Gliosarcoma
Brain Neoplasms
Rats, Inbred F344
Glioma
Chondroblastoma
Elementary Particle Interactions
Reticulin
Glioblastoma
Carmustine
Neoplasm Transplantation
Astrocytoma
Dacarbazine
Antineoplastic Agents, Alkylating
Deletion of multiple immediate-early genes from herpes simplex virus reduces cytotoxicity and permits long-term gene expression in neurons. (1/145)
Herpes simplex virus type 1 (HSV-1) has many attractive features that suggest its utility for gene transfer to neurons. However, viral cytotoxicity and transient transgene expression limit practical applications even in the absence of viral replication. Mutant viruses deleted for the immediate early (IE) gene, ICP4, an essential transcriptional transactivator, are toxic to many cell types in culture in which only the remaining IE genes are expressed. In order to test directly the toxicity of other IE gene products in neurons and develop a mutant background capable of longterm transgene expression, we generated mutants deleted for multiple IE genes in various combinations and tested their relative cytotoxicity in 9L rat gliosarcoma cells, Vero monkey kidney cells, and primary rat cortical and dorsal root neurons in culture. Viral mutants deleted simultaneously for the IE genes encoding ICP4, ICP22 and ICP27 showed substantially reduced cytotoxicity compared with viruses deleted for ICP4 alone or ICP4 in combination with either ICP22, ICP27 or ICP47. Infection of neurons in culture with these triple IE deletion mutants substantially enhanced cell survival and permitted transgene expression for over 21 days. Such mutants may prove useful for efficient gene transfer and extended transgene expression in neurons in vitro and in vivo. (+info)In vivo modulation of alternative pathways of P-450-catalyzed cyclophosphamide metabolism: impact on pharmacokinetics and antitumor activity. (2/145)
The widely used anticancer prodrug cyclophosphamide (CPA) is activated in liver by a 4-hydroxylation reaction primarily catalyzed by cytochrome P-4502B and P-4502C enzymes. An alternative metabolic pathway involves CPA N-dechloroethylation to yield chloroacetaldehyde (CA), a P-4503A-catalyzed deactivation/neurotoxication reaction. The in vivo modulation of these alternative, competing pathways of P-450 metabolism was investigated in pharmacokinetic studies carried out in the rat model. Peak plasma concentrations (Cmax) for 4-OH-CPA and CA were increased by 3- to 4-fold, and apparent plasma half-lives of both metabolites were correspondingly shortened in rats pretreated with phenobarbital (PB), an inducer of P-4502B and P-4503A enzymes. However, PB had no net impact on the extent of drug activation or its partitioning between these alternative metabolic pathways, as judged from AUC values (area-under-the-plasma concentration x time curve) for 4-OH-CPA and CA. The P-4503A inhibitor troleandomycin (TAO) decreased plasma Cmax and AUC of CA (80-85% decrease) without changing the Cmax or AUC of 4-OH-CPA in uninduced rats. In PB-induced rats, TAO decreased AUCCA by 73%, whereas it increased AUC4-OH-CPA by 93%. TAO thus selectively suppresses CPA N-dechloroethylation, thereby increasing the availability of drug for P-450 activation via 4-hydroxylation. By contrast, dexamethasone, a P-4503A inducer and antiemetic widely used in patients with cancer, stimulated large, undesirable increases in the Cmax and AUC of CA (8- and 4-fold, respectively) while reducing the AUC of the 4-hydroxylation pathway by approximately 60%. Tumor excision/in vitro colony formation and tumor growth delay assays using an in vivo 9L gliosarcoma solid tumor model revealed that TAO suppression of CPA N-dechloroethylation could be achieved without compromising the antitumor effect of CPA. The combination of PB with TAO did not, however, enhance the antitumor activity of CPA, despite the approximately 2-fold increase in AUC4-OH-CPA, suggesting that other PB-inducible activities, such as aldehyde dehydrogenase, may counter this increase through enhanced deactivation of the 4-hydroxy metabolite. Together, these studies demonstrate that the P-4503A inhibitor TAO can be used to effectively modulate CPA metabolism and pharmacokinetics in vivo in a manner that decreases the formation of toxic metabolites that do not contribute to antitumor activity. (+info)Gliosarcoma: a case with unusual epithelial feature. (3/145)
Astrocytic tumors, particularly gliosarcoma, may contain epithelial features in the form of trabecular, adenoid, papillary arrangement, and squamous metaplasia. A case of gliosarcoma with unusual epithelial feature is described. The patient was a 60-year-old male with frequent seizures. The mass was 4 cm and in the left frontal lobe. Trabecular or rarely adenoid arrangement of neoplastic astrocytes was present in the mucinous stroma, and there was a distinctive transition between the trabecular area and typical anaplastic astrocytoma. The tumor cells in the trabecular area showed positive immunostain for glial fibrillary acidic protein, but did not react with various kinds of cytokeratin. The sarcomatous area was undifferentiated and was not labeled by factor-VIII, desmin, and anti-smooth muscle actin. Occurrence and histogenesis of epithelial features in gliosarcoma are reviewed. The importance to recognize the existence of epithelial feature in malignant astrocytic tumor is emphasized. (+info)Enhanced uptake of [11C]TPMP in canine brain tumor: a PET study. (4/145)
In vitro studies have demonstrated the membrane potential-dependent enhanced uptake of phosphonium salts, including [3H]triphenylmethylphosphonium (TPMP), into mitochondria of carcinoma and glioma-derived tumor cells, suggesting the potential use of phosphonium salts as tracers for tumor imaging. This study characterizes the in vivo uptake of [11C]TPMP in canine brain glioma using PET. METHODS: Dynamic paired PET studies of [11C]TPMP followed by [68Ga]ethylenediaminetetraacetic acid (EDTA) were performed 4 d before and 9 d after tumor cell inoculation. Graphical analysis was used to evaluate [11C]TPMP retention in tumor tissue. Distribution of tracer uptake was compared with tumor histological sections. RESULTS: [11C]TPMP exhibited enhanced uptake and prolonged retention in tumor cells. Patlak plot was linear over the 20- to 95-min postinjection period (r = 0.97 +/- 0.1). [68Ga]EDTA exhibited a gradual washout from the tumor tissue. The tumor-to-normal brain uptake ratio at 55 to 95 min postinjection was 47.5 for [11C]TPMP and 8.1 for [68Ga]EDTA. Qualitative comparison with histological sections indicated that [11C]TPMP enhanced uptake was restricted to the tumor area. CONCLUSION: The enhanced uptake and prolonged retention in tumor suggest [11C]TPMP as a promising means for imaging of gliomas in dogs. The need for studies in humans is indicated. (+info)B-myb promoter retargeting of herpes simplex virus gamma34.5 gene-mediated virulence toward tumor and cycling cells. (5/145)
Deletion of the gamma34.5 gene coding for virulence markedly reduces cytotoxicity mediated by herpes simplex virus type 1 (HSV-1) (J. M. Markert et al., Neurosurgery 32:597-603, 1993; N. S. Markovitz et al. , J. Virol. 71:5560-5569, 1997). To target lytic virulence to tumors, we have created a novel HSV-1 mutant, designated Myb34.5. This viral mutant is characterized by a deletion of the gene for infected cell polypeptide 6 (ICP6; also known as UL39 or ribonucleotide reductase) and of the two endogenous copies of the gamma34.5 gene (RL1) and by reintroduction of one copy of gamma34.5 under control of the E2F-responsive, cellular B-myb promoter. On direct intracerebral inoculation in BALB/c mice, the 50% lethal dose (LD(50)) for Myb34.5 was 2.7 x 10(7) PFU while that for HSVs with mutations in the gamma34.5 gene could not be technically achieved with available viral stocks and it was estimated as >1 x 10(7) PFU. The LD(50) for an HSV with a single defect in ICP6 function was 1.3 x 10(6) PFU. Conversely, Myb34.5's oncolytic efficacy against a variety of human glioma cells in culture and in vivo was enhanced compared to that of HSVs with gamma34.5 mutations, and in fact, it was comparable to that of the wild-type F strain and of viral mutants that possess a wild-type gamma34.5 gene. The characteristic shutoff of host protein synthesis, occurring after infection of human SK-N-SH neuroblastoma cells by gamma34.5 mutant viruses (J. Chou and B. Roizman, Proc. Natl. Acad. Sci. USA 89:3266-3270, 1992), was not present after infection with Myb34.5. There was an increase of almost 3 logarithmic units in the production of progeny virus in arrested fibroblasts compared to that in cycling fibroblasts infected with Myb34.5. These results suggest that transcriptional regulation of gamma34.5 by cell cycle-regulated promoters can be used to target HSV-1 virulence toward tumors while maintaining the desirable neuroattenuated phenotype of a gamma34.5 mutant. (+info)Genetic profile of gliosarcomas. (6/145)
There are distinct genetic pathways leading to the glioblastoma, the most malignant astrocytic brain tumor. Primary (de novo) glioblastomas develop in older patients and are characterized by epidermal growth factor (EGF) receptor amplification/overexpression, p16 deletion, and PTEN mutations, whereas secondary glioblastomas that progressed from low-grade or anaplastic astrocytoma develop in younger patients and frequently contain p53 mutations. In this study, we assessed the genetic profile of gliosarcoma, a rare glioblastoma variant characterized by a biphasic tissue pattern with alternating areas displaying glial and mesenchymal differentiation. Single-strand conformation polymorphism followed by direct DNA sequencing revealed p53 mutations in five of 19 gliosarcomas (26%) and PTEN mutations in seven cases (37%). Homozygous p16 deletion was detected by differential polymerase chain reaction in seven (37%) gliosarcomas. The overall incidence of alterations in the Rb pathway (p16 deletion, CDK4 amplification, or loss of pRb immunoreactivity) was 53%, and these changes were mutually exclusive. Coamplification of CDK4 and MDM2 was detected in one gliosarcoma. None of the gliosarcomas showed amplification or overexpression of the EGF receptor. Thus gliosarcomas exhibit a genetic profile similar to that of primary (de novo) glioblastomas, except for the absence of EGFR amplification/overexpression. Identical PTEN mutations in the gliomatous and sarcomatous tumor components were found in two cases. Other biopsies contained p16 deletions, an identical p53 mutation, or coamplification of MDM2 and CDK4 in both tumor areas. This strongly supports the concept of a monoclonal origin of gliosarcomas and an evolution of the sarcomatous component due to aberrant mesenchymal differentiation in a highly malignant astrocytic neoplasm. (+info)Vascular protection by chloroquine during brain tumor therapy with Tf-CRM107. (7/145)
Tf-CRM107 is a conjugate of transferrin and a point mutant of diphtheria toxin that selectively kills cells expressing high levels of the transferrin receptor. Tf-CRM107 has been infused intratumorally into patients with malignant brain tumors. Although approximately half of the patients exhibit tumor responses, patients receiving higher doses of Tf-CRM107 may develop magnetic resonance image (MRI) evidence of toxicity indicative of small vessel thrombosis or petechial hemorrhage. Consistent with these clinical results we found that intracerebral injection of Tf-CRM107 into rats at total doses > or =0.025 microg causes brain damage detectable by MRI and histology. To widen the therapeutic window of Tf-CRM107, we explored ways to prevent this damage to the vasculature. We reasoned that the vasculature may be protected to a greater extent than tumor from Tf-CRM107 infused into brain parenchyma by i.v. injection of reagents with low blood-brain barrier permeability that block the toxicity of Tf-CRM107. Chloroquine, a well-characterized antimalarial drug, blocks the toxicity of diphtheria toxin and Tf-CRM107. Systemic administration of chloroquine blocked the toxicity of Tf-CRM107 infused intracerebrally in rats and changed the maximum tolerated dose of Tf-CRM107 from 0.2 to 0.3 microg. Moreover, chloroquine treatment completely blocked the brain damage detected by MRI caused by intracerebral infusion of 0.05 microg of Tf-CRM107. In nude mice bearing s.c. U251 gliomas, chloroquine treatment had little effect on the antitumor efficacy of Tf-CRM107. Thus, chloroquine treatment may be useful to reduce the toxicity of Tf-CRM107 for normal brain without inhibiting antitumor efficacy and increase the therapeutic window of Tf-CRM107 for brain tumor therapy. (+info)Cytokine gene therapy of gliomas: induction of reactive CD4+ T cells by interleukin-4-transfected 9L gliosarcoma is essential for protective immunity. (8/145)
Tumor cells genetically modified to secrete cytokines stimulate potent immune responses against peripheral and central nervous system tumors; however, variable results on the efficacy of this strategy for therapeutic intervention against established intracranial neoplasia have been reported. We have found that vaccination with rat 9L gliosarcoma cells expressing interleukin 4 (9LmIL4) induced a specific, protective, immune response against rechallenge with parental 9L tumors. In naive rats, sham-transfected 9L (9Lneo) tumors and 9LmIL4 tumors grew at comparable rates for 12-14 days, and then 9LmIL4 tumors regressed. After regression of 9LmIL4 tumors, rats were resistant to rechallenge with parental 9L cells. To investigate the mechanism(s) responsible for 9LmIL4-induced immunity, the phenotype and function of tumor-infiltrating lymphocytes (TILs) in 9Lneo and 9LmIL4 tumors were compared. In flow cytometric analyses, it was determined that CD4+ T cells were the predominant cell type in both 9Lneo and 9LmIL4 tumors at day 10. However, at the onset of regression (day 14), 9LmIL4 tumors were infiltrated predominantly by CD8+ T cells. To investigate functional aspects of the anti-9L tumor responses, we assessed the capacity of 9LmIL4 TILs to mediate specific lytic function or production of cytokines. In response to parental 9L, TILs isolated from day 14 9LmIL4 tumors were demonstrated to produce substantially greater amounts of IFN-gamma than did TILs from 9Lneo tumors. Although freshly isolated TILs from 9LmIL4 or control tumors did not lyse 9L cells in 51Cr-release cytotoxicity assays, specific cytotoxicity was demonstrable using TILs from day 14 9LmIL4 or splenocytes from 9LmIL4-bearing rats after their restimulation for 5 days with parental 9L tumor cells in vitro. Antibody blocking studies demonstrated that cytokine production and lytic activity by TILs, or splenocytes from 9LmIL4-immunized rats, were mediated in a T-cell receptor-dependent fashion. Because interleukin-4 also promotes humoral responses, quantity and isotype of immunoglobulins in sera from 9Lneo or 9LmIL4-immunized rats were compared. The amount of IgG1 antibodies was significantly increased in sera from 9LmIL4-immunized rats compared to sera from 9Lneo-bearing rats. Experiments using sublethally irradiated, naive rats adoptively transferred with splenocytes and/or sera from 9LmIL4-immunized or naive rats demonstrated that immune cells, with or without immune sera, protected recipients from challenge with parental 9L. Immune sera provided no protection when given with lymphocytes from naive rats, and it did not enhance protection against parental 9L when given in conjunction with lymphocytes for 9LmIL4-immunized rats. In additional adoptive transfer experiments, an essential role for CD4+ T cells in immunity was observed because their depletion from among splenocytes of 9LmIL4-immunized rats eliminated the protective effective against 9L, whereas depletion of CD8+ cells resulted in a more limited effect on protection against 9L. These data suggest that strategies for inducing systemic, long-term tumor-specific reactivity among CD4+ T cells will be critical for the development of immunotherapy of gliomas. (+info)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.
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.
F344 is a strain code used to designate an outbred stock of rats that has been inbreeded for over 100 generations. The F344 rats, also known as Fischer 344 rats, were originally developed at the National Institutes of Health (NIH) and are now widely used in biomedical research due to their consistent and reliable genetic background.
Inbred strains, like the F344, are created by mating genetically identical individuals (siblings or parents and offspring) for many generations until a state of complete homozygosity is reached, meaning that all members of the strain have identical genomes. This genetic uniformity makes inbred strains ideal for use in studies where consistent and reproducible results are important.
F344 rats are known for their longevity, with a median lifespan of around 27-31 months, making them useful for aging research. They also have a relatively low incidence of spontaneous tumors compared to other rat strains. However, they may be more susceptible to certain types of cancer and other diseases due to their inbred status.
It's important to note that while F344 rats are often used as a standard laboratory rat strain, there can still be some genetic variation between individual animals within the same strain, particularly if they come from different suppliers or breeding colonies. Therefore, it's always important to consider the source and history of any animal model when designing experiments and interpreting results.
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.
Chondroblastoma is a rare, benign (non-cancerous) bone tumor that typically develops in the epiphysis, which is the rounded end of a long bone near a joint. It primarily affects children and adolescents, with around 90% of cases occurring before the age of 20.
The tumor arises from chondroblasts, cells responsible for producing cartilage during bone growth. Chondroblastoma is usually slow-growing and typically causes localized pain, swelling, or tenderness in the affected area. In some cases, it may weaken the bone and lead to fractures.
Treatment generally involves surgical removal of the tumor, followed by curettage (scraping) of the surrounding bone tissue and replacement with bone grafts or substitutes. Recurrence is possible but rare, and long-term prognosis is usually favorable.
Elementary particle interactions refer to the fundamental forces that govern how elementary particles, which are the basic building blocks of matter, interact with each other. There are four fundamental forces in nature: gravity, electromagnetism, the strong nuclear force, and the weak nuclear force. Each of these forces is associated with a specific type of particle interaction.
1. Gravity: This force is associated with the interaction between massive objects, such as planets and stars. However, at the level of elementary particles, gravity is too weak to be observed directly, and its effects are not well understood.
2. Electromagnetism: This force is responsible for the interactions between charged particles, such as electrons and protons. It is mediated by the exchange of photons, which are massless particles that carry the electromagnetic force.
3. Strong Nuclear Force: This force is responsible for holding atomic nuclei together. It is mediated by the exchange of gluons, which are massless particles that carry the strong nuclear force. The strong nuclear force is about 100 times stronger than electromagnetism but only operates at very short distances, typically less than the size of a proton.
4. Weak Nuclear Force: This force is responsible for certain types of radioactive decay and other processes that involve the transformation of particles. It is mediated by the exchange of W and Z bosons, which are massive particles that carry the weak nuclear force. The weak nuclear force is much weaker than both electromagnetism and the strong nuclear force but has a longer range.
These particle interactions can be studied using high-energy particle accelerators, such as the Large Hadron Collider (LHC) at CERN, where particles are accelerated to very high speeds and then collided together. By analyzing the products of these collisions, scientists can learn more about the fundamental nature of matter and the forces that govern its behavior.
Reticulin is a type of protein fiber that forms part of the extracellular matrix in various connective tissues in the body. It is composed of collagenous and non-collagenous proteins, and it has a reticular or network-like structure when viewed under a microscope. In histology (the study of the microscopic structure of tissues), reticulin fibers are often stained to help identify certain types of cells or structures.
In particular, reticulin fibers are often found in close association with certain types of cells, such as hematopoietic stem cells and neurons. They provide structural support and help regulate the function of these cells. In addition, reticulin fibers play a role in the immune response, wound healing, and tissue repair.
Abnormal accumulations of reticulin fibers can be seen in various disease states, such as fibrosis (excessive scarring) and certain types of cancer. For example, increased reticulin fibers are often found in the liver in patients with cirrhosis, a condition characterized by extensive scarring and damage to the liver. Similarly, abnormal reticulin fiber deposition is seen in some forms of lymphoma, a type of cancer that affects the lymphatic system.
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.
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.
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.
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.
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.
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.
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.
Gliosarcoma
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University of California Health Glioma Clinical Trials for 2023 - California
Glioma3
- Gliosarcoma is a rare type of glioma, a cancer of the brain that comes from glial, or supportive, brain cells, as opposed to the neural brain cells. (wikipedia.org)
- In the current study, 25 patients were enrolled with confirmed high-grade glioma, 17 had GBM or gliosarcoma. (salesandmarketingnetwork.com)
- Marizomib (NPI-0052) is under development for the treatment of pediatric patients with diffuse intrinsic pontine glioma (DIPG), newly diagnosed malignant glioma and relapsed malignant glioma including glioblastoma and gliosarcoma. (pharmaceutical-technology.com)
Tumor6
- Primary gliosarcoma (PGS) is classified as a grade IV tumor and a subtype of glioblastoma multiforme in the 2007 World Health Organization classification system (GBM). (wikipedia.org)
- Feigin's early reports components of perivascular sarcomatous and hyperplastic arteries in gliosarcoma offered evidence for the "collision tumor" hypothesis. (wikipedia.org)
- In this report, we illustrate a case of gliosarcoma with extensive extracranial metastases with confirmation of histological and molecular concordance between the primary tumor and a metastatic lesion of the lung. (bvsalud.org)
- Pathological analysis of the tumor removal specimen revealed gliosarcoma, with a glial component resembling pleomorphic xanthoastrocytoma. (bvsalud.org)
- Pathological analysis of the first tumor removal specimen identified gliosarcoma, with a glial component characterized by large tumor cells. (bvsalud.org)
- Variants of the tumor include gliosarcoma, multifocal GBM, or gliomatosis cerebri (in which the entire brain may be infiltrated with tumor cells). (medscape.com)
Glioblastoma multiforme2
- This phase II clinical trial studies how well ERC1671 plus Granulocyte-macrophage colony-stimulating factor (GM-CSF) plus Cyclophosphamide with Bevacizumab works compared to Placebo Injection plus Placebo Pill with Bevacizumab in treating patients with recurrent/progressive, bevacizumab naïve glioblastoma multiforme and gliosarcoma (World Health Organization (WHO) grade IV malignant gliomas, GBM). (uci.edu)
- It is also called as Glioblastoma multiforme, it has variants of giant cell Glioblastoma and gliosarcoma found in cerebral hemisphere of brain. (pharmiweb.com)
Malignant2
- Gliosarcoma is a malignant cancer, and is defined as a glioblastoma consisting of gliomatous and sarcomatous components. (wikipedia.org)
- An alternative view that has recently gained support suggests that both gliosarcoma components have a monoclonal origin, with the sarcomatous component deriving from abnormal differentiation of malignant gliomal mesenchyma. (wikipedia.org)
Extracranial metastases1
- Most gliosarcoma extracranial metastases are found in the lung and liver, but there have been reports of metastases elsewhere as well, including evidence of intramedullary metastases to the cervical spine. (wikipedia.org)
Genetic3
- Other scientists then noted that both gliosarcoma components had similar genetic changes and chromosomal abnormalities of the kind often seen in GBM. (wikipedia.org)
- Despite their bi-phasic histology, genetic analyses of adult gliosarcoma cases suggest not only a molecular profile similar to glioblastoma, but also a monoclonal histogenesis for the glial and sarcomatous elements. (touchoncology.com)
- It is essential to continue histopathological evaluation of glial components, and further genetic evaluation on gliosarcoma is required. (bvsalud.org)
Glial2
- Because of a lack of specific and clear diagnostic criteria, the word "gliosarcoma" was frequently used to refer to glial tumours with mesenchymal properties, such as the ability to make collagen and reticulin. (wikipedia.org)
- Gliosarcoma is characterized by the presence of alternating lesions of glial and mesenchymal components. (bvsalud.org)
Temozolomide1
- This phase 1/2 study measured if vorinostat, given with isotretinoin and temozolomide, helped to control glioblastoma or gliosarcoma. (cancer.gov)
Patients1
- Resection (all patients): Patients undergo maximal resection (en bloc, if feasible) followed by placement of 2-3 peritumoral catheters (4 days after completion of pre-resection infusion for the initial cohorts of patients and at study entry for subsequent cohorts of patients). (knowcancer.com)
Brain cancer2
- Tony was diagnosed with a grade 4 Gliosarcoma (brain cancer) in early January 2018. (caringbridge.org)
- The nanoparticles have selective toxicity towards gliosarcoma brain cancer cells," she says. (innovationcampus.com.au)
Cases1
- We here report two cases of gliosarcoma. (bvsalud.org)
Rare1
- Gliosarcoma is a rare histopathological subtype of glioblastoma. (bvsalud.org)
Study1
- The pathways and copy number alterations detected in this study may represent key drivers in gliosarcoma oncogenesis and may provide a starting point toward targeted oncologic analysis with therapeutic potential. (bvsalud.org)
Glioblastoma7
- Gliosarcoma is a malignant cancer, and is defined as a glioblastoma consisting of gliomatous and sarcomatous components. (wikipedia.org)
- Primary gliosarcoma (PGS) is classified as a grade IV tumor and a subtype of glioblastoma multiforme in the 2007 World Health Organization classification system (GBM). (wikipedia.org)
- Gliosarcoma is a rare variant of glioblastoma that arises most frequently as a primary tumor, and has equal or worse survival and an increased propensity for extracranial metastases compared with other Grade 4 gliomas. (nih.gov)
- Patients must have pathologic diagnosis of anaplastic astrocytoma defined as WHO grade III or glioblastoma/gliosarcoma, WHO grade IV, which are confirmed by NCI Laboratory of Pathology. (nih.gov)
- Gliosarcoma is a variant of glioblastoma multiforme, which is characterized by the presence of both glial and mesenchymal components. (bvsalud.org)
- Besides these common features, several well-recognized histological subtypes include giant cell glioblastoma, granular cell glioblastoma, gliosarcoma, glioblastoma with a primitive neuronal component, small cell glioblastoma, and epithelioid glioblastoma. (wustl.edu)
- Demographic, radiographic, molecular and clinical characteristics of primary gliosarcoma and differences to glioblastoma. (cdc.gov)
Tumors1
- Has anyone heard of DORMANT TUMORS which are tiny - our understanding is that both GBM and GLIOSARCOMA comes back with a vengeance and it grows to 20 mm size in a very short period (three months). (cancer.org)
Sarcomatous component2
- An alternative view that has recently gained support suggests that both gliosarcoma components have a monoclonal origin, with the sarcomatous component deriving from abnormal differentiation of malignant gliomal mesenchyma. (wikipedia.org)
- 18. Gliosarcoma cerebri with a myxoid matrix of the sarcomatous component. (nih.gov)
Astrocytoma1
- 8. Transformation of intracranial anaplastic astrocytoma associated with neurofibromatosis type I into gliosarcoma: case report. (nih.gov)
Giant2
Metastases2
- Most gliosarcoma extracranial metastases are found in the lung and liver, but there have been reports of metastases elsewhere as well, including evidence of intramedullary metastases to the cervical spine. (wikipedia.org)
- 16. [Multiple gliosarcoma metastases in the cauda equina roots]. (nih.gov)
Differentiation5
- 5. Immunohistochemistry of gliosarcoma with liposarcomatous differentiation. (nih.gov)
- 10. Cytopatholologic features of gliosarcoma with areas of primitive neuroepithelial differentiation of the brain in squash smears. (nih.gov)
- 13. Gliosarcoma with ependymal and PNET-like differentiation. (nih.gov)
- 15. Gliosarcoma with primitive neuroectodermal, osseous, cartilage and adipocyte differentiation: a case report. (nih.gov)
- 20. Gliosarcoma with chondroid and osseous differentiation. (nih.gov)
Primary1
- The authors present the case of a primary gliosarcoma with an isocitrate dehydrogenase-1 (IDH1) mutation. (nih.gov)
Disease1
- 19. [Gliosarcoma associated with von Recklinghausen's disease: a case report]. (nih.gov)
Radiation2
Case report1
- 2. [Gliosarcoma--a case report]. (nih.gov)
Review of the literature1
- 1. Infantile gliosarcoma: a case and a review of the literature. (nih.gov)
Report1
- 4. Gliosarcoma with chondroblastic osteosarcomatous differentation: report of two case with clinicopathologic and immunohistochemical features. (nih.gov)