Neuroblastoma
Ganglioneuroma
Tumor Cells, Cultured
Oncogene Proteins
3-Iodobenzylguanidine
Genes, myc
Ganglioneuroblastoma
Vanilmandelic Acid
Esthesioneuroblastoma, Olfactory
Gene Amplification
Abdominal Neoplasms
Nervous System Neoplasms
Gangliosides
Apoptosis
Gene Expression Regulation, Neoplastic
Bone Marrow Neoplasms
Tretinoin
Cell Differentiation
Neurons
Iodobenzenes
Hybrid Cells
Cell Survival
Proto-Oncogene Proteins c-myc
Nuclear Proteins
Neuroectodermal Tumors, Primitive, Peripheral
Chromosomes, Human, Pair 1
Neurites
RNA, Messenger
Transfection
Mice, Nude
Brain Neoplasms
Neoplasm Staging
Fenretinide
Reverse Transcriptase Polymerase Chain Reaction
Blotting, Western
Homovanillic Acid
Prognosis
Isotretinoin
Sympathetic Nervous System
Induced Pluripotent Stem Cells
Glycopeptides from the surgace of human neuroblastoma cells. (1/5127)
Glycopeptides suggesting a complex oligosaccharide composition are present on the surface of cells from human neuroblastoma tumors and several cell lines derived from the tumors. The glycopeptides, labeled with radioactive L-fucose, were removed from the cell surface with trypsin, digested with Pronase, and examined by chromatography on Sephadex G-50. Human skin fibroblasts, brain cells, and a fibroblast line derived from neuroblastoma tumor tissue show less complex glycopeptides. Although some differences exist between the cell lines and the primary tumor cells, the similarities between these human tumors and animal tumors examined previously are striking. (+info)Expression of the naturally occurring truncated trkB neurotrophin receptor induces outgrowth of filopodia and processes in neuroblastoma cells. (2/5127)
We have investigated the effects of the truncated trkB receptor isoform T1 (trkB.T1) by transient transfection into mouse N2a neuroblastoma cells. We observed that expression of trkB.T1 leads to a striking change in cell morphology characterized by outgrowth of filopodia and processes. A similar morphological response was also observed in SH-SY5Y human neuroblastoma cells and NIH3T3 fibroblasts transfected with trkB.T1. N2a cells lack endogenous expression of trkB isoforms, but express barely detectable amounts of its ligands, brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT-4). The morphological change was ligand-independent, since addition of exogenous BDNF or NT-4 or blockade of endogenous trkB ligands did not influence this response. Filopodia and process outgrowth was significantly suppressed when full-length trkB.TK+ was cotransfected together with trkB.T1 and this inhibitory effect was blocked by tyrosine kinase inhibitor K252a. Transfection of trkB.T1 deletion mutants showed that the morphological response is dependent on the extracellular, but not the intracellular domain of the receptor. Our results suggest a novel ligand-independent role for truncated trkB in the regulation of cellular morphology. (+info)p73 at chromosome 1p36.3 is lost in advanced stage neuroblastoma but its mutation is infrequent. (3/5127)
p73, a novel p53 family member, is a recently identified candidate neuroblastoma (NBL) suppressor gene mapped at chromosome 1p36.33 and was found to inhibit growth and induce apoptosis in cell lines. To test the hypothesis that p73 is a NBL suppressor gene, we analysed the p73 gene in primary human NBLs. Loss of heterozygosity (LOH) for p73 was observed in 19% (28/151) of informative cases which included 92 mass-screening (MS) tumors. The high frequency of p73 LOH was significantly associated with sporadic NBLs (9% vs 34%, P<0.001), N-myc amplification (10% vs 71%, P<0.001), and advanced stage (14% vs 28%, P<0.05). Both p73alpha and p73beta transcripts were detectable in only 46 of 134 (34%) NBLs at low levels by RT-PCR methods, while they were easily detectable in most breast cancers and colorectal cancers under the same conditions. They found no correlation between p73 LOH and its expression levels (P>0.1). We found two mutations out of 140 NBLs, one somatic and one germline, which result in amino acid substitutions in the C-terminal region of p73 which may affect transactivation functions, though, in the same tumor samples, no mutation of the p53 gene was observed as reported previously. These results suggest that allelic loss of the p73 gene may be a later event in NBL tumorigenesis. However, p73 is infrequently mutated in primary NBLs and may hardly function as a tumor suppressor in a classic Knudson's manner. (+info)Cadmium-mediated activation of the metal response element in human neuroblastoma cells lacking functional metal response element-binding transcription factor-1. (4/5127)
Metal response element-binding transcription factor-1 (MTF-1) binds specifically to metal response elements (MREs) and transactivates metallothionein (MT) gene expression in response to zinc and cadmium. This investigation contrasts the mechanism of mouse MT gene (mMT-I) promoter activation by cadmium and zinc in IMR-32 human neuroblastoma cells to determine whether MTF-1 binding to the MRE is necessary for activation by these metals. Cadmium activated a mMT-1 promoter (-150 base pairs) luciferase reporter 20-25-fold through a MRE-dependent mechanism. In contrast, zinc had little effect on the mMT-1 luciferase reporter. IMR-32 cells lacked MRE binding activity, and treatment with zinc in vitro or in vivo did not generate a MTF-1. MRE complex, suggesting that IMR-32 cells lack functional MTF-1. Overexpression of mMTF-1 regenerated a zinc-mediated induction of the MRE without affecting cadmium activation. Because no other transition metals tested activated the MRE, this effect appeared to be cadmium-specific. These data demonstrate that in IMR-32 human neuroblastoma cells, zinc and cadmium can use independent mechanisms for activation of the mMT-I promoter and cadmium-mediated MRE activation is independent of MTF-1 and zinc. (+info)Inhibition of angiogenesis induces chromaffin differentiation and apoptosis in neuroblastoma. (5/5127)
Inhibition of angiogenesis has been shown to reduce tumor growth, metastasis, and tumor microvascular density in experimental models. To these effects we would now like to add induction of differentiation, based on biological analysis of xenografted human neuroblastoma (SH-SY5Y, WAG rnu/rnu) treated with the angiogenesis inhibitor TNP-470. Treatment with TNP-470 (10 mg/kg s.c., n = 15) reduced the tumor growth by 66% and stereological vascular parameters (Lv, Vv, Sv) by 36-45%. The tumor cell apoptotic fraction increased more than threefold, resulting in a decrease in viable tumor cells by 33%. In contrast, the mean vascular diameter (29 microm) and the mean tumor cell proliferative index (49%) were unaffected. TNP-470-treated tumors exhibited striking chromaffin differentiation of neuroblastoma cells, observed as increased expression of insulin-like growth factor II gene (+88%), tyrosine hydroxylase (+96%), chromogranin A, and cellular processes. Statistical analysis revealed an inverse correlation between differentiation and angiogenesis. It is suggested that by inhibiting angiogenesis, TNP-470 induces metabolic stress, resulting in chromaffin differentiation and apoptosis in neuroblastoma. Such agonal differentiation may be the link between angiostatic therapy and tumor cell apoptosis. (+info)Binding partners for the myelin-associated glycoprotein of N2A neuroblastoma cells. (6/5127)
The myelin-associated glycoprotein (MAG) has been proposed to be important for the integrity of myelinated axons. For a better understanding of the interactions involved in the binding of MAG to neuronal axons, we performed this study to identify the binding partners for MAG on neuronal cells. Experiments with glycosylation inhibitors revealed that sialylated N-glycans of glycoproteins represent the major binding sites for MAG on the neuroblastoma cell line N2A. From extracts of [3H]glucosamine-labelled N2A cells several glycoproteins with molecular weights between 20 and 230 kDa were affinity-precipitated using immobilised MAG. The interactions of these proteins with MAG were sialic acid-dependent and specific for MAG. (+info)Comparison of two in vitro activation systems for protoxicant organophosphorous esterase inhibitors. (7/5127)
In order to perform in vitro testing of esterase inhibition caused by organophosphorous (OP) protoxicants, simple, reliable methods are needed to convert protoxicants to their esterase-inhibiting forms. Incubation of parathion or chlorpyrifos with 0.05% bromine solution or uninduced rat liver microsomes (RLM) resulted in production of the corresponding oxygen analogs of these OP compounds and markedly increased esterase inhibition in SH-SY5Y human neuroblastoma cells. Neither activation system affected cell viability or the activity of AChE or NTE in the absence of OP compounds. Although parathion and chlorpyrifos were activated by RLM, bromine activation required fewer steps and produced more esterase inhibition for a given concentration of chlorpyrifos. However, RLM activation of OP protoxicants produced metabolites other than oxygen analogs and may, therefore, be more relevant as a surrogate for OP biotransformation in vivo. This methodology makes the use of intact cells for in vitro testing of esterase inhibition caused by protoxicant organophosphate compounds a viable alternative to in vivo tests. (+info)MycN sensitizes neuroblastoma cells for drug-induced apoptosis. (8/5127)
Amplification of the MYCN gene is found in a large proportion of neuroblastoma and considered as an adverse prognostic factor. To investigate the effect of ectopic MycN expression on the susceptibility of neuroblastoma cells to cytotoxic drugs we used a human neuroblastoma cell line harboring tetracycline-controlled expression of MycN. Neither conditional expression of MycN alone nor low drug concentrations triggered apoptosis. However, when acting in concert, MycN and cytotoxic drugs efficiently induced cell death. Apoptosis depended on mitochondrial permeability transition and activation of caspases, since the mitochondrion-specific inhibitor bongkrekic acid and the caspase inhibitor zVAD-fmk almost completely abrogated apoptosis. Loss of mitochondrial transmembrane potential and release of cytochrome c from mitochondria preceded activation of caspase-8 and caspase-3 and cleavage of PARP. CD95 expression was upregulated by treatment with cytotoxic drugs, while MycN cooperated with cytotoxic drugs to increase sensitivity to CD95-induced apoptosis and enhancing CD95-L expression. MycN overexpression and cytotoxic drugs also synergized to induce p53 and Bax protein expression, while Bcl-2 and Bcl-X(L) protein levels remained unchanged. Since amplification of MYCN is usually associated with a poor prognosis, these findings suggest that dysfunctions in apoptosis pathways may be a mechanism by which MycN-induced apoptosis of neuroblastoma cells is inhibited. (+info)Neuroblastoma is defined as a type of cancer that develops from immature nerve cells found in the fetal or early postnatal period, called neuroblasts. It typically occurs in infants and young children, with around 90% of cases diagnosed before age five. The tumors often originate in the adrenal glands but can also arise in the neck, chest, abdomen, or spine. Neuroblastoma is characterized by its ability to spread (metastasize) to other parts of the body, including bones, bone marrow, lymph nodes, and skin. The severity and prognosis of neuroblastoma can vary widely, depending on factors such as the patient's age at diagnosis, stage of the disease, and specific genetic features of the tumor.
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.
A ganglioneuroma is a type of benign (noncancerous) tumor that arises from the nerve cells called ganglia in the autonomic nervous system. These tumors typically develop in the abdomen or chest and are most commonly found in children and adolescents, although they can occur at any age.
Ganglioneuromas are composed of mature nerve cells (ganglion cells) and supporting tissue called stroma. They tend to grow slowly and usually do not cause any symptoms unless they become very large or press on nearby organs. In some cases, ganglioneuromas may produce hormones that can cause symptoms such as diarrhea, flushing, or heart palpitations.
While ganglioneuromas are generally benign, there is a small risk that they may become malignant (cancerous) and develop into a type of tumor called a ganglioneuroblastoma or neuroblastoma. For this reason, it is important to monitor these tumors closely and remove them if they grow too large or cause symptoms.
Treatment for ganglioneuromas typically involves surgical removal of the tumor. In some cases, radiation therapy or chemotherapy may also be recommended, particularly if there is a risk of malignant transformation.
'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.
Oncogene proteins are derived from oncogenes, which are genes that have the potential to cause cancer. Normally, these genes help regulate cell growth and division, but when they become altered or mutated, they can become overactive and lead to uncontrolled cell growth and division, which is a hallmark of cancer. Oncogene proteins can contribute to tumor formation and progression by promoting processes such as cell proliferation, survival, angiogenesis, and metastasis. Examples of oncogene proteins include HER2/neu, EGFR, and BCR-ABL.
3-Iodobenzylguanidine (3-IBG) is a radioactive tracer drug that is used in nuclear medicine to help diagnose and evaluate pheochromocytomas and paragangliomas, which are rare tumors of the adrenal glands or nearby nerve tissue. It works by accumulating in the cells of these tumors, allowing them to be detected through imaging techniques such as single-photon emission computed tomography (SPECT) scans.
The drug contains a radioactive isotope of iodine (I-123 or I-131) that emits gamma rays, which can be detected by a gamma camera during the imaging procedure. The 3-IBG molecule also includes a guanidine group, which selectively binds to the norepinephrine transporter (NET) on the surface of the tumor cells, allowing the drug to accumulate within the tumor tissue.
It is important to note that the use of 3-IBG should be under the supervision of a qualified healthcare professional, as it involves exposure to radiation and may have potential side effects.
I'm sorry for any confusion, but "Genes, myc" is not a recognized medical term or abbreviation. It seems like there might be a misunderstanding or a missing word in the request. "Myc" could refer to the Myc family of transcription factors that are involved in cell growth and division, and are often deregulated in cancer. However, without more context, it's difficult to provide an accurate definition. If you could provide more information or clarify your question, I would be happy to help further!
Ganglioneuroblastoma is a rare tumor that arises from the neural crest cells, which are immature cells in the sympathetic nervous system. It typically occurs in children who are younger than 10 years old, with most diagnoses occurring within the first year of life. The tumor can develop anywhere along the sympathetic nervous system but is most commonly found in the adrenal glands (small glands located on top of each kidney) or along the spine.
Ganglioneuroblastoma is a type of neuroblastoma, which is a broader category of tumors that also arise from neural crest cells. Ganglioneuroblastomas are unique within this group because they have a mix of both mature and immature cells. The presence of these more mature cells can make ganglioneuroblastomas less aggressive than other neuroblastomas, although the behavior of the tumor can vary widely depending on factors such as its size, location, and whether it has spread to other parts of the body (metastasized).
Treatment for ganglioneuroblastoma typically involves a combination of surgery, chemotherapy, and radiation therapy. The specific approach will depend on various factors, including the patient's age, overall health, and the stage and aggressiveness of the tumor. With appropriate treatment, many children with ganglioneuroblastoma can achieve long-term survival and even cure.
Vanilmandelic acid (VMA) is a metabolite produced in the body as a result of the breakdown of catecholamines, which are hormones such as dopamine, norepinephrine, and epinephrine. Specifically, VMA is the major end product of epinephrine and norepinephrine metabolism.
In clinical medicine, measurement of VMA in urine is often used as a diagnostic test for pheochromocytoma, a rare tumor that arises from the chromaffin cells of the adrenal gland and can cause excessive production of catecholamines. Elevated levels of VMA in the urine may indicate the presence of a pheochromocytoma or other conditions associated with increased catecholamine secretion, such as neuroblastoma or ganglioneuroma.
It's important to note that while VMA is a useful diagnostic marker for pheochromocytoma and related conditions, it is not specific to these disorders and can be elevated in other medical conditions as well. Therefore, the test should be interpreted in conjunction with other clinical findings and diagnostic tests.
Esthesioneuroblastoma, also known as olfactory neuroblastoma, is a rare type of malignant tumor that develops in the upper part of the nasal cavity, near the area responsible for the sense of smell (olfaction). It arises from the olfactory nerve cells and typically affects adults between 20 to 50 years old, although it can occur at any age.
Esthesioneuroblastomas are characterized by their aggressive growth and potential to spread to other parts of the head and neck, as well as distant organs such as the lungs, bones, and bone marrow. Symptoms may include nasal congestion, nosebleeds, loss of smell, facial pain or numbness, bulging eyes, and visual disturbances.
Diagnosis is usually made through a combination of clinical examination, imaging studies (such as MRI or CT scans), and biopsy. Treatment typically involves surgical resection of the tumor, followed by radiation therapy and/or chemotherapy to reduce the risk of recurrence. Regular follow-up care is essential due to the possibility of late relapse.
Overall, prognosis varies depending on factors such as the stage of the disease at diagnosis, the patient's age, and the effectiveness of treatment. While some individuals may experience long-term survival or even cure, others may face more aggressive tumor behavior and a higher risk of recurrence.
Gene amplification is a process in molecular biology where a specific gene or set of genes are copied multiple times, leading to an increased number of copies of that gene within the genome. This can occur naturally in cells as a response to various stimuli, such as stress or exposure to certain chemicals, but it can also be induced artificially through laboratory techniques for research purposes.
In cancer biology, gene amplification is often associated with tumor development and progression, where the amplified genes can contribute to increased cell growth, survival, and drug resistance. For example, the overamplification of the HER2/neu gene in breast cancer has been linked to more aggressive tumors and poorer patient outcomes.
In diagnostic and research settings, gene amplification techniques like polymerase chain reaction (PCR) are commonly used to detect and analyze specific genes or genetic sequences of interest. These methods allow researchers to quickly and efficiently generate many copies of a particular DNA sequence, facilitating downstream analysis and detection of low-abundance targets.
Abdominal neoplasms refer to abnormal growths or tumors in the abdomen that can be benign (non-cancerous) or malignant (cancerous). These growths can occur in any of the organs within the abdominal cavity, including the stomach, small intestine, large intestine, liver, pancreas, spleen, and kidneys.
Abdominal neoplasms can cause various symptoms depending on their size, location, and type. Some common symptoms include abdominal pain or discomfort, bloating, changes in bowel habits, unexplained weight loss, fatigue, and fever. In some cases, abdominal neoplasms may not cause any symptoms until they have grown quite large or spread to other parts of the body.
The diagnosis of abdominal neoplasms typically involves a combination of physical exam, medical history, imaging studies such as CT scans or MRIs, and sometimes biopsy to confirm the type of tumor. Treatment options depend on the type, stage, and location of the neoplasm but may include surgery, radiation therapy, chemotherapy, targeted therapy, or a combination of these approaches.
Nervous system neoplasms are abnormal growths or tumors that occur within the nervous system, which includes the brain, spinal cord, and peripheral nerves. These tumors can be benign (non-cancerous) or malignant (cancerous), and their growth can compress or infiltrate surrounding tissues, leading to various neurological symptoms. The causes of nervous system neoplasms are not fully understood but may involve genetic factors, exposure to certain chemicals or radiation, and certain viral infections. Treatment options depend on the type, location, and size of the tumor and can include surgery, radiation therapy, chemotherapy, or a combination of these approaches.
Gangliosides are a type of complex lipid molecule known as sialic acid-containing glycosphingolipids. They are predominantly found in the outer leaflet of the cell membrane, particularly in the nervous system. Gangliosides play crucial roles in various biological processes, including cell recognition, signal transduction, and cell adhesion. They are especially abundant in the ganglia (nerve cell clusters) of the peripheral and central nervous systems, hence their name.
Gangliosides consist of a hydrophobic ceramide portion and a hydrophilic oligosaccharide chain that contains one or more sialic acid residues. The composition and structure of these oligosaccharide chains can vary significantly among different gangliosides, leading to the classification of various subtypes, such as GM1, GD1a, GD1b, GT1b, and GQ1b.
Abnormalities in ganglioside metabolism or expression have been implicated in several neurological disorders, including Parkinson's disease, Alzheimer's disease, and various lysosomal storage diseases like Tay-Sachs and Gaucher's diseases. Additionally, certain bacterial toxins, such as botulinum neurotoxin and tetanus toxin, target gangliosides to gain entry into neuronal cells, causing their toxic effects.
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).
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.
Bone marrow neoplasms are a type of cancer that originates in the bone marrow, which is the spongy tissue inside bones where blood cells are produced. These neoplasms can be divided into two main categories: hematologic (or liquid) malignancies and solid tumors.
Hematologic malignancies include leukemias, lymphomas, and multiple myeloma. Leukemias are cancers of the white blood cells, which normally fight infections. In leukemia, the bone marrow produces abnormal white blood cells that do not function properly, leading to an increased risk of infection, anemia, and bleeding.
Lymphomas are cancers of the lymphatic system, which helps to fight infections and remove waste from the body. Lymphoma can affect the lymph nodes, spleen, thymus gland, and bone marrow. There are two main types of lymphoma: Hodgkin's lymphoma and non-Hodgkin's lymphoma.
Multiple myeloma is a cancer of the plasma cells, which are a type of white blood cell that produces antibodies to help fight infections. In multiple myeloma, abnormal plasma cells accumulate in the bone marrow and produce large amounts of abnormal antibodies, leading to bone damage, anemia, and an increased risk of infection.
Solid tumors of the bone marrow are rare and include conditions such as chordomas, Ewing sarcomas, and osteosarcomas. These cancers originate in the bones themselves or in other tissues that support the bones, but they can also spread to the bone marrow.
Treatment for bone marrow neoplasms depends on the type and stage of cancer, as well as the patient's overall health. Treatment options may include chemotherapy, radiation therapy, stem cell transplantation, targeted therapy, or a combination of these approaches.
Adrenal gland neoplasms refer to abnormal growths or tumors in the adrenal glands. These glands are located on top of each kidney and are responsible for producing hormones that regulate various bodily functions such as metabolism, blood pressure, and stress response. Adrenal gland neoplasms can be benign (non-cancerous) or malignant (cancerous).
Benign adrenal tumors are called adenomas and are usually small and asymptomatic. However, some adenomas may produce excessive amounts of hormones, leading to symptoms such as high blood pressure, weight gain, and mood changes.
Malignant adrenal tumors are called adrenocortical carcinomas and are rare but aggressive cancers that can spread to other parts of the body. Symptoms of adrenocortical carcinoma may include abdominal pain, weight loss, and hormonal imbalances.
It is important to diagnose and treat adrenal gland neoplasms early to prevent complications and improve outcomes. Diagnostic tests may include imaging studies such as CT scans or MRIs, as well as hormone level testing and biopsy. Treatment options may include surgery, radiation therapy, chemotherapy, or a combination of these approaches.
Tretinoin is a form of vitamin A that is used in the treatment of acne vulgaris, fine wrinkles, and dark spots caused by aging or sun damage. It works by increasing the turnover of skin cells, helping to unclog pores and promote the growth of new skin cells. Tretinoin is available as a cream, gel, or liquid, and is usually applied to the affected area once a day in the evening. Common side effects include redness, dryness, and peeling of the skin. It is important to avoid sunlight and use sunscreen while using tretinoin, as it can make the skin more sensitive to the sun.
Cell differentiation is the process by which a less specialized cell, or stem cell, becomes a more specialized cell type with specific functions and structures. This process involves changes in gene expression, which are regulated by various intracellular signaling pathways and transcription factors. Differentiation results in the development of distinct cell types that make up tissues and organs in multicellular organisms. It is a crucial aspect of embryonic development, tissue repair, and maintenance of homeostasis in the body.
Neurons, also known as nerve cells or neurocytes, are specialized cells that constitute the basic unit of the nervous system. They are responsible for receiving, processing, and transmitting information and signals within the body. Neurons have three main parts: the dendrites, the cell body (soma), and the axon. The dendrites receive signals from other neurons or sensory receptors, while the axon transmits these signals to other neurons, muscles, or glands. The junction between two neurons is called a synapse, where neurotransmitters are released to transmit the signal across the gap (synaptic cleft) to the next neuron. Neurons vary in size, shape, and structure depending on their function and location within the nervous system.
Iodobenzenes are organic compounds that contain a iodine atom (I) attached to a benzene ring. The general formula for iodobenzenes is C6H5I. They can be considered as aryl halides and can undergo various chemical reactions such as nucleophilic substitution, electrophilic aromatic substitution, and reduction. Iodobenzenes are less reactive than other aryl halides due to the larger size and lower electronegativity of iodine compared to other halogens. They are used in organic synthesis as building blocks or reagents for various chemical transformations.
A cell line is a culture of cells that are grown in a laboratory for use in research. These cells are usually taken from a single cell or group of cells, and they are able to divide and grow continuously in the lab. Cell lines can come from many different sources, including animals, plants, and humans. They are often used in scientific research to study cellular processes, disease mechanisms, and to test new drugs or treatments. Some common types of human cell lines include HeLa cells (which come from a cancer patient named Henrietta Lacks), HEK293 cells (which come from embryonic kidney cells), and HUVEC cells (which come from umbilical vein endothelial cells). It is important to note that cell lines are not the same as primary cells, which are cells that are taken directly from a living organism and have not been grown in the lab.
I'm sorry for any confusion, but "hybrid cells" is not a standard medical term with a widely accepted or specific definition in the field of medicine. The term "hybrid" is used in various scientific and medical contexts to describe combinations or mixtures of different elements, such as hybridoma cells (a type of fusion cell used in research, created by combining a B cell and a tumor cell) or hybridization (in genetics, the process of combining DNA from two different sources).
Without more specific context, it's difficult to provide an accurate medical definition for "hybrid cells." If you could provide more information about the context in which this term was used, I would be happy to help you further!
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.
Proto-oncogene proteins, such as c-Myc, are crucial regulators of normal cell growth, differentiation, and apoptosis (programmed cell death). When proto-oncogenes undergo mutations or alterations in their regulation, they can become overactive or overexpressed, leading to the formation of oncogenes. Oncogenic forms of c-Myc contribute to uncontrolled cell growth and division, which can ultimately result in cancer development.
The c-Myc protein is a transcription factor that binds to specific DNA sequences, influencing the expression of target genes involved in various cellular processes, such as:
1. Cell cycle progression: c-Myc promotes the expression of genes required for the G1 to S phase transition, driving cells into the DNA synthesis and division phase.
2. Metabolism: c-Myc regulates genes associated with glucose metabolism, glycolysis, and mitochondrial function, enhancing energy production in rapidly dividing cells.
3. Apoptosis: c-Myc can either promote or inhibit apoptosis, depending on the cellular context and the presence of other regulatory factors.
4. Differentiation: c-Myc generally inhibits differentiation by repressing genes that are necessary for specialized cell functions.
5. Angiogenesis: c-Myc can induce the expression of pro-angiogenic factors, promoting the formation of new blood vessels to support tumor growth.
Dysregulation of c-Myc is frequently observed in various types of cancer, making it an important therapeutic target for cancer treatment.
Nuclear proteins are a category of proteins that are primarily found in the nucleus of a eukaryotic cell. They play crucial roles in various nuclear functions, such as DNA replication, transcription, repair, and RNA processing. This group includes structural proteins like lamins, which form the nuclear lamina, and regulatory proteins, such as histones and transcription factors, that are involved in gene expression. Nuclear localization signals (NLS) often help target these proteins to the nucleus by interacting with importin proteins during active transport across the nuclear membrane.
Neuroectodermal tumors, primitive, peripheral (PNET) are a group of rare and aggressive malignancies that primarily affect children and young adults. These tumors arise from the primitive neuroectodermal cells, which are the precursors to the nervous system. PNETs can occur in various locations throughout the body, but when they occur outside the central nervous system (CNS), they are referred to as peripheral PNETs (pPNETs).
Peripheral PNETs are similar to Ewing sarcoma, another type of small, round blue cell tumor that arises from primitive neuroectodermal cells. In fact, some researchers consider pPNETs and Ewing sarcomas to be part of the same disease spectrum, known as the Ewing family of tumors (EFT).
Peripheral PNETs can occur in any part of the body, but they most commonly affect the bones and soft tissues of the trunk, extremities, and head and neck region. The symptoms of pPNET depend on the location and size of the tumor, but they may include pain, swelling, decreased mobility, and systemic symptoms such as fever and weight loss.
The diagnosis of pPNET typically involves a combination of imaging studies (such as MRI or CT scans), biopsy, and molecular testing. The treatment usually involves a multimodal approach that includes surgery, chemotherapy, and radiation therapy. Despite aggressive treatment, the prognosis for patients with pPNET remains poor, with a five-year survival rate of approximately 30%.
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.
Human chromosome pair 1 refers to the first pair of chromosomes in a set of 23 pairs found in the cells of the human body, excluding sex cells (sperm and eggs). Each cell in the human body, except for the gametes, contains 46 chromosomes arranged in 23 pairs. These chromosomes are rod-shaped structures that contain genetic information in the form of DNA.
Chromosome pair 1 is the largest pair, making up about 8% of the total DNA in a cell. Each chromosome in the pair consists of two arms - a shorter p arm and a longer q arm - connected at a centromere. Chromosome 1 carries an estimated 2,000-2,500 genes, which are segments of DNA that contain instructions for making proteins or regulating gene expression.
Defects or mutations in the genes located on chromosome 1 can lead to various genetic disorders and diseases, such as Charcot-Marie-Tooth disease type 1A, Huntington's disease, and certain types of cancer.
Neurites are extensions of a neuron (a type of cell in the nervous system) that can be either an axon or a dendrite. An axon is a thin, cable-like extension that carries signals away from the cell body, while a dendrite is a branching extension that receives signals from other neurons. Neurites play a crucial role in the communication between neurons and the formation of neural networks. They are involved in the transmission of electrical and chemical signals, as well as in the growth and development of the nervous system.
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.
Transfection is a term used in molecular biology that refers to the process of deliberately introducing foreign genetic material (DNA, RNA or artificial gene constructs) into cells. This is typically done using chemical or physical methods, such as lipofection or electroporation. Transfection is widely used in research and medical settings for various purposes, including studying gene function, producing proteins, developing gene therapies, and creating genetically modified organisms. It's important to note that transfection is different from transduction, which is the process of introducing genetic material into cells using viruses as vectors.
"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.
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.
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.
Neoplasm staging is a systematic process used in medicine to describe the extent of spread of a cancer, including the size and location of the original (primary) tumor and whether it has metastasized (spread) to other parts of the body. The most widely accepted system for this purpose is the TNM classification system developed by the American Joint Committee on Cancer (AJCC) and the Union for International Cancer Control (UICC).
In this system, T stands for tumor, and it describes the size and extent of the primary tumor. N stands for nodes, and it indicates whether the cancer has spread to nearby lymph nodes. M stands for metastasis, and it shows whether the cancer has spread to distant parts of the body.
Each letter is followed by a number that provides more details about the extent of the disease. For example, a T1N0M0 cancer means that the primary tumor is small and has not spread to nearby lymph nodes or distant sites. The higher the numbers, the more advanced the cancer.
Staging helps doctors determine the most appropriate treatment for each patient and estimate the patient's prognosis. It is an essential tool for communication among members of the healthcare team and for comparing outcomes of treatments in clinical trials.
Fenretinide is a synthetic retinoid, which is a class of compounds related to vitamin A. It is a medication that has been studied in clinical trials for the prevention and treatment of various types of cancer. Fenretinide works by interfering with the way that cancer cells grow and multiply.
Fenretinide has been shown to have anti-cancer effects in laboratory studies, and it has been tested in several clinical trials as a potential cancer treatment. However, the results of these studies have been mixed, and fenretinide is not currently approved by the U.S. Food and Drug Administration (FDA) for the treatment of any type of cancer.
Like other retinoids, fenretinide can cause side effects such as dry skin, dry eyes, and changes in vision. It may also cause more serious side effects, such as liver damage and increased pressure in the brain. Fenretinide should be used with caution and under the close supervision of a healthcare provider.
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.
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.
Homovanillic acid (HVA) is a major metabolite of dopamine, a neurotransmitter in the human body. It is formed in the body when an enzyme called catechol-O-methyltransferase (COMT) breaks down dopamine. HVA can be measured in body fluids such as urine, cerebrospinal fluid, and plasma to assess the activity of dopamine and the integrity of the dopaminergic system. Increased levels of HVA are associated with certain neurological disorders, including Parkinson's disease, while decreased levels may indicate dopamine deficiency or other conditions affecting the nervous system.
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.
Isotretinoin is a derivative of vitamin A, used in the treatment of severe recalcitrant nodular acne that has not responded to other therapies. It is a potent inhibitor of sebaceous gland function and keratinization. Isotretinoin is also known to have anti-inflammatory properties. It is taken orally in the form of capsules and its use requires careful monitoring due to potential teratogenic effects and other side effects, such as dryness of the skin and mucous membranes, mood changes, and liver enzyme abnormalities.
The sympathetic nervous system (SNS) is a part of the autonomic nervous system that operates largely below the level of consciousness, and it functions to produce appropriate physiological responses to perceived danger. It's often associated with the "fight or flight" response. The SNS uses nerve impulses to stimulate target organs, causing them to speed up (e.g., increased heart rate), prepare for action, or otherwise respond to stressful situations.
The sympathetic nervous system is activated due to stressful emotional or physical situations and it prepares the body for immediate actions. It dilates the pupils, increases heart rate and blood pressure, accelerates breathing, and slows down digestion. The primary neurotransmitter involved in this system is norepinephrine (also known as noradrenaline).
Induced Pluripotent Stem Cells (iPSCs) are a type of pluripotent stem cells that are generated from somatic cells, such as skin or blood cells, through the introduction of specific genes encoding transcription factors. These reprogrammed cells exhibit similar characteristics to embryonic stem cells, including the ability to differentiate into any cell type of the three germ layers (endoderm, mesoderm, and ectoderm). The discovery and development of iPSCs have opened up new possibilities in regenerative medicine, drug testing and development, and disease modeling, while avoiding ethical concerns associated with embryonic stem cells.
Pluripotent stem cells are a type of undifferentiated stem cell that have the ability to differentiate into any cell type of the three germ layers (endoderm, mesoderm, and ectoderm) of a developing embryo. These cells can give rise to all the cell types that make up the human body, with the exception of those that form the extra-embryonic tissues such as the placenta.
Pluripotent stem cells are characterized by their ability to self-renew, which means they can divide and produce more pluripotent stem cells, and differentiate, which means they can give rise to specialized cell types with specific functions. Pluripotent stem cells can be derived from embryos at the blastocyst stage of development or generated in the lab through a process called induced pluripotency, where adult cells are reprogrammed to have the properties of embryonic stem cells.
Pluripotent stem cells hold great promise for regenerative medicine and tissue engineering because they can be used to generate large numbers of specific cell types that can potentially replace or repair damaged or diseased tissues in the body. However, their use is still a subject of ethical debate due to concerns about the source of embryonic stem cells and the potential risks associated with their use in clinical applications.