434 cells share some cytogenetic abnormalities with Hu-O-2A/Gb1 cells, despite their apparent derivation from a different biological origin, but also have translocations involving the long and short arms of chromosome 1 and the long arm of chromosome 7, and deletion of chromosome 13 at bands 13q12-21.  (+info)

Simultaneous alterations of retinoblastoma and p53 protein expression in astrocytic tumors. (8/4101)

The genetic alterations frequently involved in glial malignancies are in the tumor suppressor genes, Rb and p53. An altered Rb expression or p53 overexpression is thought to indicate defective tumor suppression and subsequently more aggressive tumors. Therefore, to assess the alterations in the conjoint expression of Rb and p53 proteins in formalin fixed paraffin embedded sections, 64 astrocytic tumors were studied (16 astrocytomas,7 gemistocytic astrocytomas, 19 anaplastic astrocytomas and 22 glioblastomas) using the avidin biotin immunoperoxidase technique. Fifty two cases (81.25%) were found to be positive for p53 protein. Seventeen of these showed aberrant heterogenous staining for pRb, of which 7 were glioblastomas. Only one case of astrocytoma showed aberrant expression of both p53 and Rb. Thus, of the 64 tumors, simultaneous aberrant expression of both p53 and Rb was seen in 21.9% of cases. This was more commonly observed among glioblastoma cases (7/22). No statistical difference was found between the survival rate of heterogenous pRb and p53 positivity in different grades of tumors. In glioblastomas, the survival rate appeared to be less in patients expressing heterogenous pRb, but this was not statistically significant. These results lead us to suspect that p53 and pRb pathways are inactivated, either through mutation or as part of the neoplastic process in astrocytic tumors.  (+info)

Glioblastoma, also known as Glioblastoma multiforme (GBM), is a highly aggressive and malignant type of brain tumor that arises from the glial cells in the brain. These tumors are characterized by their rapid growth, invasion into surrounding brain tissue, and resistance to treatment.

Glioblastomas are composed of various cell types, including astrocytes and other glial cells, which make them highly heterogeneous and difficult to treat. They typically have a poor prognosis, with a median survival rate of 14-15 months from the time of diagnosis, even with aggressive treatment.

Symptoms of glioblastoma can vary depending on the location and size of the tumor but may include headaches, seizures, nausea, vomiting, memory loss, difficulty speaking or understanding speech, changes in personality or behavior, and weakness or paralysis on one side of the body.

Standard treatment for glioblastoma typically involves surgical resection of the tumor, followed by radiation therapy and chemotherapy with temozolomide. However, despite these treatments, glioblastomas often recur, leading to a poor overall prognosis.

Brain neoplasms, also known as brain tumors, are abnormal growths of cells within the brain. These growths can be benign (non-cancerous) or malignant (cancerous). Benign brain tumors typically grow slowly and do not spread to other parts of the body. However, they can still cause serious problems if they press on sensitive areas of the brain. Malignant brain tumors, on the other hand, are cancerous and can grow quickly, invading surrounding brain tissue and spreading to other parts of the brain or spinal cord.

Brain neoplasms can arise from various types of cells within the brain, including glial cells (which provide support and insulation for nerve cells), neurons (nerve cells that transmit signals in the brain), and meninges (the membranes that cover the brain and spinal cord). They can also result from the spread of cancer cells from other parts of the body, known as metastatic brain tumors.

Symptoms of brain neoplasms may vary depending on their size, location, and growth rate. Common symptoms include headaches, seizures, weakness or paralysis in the limbs, difficulty with balance and coordination, changes in speech or vision, confusion, memory loss, and changes in behavior or personality.

Treatment for brain neoplasms depends on several factors, including the type, size, location, and grade of the tumor, as well as the patient's age and overall health. Treatment options may include surgery, radiation therapy, chemotherapy, targeted therapy, or a combination of these approaches. Regular follow-up care is essential to monitor for recurrence and manage any long-term effects of treatment.

Dacarbazine is a medical term that refers to a chemotherapeutic agent used in the treatment of various types of cancer. It is an alkylating agent, which means it works by modifying the DNA of cancer cells, preventing them from dividing and growing. Dacarbazine is often used to treat malignant melanoma, Hodgkin's lymphoma, and soft tissue sarcomas.

The drug is typically administered intravenously in a hospital or clinic setting, and the dosage and schedule may vary depending on the type and stage of cancer being treated, as well as the patient's overall health and response to treatment. Common side effects of dacarbazine include nausea, vomiting, loss of appetite, and weakness or fatigue. More serious side effects, such as low white blood cell counts, anemia, and liver damage, may also occur.

It is important for patients receiving dacarbazine to follow their doctor's instructions carefully and report any unusual symptoms or side effects promptly. Regular monitoring of blood counts and other laboratory tests may be necessary to ensure safe and effective treatment.

A glioma is a type of tumor that originates from the glial cells in the brain. Glial cells are non-neuronal cells that provide support and protection for nerve cells (neurons) within the central nervous system, including providing nutrients, maintaining homeostasis, and insulating neurons.

Gliomas can be classified into several types based on the specific type of glial cell from which they originate. The most common types include:

1. Astrocytoma: Arises from astrocytes, a type of star-shaped glial cells that provide structural support to neurons.
2. Oligodendroglioma: Develops from oligodendrocytes, which produce the myelin sheath that insulates nerve fibers.
3. Ependymoma: Originate from ependymal cells, which line the ventricles (fluid-filled spaces) in the brain and spinal cord.
4. Glioblastoma multiforme (GBM): A highly aggressive and malignant type of astrocytoma that tends to spread quickly within the brain.

Gliomas can be further classified based on their grade, which indicates how aggressive and fast-growing they are. Lower-grade gliomas tend to grow more slowly and may be less aggressive, while higher-grade gliomas are more likely to be aggressive and rapidly growing.

Symptoms of gliomas depend on the location and size of the tumor but can include headaches, seizures, cognitive changes, and neurological deficits such as weakness or paralysis in certain parts of the body. Treatment options for gliomas may include surgery, radiation therapy, chemotherapy, or a combination of these approaches.

A cell line that is derived from tumor cells and has been adapted to grow in culture. These cell lines are often used in research to study the characteristics of cancer cells, including their growth patterns, genetic changes, and responses to various treatments. They can be established from many different types of tumors, such as carcinomas, sarcomas, and leukemias. Once established, these cell lines can be grown and maintained indefinitely in the laboratory, allowing researchers to conduct experiments and studies that would not be feasible using primary tumor cells. It is important to note that tumor cell lines may not always accurately represent the behavior of the original tumor, as they can undergo genetic changes during their time in culture.

Astrocytoma is a type of brain tumor that arises from astrocytes, which are star-shaped glial cells in the brain. These tumors can occur in various parts of the brain and can have different grades of malignancy, ranging from low-grade (I or II) to high-grade (III or IV). Low-grade astrocytomas tend to grow slowly and may not cause any symptoms for a long time, while high-grade astrocytomas are more aggressive and can grow quickly, causing neurological problems.

Symptoms of astrocytoma depend on the location and size of the tumor but may include headaches, seizures, weakness or numbness in the limbs, difficulty speaking or swallowing, changes in vision or behavior, and memory loss. Treatment options for astrocytomas include surgery, radiation therapy, chemotherapy, or a combination of these approaches. The prognosis for astrocytoma varies widely depending on the grade and location of the tumor, as well as the age and overall health of the patient.

Antineoplastic agents, alkylating, are a class of chemotherapeutic drugs that work by alkylating (adding alkyl groups) to DNA, which can lead to the death or dysfunction of cancer cells. These agents can form cross-links between strands of DNA, preventing DNA replication and transcription, ultimately leading to cell cycle arrest and apoptosis (programmed cell death). Examples of alkylating agents include cyclophosphamide, melphalan, and cisplatin. While these drugs are designed to target rapidly dividing cancer cells, they can also affect normal cells that divide quickly, such as those in the bone marrow and digestive tract, leading to side effects like anemia, neutropenia, thrombocytopenia, and nausea/vomiting.

DNA modification methylases are a type of enzyme that catalyze the transfer of methyl groups (-CH3) to specific nucleotides in DNA, usually cytosine or adenine residues. This process is known as DNA methylation and is an important epigenetic mechanism that regulates gene expression, genome stability, and other cellular processes.

There are several types of DNA modification methylases, including:

1. Cytosine-5 methyltransferases (CNMTs or DNMTs): These enzymes catalyze the transfer of a methyl group to the fifth carbon atom of cytosine residues in DNA, forming 5-methylcytosine (5mC). This is the most common type of DNA methylation and plays a crucial role in gene silencing, X-chromosome inactivation, and genomic imprinting.
2. N6-adenine methyltransferases (MTases): These enzymes catalyze the transfer of a methyl group to the sixth nitrogen atom of adenine residues in DNA, forming N6-methyladenine (6mA). This type of DNA methylation is less common than 5mC but has been found to be involved in various cellular processes, such as transcriptional regulation and DNA repair.
3. GpC methyltransferases: These enzymes catalyze the transfer of a methyl group to the second carbon atom of guanine residues in DNA, forming N4-methylcytosine (4mC). This type of DNA methylation is relatively rare and has been found mainly in prokaryotic genomes.

Dysregulation of DNA modification methylases has been implicated in various diseases, including cancer, neurological disorders, and immunological diseases. Therefore, understanding the function and regulation of these enzymes is essential for developing novel therapeutic strategies to treat these conditions.

Neoplastic stem cells, also known as cancer stem cells (CSCs), are a subpopulation of cells within a tumor that are capable of self-renewal and generating the heterogeneous lineages of cells that comprise the tumor. These cells are believed to be responsible for the initiation, maintenance, and progression of cancer, as well as its recurrence and resistance to therapy.

CSCs share some similarities with normal stem cells, such as their ability to divide asymmetrically and give rise to differentiated progeny. However, they also have distinct characteristics that distinguish them from their normal counterparts, including aberrant gene expression, altered signaling pathways, and increased resistance to apoptosis (programmed cell death).

The existence of CSCs has important implications for cancer diagnosis, treatment, and prevention. Targeting these cells specifically may be necessary to achieve durable remissions and prevent relapse, as they are thought to survive conventional therapies that target the bulk of the tumor. Further research is needed to better understand the biology of CSCs and develop effective strategies for their elimination.

"Nude mice" is a term used in the field of laboratory research to describe a strain of mice that have been genetically engineered to lack a functional immune system. Specifically, nude mice lack a thymus gland and have a mutation in the FOXN1 gene, which results in a failure to develop a mature T-cell population. This means that they are unable to mount an effective immune response against foreign substances or organisms.

The name "nude" refers to the fact that these mice also have a lack of functional hair follicles, resulting in a hairless or partially hairless phenotype. This feature is actually a secondary consequence of the same genetic mutation that causes their immune deficiency.

Nude mice are commonly used in research because their weakened immune system makes them an ideal host for transplanted tumors, tissues, and cells from other species, including humans. This allows researchers to study the behavior of these foreign substances in a living organism without the complication of an immune response. However, it's important to note that because nude mice lack a functional immune system, they must be kept in sterile conditions and are more susceptible to infection than normal mice.

Neoplastic gene expression regulation refers to the processes that control the production of proteins and other molecules from genes in neoplastic cells, or cells that are part of a tumor or cancer. In a normal cell, gene expression is tightly regulated to ensure that the right genes are turned on or off at the right time. However, in cancer cells, this regulation can be disrupted, leading to the overexpression or underexpression of certain genes.

Neoplastic gene expression regulation can be affected by a variety of factors, including genetic mutations, epigenetic changes, and signals from the tumor microenvironment. These changes can lead to the activation of oncogenes (genes that promote cancer growth and development) or the inactivation of tumor suppressor genes (genes that prevent cancer).

Understanding neoplastic gene expression regulation is important for developing new therapies for cancer, as targeting specific genes or pathways involved in this process can help to inhibit cancer growth and progression.

'Tumor cells, cultured' refers to the process of removing cancerous cells from a tumor and growing them in controlled laboratory conditions. This is typically done by isolating the tumor cells from a patient's tissue sample, then placing them in a nutrient-rich environment that promotes their growth and multiplication.

The resulting cultured tumor cells can be used for various research purposes, including the study of cancer biology, drug development, and toxicity testing. They provide a valuable tool for researchers to better understand the behavior and characteristics of cancer cells outside of the human body, which can lead to the development of more effective cancer treatments.

It is important to note that cultured tumor cells may not always behave exactly the same way as they do in the human body, so findings from cell culture studies must be validated through further research, such as animal models or clinical trials.

A xenograft model antitumor assay is a type of preclinical cancer research study that involves transplanting human tumor cells or tissues into an immunodeficient mouse. This model allows researchers to study the effects of various treatments, such as drugs or immune therapies, on human tumors in a living organism.

In this assay, human tumor cells or tissues are implanted into the mouse, typically under the skin or in another organ, where they grow and form a tumor. Once the tumor has established, the mouse is treated with the experimental therapy, and the tumor's growth is monitored over time. The response of the tumor to the treatment is then assessed by measuring changes in tumor size or weight, as well as other parameters such as survival rate and metastasis.

Xenograft model antitumor assays are useful for evaluating the efficacy and safety of new cancer therapies before they are tested in human clinical trials. They provide valuable information on how the tumors respond to treatment, drug pharmacokinetics, and toxicity, which can help researchers optimize dosing regimens and identify potential side effects. However, it is important to note that xenograft models have limitations, such as differences in tumor biology between mice and humans, and may not always predict how well a therapy will work in human patients.

Cell proliferation is the process by which cells increase in number, typically through the process of cell division. In the context of biology and medicine, it refers to the reproduction of cells that makes up living tissue, allowing growth, maintenance, and repair. It involves several stages including the transition from a phase of quiescence (G0 phase) to an active phase (G1 phase), DNA replication in the S phase, and mitosis or M phase, where the cell divides into two daughter cells.

Abnormal or uncontrolled cell proliferation is a characteristic feature of many diseases, including cancer, where deregulated cell cycle control leads to excessive and unregulated growth of cells, forming tumors that can invade surrounding tissues and metastasize to distant sites in the body.

Neoplasm invasiveness is a term used in pathology and oncology to describe the aggressive behavior of cancer cells as they invade surrounding tissues and organs. This process involves the loss of cell-to-cell adhesion, increased motility and migration, and the ability of cancer cells to degrade the extracellular matrix (ECM) through the production of enzymes such as matrix metalloproteinases (MMPs).

Invasive neoplasms are cancers that have spread beyond the original site where they first developed and have infiltrated adjacent tissues or structures. This is in contrast to non-invasive or in situ neoplasms, which are confined to the epithelial layer where they originated and have not yet invaded the underlying basement membrane.

The invasiveness of a neoplasm is an important prognostic factor in cancer diagnosis and treatment, as it can indicate the likelihood of metastasis and the potential effectiveness of various therapies. In general, more invasive cancers are associated with worse outcomes and require more aggressive treatment approaches.

Supratentorial neoplasms refer to tumors that originate in the region of the brain located above the tentorium cerebelli, which is a dual layer of dura mater (the protective outer covering of the brain) that separates the cerebrum from the cerebellum. This area includes the cerebral hemispheres, basal ganglia, thalamus, hypothalamus, and pineal gland. Supratentorial neoplasms can be benign or malignant and may arise from various cell types such as neurons, glial cells, meninges, or blood vessels. They can cause a variety of neurological symptoms depending on their size, location, and rate of growth.

Central nervous system (CNS) neoplasms refer to a group of abnormal growths or tumors that develop within the brain or spinal cord. These tumors can be benign or malignant, and their growth can compress or disrupt the normal functioning of surrounding brain or spinal cord tissue.

Benign CNS neoplasms are slow-growing and rarely spread to other parts of the body. However, they can still cause significant problems if they grow large enough to put pressure on vital structures within the brain or spinal cord. Malignant CNS neoplasms, on the other hand, are aggressive tumors that can invade and destroy surrounding tissue. They may also spread to other parts of the CNS or, rarely, to other organs in the body.

CNS neoplasms can arise from various types of cells within the brain or spinal cord, including nerve cells, glial cells (which provide support and insulation for nerve cells), and supportive tissues such as blood vessels. The specific type of CNS neoplasm is often used to help guide treatment decisions and determine prognosis.

Symptoms of CNS neoplasms can vary widely depending on the location and size of the tumor, but may include headaches, seizures, weakness or paralysis, vision or hearing changes, balance problems, memory loss, and changes in behavior or personality. Treatment options for CNS neoplasms may include surgery, radiation therapy, chemotherapy, or a combination of these approaches.

Heterologous transplantation is a type of transplantation where an organ or tissue is transferred from one species to another. This is in contrast to allogeneic transplantation, where the donor and recipient are of the same species, or autologous transplantation, where the donor and recipient are the same individual.

In heterologous transplantation, the immune systems of the donor and recipient are significantly different, which can lead to a strong immune response against the transplanted organ or tissue. This is known as a graft-versus-host disease (GVHD), where the immune cells in the transplanted tissue attack the recipient's body.

Heterologous transplantation is not commonly performed in clinical medicine due to the high risk of rejection and GVHD. However, it may be used in research settings to study the biology of transplantation and to develop new therapies for transplant rejection.

Apoptosis is a programmed and controlled cell death process that occurs in multicellular organisms. It is a natural process that helps maintain tissue homeostasis by eliminating damaged, infected, or unwanted cells. During apoptosis, the cell undergoes a series of morphological changes, including cell shrinkage, chromatin condensation, and fragmentation into membrane-bound vesicles called apoptotic bodies. These bodies are then recognized and engulfed by neighboring cells or phagocytic cells, preventing an inflammatory response. Apoptosis is regulated by a complex network of intracellular signaling pathways that involve proteins such as caspases, Bcl-2 family members, and inhibitors of apoptosis (IAPs).

Neoplasm transplantation is not a recognized or established medical procedure in the field of oncology. The term "neoplasm" refers to an abnormal growth of cells, which can be benign or malignant (cancerous). "Transplantation" typically refers to the surgical transfer of living cells, tissues, or organs from one part of the body to another or between individuals.

The concept of neoplasm transplantation may imply the transfer of cancerous cells or tissues from a donor to a recipient, which is not a standard practice due to ethical considerations and the potential harm it could cause to the recipient. In some rare instances, researchers might use laboratory animals to study the transmission and growth of human cancer cells, but this is done for scientific research purposes only and under strict regulatory guidelines.

In summary, there is no medical definition for 'Neoplasm Transplantation' as it does not represent a standard or ethical medical practice.

The Karnofsky Performance Status (KPS) is a clinical tool used by healthcare professionals to assess the functional impairment and overall health of a patient with a chronic illness or malignancy. It was originally developed in 1948 by Dr. David A. Karnofsky and Dr. Joseph H. Burchenal to evaluate the ability of cancer patients to undergo specific treatments.

The KPS scale ranges from 0 to 100, with increments of 10, and it is based on the patient's ability to perform daily activities independently and their need for assistance or medical intervention. The following is a brief overview of the KPS scale:

* 100: Normal; no complaints; no evidence of disease
* 90: Able to carry on normal activity; minor symptoms of disease
* 80: Normal activity with effort; some symptoms of disease
* 70: Cares for self; unable to carry on normal activity or do active work
* 60: Requires occasional assistance but can take care of most needs
* 50: Requires considerable assistance and frequent medical care
* 40: Disabled; requires special care and assistance
* 30: Severely disabled; hospitalization is indicated although death not imminent
* 20: Very sick; hospitalization necessary; active supportive treatment required
* 10: Moribund; fatal processes progressing rapidly
* 0: Dead

The KPS score helps healthcare professionals determine the appropriate treatment plan, prognosis, and potential for recovery in patients with various medical conditions. It is widely used in oncology, palliative care, and clinical trials to assess the overall health status of patients and their ability to tolerate specific therapies.

DNA repair enzymes are a group of enzymes that are responsible for identifying and correcting damage to the DNA molecule. These enzymes play a critical role in maintaining the integrity of an organism's genetic material, as they help to ensure that the information stored in DNA is accurately transmitted during cell division and reproduction.

There are several different types of DNA repair enzymes, each responsible for correcting specific types of damage. For example, base excision repair enzymes remove and replace damaged or incorrect bases, while nucleotide excision repair enzymes remove larger sections of damaged DNA and replace them with new nucleotides. Other types of DNA repair enzymes include mismatch repair enzymes, which correct errors that occur during DNA replication, and double-strand break repair enzymes, which are responsible for fixing breaks in both strands of the DNA molecule.

Defects in DNA repair enzymes have been linked to a variety of diseases, including cancer, neurological disorders, and premature aging. For example, individuals with xeroderma pigmentosum, a rare genetic disorder characterized by an increased risk of skin cancer, have mutations in genes that encode nucleotide excision repair enzymes. Similarly, defects in mismatch repair enzymes have been linked to hereditary nonpolyposis colorectal cancer, a type of colon cancer that is inherited and tends to occur at a younger age than sporadic colon cancer.

Overall, DNA repair enzymes play a critical role in maintaining the stability and integrity of an organism's genetic material, and defects in these enzymes can have serious consequences for human health.

Antineoplastic agents are a class of drugs used to treat malignant neoplasms or cancer. These agents work by inhibiting the growth and proliferation of cancer cells, either by killing them or preventing their division and replication. Antineoplastic agents can be classified based on their mechanism of action, such as alkylating agents, antimetabolites, topoisomerase inhibitors, mitotic inhibitors, and targeted therapy agents.

Alkylating agents work by adding alkyl groups to DNA, which can cause cross-linking of DNA strands and ultimately lead to cell death. Antimetabolites interfere with the metabolic processes necessary for DNA synthesis and replication, while topoisomerase inhibitors prevent the relaxation of supercoiled DNA during replication. Mitotic inhibitors disrupt the normal functioning of the mitotic spindle, which is essential for cell division. Targeted therapy agents are designed to target specific molecular abnormalities in cancer cells, such as mutated oncogenes or dysregulated signaling pathways.

It's important to note that antineoplastic agents can also affect normal cells and tissues, leading to various side effects such as nausea, vomiting, hair loss, and myelosuppression (suppression of bone marrow function). Therefore, the use of these drugs requires careful monitoring and management of their potential adverse effects.

The Epidermal Growth Factor Receptor (EGFR) is a type of receptor found on the surface of many cells in the body, including those of the epidermis or outer layer of the skin. It is a transmembrane protein that has an extracellular ligand-binding domain and an intracellular tyrosine kinase domain.

EGFR plays a crucial role in various cellular processes such as proliferation, differentiation, migration, and survival. When EGF (Epidermal Growth Factor) or other ligands bind to the extracellular domain of EGFR, it causes the receptor to dimerize and activate its intrinsic tyrosine kinase activity. This leads to the autophosphorylation of specific tyrosine residues on the receptor, which in turn recruits and activates various downstream signaling molecules, resulting in a cascade of intracellular signaling events that ultimately regulate gene expression and cell behavior.

Abnormal activation of EGFR has been implicated in several human diseases, including cancer. Overexpression or mutation of EGFR can lead to uncontrolled cell growth and division, angiogenesis, and metastasis, making it an important target for cancer therapy.

PTEN phosphohydrolase, also known as PTEN protein or phosphatase and tensin homolog deleted on chromosome ten, is a tumor suppressor protein that plays a crucial role in regulating cell growth and division. It works by dephosphorylating (removing a phosphate group from) the lipid second messenger PIP3, which is involved in signaling pathways that promote cell proliferation and survival. By negatively regulating these pathways, PTEN helps to prevent uncontrolled cell growth and tumor formation. Mutations in the PTEN gene can lead to a variety of cancer types, including breast, prostate, and endometrial cancer.

Combined modality therapy (CMT) is a medical treatment approach that utilizes more than one method or type of therapy simultaneously or in close succession, with the goal of enhancing the overall effectiveness of the treatment. In the context of cancer care, CMT often refers to the combination of two or more primary treatment modalities, such as surgery, radiation therapy, and systemic therapies (chemotherapy, immunotherapy, targeted therapy, etc.).

The rationale behind using combined modality therapy is that each treatment method can target cancer cells in different ways, potentially increasing the likelihood of eliminating all cancer cells and reducing the risk of recurrence. The specific combination and sequence of treatments will depend on various factors, including the type and stage of cancer, patient's overall health, and individual preferences.

For example, a common CMT approach for locally advanced rectal cancer may involve preoperative (neoadjuvant) chemoradiation therapy, followed by surgery to remove the tumor, and then postoperative (adjuvant) chemotherapy. This combined approach allows for the reduction of the tumor size before surgery, increases the likelihood of complete tumor removal, and targets any remaining microscopic cancer cells with systemic chemotherapy.

It is essential to consult with a multidisciplinary team of healthcare professionals to determine the most appropriate CMT plan for each individual patient, considering both the potential benefits and risks associated with each treatment method.

Nimustine is a medical term for a specific anti-cancer drug, also known as a cytotoxic chemotherapeutic agent. Its chemical name is nimustine hydrochloride and it belongs to the class of alkylating agents. It works by interfering with the DNA of cancer cells, preventing them from dividing and growing. Nimustine is used in the treatment of various types of cancers, including brain tumors and Hodgkin's lymphoma.

The drug is administered intravenously under the supervision of a healthcare professional, as it can have serious side effects, such as bone marrow suppression, nausea, vomiting, and hair loss. It is important for patients to be closely monitored during treatment with nimustine and to receive appropriate supportive care to manage these side effects.

It's worth noting that the use of nimustine should be based on a thorough evaluation of the patient's medical condition, the type and stage of cancer, and other factors. The decision to use this drug should be made by a qualified healthcare professional in consultation with the patient.

Gliosarcoma is a rare and aggressive type of brain tumor that arises from glial cells, which are the supportive cells in the brain. It is a subtype of glioblastoma multiforme (GBM), which is the most common and malignant primary brain tumor in adults.

Gliosarcoma is characterized by the presence of both glial and sarcomatous components, with the latter resembling mesenchymal tissue such as bone, cartilage, or muscle. The tumor typically grows rapidly and can invade surrounding brain tissue, making it difficult to completely remove with surgery.

The exact cause of gliosarcoma is not known, but risk factors may include exposure to ionizing radiation, certain genetic conditions, and a history of other types of brain tumors. Symptoms can vary depending on the location and size of the tumor, but may include headaches, seizures, weakness, numbness, or changes in vision, speech, or behavior.

Treatment for gliosarcoma typically involves surgery to remove as much of the tumor as possible, followed by radiation therapy and chemotherapy. However, despite aggressive treatment, the prognosis for patients with gliosarcoma is generally poor, with a median survival time of less than one year.

Signal transduction is the process by which a cell converts an extracellular signal, such as a hormone or neurotransmitter, into an intracellular response. This involves a series of molecular events that transmit the signal from the cell surface to the interior of the cell, ultimately resulting in changes in gene expression, protein activity, or metabolism.

The process typically begins with the binding of the extracellular signal to a receptor located on the cell membrane. This binding event activates the receptor, which then triggers a cascade of intracellular signaling molecules, such as second messengers, protein kinases, and ion channels. These molecules amplify and propagate the signal, ultimately leading to the activation or inhibition of specific cellular responses.

Signal transduction pathways are highly regulated and can be modulated by various factors, including other signaling molecules, post-translational modifications, and feedback mechanisms. Dysregulation of these pathways has been implicated in a variety of diseases, including cancer, diabetes, and neurological disorders.

Cell movement, also known as cell motility, refers to the ability of cells to move independently and change their location within tissue or inside the body. This process is essential for various biological functions, including embryonic development, wound healing, immune responses, and cancer metastasis.

There are several types of cell movement, including:

1. **Crawling or mesenchymal migration:** Cells move by extending and retracting protrusions called pseudopodia or filopodia, which contain actin filaments. This type of movement is common in fibroblasts, immune cells, and cancer cells during tissue invasion and metastasis.
2. **Amoeboid migration:** Cells move by changing their shape and squeezing through tight spaces without forming protrusions. This type of movement is often observed in white blood cells (leukocytes) as they migrate through the body to fight infections.
3. **Pseudopodial extension:** Cells extend pseudopodia, which are temporary cytoplasmic projections containing actin filaments. These protrusions help the cell explore its environment and move forward.
4. **Bacterial flagellar motion:** Bacteria use a whip-like structure called a flagellum to propel themselves through their environment. The rotation of the flagellum is driven by a molecular motor in the bacterial cell membrane.
5. **Ciliary and ependymal movement:** Ciliated cells, such as those lining the respiratory tract and fallopian tubes, have hair-like structures called cilia that beat in coordinated waves to move fluids or mucus across the cell surface.

Cell movement is regulated by a complex interplay of signaling pathways, cytoskeletal rearrangements, and adhesion molecules, which enable cells to respond to environmental cues and navigate through tissues.

Pathologic neovascularization is the abnormal growth of new blood vessels in previously avascular tissue or excessive growth within existing vasculature, which occurs as a result of hypoxia, inflammation, or angiogenic stimuli. These newly formed vessels are often disorganized, fragile, and lack proper vessel hierarchy, leading to impaired blood flow and increased vascular permeability. Pathologic neovascularization can be observed in various diseases such as cancer, diabetic retinopathy, age-related macular degeneration, and chronic inflammation. This process contributes to disease progression by promoting tumor growth, metastasis, and edema formation, ultimately leading to tissue damage and organ dysfunction.

Oligodendroglioma is a type of brain tumor that originates from the glial cells, specifically the oligodendrocytes, which normally provide support and protection for the nerve cells (neurons) within the brain. This type of tumor is typically slow-growing and located in the cerebrum, particularly in the frontal or temporal lobes.

Oligodendrogliomas are characterized by their distinct appearance under a microscope, where the tumor cells have a round nucleus with a clear halo around it, resembling a "fried egg." They often contain calcifications and have a tendency to infiltrate the brain tissue, making them difficult to completely remove through surgery.

Oligodendrogliomas are classified based on their genetic profile, which includes the presence or absence of certain chromosomal abnormalities like 1p/19q co-deletion. This genetic information can help predict the tumor's behavior and response to specific treatments. Overall, oligodendrogliomas tend to have a better prognosis compared to other types of brain tumors, but their treatment and management depend on various factors, including the patient's age, overall health, and the extent of the tumor.

Local neoplasm recurrence is the return or regrowth of a tumor in the same location where it was originally removed or treated. This means that cancer cells have survived the initial treatment and started to grow again in the same area. It's essential to monitor and detect any local recurrence as early as possible, as it can affect the prognosis and may require additional treatment.

Small interfering RNA (siRNA) is a type of short, double-stranded RNA molecule that plays a role in the RNA interference (RNAi) pathway. The RNAi pathway is a natural cellular process that regulates gene expression by targeting and destroying specific messenger RNA (mRNA) molecules, thereby preventing the translation of those mRNAs into proteins.

SiRNAs are typically 20-25 base pairs in length and are generated from longer double-stranded RNA precursors called hairpin RNAs or dsRNAs by an enzyme called Dicer. Once generated, siRNAs associate with a protein complex called the RNA-induced silencing complex (RISC), which uses one strand of the siRNA (the guide strand) to recognize and bind to complementary sequences in the target mRNA. The RISC then cleaves the target mRNA, leading to its degradation and the inhibition of protein synthesis.

SiRNAs have emerged as a powerful tool for studying gene function and have shown promise as therapeutic agents for a variety of diseases, including viral infections, cancer, and genetic disorders. However, their use as therapeutics is still in the early stages of development, and there are challenges associated with delivering siRNAs to specific cells and tissues in the body.

'Cellular spheroids' refer to three-dimensional (3D) aggregates of cells that come together to form spherical structures. These spheroids can be formed by various cell types, including cancer cells, stem cells, and primary cells, and they are often used as models to study cell-cell interactions, cell signaling, drug development, and tumor biology in a more physiologically relevant context compared to traditional two-dimensional (2D) cell cultures.

Cellular spheroids can form spontaneously under certain conditions or be induced through various methods such as hanging drop, spinner flask, or microfluidic devices. The formation of spheroids allows cells to interact with each other and the extracellular matrix in a more natural way, leading to the creation of complex structures that mimic the organization and behavior of tissues in vivo.

Studying cellular spheroids has several advantages over traditional 2D cultures, including better preservation of cell-cell interactions, improved modeling of drug penetration and resistance, and enhanced ability to recapitulate the complexity of tumor microenvironments. As a result, cellular spheroids have become an important tool in various areas of biomedical research, including cancer biology, tissue engineering, and regenerative medicine.

'Rats, Nude' is not a standard medical term or condition. The term 'nude' in the context of laboratory animals like rats usually refers to a strain of rats that are hairless due to a genetic mutation. This can make them useful for studies involving skin disorders, wound healing, and other conditions where fur might interfere with observations or procedures. However, 'Rats, Nude' is not a recognized or established term in medical literature or taxonomy.

Isocitrate Dehydrogenase (IDH) is an enzyme that catalyzes the oxidative decarboxylation of isocitrate to α-ketoglutarate in the presence of NAD+ or NADP+, producing NADH or NADPH respectively. This reaction occurs in the citric acid cycle, also known as the Krebs cycle or tricarboxylic acid (TCA) cycle, which is a crucial metabolic pathway in the cell's energy production and biosynthesis of various molecules. There are three isoforms of IDH found in humans: IDH1 located in the cytosol, IDH2 in the mitochondrial matrix, and IDH3 within the mitochondria. Mutations in IDH1 and IDH2 have been associated with several types of cancer, such as gliomas and acute myeloid leukemia (AML), leading to abnormal accumulation of 2-hydroxyglutarate, which can contribute to tumorigenesis.

Western blotting is a laboratory technique used in molecular biology to detect and quantify specific proteins in a mixture of many different proteins. This technique is commonly used to confirm the expression of a protein of interest, determine its size, and investigate its post-translational modifications. The name "Western" blotting distinguishes this technique from Southern blotting (for DNA) and Northern blotting (for RNA).

The Western blotting procedure involves several steps:

1. Protein extraction: The sample containing the proteins of interest is first extracted, often by breaking open cells or tissues and using a buffer to extract the proteins.
2. Separation of proteins by electrophoresis: The extracted proteins are then separated based on their size by loading them onto a polyacrylamide gel and running an electric current through the gel (a process called sodium dodecyl sulfate-polyacrylamide gel electrophoresis or SDS-PAGE). This separates the proteins according to their molecular weight, with smaller proteins migrating faster than larger ones.
3. Transfer of proteins to a membrane: After separation, the proteins are transferred from the gel onto a nitrocellulose or polyvinylidene fluoride (PVDF) membrane using an electric current in a process called blotting. This creates a replica of the protein pattern on the gel but now immobilized on the membrane for further analysis.
4. Blocking: The membrane is then blocked with a blocking agent, such as non-fat dry milk or bovine serum albumin (BSA), to prevent non-specific binding of antibodies in subsequent steps.
5. Primary antibody incubation: A primary antibody that specifically recognizes the protein of interest is added and allowed to bind to its target protein on the membrane. This step may be performed at room temperature or 4°C overnight, depending on the antibody's properties.
6. Washing: The membrane is washed with a buffer to remove unbound primary antibodies.
7. Secondary antibody incubation: A secondary antibody that recognizes the primary antibody (often coupled to an enzyme or fluorophore) is added and allowed to bind to the primary antibody. This step may involve using a horseradish peroxidase (HRP)-conjugated or alkaline phosphatase (AP)-conjugated secondary antibody, depending on the detection method used later.
8. Washing: The membrane is washed again to remove unbound secondary antibodies.
9. Detection: A detection reagent is added to visualize the protein of interest by detecting the signal generated from the enzyme-conjugated or fluorophore-conjugated secondary antibody. This can be done using chemiluminescent, colorimetric, or fluorescent methods.
10. Analysis: The resulting image is analyzed to determine the presence and quantity of the protein of interest in the sample.

Western blotting is a powerful technique for identifying and quantifying specific proteins within complex mixtures. It can be used to study protein expression, post-translational modifications, protein-protein interactions, and more. However, it requires careful optimization and validation to ensure accurate and reproducible results.

Tumor suppressor proteins are a type of regulatory protein that helps control the cell cycle and prevent cells from dividing and growing in an uncontrolled manner. They work to inhibit tumor growth by preventing the formation of tumors or slowing down their progression. These proteins can repair damaged DNA, regulate gene expression, and initiate programmed cell death (apoptosis) if the damage is too severe for repair.

Mutations in tumor suppressor genes, which provide the code for these proteins, can lead to a decrease or loss of function in the resulting protein. This can result in uncontrolled cell growth and division, leading to the formation of tumors and cancer. Examples of tumor suppressor proteins include p53, Rb (retinoblastoma), and BRCA1/2.

Carmustine is a chemotherapy drug used to treat various types of cancer, including brain tumors, multiple myeloma, and Hodgkin's lymphoma. It belongs to a class of drugs called alkylating agents, which work by damaging the DNA in cancer cells, preventing them from dividing and growing.

Carmustine is available as an injectable solution that is administered intravenously (into a vein) or as implantable wafers that are placed directly into the brain during surgery. The drug can cause side effects such as nausea, vomiting, hair loss, and low blood cell counts, among others. It may also increase the risk of certain infections and bleeding complications.

As with all chemotherapy drugs, carmustine can have serious and potentially life-threatening side effects, and it should only be administered under the close supervision of a qualified healthcare professional. Patients receiving carmustine treatment should be closely monitored for signs of toxicity and other adverse reactions.

Immunohistochemistry (IHC) is a technique used in pathology and laboratory medicine to identify specific proteins or antigens in tissue sections. It combines the principles of immunology and histology to detect the presence and location of these target molecules within cells and tissues. This technique utilizes antibodies that are specific to the protein or antigen of interest, which are then tagged with a detection system such as a chromogen or fluorophore. The stained tissue sections can be examined under a microscope, allowing for the visualization and analysis of the distribution and expression patterns of the target molecule in the context of the tissue architecture. Immunohistochemistry is widely used in diagnostic pathology to help identify various diseases, including cancer, infectious diseases, and immune-mediated disorders.

Medical Definition:

Magnetic Resonance Imaging (MRI) is a non-invasive diagnostic imaging technique that uses a strong magnetic field and radio waves to create detailed cross-sectional or three-dimensional images of the internal structures of the body. The patient lies within a large, cylindrical magnet, and the scanner detects changes in the direction of the magnetic field caused by protons in the body. These changes are then converted into detailed images that help medical professionals to diagnose and monitor various medical conditions, such as tumors, injuries, or diseases affecting the brain, spinal cord, heart, blood vessels, joints, and other internal organs. MRI does not use radiation like computed tomography (CT) scans.

Prognosis is a medical term that refers to the prediction of the likely outcome or course of a disease, including the chances of recovery or recurrence, based on the patient's symptoms, medical history, physical examination, and diagnostic tests. It is an important aspect of clinical decision-making and patient communication, as it helps doctors and patients make informed decisions about treatment options, set realistic expectations, and plan for future care.

Prognosis can be expressed in various ways, such as percentages, categories (e.g., good, fair, poor), or survival rates, depending on the nature of the disease and the available evidence. However, it is important to note that prognosis is not an exact science and may vary depending on individual factors, such as age, overall health status, and response to treatment. Therefore, it should be used as a guide rather than a definitive forecast.

Cell survival refers to the ability of a cell to continue living and functioning normally, despite being exposed to potentially harmful conditions or treatments. This can include exposure to toxins, radiation, chemotherapeutic drugs, or other stressors that can damage cells or interfere with their normal processes.

In scientific research, measures of cell survival are often used to evaluate the effectiveness of various therapies or treatments. For example, researchers may expose cells to a particular drug or treatment and then measure the percentage of cells that survive to assess its potential therapeutic value. Similarly, in toxicology studies, measures of cell survival can help to determine the safety of various chemicals or substances.

It's important to note that cell survival is not the same as cell proliferation, which refers to the ability of cells to divide and multiply. While some treatments may promote cell survival, they may also inhibit cell proliferation, making them useful for treating diseases such as cancer. Conversely, other treatments may be designed to specifically target and kill cancer cells, even if it means sacrificing some healthy cells in the process.

Gene expression profiling is a laboratory technique used to measure the activity (expression) of thousands of genes at once. This technique allows researchers and clinicians to identify which genes are turned on or off in a particular cell, tissue, or organism under specific conditions, such as during health, disease, development, or in response to various treatments.

The process typically involves isolating RNA from the cells or tissues of interest, converting it into complementary DNA (cDNA), and then using microarray or high-throughput sequencing technologies to determine which genes are expressed and at what levels. The resulting data can be used to identify patterns of gene expression that are associated with specific biological states or processes, providing valuable insights into the underlying molecular mechanisms of diseases and potential targets for therapeutic intervention.

In recent years, gene expression profiling has become an essential tool in various fields, including cancer research, drug discovery, and personalized medicine, where it is used to identify biomarkers of disease, predict patient outcomes, and guide treatment decisions.

SCID mice is an acronym for Severe Combined Immunodeficiency mice. These are genetically modified mice that lack a functional immune system due to the mutation or knockout of several key genes required for immunity. This makes them ideal for studying the human immune system, infectious diseases, and cancer, as well as testing new therapies and treatments in a controlled environment without the risk of interference from the mouse's own immune system. SCID mice are often used in xenotransplantation studies, where human cells or tissues are transplanted into the mouse to study their behavior and interactions with the human immune system.

Gene knockdown techniques are methods used to reduce the expression or function of specific genes in order to study their role in biological processes. These techniques typically involve the use of small RNA molecules, such as siRNAs (small interfering RNAs) or shRNAs (short hairpin RNAs), which bind to and promote the degradation of complementary mRNA transcripts. This results in a decrease in the production of the protein encoded by the targeted gene.

Gene knockdown techniques are often used as an alternative to traditional gene knockout methods, which involve completely removing or disrupting the function of a gene. Knockdown techniques allow for more subtle and reversible manipulation of gene expression, making them useful for studying genes that are essential for cell survival or have redundant functions.

These techniques are widely used in molecular biology research to investigate gene function, genetic interactions, and disease mechanisms. However, it is important to note that gene knockdown can have off-target effects and may not completely eliminate the expression of the targeted gene, so results should be interpreted with caution.

Angiogenesis inhibitors are a class of drugs that block the growth of new blood vessels (angiogenesis). They work by targeting specific molecules involved in the process of angiogenesis, such as vascular endothelial growth factor (VEGF) and its receptors. By blocking these molecules, angiogenesis inhibitors can prevent the development of new blood vessels that feed tumors, thereby slowing or stopping their growth.

Angiogenesis inhibitors are used in the treatment of various types of cancer, including colon, lung, breast, kidney, and ovarian cancer. They may be given alone or in combination with other cancer treatments, such as chemotherapy or radiation therapy. Some examples of angiogenesis inhibitors include bevacizumab (Avastin), sorafenib (Nexavar), sunitinib (Sutent), and pazopanib (Votrient).

It's important to note that while angiogenesis inhibitors can be effective in treating cancer, they can also have serious side effects, such as high blood pressure, bleeding, and damage to the heart or kidneys. Therefore, it's essential that patients receive careful monitoring and management of these potential side effects while undergoing treatment with angiogenesis inhibitors.

Interleukin-13 receptor alpha2 subunit (IL-13Rα2) is a protein that forms part of a complex with other proteins to create a type II cytokine receptor. This receptor binds the cytokine interleukin-13 (IL-13), which is involved in the regulation of immune responses and inflammation.

IL-13Rα2 has a high affinity for IL-13, but its physiological role remains unclear because it does not seem to signal through the same pathways as other IL-13 receptors. Instead, IL-13Rα2 may act as a decoy receptor that modulates IL-13 activity by preventing it from binding to other receptors and initiating signaling.

IL-13Rα2 is overexpressed in several types of cancer, including glioblastoma multiforme, ovarian cancer, and colorectal cancer. This overexpression has been associated with increased tumor growth, invasion, and resistance to chemotherapy. Therefore, IL-13Rα2 has emerged as a potential therapeutic target for cancer treatment.

Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) is a laboratory technique used in molecular biology to amplify and detect specific DNA sequences. This technique is particularly useful for the detection and quantification of RNA viruses, as well as for the analysis of gene expression.

The process involves two main steps: reverse transcription and polymerase chain reaction (PCR). In the first step, reverse transcriptase enzyme is used to convert RNA into complementary DNA (cDNA) by reading the template provided by the RNA molecule. This cDNA then serves as a template for the PCR amplification step.

In the second step, the PCR reaction uses two primers that flank the target DNA sequence and a thermostable polymerase enzyme to repeatedly copy the targeted cDNA sequence. The reaction mixture is heated and cooled in cycles, allowing the primers to anneal to the template, and the polymerase to extend the new strand. This results in exponential amplification of the target DNA sequence, making it possible to detect even small amounts of RNA or cDNA.

RT-PCR is a sensitive and specific technique that has many applications in medical research and diagnostics, including the detection of viruses such as HIV, hepatitis C virus, and SARS-CoV-2 (the virus that causes COVID-19). It can also be used to study gene expression, identify genetic mutations, and diagnose genetic disorders.

The Kaplan-Meier estimate is a statistical method used to calculate the survival probability over time in a population. It is commonly used in medical research to analyze time-to-event data, such as the time until a patient experiences a specific event like disease progression or death. The Kaplan-Meier estimate takes into account censored data, which occurs when some individuals are lost to follow-up before experiencing the event of interest.

The method involves constructing a survival curve that shows the proportion of subjects still surviving at different time points. At each time point, the survival probability is calculated as the product of the conditional probabilities of surviving from one time point to the next. The Kaplan-Meier estimate provides an unbiased and consistent estimator of the survival function, even when censoring is present.

In summary, the Kaplan-Meier estimate is a crucial tool in medical research for analyzing time-to-event data and estimating survival probabilities over time while accounting for censored observations.

ERBB-1, also known as EGFR (Epidermal Growth Factor Receptor), is a gene that provides instructions for making a receptor protein involved in cell growth, division, and survival. This gene belongs to the ERBB family of genes, which encode receptors with intrinsic tyrosine kinase activity.

The erbB-1/EGFR protein spans the cell membrane, with one part (the extracellular domain) extending outside the cell and another part (the intracellular domain) inside the cell. When a specific growth factor binds to the extracellular domain, it triggers a series of reactions that activate the tyrosine kinase activity within the intracellular domain. This activation leads to signal transduction pathways that promote cell growth, division, and survival.

Mutations in the erbB-1/EGFR gene have been associated with various types of cancer, such as lung, colon, breast, and brain cancers. These mutations often result in overactive receptors, leading to uncontrolled cell growth and division, ultimately contributing to tumor formation and progression.

Tumor markers are substances that can be found in the body and their presence can indicate the presence of certain types of cancer or other conditions. Biological tumor markers refer to those substances that are produced by cancer cells or by other cells in response to cancer or certain benign (non-cancerous) conditions. These markers can be found in various bodily fluids such as blood, urine, or tissue samples.

Examples of biological tumor markers include:

1. Proteins: Some tumor markers are proteins that are produced by cancer cells or by other cells in response to the presence of cancer. For example, prostate-specific antigen (PSA) is a protein produced by normal prostate cells and in higher amounts by prostate cancer cells.
2. Genetic material: Tumor markers can also include genetic material such as DNA, RNA, or microRNA that are shed by cancer cells into bodily fluids. For example, circulating tumor DNA (ctDNA) is genetic material from cancer cells that can be found in the bloodstream.
3. Metabolites: Tumor markers can also include metabolic products produced by cancer cells or by other cells in response to cancer. For example, lactate dehydrogenase (LDH) is an enzyme that is released into the bloodstream when cancer cells break down glucose for energy.

It's important to note that tumor markers are not specific to cancer and can be elevated in non-cancerous conditions as well. Therefore, they should not be used alone to diagnose cancer but rather as a tool in conjunction with other diagnostic tests and clinical evaluations.

Astrocytes are a type of star-shaped glial cell found in the central nervous system (CNS), including the brain and spinal cord. They play crucial roles in supporting and maintaining the health and function of neurons, which are the primary cells responsible for transmitting information in the CNS.

Some of the essential functions of astrocytes include:

1. Supporting neuronal structure and function: Astrocytes provide structural support to neurons by ensheathing them and maintaining the integrity of the blood-brain barrier, which helps regulate the entry and exit of substances into the CNS.
2. Regulating neurotransmitter levels: Astrocytes help control the levels of neurotransmitters in the synaptic cleft (the space between two neurons) by taking up excess neurotransmitters and breaking them down, thus preventing excessive or prolonged activation of neuronal receptors.
3. Providing nutrients to neurons: Astrocytes help supply energy metabolites, such as lactate, to neurons, which are essential for their survival and function.
4. Modulating synaptic activity: Through the release of various signaling molecules, astrocytes can modulate synaptic strength and plasticity, contributing to learning and memory processes.
5. Participating in immune responses: Astrocytes can respond to CNS injuries or infections by releasing pro-inflammatory cytokines and chemokines, which help recruit immune cells to the site of injury or infection.
6. Promoting neuronal survival and repair: In response to injury or disease, astrocytes can become reactive and undergo morphological changes that aid in forming a glial scar, which helps contain damage and promote tissue repair. Additionally, they release growth factors and other molecules that support the survival and regeneration of injured neurons.

Dysfunction or damage to astrocytes has been implicated in several neurological disorders, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS).

Survival analysis is a branch of statistics that deals with the analysis of time to event data. It is used to estimate the time it takes for a certain event of interest to occur, such as death, disease recurrence, or treatment failure. The event of interest is called the "failure" event, and survival analysis estimates the probability of not experiencing the failure event until a certain point in time, also known as the "survival" probability.

Survival analysis can provide important information about the effectiveness of treatments, the prognosis of patients, and the identification of risk factors associated with the event of interest. It can handle censored data, which is common in medical research where some participants may drop out or be lost to follow-up before the event of interest occurs.

Survival analysis typically involves estimating the survival function, which describes the probability of surviving beyond a certain time point, as well as hazard functions, which describe the instantaneous rate of failure at a given time point. Other important concepts in survival analysis include median survival times, restricted mean survival times, and various statistical tests to compare survival curves between groups.

Radiation tolerance, in the context of medicine and particularly radiation oncology, refers to the ability of tissues or organs to withstand and recover from exposure to ionizing radiation without experiencing significant damage or loss of function. It is often used to describe the maximum dose of radiation that can be safely delivered to a specific area of the body during radiotherapy treatments.

Radiation tolerance varies depending on the type and location of the tissue or organ. For example, some tissues such as the brain, spinal cord, and lungs have lower radiation tolerance than others like the skin or bone. Factors that can affect radiation tolerance include the total dose of radiation, the fractionation schedule (the number and size of radiation doses), the volume of tissue treated, and the individual patient's overall health and genetic factors.

Assessing radiation tolerance is critical in designing safe and effective radiotherapy plans for cancer patients, as excessive radiation exposure can lead to serious side effects such as radiation-induced injury, fibrosis, or even secondary malignancies.

Drug resistance in neoplasms (also known as cancer drug resistance) refers to the ability of cancer cells to withstand the effects of chemotherapeutic agents or medications designed to kill or inhibit the growth of cancer cells. This can occur due to various mechanisms, including changes in the cancer cell's genetic makeup, alterations in drug targets, increased activity of drug efflux pumps, and activation of survival pathways.

Drug resistance can be intrinsic (present at the beginning of treatment) or acquired (developed during the course of treatment). It is a significant challenge in cancer therapy as it often leads to reduced treatment effectiveness, disease progression, and poor patient outcomes. Strategies to overcome drug resistance include the use of combination therapies, development of new drugs that target different mechanisms, and personalized medicine approaches that consider individual patient and tumor characteristics.

Cell growth processes refer to the series of events that occur within a cell leading to an increase in its size, mass, and number of organelles. These processes are essential for the development, maintenance, and reproduction of all living organisms. The main cell growth processes include:

1. Cell Cycle: It is the sequence of events that a eukaryotic cell goes through from one cell division (mitosis) to the next. The cell cycle consists of four distinct phases: G1 phase (growth and preparation for DNA replication), S phase (DNA synthesis), G2 phase (preparation for mitosis), and M phase (mitosis or meiosis).

2. DNA Replication: It is the process by which a cell makes an identical copy of its DNA molecule before cell division. This ensures that each daughter cell receives an exact replica of the parent cell's genetic material.

3. Protein Synthesis: Cells grow by increasing their protein content, which is achieved through the process of protein synthesis. This involves transcribing DNA into mRNA (transcription) and then translating that mRNA into a specific protein sequence (translation).

4. Cellular Metabolism: It refers to the sum total of all chemical reactions that occur within a cell to maintain life. These reactions include catabolic processes, which break down nutrients to release energy, and anabolic processes, which use energy to build complex molecules like proteins, lipids, and carbohydrates.

5. Cell Signaling: Cells communicate with each other through intricate signaling pathways that help coordinate growth, differentiation, and survival. These signals can come from within the cell (intracellular) or from outside the cell (extracellular).

6. Cell Division: Also known as mitosis, it is the process by which a single cell divides into two identical daughter cells. This ensures that each new cell contains an exact copy of the parent cell's genetic material and allows for growth and repair of tissues.

7. Apoptosis: It is a programmed cell death process that helps maintain tissue homeostasis by eliminating damaged or unnecessary cells. Dysregulation of apoptosis can lead to diseases such as cancer and autoimmune disorders.

Radiation-sensitizing agents are drugs that make cancer cells more sensitive to radiation therapy. These agents work by increasing the ability of radiation to damage the DNA of cancer cells, which can lead to more effective tumor cell death. This means that lower doses of radiation may be required to achieve the same therapeutic effect, reducing the potential for damage to normal tissues surrounding the tumor.

Radiation-sensitizing agents are often used in conjunction with radiation therapy to improve treatment outcomes for patients with various types of cancer. They can be given either systemically (through the bloodstream) or locally (directly to the tumor site). The choice of agent and the timing of administration depend on several factors, including the type and stage of cancer, the patient's overall health, and the specific radiation therapy protocol being used.

It is important to note that while radiation-sensitizing agents can enhance the effectiveness of radiation therapy, they may also increase the risk of side effects. Therefore, careful monitoring and management of potential toxicities are essential during treatment.

Messenger RNA (mRNA) is a type of RNA (ribonucleic acid) that carries genetic information copied from DNA in the form of a series of three-base code "words," each of which specifies a particular amino acid. This information is used by the cell's machinery to construct proteins, a process known as translation. After being transcribed from DNA, mRNA travels out of the nucleus to the ribosomes in the cytoplasm where protein synthesis occurs. Once the protein has been synthesized, the mRNA may be degraded and recycled. Post-transcriptional modifications can also occur to mRNA, such as alternative splicing and addition of a 5' cap and a poly(A) tail, which can affect its stability, localization, and translation efficiency.

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The Glioblastoma Foundation funds research on discovering new and more effective treatments for glioblastoma patients. Grants ... The Glioblastoma Foundation extends support to glioblastoma patients and their families through initiatives including The ... The Glioblastoma Foundation is also involved in supporting the development of a generic version of the chemotherapy drug ... The Glioblastoma Foundation (GF) is a United States non-profit charitable organization established in June 2016 in Durham, ...
The giant-cell glioblastoma is a histological variant of glioblastoma, presenting a prevalence of bizarre, multinucleated (more ... The giant-cell glioblastoma affects males more frequently. (The M/F ratio is 1.6.) Most patients with giant-cell glioblastoma ... The giant-cell glioblastoma is a rare neoplasia: its incidence is less than 1% of all brain tumors. It represents up to 5% of ... Glioblastoma WHO classification of the tumors of the central nervous system Grading of the tumors of the central nervous system ...
Brem authored the comprehensive glioblastoma textbook "Glioblastoma". "Raising Hope". Archived from the original on 2021-09-22 ... Brem, Steven; Abdullah, Kalil (September 22, 2016). Glioblastoma. Elsevier. ISBN 9780323476607. Portals: Biography United ...
"Glioblastoma microvesicles". Nature Cell Biology. 10 (12): 1470-6. doi:10.1038/ncb1800. PMC 3423894. PMID 19011622. "Executive ...
"Team - Cure Glioblastoma". Cure Glioblastoma. Archived from the original on October 21, 2020. Retrieved October 19, 2020. Jones ... Shawn Carbonell and Luzanne Otte named Cure Glioblastoma, the same disease her father died from. The purpose of the charity is ...
The tumour evolved into glioblastoma, with which she was diagnosed in October 2018. Berns died from brain cancer on 13 ... Berns, Magdalen (7 October 2018). My ladybrain update #2 , Glioblastoma (Videotape). United Kingdom: YouTube. Retrieved 5 ... Deaths from glioblastoma, Feminism and transgender, GNOME developers, Lesbian feminists, Lesbian sportswomen, LGBT boxers, LGBT ...
CYP1B1 Glioblastoma, somatic; 137800; ERBB2 Globozoospermia; 102530; GOPC Globozoospermia; 102530; SPATA16 Glomerulocystic ...
Gene rearrangements involving the ROS1 gene were first detected in glioblastoma tumors and cell lines. In 2007 a ROS1 ... Birchmeier C, Sharma S, Wigler M (December 1987). "Expression and rearrangement of the ROS1 gene in human glioblastoma cells". ... ROS1 fusions were also identified in approximately 2% of adenocarcinomas and 1% of glioblastoma samples in an assessment of ... fused in glioblastoma; SDC4; LRIG3; leucine-rich repeats and immunoglobulin-like domains 3; SDC; syndecan 4; SLC34A2; solute ...
"Home :: Ivy Glioblastoma Atlas Project". glioblastoma.alleninstitute.org. Retrieved July 16, 2018. alleninstitute.org, "Public ... The Ivy Glioblastoma Atlas Project (Ivy GAP), a platform for exploring the anatomic and genetic basis of glioblastoma at the ...
Urbańska, K., Sokołowska, J., Szmidt, M., & Sysa, P. (2014). Glioblastoma multiforme - an overview. Contemporary Oncology, 18(5 ...
In Glioblastoma multiforme, upregulation of gBK potassium channels and ClC-3 chloride channels enables glioblastoma cells to ... Molenaar RJ (2011). "Ion channels in glioblastoma". ISRN Neurology. 2011: 590249. doi:10.5402/2011/590249. PMC 3263536. PMID ...
In glioblastoma, the difference is larger. There, IDH1/2 wild-type glioblastoma have a median overall survival of 1 year, ... found, in the glioblastomas without methylated MGMT promoters, that the level of microRNA miR-181d is inversely correlated with ... For instance, methylation of the DNA repair gene MGMT promoter was observed in 51% to 66% of glioblastoma specimens. In ... July 2020). "Management of glioblastoma: State of the art and future directions". CA: A Cancer Journal for Clinicians. 70 (4): ...
"Gary Carter has glioblastoma". sports.espn.go.com. June 1, 2011. "Gary Carter makes team's opener". February 3, 2012. Retrieved ... Doctors confirmed that he had a grade IV primary brain tumor known as glioblastoma multiforme. Doctors said that the extremely ... Deaths from glioblastoma, Florida Marlins announcers, Gold Glove Award winners, Long Island Ducks coaches, Los Angeles Dodgers ...
... and when blocked in glioblastoma it attenuates tumor growth and improves the efficacy of typical glioblastoma treatment, EGFR ... Alzheimer's Disease, and glioblastoma. Since rare mutations in the NHE gene had been associated with autism, Rao probed the ... The Rao Lab then discovered that NHE9 expression in glioblastoma is associated with poor clinical prognosis. NHE9 is an ... A leak pathway for luminal protons in endosomes drives oncogenic signaling in glioblastoma. Nature Communications 6 Article ...
Glioblastoma multiforme is a form of malignant, grade IV tumor of the central nervous system. Most of diagnosed glioblastoma ... Glioblastoma has been linked to certain genetic alterations and deregulations, but it mostly occurs spontaneously and its ... Urbańska K, Sokołowska J, Szmidt M, Sysa P (2014). "Glioblastoma multiforme - an overview". Contemporary Oncology. 18 (5): 307- ... glioblastoma multiforme and gonadoblastoma. Hepatoblastoma (HBL) is the first and most common malignancy in children, often ...
Glioblastoma multiforme is the most common and deadly brain tumor in adults, but only affects 10,000-17,000 people in the US. ... "Glioblastoma patient is first to receive treatment under Right to Try. Our question is Why? - The Cancer Letter". The Cancer ... Sitoiganap (EU)/Gliovac/ERC1671 is an immunotherapy vaccine that trains the body's immune system to attack a Glioblastoma ( ... Lassen, Ulrik; Mau-Sørensen, Morten; Poulsen, Hans Skovgaard (2014-11-14). "Orphan drugs in glioblastoma multiforme: a review ...
"Treatment of glioblastoma multiforme". U.S. Food and Drug Administration (FDA). 2012-07-24. "Treatment of Myelodysplastic ... is a soluble CD95-Fc fusion protein which is in clinical development for the treatment of glioblastoma multiforme (GBM) and ... reirradiation versus reirradiation in progressive glioblastoma". Clin Cancer Res. 15 (24): 6304-13. doi:10.1158/1078-0432.CCR- ...
... glioblastomas. Mutations in catenin genes can cause loss of contact inhibition that can promote cancer development and tumor ...
Molecular Genetics of Secondary Glioblastoma. Brisbane (AU): Codon Publications. doi:10.15586/codon.glioblastoma.2017.ch2. ISBN ...
Of those agents that are able to reach the tumor, glioblastomas have shown to be resistant to most cytotoxic agents and to ... "Recurrent Glioblastoma - ReSPECTâ„¢ Clinical Trials". Respect-trials.com. Retrieved 29 May 2022. "Maximum Tolerated Dose, Safety ... According to the most recent CBTRUS Statistical Report, annually there are approximately 12,900 cases of glioblastoma diagnosed ... The infiltrative nature of glioblastoma results in difficulty eliminating microscopic disease despite macroscopic gross-total ...
Magdalen Berns, 36, Scottish YouTuber, glioblastoma. Cynthia Cockburn, 85, British feminist and peace activist. Paul Cronin, 81 ... Louis Cardinals), World Series champion (2006), glioblastoma. Chandrasiri Gajadeera, 73, Sri Lankan politician, MP (1994-2001, ... ", "Summer Nights") and music producer, glioblastoma. John D'Arcy, 84, Australian football player (Richmond). Patsy Elsener, 89 ...
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Smoll NR, Schaller K, Gautschi OP (2012). "The Cure Fraction of Glioblastoma Multiforme". Neuroepidemiology. 39 (1): 63-9. doi: ...
"Entrez Gene: GBAS glioblastoma amplified sequence". Mehrle A, Rosenfelder H, Schupp I, et al. (2006). "The LIFEdb database in ... Chromosomal region 7p12, which contains GBAS, is amplified in approximately 40% of glioblastomas, the most common and malignant ...
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Rhodes Center for Glioblastoma at NewYork-Presbyterian Hospital Appearances on C-SPAN Articles Book Review: Banker To the World ... In 2017, Rhodes established the William Rhodes and Louise Tilzer-Rhodes Center for Glioblastoma at New York-Presbyterian. The ... "NewYork-Presbyterian establishes glioblastoma research center". Healio. SLACK Incorporated. Retrieved 29 June 2017. "Debt ... center will conduct research and provide treatment and therapies to patients with glioblastoma. Bionic Site 1992 American ...
The only monitored in vivo dosage of five human patients with glioblastoma with DCA was not designed to test its efficacy ... "Metabolic Modulation of Glioblastoma with Dichloroacetate". Science Translational Medicine. 2 (31): 31ra34. doi:10.1126/ ... those five patients suggest that DCA might act against cancer cells by depolarising abnormal mitochondria found in glioblastoma ...
Kenneth Aldape; Gelareh Zadeh; Sheila Mansouri; Guido Reifenberger; Andreas von Deimling (6 May 2015). "Glioblastoma: pathology ...
Drake, Lindsey R.; Hillmer, Ansel T.; Cai, Zhengxin (28 January 2020). "Approaches to PET Imaging of Glioblastoma". Molecules. ...
... glioblastoma cancer stem cells) have been found in glioblastomas. Their presence, coupled with the glioblastomas diffuse ... Glioblastoma, previously known as glioblastoma multiforme (GBM), is the most aggressive and most common type of cancer that ... CD44 can also be used as a cancer stem cell marker in a subset of glioblastoma tumour cells. Glioblastoma cancer stem cells ... The cellular origin of glioblastoma is unknown. Because of the similarities in immunostaining of glial cells and glioblastoma, ...
To investigate the CSCs diversity, we established 4 subclones from a glioblastoma patient. These subclones were subsequently ... Single-cell molecular profiling using ex vivo functional readouts fuels precision oncology in glioblastoma *Dena Panovska ... In this study, we established 4 subclones from a glioblastoma patient and demonstrated clear evidence that a brain tumor ... The median survival of patients with glioblastoma multiforme (GBM), the most aggressive malignant brain tumor, is typically ...
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We investigate two cell lines for glioblastoma and medulloblastoma (U87mg & DAOY, respectively), plated as spheroidal ... Lyon, J.G., Carroll, S.L., Mokarram, N. et al. Electrotaxis of Glioblastoma and Medulloblastoma Spheroidal Aggregates. Sci Rep ... Electrotaxis of Glioblastoma and Medulloblastoma Spheroidal Aggregates. *Johnathan G. Lyon. ORCID: orcid.org/0000-0002-0926- ... U87 mg (human glioblastoma, ATCC HTB-14), DAOY (human medulloblastoma, ATCC HTB-186), and MatLyLu (rat prostate cancer, ATCC ...
Glioblastoma multiforme (GBM) is the most common and most aggressive of the primary brain tumors. The current World Health ... encoded search term (Neurologic Manifestations of Glioblastoma Multiforme) and Neurologic Manifestations of Glioblastoma ... Neurologic Manifestations of Glioblastoma Multiforme. Updated: Nov 07, 2021 * Author: Gaurav Gupta, MD, FAANS, FACS; Chief ... Case in Point: An Experts Approach to Caring for Patients With Glioblastoma 0.25 CME / ABIM MOC Credits Clinical Review ...
Glioblastoma (GBM) is a fast-growing brain tumor that mostly affects adults. Treatments can ease symptoms. ... Glioblastoma (GBM). Glioblastomas (GBMs) account for almost half of all cancerous brain tumors in adults. This brain cancer ... What is glioblastoma (GBM)?. Glioblastoma multiforme (GBM) is the most common type of malignant (cancerous) brain tumor in ... How is glioblastoma diagnosed?. If your healthcare provider suspects a brain tumor, you may get these tests:. *MRI or CT scan ...
Home Topics Bioprocessing ImmunoCellular Therapeutics Chooses PCT for Supply of Glioblastoma Vaccine Candidate ... ImmunoCellular Therapeutics has decided to use Progenitor Cell Therapy (PCT) to produce its Phase II glioblastoma vaccine, ICT- ... Brain cancerCancer vaccineCancersCell therapyChemotherapyDrug therapyGenetic Engineering and BiotechnologyGlioblastoma ...
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Glioblastoma multiforme (GBM) is the most malignant human primary brain tumor, and its infiltrative nature represents the ... Silencing of Eps8 blocks migration and invasion in human glioblastoma cell lines Exp Cell Res. 2012 Sep 10;318(15):1901-12. doi ... Glioblastoma multiforme (GBM) is the most malignant human primary brain tumor, and its infiltrative nature represents the ...
Objective: Glioblastoma multiforme (GBM) is the most malignant and most common primary brain tumour worldwide. This study was ... Glioblastoma multiforme is the most malignant and the most common primary brain tumour worldwide. This initial study was ...
This review focuses on clinical developments and management of newly diagnosed glioblastoma, and includes a discussion about ... Secondary glioblastoma/IDH-mutated glioblastoma. Up to 10% of patients with glioblastoma harbor a mutation in the IDH1 or IDH2 ... Primary glioblastoma/IDH wild-type glioblastoma. The majority of glioblastomas are IDH wild-type and correspond to the ... Since these glioblastomas often arise from a prior lower-grade glioma, they are considered secondary glioblastomas. In the past ...
Phase II Study: Systemic Treatment With iv ZK219477-Epothilone in Recurrent Glioblastoma Patients. Trial Phase:. Phase 2. ... Study Population: 15 recurrent glioblastoma. patients previously treated by surgery, conventional radiotherapy and chemotherapy ... Phase II Study: Systemic Treatment With iv ZK219477-Epothilone in Recurrent Glioblastoma Patients ...
Emily has glioblastoma and was given just three months to live. Its a tough cancer to treat and options are limited, so ... Experimental Drug Being Tested On Dogs Could Hold Promise For People Battling Glioblastoma. August 27, 2018 / 5:23 PM. / CBS ... McCain had glioblastoma, which is the deadliest kind of brain cancer. It also killed Ted Kennedy and Beau Biden. ... In partnership with Wake Forest University, Virginia-Maryland Veterinary College is still accepting dogs with glioblastoma into ...
Adult glioblastoma. J Clin Oncol. 2017;35(21):2402-2409.. View this article via: PubMed CrossRef Google Scholar ... Osteopontin mediates glioblastoma-associated macrophage infiltration and is a potential therapeutic target. Jun Wei,1 Anantha ... Immune heterogeneity of glioblastoma subtypes: extrapolation from the cancer genome atlas. Cancer Immunol Res. 2013;1(2):112- ... Glioblastoma-infiltrated innate immune cells resemble M0 macrophage phenotype. JCI Insight. 2016;1(2):e85841. View this article ...
5-30-09 My sister was recently diagnosed with Glioblastoma and we are wanting to know as much as possible on treatment options ... Glioblastoma. Hi Beth,. I just started a blog and read yours which gave me hope. My boyfriend has GBM stage 4 - has had surgery ... glioblastoma muliforme. Hi Csharger,. My husband was diagnosed with an astrocytoma on April 23rd. We are now getting ready to ... glioblastoma muliforme. Hi Csharger,. My husband was diagnosed with an astrocytoma on April 23rd. We are now getting ready to ...
Glioblastoma (GBM) adaptive, global, innovative learning environment (GBM AGILE) is an international, seamless Phase II/III ... Glioblastoma (GBM) adaptive, global, innovative learning environment (GBM AGILE) is an. international, seamless Phase II/III ...
... in glioblastomas.6 However, the value of CD133 as a single marker of glioblastoma TICs remains controversial, partly because ... glioblastomas harbouring the G-CIMP phenotype tend to be more benign. Correspondingly, patients with G-CIMP glioblastomas ... Transdifferentiation of glioblastoma cells into vascular endothelial cells. Proc Natl Acad Sci U S A 2011;108:4274-80. ... Glioblastoma is the most common form of primary brain tumour. The incidence of this tumour is fairly low, with two to three ...
Proceeds will go to the Glioblastoma Foundation Glioblastomafoundation.org ... Proceeds will go to the Glioblastoma Foundation Glioblastomafoundation.org ...
Anticancer effect in human glioblastoma and antioxidant activity of Petroselinum crispum. ... Diseases : Glioblastoma : CK(545) : AC(272). Pharmacological Actions : Antioxidants : CK(21528) : AC(8856), Antiproliferative ... Anticancer effect in human glioblastoma and antioxidant activity of Petroselinum crispum. - GreenMedInfo Summary ... antioxidant and anticancer activity ofaqueous and methanol extracts against Human glioblastoma cells U87MG. Adhesion assay was ...
glioblastoma stem cells from Neuroscience News features breaking science news from research labs, scientists and colleges ... A new study in the Journal of Experimental Medicine report Zika virus could be used to target and treat glioblastoma brain ... Researchers found a mouse adapted strain of Zika slowed tumor growth and extended life span in mice with glioblastoma.. Read ... Engineered Nk Cells Can Eliminate Glioblastoma Stem Cells. Engineering NK cells to resist immune suppression could be a path ...
Glioblastoma multiforme (GBM) represents the most frequent and aggressive type of primary brain tumours in adults. Despite ... Glioblastoma multiforme (GBM) represents the most frequent and aggressive type of primary brain tumours in adults. Despite ... Unravelling mitochondrias role in glioblastoma. Cancer cells display an altered metabolism as a result of genetic mutations, ... the MITIG project aims to understand how this process affects metabolism and tumour development of glioblastoma multiforme (GBM ...
15-20 months for glioblastoma (GBM) with the current standard of care (SOC) which is concurrent temozolomide (TMZ) and ... AMP kinase promotes glioblastoma bioenergetics and tumour growth. Nat. Cell Biol. 2018, 20, 823-835. [Google Scholar] [CrossRef ... Glioblastoma (GBM) is the most lethal and primary malignant brain tumor with median survivals of 15-20 months [1,2]. Introduced ... Glioblastoma cell lines LN229 (ATCC CRL-2611), T98G (ATCC CRL-1690) and U87MG (ATCC HTB-14) were procured from ATCC, USA and ...
Glioblastoma accounts for nearly half of all brain tumors, and little effective treatment is currently available. The National ... Stanford University and The Invus Group, an investment firm, have formed a collaboration to develop treatments for glioblastoma ... Brain Tumor Society estimates that more than 13,000 U.S. residents will be diagnosed with glioblastoma this year; the average ... collaboration between Stanford University and The Invus Group will enable the development of medication to treat glioblastoma, ...
i] GBM, glioblastoma; PD-1, programmed cell death 1; PD-L1, PD-1 ligand 1; PVSRIPO, polio-rhinovirus chimera; HDAC, histone ... The heterogeneity of glioblastoma can suppress immune cell function and lead to immune evasion, which presents a challenge in ... Glioblastoma-produced cfDNA, ctDNA and mtDNA, detected by NGS monitoring in blood or cerebrospinal fluid, may provide a ... Glioblastoma is known for its anti-radiation properties, which are attributed to various mechanisms, such as microRNA, tumor ...
... , Health Newstrack ... Glioblastoma is both the most common and lethal form of brain ... Bevacizumab offers no benefit for glioblastoma , Health Newstrack , ... Tags Brain, Genes, Glioblastoma, Pulmonary embolism, Quality of life, Radiation, Surgery. Crohns disease - accelerated step- ... "Obviously, glioblastoma is a cancer with too few effective therapies," said Gilbert, who also holds the Blanche Bender ...
Glioblastoma multiforme (GBM) may be termed as the most common and aggressive form of brain tumor in humans. It now seems that ... Glioblastoma multiforme (GBM) may be termed as the most common and aggressive form of brain tumor in humans. It now seems that ... MNK1-regulated events were also inspected to analyze the role of MNK1 in glioblastoma. MNK1 was allegedly linked with the ... What we have done is the basic characterization of what we believe is an important signaling pathway in glioblastoma." ...
... is a lead researcher at the City of Hope National Medical Center with a clinical focus on glioblastoma. She plays an integral ... What is glioblastoma?. Glioblastoma is a cancer of the central nervous system (brain and spinal cord). Tumors in the brain and ... Can we count on CAR T cells against glioblastoma?. The lack of safe and effective therapies for glioblastoma is why many cancer ... Home Who We Are In the News ACGT Scientific Advisory Council member Christine Brown, PhD, leads trial for glioblastoma ...
... on survival in patients with newly diagnosed primary glioblastoma (GBM) treated with the same therapeutical protocol. Patients ... Glioblastoma (GBM) is both the most common and lethal primary brain tumor in adults [1, 2]. The standard of care for patients ... Li YM, Suki D, Hess K, Sawaya R. The influence of maximum safe resection of glioblastoma on survival in 1229 patients: can we ... The effect of initiation of RT on survival of glioblastoma patients has been a matter of debate for a long time. ...
  • Glioblastoma, previously known as glioblastoma multiforme (GBM), is the most aggressive and most common type of cancer that originates in the brain, and has very poor prognosis for survival. (wikipedia.org)
  • The median survival of patients with glioblastoma multiforme (GBM), the most aggressive malignant brain tumor, is typically less than 2 years 1 . (nature.com)
  • There's no cure for glioblastoma, which is also known as glioblastoma multiforme. (mayoclinic.org)
  • Persons with the most common pediatric brain malignancy, medulloblastoma, fare only slightly better than average, with a 71.9% 5-year survival, though the most common adult brain tumor, glioblastoma multiforme (GBM), incurs a mere 5.1% 5-year survival rate 2 . (nature.com)
  • Glioblastoma multiforme (GBM) is the most common and most aggressive of the primary brain tumors. (medscape.com)
  • Glioblastoma multiforme (GBM) is the most common type of malignant (cancerous) brain tumor in adults. (clevelandclinic.org)
  • Glioblastoma multiforme (GBM) is the most malignant human primary brain tumor, and its infiltrative nature represents the leading cause for the failure of therapies and tumor recurrences. (nih.gov)
  • Glioblastoma multiforme is the most malignant and the most common primary brain tumour worldwide. (uwi.edu)
  • Glioblastoma, previously known as glioblastoma multiforme, is the most aggressive among infiltrative gliomas, a group of primary tumors arising from the central nervous system (CNS). (cancernetwork.com)
  • The term 'glioblastoma multiforme' was introduced in the 1926 classification system devised by Cushing and Bailey. (cancernetwork.com)
  • 1] 'Multiforme,' which refers to a heterogenous histologic appearance and proliferation of multiple cell types, was abandoned from the revised nomenclature in the 2007 World Health Organization Classification of Tumors of the Central Nervous System, and is now simply called 'glioblastoma. (cancernetwork.com)
  • Funded by the Marie SkÅ‚odowska-Curie Actions programme, the MITIG project aims to understand how this process affects metabolism and tumour development of glioblastoma multiforme (GBM), a common and aggressive brain tumour in adults. (europa.eu)
  • Glioblastoma multiforme (GBM) represents the most frequent and aggressive type of primary brain tumours in adults. (europa.eu)
  • Glioblastoma multiforme (GBM) may be termed as the most common and aggressive form of brain tumor in humans. (healthjockey.com)
  • Glioblastoma multiforme (GBM) is the most common malignant tumor with high morbidity and mortality. (spandidos-publications.com)
  • Glioblastoma multiforme (GBM) is a World Health Organization grade IV glioma ( 3 ). (spandidos-publications.com)
  • It is also called as Glioblastoma multiforme, it has variants of giant cell Glioblastoma and gliosarcoma found in cerebral hemisphere of brain. (pharmiweb.com)
  • Penn Medicine has announced a new Translational Center of Excellence in the Abramson Cancer Center, focused on glioblastoma multiforme. (ascopost.com)
  • Paclitaxel is under clinical development by Serb and currently in Phase II for Glioblastoma Multiforme (GBM). (pharmaceutical-technology.com)
  • According to GlobalData, Phase II drugs for Glioblastoma Multiforme (GBM) have a 23% phase transition success rate (PTSR) indication benchmark for progressing into Phase III. (pharmaceutical-technology.com)
  • In the case of glioblastoma multiforme, the deadliest type of brain cancer, researchers have discovered that the molecule CD44s seems to give cancer cells a survival advantage. (neurosciencenews.com)
  • Treatment with erlotinib attempts to kill cancer cells by inhibiting EGFR signaling, a cellular mechanism that is hyperactive in most cases of glioblastoma multiforme and associated with poor prognosis," said senior author Dr. Chonghui Cheng, associate professor of molecular and human genetics and of molecular and cellular biology at Baylor College of Medicine. (neurosciencenews.com)
  • In this study, we discovered a mechanism by which CD44s helps maintain the EGFR signaling activated in glioblastoma multiforme," said Cheng, who also is an associate professor in the Lester and Sue Smith Breast Center at Baylor, part of the NCI-designated Dan L Duncan Comprehensive Cancer Center. (neurosciencenews.com)
  • My dad has a glioblastoma multiforme stage four. (cancer.org)
  • Glioblastoma multiforme (GBM) remains incurable despite aggressive implementation of multimodal treatments after surgical debulking. (nih.gov)
  • Here we present a case study of a patient with advanced multifocal, and rapidly progressing Glioblastoma Multiforme treated with STUPP protocol in combination with IV Quercetin. (scirp.org)
  • Histopathologic slide demonstrating a glioblastoma multiforme (GBM). (medscape.com)
  • A pooled analysis was conducted to examine the association between select variants in DNA repair genes and glioblastoma multiforme, the most common and deadliest form of adult brain tumors. (cdc.gov)
  • Genetic data for approximately 1,000 glioblastoma multiforme cases and 2,000 controls were combined from four centers in the United States that have conducted case-control studies on adult glioblastoma multiforme, including the National Cancer Institute, the National Institute for Occupational Safety and Health, the University of Texas M. D. Anderson Cancer Center, and the University of California at San Francisco. (cdc.gov)
  • Few studies have reported on the associations between variants in DNA repair genes and brain tumors, and few specifically have examined their impact on glioblastoma multiforme. (cdc.gov)
  • Our results suggest that common variation in DNA repair genes may be associated with risk for glioblastoma multiforme. (cdc.gov)
  • Study Population: 15 recurrent glioblastoma patients previously treated by surgery, conventional radiotherapy and chemotherapy with temozolomide (TMZ. (knowcancer.com)
  • Glioblastoma (GBM) adaptive, global, innovative learning environment (GBM AGILE) is an international, seamless Phase II/III response adaptive randomization platform trial designed to evaluate multiple therapies in newly diagnosed (ND) and recurrent GBM. (dana-farber.org)
  • Whereas previous studies in recurrent glioblastoma have demonstrated clinical benefit leading to FDA approval of the therapy, our study did not find a benefit using bevazicumab in the frontline," said Gilbert. (healthnewstrack.com)
  • She and her team in Duarte, California, are running an early phase clinical trial involving CAR T-cell therapy for recurrent glioblastoma - with promising early results. (acgtfoundation.org)
  • The presentation entitled "EO2401 peptide immunotherapy + nivolumab +/- bevacizumab in first recurrent glioblastoma: the Phase 1/2 EOGBM1-18/ROSALIE study" was delivered by David Reardon, M.D., Professor of Medicine at Harvard Medical School and Clinical Director of the Center for Neuro-Oncology at Dana-Farber Cancer Institute. (mywabashvalley.com)
  • Recurrent glioblastoma is one of the most challenging cancers to treat. (mywabashvalley.com)
  • EO2401 in combination with nivolumab and bevacizumab, as administered to 26 patients with recurrent glioblastoma comprising Cohort 3 of the ROSALIE study, was well tolerated with a safety profile consistent with the profile of nivolumab and bevacizumab, with the addition of local administration site reaction. (mywabashvalley.com)
  • This review focuses on clinical developments and management of newly diagnosed glioblastoma, and includes a discussion about the incorporation of molecular features into the classification of this disease. (cancernetwork.com)
  • The randomized, double-blind, placebo-controlled study registered 978 and enrolled 637 patients, respectively, all of whom were newly diagnosed with glioblastoma. (healthnewstrack.com)
  • To evaluate the effect of timing of radiotherapy (RT) on survival in patients with newly diagnosed primary glioblastoma (GBM) treated with the same therapeutical protocol. (springer.com)
  • This controversy has become critical as multiple phase III trials of anti-VEGF agents combined with cytotoxics failed to show overall survival benefit in newly diagnosed glioblastoma (nGBM) patients and several other cancers. (mit.edu)
  • The phase 2B randomized SURVIVE trial is currently underway at Roswell Park and other centers, open to newly diagnosed adult glioblastoma patients who meet eligibility criteria. (roswellpark.org)
  • One approved indication for temozolomide remains the same: treatment of adults with newly diagnosed glioblastoma , alongside radiotherapy, and then as maintenance treatment. (medscape.com)
  • The FDA also updated temozolomide's dosage regimen for newly diagnosed glioblastoma and refractory anaplastic astrocytoma, added information on risks from exposure to opened capsules, and updated patient counseling information and the Patient Information document. (medscape.com)
  • The cause of most cases of glioblastoma is not known. (wikipedia.org)
  • The market for Glioblastoma treatment drugs will grow significantly as the increasing cases of glioblastoma where doctors are looking for newer drugs and treatment methods to overcome the disease. (pharmiweb.com)
  • Since these glioblastomas often arise from a prior lower-grade glioma, they are considered secondary glioblastomas. (cancernetwork.com)
  • WHO grade 4 glioma is essentially synonymous with glioblastoma. (bmj.com)
  • Other types of chemotherapy given through a vein might be the treatment for glioblastoma that returns. (mayoclinic.org)
  • The study involved people with relapsed glioblastoma - a tumor that returned following standard treatment, such as chemotherapy. (acgtfoundation.org)
  • This result is an improvement from standard-of-care chemotherapy of 5-9 months for glioblastoma. (acgtfoundation.org)
  • In comparison, murine models of glioblastoma treated with chemotherapy relapsed within 100 days. (euroweeklynews.com)
  • Recently it has become a focus of interest, in treatment of Glioblastoma along with different forms of radiation and chemotherapy. (scirp.org)
  • Preliminary data have shown that the modified diet appears to make glioblastoma tumors more sensitive to treatment with radiation and chemotherapy. (medscape.com)
  • Special tests of the cancer cells can give your health care team more information about your glioblastoma and your prognosis. (mayoclinic.org)
  • Glioblastoma (GBM) is a highly aggressive and invasive brain tumor with a poor prognosis despite extensive treatment . (bvsalud.org)
  • Because of the similarities in immunostaining of glial cells and glioblastoma, gliomas such as glioblastoma have long been assumed to originate from glial-type stem cells found in the subventricular zone. (wikipedia.org)
  • The best available evidence suggests that glioblastomas originate from cells that give rise to glial cells. (bmj.com)
  • Dr. Brown, a member of the Alliance for Cancer Gene Therapy Scientific Advisory Council, is a lead researcher at the City of Hope National Medical Center with a clinical focus on glioblastoma. (acgtfoundation.org)
  • And he now researches cancer with a focus on glioblastoma, a brain cancer that currently remains almost untreatable. (jax.org)
  • Her mission to find a cure for glioblastoma stretches to her membership on ACGT's Scientific Advisory Council. (acgtfoundation.org)
  • This is clearly a tough problem and an unmet medical need, as malignant brain tumors - and particularly glioblastoma - pose many challenges to immunotherapy. (acgtfoundation.org)
  • We are very pleased to present extensive data from the Phase 1/2 ROSALIE study of EO2401, our lead OncoMimics â„¢ peptide-based immunotherapy, in glioblastoma," said Pierre Belichard, Chief Executive Officer of Enterome. (mywabashvalley.com)
  • We then outline preclinical approaches that employ CAR-NK cells for GB immunotherapy, and give an overview on the ongoing clinical development of ErbB2 (HER2)-specific CAR-NK cells currently applied in a phase I clinical trial in glioblastoma patients. (frontiersin.org)
  • My sister was recently diagnosed with Glioblastoma and we are wanting to know as much as possible on treatment options, effects of , and alternative therapies. (cancer.org)
  • Beth, Please send any info on the alternative therapies used for Glioblastoma Grade IV. (cancer.org)
  • The heterogeneity of glioblastoma can suppress immune cell function and lead to immune evasion, which presents a challenge in developing effective molecular therapies for tumor cells. (spandidos-publications.com)
  • Obviously, glioblastoma is a cancer with too few effective therapies," said Gilbert, who also holds the Blanche Bender Professorship in Cancer Research. (healthnewstrack.com)
  • The lack of safe and effective therapies for glioblastoma is why many cancer experts are interested in testing different cancer cell and gene therapies , like CAR T cells. (acgtfoundation.org)
  • The use of gold nanorods in hyperthermal therapies is very effective in eliminating glioblastoma cells, and therefore represents an important area of research for therapeutic development. (dovepress.com)
  • For long term survival of in glioblastoma, there are newer combination therapies studied and various clinical trials are in order to fight against these disease. (pharmiweb.com)
  • The team will investigate new immune therapies for glioblastoma and, in particular, design and test new chimeric antigen receptor (CAR) T-cell therapies. (ascopost.com)
  • Glioblastoma is a type of cancer that starts in cells called astrocytes that support nerve cells. (mayoclinic.org)
  • Glioblastoma is a type of cancer that starts as a growth of cells in the brain or spinal cord. (mayoclinic.org)
  • Glioblastoma forms from cells called astrocytes that support nerve cells. (mayoclinic.org)
  • Tests can tell whether the cells are cancerous and if they're glioblastoma cells. (mayoclinic.org)
  • Glioblastoma often grows into the healthy brain tissue, so it might not be possible to remove all of the cancer cells. (mayoclinic.org)
  • 2] Glioblastoma is histologically defined by neoplastic cells with astrocytic characteristics and the presence of either endothelial proliferation-often in a glomeruloid morphology-and/or necrosis, which may resemble a pseudopalisading pattern (a false fence of neoplastic cells surrounding an area of necrotic tissue). (cancernetwork.com)
  • The majority of glioblastomas are IDH wild-type and correspond to the longstanding clinical description of primary glioblastomas, which arise rapidly from non-neoplastic brain cells and progress quickly. (cancernetwork.com)
  • The aim of the present study was to evaluate the phytochemical composition, antioxidant and anticancer activity ofaqueous and methanol extracts against Human glioblastoma cells U87MG. (greenmedinfo.com)
  • Engineering NK cells to resist immune suppression could be a path toward using NK cell-based immunotherapies for glioblastoma brain cancer. (neurosciencenews.com)
  • Glioblastoma (GBM) is characterized by significant genetic heterogeneity among tumor cells. (spandidos-publications.com)
  • Can we count on CAR T cells against glioblastoma? (acgtfoundation.org)
  • In this study, we developed an optical hyperthermia method capable of inducing in vitro death of glioblastoma cells. (dovepress.com)
  • The effectiveness of the method was determined by measuring changes in cell viability after laser irradiation of glioblastoma cells in the presence of gold nanorods. (dovepress.com)
  • Previous methods looked at cancer cells en masse, which could provide accurate data about what the "average" cell - and its genetic mutations - looked like. (jax.org)
  • It provides detailed analyses of both the glioblastoma cells and their microenvironments, the tissues and cells (including immune cells) that surround the tumor in the body. (jax.org)
  • Glioblastoma (GBM) is most common grade four tumor, is malignant and contains dead tumor cells. (pharmiweb.com)
  • Glioblastoma is also difficult to treat because of number of different types of cells and thus combines various treatment plans combined. (pharmiweb.com)
  • With a pilot mass cytometry dataset of 2 million cells from 28 glioblastomas, RAPID identified tumor cells whose abundance independently and continuously stratified patient survival. (elifesciences.org)
  • Glioblastomas and most other types of cancer produce a molecule called survivin , which helps the cancer cells survive. (roswellpark.org)
  • Summary: A new Baylor study reveals the CD44s molecule gives glioblastoma brain cancer cells a survival advantage. (neurosciencenews.com)
  • In an orthotopic patient-derived glioblastoma humanized mouse model, the combined treatment with nanoporter-hydrogel superstructure and CD47 antibody increased the frequency of positive immune responding cells and suppressed the negative immune regulating cells, conferring a robust tumoricidal immunity surrounding the postsurgical cavity and inhibiting postoperative glioblastoma relapse. (nih.gov)
  • While a few studies have attempted reprogramming of glioblastoma (GBM) cells toward a neuronal fate, this approach has not yet been used to induce differentiation into other lineages and in vivo data on reduction in tumorigenicity are limited. (lu.se)
  • They used human-derived glioblastoma cells in a mouse model. (medscape.com)
  • Glycation Leads to Increased Invasion of Glioblastoma Cells. (bvsalud.org)
  • A new study in the Journal of Experimental Medicine report Zika virus could be used to target and treat glioblastoma brain cancer. (neurosciencenews.com)
  • The collaboration between Stanford University and The Invus Group will enable the development of medication to treat glioblastoma, a form of brain cancer. (stanford.edu)
  • Anticancer Effect in Human Glioblastoma and Antioxidant Activity ofL. (greenmedinfo.com)
  • In the past, both primary and secondary glioblastomas were considered to be the same clinical entity. (cancernetwork.com)
  • As such, secondary glioblastomas are to be classified as a distinct biological and molecular entity for which different treatment strategies will ultimately be proposed. (cancernetwork.com)
  • Glioblastomas (GBMs) account for almost half of all cancerous brain tumors in adults. (clevelandclinic.org)
  • Glioblastomas (GBMs) are an aggressive type of malignant brain tumor. (fusfoundation.org)
  • She is thankful to be a part of the glioblastoma IMPT clinical trial and hopes that it will help other patients, and possibly her own family. (mdanderson.org)
  • Up to 10% of patients with glioblastoma harbor a mutation in the IDH1 or IDH2 genes, an early event in gliomagenesis. (cancernetwork.com)
  • There is a critical need to identify readily translatable adjuncts to potentiate the dismal median survivals of only 15-20 months in glioblastoma (GBM) patients after standard of care, i.e., concurrent Temozolomide (TMZ) and radiation (XRT) therapy. (mdpi.com)
  • Using liquid biopsy technology as a new diagnostic method, innovative treatment strategies may be implemented for patients with glioblastoma to improve their outcomes. (spandidos-publications.com)
  • Avastin - bevacizumab failed to increase overall survival (OS) or statistically significant progression-free survival (PFS) for glioblastoma patients in the frontline setting. (healthnewstrack.com)
  • In conclusion, tumor perfusion changes after antiangiogenic therapy may distinguish responders vs. nonresponders early in the course of this expensive and potentially toxic form of therapy, and these results may provide new insight into the selection of glioblastoma patients most likely to benefit from anti-VEGF treatments. (mit.edu)
  • There are various organizations which are supporting Glioblastoma patients and efforts are being taken to improvise the treatments related to it. (pharmiweb.com)
  • Biological validation used an orthogonal platform, immunohistochemistry, and a larger cohort of 73 glioblastoma patients to confirm the findings from the pilot cohort. (elifesciences.org)
  • Penn Medicine is at the cutting edge of research and clinical care for patients with glioblastoma, and our [Translational Center] will help accelerate this mission-critical work," said Donald M. O'Rourke, MD , John Templeton, Jr, MD, Associate Professor in Neurosurgery in the Perelman School of Medicine at the University of Pennsylvania, who will lead the Translational Center (a partnership of the Abramson Cancer Center and the Department of Neurosurgery). (ascopost.com)
  • ROSALIE (EOGBM1-18) is a multicenter, open-label, first-in-human, Phase 1/2 study of EO2401 in combination with an immune checkpoint inhibitor (nivolumab, Opdivo®) +/- bevacizumab for the treatment of patients with first progression/recurrence of glioblastoma. (mywabashvalley.com)
  • Despite this aggressive treatment, median survival of glioblastoma patients is only about 15 months, and recurrence remains almost inevitable ( 1 , 2 ). (frontiersin.org)
  • BACKGROUND: Src signaling is markedly upregulated in patients with invasive glioblastoma (GBM) after the administration of bevacizumab. (healthpartners.com)
  • It is our recommendation to investigate such combinational approach in patients with Glioblastoma, as in our case it proved to be safe and effective with improved quality of life and performance as well as clinical response and survival. (scirp.org)
  • There are ongoing studies of many other treatments for glioblastoma. (mayoclinic.org)
  • Stanford University and The Invus Group, an investment firm, have formed a collaboration to develop treatments for glioblastoma, a type of brain cancer. (stanford.edu)
  • Glioblastoma Treatment Drugs Market: Drivers & Restraints Glioblastoma is a complicated disease and thus the treatment for it involves various approaches combining various treatments which is the major market driver for Glioblastoma treatment drugs market . (pharmiweb.com)
  • Studies carried out over the past three decades suggest that glioblastomas, like other cancers, arise secondary to the accumulation of genetic alterations. (bmj.com)
  • Although in principle this strategy does not work with other types of brain tumours, glioblastomas represent 45 per cent of all cancers that affect the brain. (euroweeklynews.com)
  • In this study, we established 4 subclones from a glioblastoma patient and demonstrated clear evidence that a brain tumor contains heterogeneous subclones that exhibit dissimilar morphologies, self-renewal, proliferative capacities and therapeutic sensitivities. (nature.com)
  • This article reviews the key principles that drive the formulation of therapeutic strategies in glioblastoma. (bmj.com)
  • This paper explores the heterogeneity of glioblastoma and the immune microenvironment, providing a therapeutic basis for individualized treatment. (spandidos-publications.com)
  • Robert Fenstermaker, MD , Chair of Neurosurgery at Roswell Park, and Michael Ciesielski, PhD , Assistant Professor of Neurosurgery, have developed a therapeutic cancer vaccine for glioblastoma, a type of aggressive brain tumor. (roswellpark.org)
  • Associations between polymorphisms in DNA repair genes and glioblastoma. (cdc.gov)
  • Deborah's glioblastoma treatment began with brain surgery to remove the tumor. (mdanderson.org)
  • In addition, a subgroup of lower-grade gliomas may carry molecular features and signatures similar to glioblastoma, with a similarly aggressive natural course,[4] for which an intensive treatment strategy is advocated. (cancernetwork.com)
  • Glioblastoma accounts for nearly half of all brain tumors, and little effective treatment is currently available. (stanford.edu)
  • This is not to say that a treatment for glioblastoma is just around the corner. (healthjockey.com)
  • Glioblastoma Treatment Drugs Market Growth Analysis, Oppo. (pharmiweb.com)
  • The key players for the Glioblastoma Treatment Drugs Market are F. Hoffmann-La Roche AG, Merck & Co., Inc., Sandoz, Arbor Pharms LLC. (pharmiweb.com)
  • Glioblastoma (GB) is the most frequent malignant primary brain tumor in adults, without any curative treatment options available at present. (frontiersin.org)
  • Hydrogel loading functionalized PAMAM/shRNA complex for postsurgical glioblastoma treatment. (physiciansweekly.com)
  • In an in vivo orthotopic U87MG postoperative tumor model, G5-BGG/shRNA871-loaded hydrogel combined with temozolomide downregulated CD47 protein expression, increased macrophage infiltration into residual tumors, and significantly prolonged the survival time of mice, indicating potential applications for glioblastoma treatment. (physiciansweekly.com)
  • The Stupp protocol has become standard of care for the treatment of glioblastoma (GBM) (since its publication in 2005) and has led to some limited survival improvements. (scirp.org)
  • Researchers from the University of Florida have published a study evaluating a high-fat, low-carbohydrate diet in the treatment of glioblastoma brain tumors. (medscape.com)
  • See Brain Lesions: 9 Cases to Test Your Management Skills , a Critical Images slideshow, to review cases including meningiomas, glioblastomas and craniopharyngiomas, and to determine the best treatment options based on the case history and images. (medscape.com)
  • After her glioblastoma diagnosis, her son took charge of researching and found information about a clinical trial at MD Anderson. (mdanderson.org)
  • Deborah is currently cancer-free, but for the next year, she'll continue to come to MD Anderson once a month as a part of the glioblastoma IMPT clinical trial. (mdanderson.org)
  • In partnership with Wake Forest University, Virginia-Maryland Veterinary College is still accepting dogs with glioblastoma into the clinical trial. (cbsnews.com)
  • To improve those numbers, far more needs to be learned about the entire molecular landscape of glioblastoma, including the mechanisms that drive disease progression. (jax.org)
  • McCain had glioblastoma , which is the deadliest kind of brain cancer. (cbsnews.com)
  • We learned two days later he had a malignant brain tumor -- a stage IV glioblastoma , the most aggressive type. (mdanderson.org)
  • In March, Barbara was diagnosed with an aggressive malignant brain tumor called a glioblastoma. (fusfoundation.org)
  • Initial signs and symptoms of glioblastoma are nonspecific. (wikipedia.org)
  • Glioblastoma symptoms include headaches that keep getting worse, nausea and vomiting, blurred or double vision, and seizures. (mayoclinic.org)
  • What are the symptoms of glioblastoma? (clevelandclinic.org)
  • Background: A more effective immune response against glioblastoma is needed in order to achieve better tumor control. (lu.se)
  • We investigate two cell lines for glioblastoma and medulloblastoma (U87mg & DAOY, respectively), plated as spheroidal aggregates in Matrigel-filled electrotaxis channels, and report opposing electrotactic responses. (nature.com)
  • Glioblastoma (GBM) is both the most common and lethal primary brain tumor in adults [ 1 , 2 ]. (springer.com)
  • Glioblastoma (GB) is the most common and aggressive primary brain tumor in adults and currently incurable. (frontiersin.org)
  • Glioblastoma is the most common form of primary brain tumour. (bmj.com)
  • ImmunoCellular Therapeutics has decided to use Progenitor Cell Therapy (PCT) to produce its Phase II glioblastoma vaccine, ICT-107. (genengnews.com)
  • Neoantigen vaccine generates intratumoral T cell responses in phase Ib glioblastoma trial. (msdmanuals.com)
  • Bevacizumab works as a monoclonal antibody against VEGF-A, which is produced by glioblastoma to stimulate blood vessel growth. (healthnewstrack.com)
  • It can be done with a needle before surgery or during surgery to remove the glioblastoma. (mayoclinic.org)
  • Surgery to remove the glioblastoma. (mayoclinic.org)
  • Glioblastoma, the most common malignant tumor of the central nervous system, readily relapses after surgery. (physiciansweekly.com)