bcl-2-Associated X Protein
Trans-Activators
Hepatitis B virus
Hepatitis B Antigens
Carcinoma, Hepatocellular
Proto-Oncogene Proteins c-bcl-2
Bornaviridae
Hepatocytes
Transcriptional Activation
Hep G2 Cells
Apoptosis
Transfection
Fragile X Mental Retardation Protein
Hepatitis B Virus, Woodchuck
Gene Expression Regulation, Viral
DNA-Binding Proteins
Hepatitis B
Marmota
Base Sequence
Transcription, Genetic
Molecular Sequence Data
Borna disease virus
Hepadnaviridae
Promoter Regions, Genetic
Chloramphenicol O-Acetyltransferase
Transcription Factors
X Chromosome
Tumor Suppressor Protein p53
Mutation
Protein Binding
Liver
Group X Phospholipases A2
Blotting, Western
Plasmids
RNA, Messenger
Signal Transduction
Viral Regulatory and Accessory Proteins
Tumor Cells, Cultured
NF-kappa B
Virus Replication
Mice, Transgenic
Amino Acid Sequence
Precipitin Tests
Gene Expression Regulation
Mitochondria
Proto-Oncogene Proteins
Genes, bcl-2
Cell Nucleus
Hepatitis B, Chronic
Binding Sites
Reverse Transcriptase Polymerase Chain Reaction
Hepatitis B Core Antigens
Proteasome Endopeptidase Complex
bcl-X Protein
Up-Regulation
Hepatocyte Nuclear Factor 1
Down-Regulation
Nuclear Proteins
RNA, Small Interfering
CARD Signaling Adaptor Proteins
Two-Hybrid System Techniques
Translocation, Genetic
Cell Survival
Gene Expression Regulation, Neoplastic
RNA Interference
Lymphoma, B-Cell
Caspase 3
Caspases
Enhancer Elements, Genetic
Fragile X Syndrome
Chromosomes, Human, Pair 14
Gene Expression
HeLa Cells
Genes, Reporter
Phosphorylation
Hepatocyte Nuclear Factor 1-alpha
Lymphoma, Large B-Cell, Diffuse
Luciferases
BH3 Interacting Domain Death Agonist Protein
Germinal Center
Recombinant Fusion Proteins
DNA, Complementary
Cyclic AMP Response Element-Binding Protein
Chromosomes, Human, Pair 18
Immunohistochemistry
Factor X
Polymerase Chain Reaction
Real-Time Polymerase Chain Reaction
Cloning, Molecular
DNA Primers
Carrier Proteins
Cell Transformation, Neoplastic
Cell Line, Transformed
Cysteine Endopeptidases
Dietary Proteins
Flow Cytometry
Gene Expression Profiling
Cell Cycle
Cells, Cultured
Restriction Mapping
Multienzyme Complexes
Cytoplasm
Protein Structure, Tertiary
Sequence Homology, Amino Acid
Mice, Knockout
Protein-Serine-Threonine Kinases
Simian virus 40
RNA-Binding Proteins
Drosophila Proteins
Mice, Nude
Protein Biosynthesis
Disease Models, Animal
Repetitive Sequences, Nucleic Acid
Enzyme Activation
Models, Biological
Cell Death
Adaptor Proteins, Signal Transducing
Cell Division
Neoplasm Proteins
Lymphoma, Follicular
Repressor Proteins
B-Lymphocytes
Gene Rearrangement
gamma-Globins
In Situ Hybridization, Fluorescence
Retinoid X Receptors
Lymphoma, B-Cell, Marginal Zone
Chromosomes, Human, Pair 3
Myeloid Cell Leukemia Sequence 1 Protein
Genes, Immunoglobulin Heavy Chain
Precursor Cells, B-Lymphoid
Immunoglobulin Heavy Chains
Proto-Oncogenes
Bacteriophage phi X 174
Genes, myc
Reticulocytosis
Cell Differentiation
Precursor Cells, T-Lymphoid
Neprilysin
Leukemia, Lymphocytic, Chronic, B-Cell
Receptors, Purinergic P2
Fetal Hemoglobin
Sperm Midpiece
Tumor Suppressor Proteins
Cyclin D2
Proto-Oncogene Proteins c-myc
Chromosome Breakage
Gene Rearrangement, B-Lymphocyte
Caspases, Effector
Oligonucleotide Array Sequence Analysis
Interferon Regulatory Factors
Chromosomes, Human, Pair 11
Prognosis
Tumor Markers, Biological
Chromosomal Puffs
Immunophenotyping
Factor X Deficiency
Nuclear Receptor Co-Repressor 2
Antibodies, Monoclonal, Murine-Derived
HEK293 Cells
Jurkat Cells
Genes, Immunoglobulin
Gene Rearrangement, B-Lymphocyte, Heavy Chain
Phenotype
delta-Globins
I-kappa B Kinase
Oncogene Proteins, Fusion
Membrane Proteins
Lymphoma, Non-Hodgkin
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
bcl-2 Homologous Antagonist-Killer Protein
beta-Globins
Polymorphism, Single Nucleotide
Oncogenes
Chromatin Immunoprecipitation
Caspase 7
T-Lymphocytes
Zinc Fingers
Receptors, CXCR5
A photodynamic pathway to apoptosis and necrosis induced by dimethyl tetrahydroxyhelianthrone and hypericin in leukaemic cells: possible relevance to photodynamic therapy. (1/4256)
The mechanism of cell death induction by dimethyl tetrahydroxyhelianthrone (DTHe), a new second-generation photodynamic sensitizer, is analysed in human leukaemic cell lines in comparison with the structurally related hypericin. DTHe has a broad range of light spectrum absorption that enables effective utilization of polychromatic light. Photosensitization of HL-60 cells with low doses of DTHe (0.65 microM DTHe and 7.2 J cm(-2) light energy) induced rapid apoptosis of > or =90% of the cells. At doses > or =2 microM, dying cells assumed morphological necrosis with perinucleolar condensation of chromatin in HL-60 and K-562 cell lines. Although nuclear fragmentation that is characteristic to apoptosis was prevented, DNA digestion to oligonucleosomes proceeded unhindered. Such incomplete apoptosis was more prevalent with the related analogue hypericin throughout most doses of photosensitization. Despite hypericin being a stronger photosensitizer, DTHe exhibited advantageous phototoxic properties to tumour cells, initiating apoptosis at concentrations about threefold lower than hypericin. Photosensitization of the cells induced dissociation of the nuclear envelope, releasing lamins into the cytosol. DTHe also differed from hypericin in effects exerted on the nuclear lamina, causing release of an 86-kDa lamin protein into the cytosol that was unique to DTHe. Within the nucleus, nuclear envelope lamin B underwent covalent polymerization, which did not affect apoptotic nuclear fragmentation at low doses of DTHe. At higher doses, polymerization may have been extensive enough to prevent nuclear collapse. Hut-78, CD4+ cells were resistant to the photodynamically activated apoptotic pathway. Beyond the tolerated levels of photodynamic damage, these cells died exclusively via necrosis. Hut-78 cells overexpress Bcl-X(L) as well as a truncated Bcl-X(L)tr isoform that could contribute to the observed resistance to apoptosis. (+info)Microsatellite instability, Epstein-Barr virus, mutation of type II transforming growth factor beta receptor and BAX in gastric carcinomas in Hong Kong Chinese. (2/4256)
Microsatellite instability (MI), the phenotypic manifestation of mismatch repair failure, is found in a proportion of gastric carcinomas. Little is known of the links between MI and Epstein-Barr virus (EBV) status and clinicopathological elements. Examination of genes mutated through the MI mechanism could also be expected to reveal important information on the carcinogenic pathway. Seventy-nine gastric carcinomas (61 EBV negative, 18 EBV positive) from local Hong Kong Chinese population, an intermediate-incidence area, were examined. Eight microsatellite loci, inclusive of the A10 tract of type II transforming growth factor beta receptor (TbetaR-II), were used to evaluate the MI status. MI in the BAX and insulin-like growth factor II receptor (IGF-IIR) genes were also examined. High-level MI (>40% unstable loci) was detected in ten cases (12.7%) and low-level MI (1-40% unstable loci) in three (3.8%). High-level MI was detected in two EBV-associated cases (11%) and the incidence was similar for the EBV-negative cases (13%). The high-level MIs were significantly associated with intestinal-type tumours (P = 0.03) and a more prominent lymphoid infiltrate (P = 0.04). Similar associations were noted in the EBV-positive carcinomas. The high-level MIs were more commonly located in the antrum, whereas the EBV-associated carcinomas were mostly located in body. Thirteen cardia cases were negative for both high-level MI and EBV. All patients aged below 55 were MI negative (P = 0.049). Of the high-level MIs, 80% had mutation in TbetaR-II, 40% in BAX and 0% in IGF-IIR. Of low-level MIs, 33% also had TbetaR-II mutation. These mutations were absent in the MI-negative cases. Of three lymphoepithelioma-like carcinomas, two cases were EBV positive and MI negative, one case was EBV negative but with high-level MI. In conclusion, high-level MIs were present regardless of the EBV status, and were found in a particular clinicopathological subset of gastric carcinoma patient. Inactivation of important growth regulatory genes observed in these carcinomas confirms the importance of MI in carcinogenesis. (+info)Role of hypoxia-induced Bax translocation and cytochrome c release in reoxygenation injury. (3/4256)
We investigated mechanisms of cell death during hypoxia/reoxygenation of cultured kidney cells. During glucose-free hypoxia, cell ATP levels declined steeply resulting in the translocation of Bax from cytosol to mitochondria. Concurrently, there was cytochrome c release and caspase activation. Cells that leaked cytochrome c underwent apoptosis after reoxygenation. ATP depletion induced by a mitochondrial uncoupler resulted in similar alterations even in the presence of oxygen. Moreover, inclusion of glucose during hypoxia prevented protein translocations and reoxygenation injury by maintaining intracellular ATP. Thus, ATP depletion, rather than hypoxia per se, was the cause of protein translocations. Overexpression of Bcl-2 prevented cytochrome c release and reoxygenation injury without ameliorating ATP depletion or Bax translocation. On the other hand, caspase inhibitors did not prevent protein translocations, but inhibited apoptosis during reoxygenation. Nevertheless, they could not confer long-term viability, since mitochondria had been damaged. Omission of glucose during reoxygenation resulted in continued failure of ATP production, and cell death with necrotic morphology. In contrast, cells expressing Bcl-2 had functional mitochondria and remained viable during reoxygenation even without glucose. Therefore, Bax translocation during hypoxia is a molecular trigger for cell death during reoxygenation. If ATP is available during reoxygenation, apoptosis develops; otherwise, death occurs by necrosis. By preserving mitochondrial integrity, BCL-2 prevents both forms of cell death and ensures cell viability. (+info)Apoptosis during breast carcinoma progression. (4/4256)
The purpose of this study was to investigate apoptosis, proliferation, and the expression of apoptosis-influencing proteins bcl-2 and bax and estrogen and progesterone receptors during breast carcinoma progression. The material consisted of 53 paired breast carcinoma samples representing primary and recurrent tumors and 24 control samples. The recurrent sample was located either in the breast scar tissue or at a distant metastatic site. Apoptosis was detected both morphologically and by 3' end labeling of fragmented DNA. Cell proliferation was evaluated immunohistochemically by the MIB index. The expressions of bcl-2, bax, and estrogen and progesterone receptors were studied immunohistochemically. There was a significant increase in the extent of apoptosis and proliferation in recurrent tumors compared to the primary lesions (P = 0.015 and P = 0.038, respectively). In primary tumors with an apoptotic index of >0.50%, the survival of the patients was significantly shorter (P = 0.015). In cases with a significant increase in apoptosis or proliferation in the recurrent tumor, the survival of the patients was significantly shorter (P = 0.009 and P = 0.003, respectively). Of the variables analyzed, bcl-2 expression and a positive estrogen receptor status were significantly associated with a low extent of apoptosis (P = 0.010 and P = 0.042, respectively). Their changes were parallel to the changes in apoptosis during tumor progression, although the associations did not reach statistical significance. The results show that increased apoptosis is associated with a worse prognosis in breast carcinoma. A significant increase in apoptosis in recurrent breast carcinoma lesions predicts a worse clinical outcome. (+info)Expression of apoptosis-related genes in human head and neck squamous cell carcinomas undergoing p53-mediated programmed cell death. (5/4256)
Human head and neck squamous cell carcinoma (HNSCC) lines infected with a replication-defective Ad5CMV-p53 vector bearing a wild-type human p53 gene were used to examine alterations in the production of proteins implicated in regulating apoptosis. Because HNSCC lines express abundant levels of c-myc, and simultaneous expression of c-myc and p53 is known to trigger apoptosis in other cells, cooperation between these two genes was examined. Surprisingly, levels of c-myc mRNA and protein were rapidly and profoundly suppressed after infection with wild-type p53. Suppression of c-myc using antisense oligodeoxynucleotides (in the absence of p53) was sufficient to trigger apoptosis in Tu-138 cells, raising the possibility that the reduction of c-myc may be involved in at least one of the cell death pathways mediated by p53. Expression of a panel of Bcl-2 homology proteins was also examined in HNSCC lines undergoing p53-mediated apoptosis. No changes in Bcl-2, Bak, or Bcl-xS were found after p53 expression. Increased levels of the apoptosis-accelerating protein Bax were found in HNSCC lines after infection with Ad5CMV-p53. Induction of the apoptosis-inhibiting protein Bcl-xL was observed in Tu-167 cells and may account for the delayed onset of apoptosis in these cells. These studies suggest that multiple pathways may regulate apoptosis after transient overexpression of p53. (+info)Long term lithium treatment suppresses p53 and Bax expression but increases Bcl-2 expression. A prominent role in neuroprotection against excitotoxicity. (6/4256)
This study was undertaken to investigate the molecular mechanisms underlying the neuroprotective actions of lithium against glutamate excitotoxicity with a focus on the role of proapoptotic and antiapoptotic genes. Long term, but not acute, treatment of cultured cerebellar granule cells with LiCl induces a concentration-dependent decrease in mRNA and protein levels of proapoptotic p53 and Bax; conversely, mRNA and protein levels of cytoprotective Bcl-2 are remarkably increased. The ratios of Bcl-2/Bax protein levels increase by approximately 5-fold after lithium treatment for 5-7 days. Exposure of cerebellar granule cells to glutamate induces a rapid increase in p53 and Bax mRNA and protein levels with no apparent effect on Bcl-2 expression. Pretreatment with LiCl for 7 days prevents glutamate-induced increase in p53 and Bax expression and maintains Bcl-2 in an elevated state. Glutamate exposure also triggers the release of cytochrome c from the mitochondria into the cytosol. Lithium pretreatment blocks glutamate-induced cytochrome c release and cleavage of lamin B1, a nuclear substrate for caspase-3. These results strongly suggest that lithium-induced Bcl-2 up-regulation and p53 and Bax down-regulation play a prominent role in neuroprotection against excitotoxicity. Our results further suggest that lithium, in addition to its use in the treatment of bipolar depressive illness, may have an expanded use in the intervention of neurodegeneration. (+info)Expression of bcl-2 and bax in glomerular disease. (7/4256)
Bcl-2 may account in part for the maintenance of hypercellularity in human glomerular diseases through preventing cell death and by counteracting bax which may be expressed to regulate excessive proliferation. This process is associated with the effect of PDGF B-chain expression. Bax expression may be important in the cell loss leading to glomerulosclerosis and TGF-beta1 participates in this process by increasing bax expression. Thus, the balance of bcl-2/bax expression may be critical in the course of human glomerular diseases. (+info)MycN sensitizes neuroblastoma cells for drug-induced apoptosis. (8/4256)
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)There are several risk factors for developing HCC, including:
* Cirrhosis, which can be caused by heavy alcohol consumption, viral hepatitis (such as hepatitis B and C), or fatty liver disease
* Family history of liver disease
* Chronic obstructive pulmonary disease (COPD)
* Diabetes
* Obesity
HCC can be challenging to diagnose, as the symptoms are non-specific and can be similar to those of other conditions. However, some common symptoms of HCC include:
* Yellowing of the skin and eyes (jaundice)
* Fatigue
* Loss of appetite
* Abdominal pain or discomfort
* Weight loss
If HCC is suspected, a doctor may perform several tests to confirm the diagnosis, including:
* Imaging tests, such as ultrasound, CT scan, or MRI, to look for tumors in the liver
* Blood tests to check for liver function and detect certain substances that are produced by the liver
* Biopsy, which involves removing a small sample of tissue from the liver to examine under a microscope
Once HCC is diagnosed, treatment options will depend on several factors, including the stage and location of the cancer, the patient's overall health, and their personal preferences. Treatment options may include:
* Surgery to remove the tumor or parts of the liver
* Ablation, which involves destroying the cancer cells using heat or cold
* Chemoembolization, which involves injecting chemotherapy drugs into the hepatic artery to reach the cancer cells
* Targeted therapy, which uses drugs or other substances to target specific molecules that are involved in the growth and spread of the cancer
Overall, the prognosis for HCC is poor, with a 5-year survival rate of approximately 20%. However, early detection and treatment can improve outcomes. It is important for individuals at high risk for HCC to be monitored regularly by a healthcare provider, and to seek medical attention if they experience any symptoms.
Liver neoplasms, also known as liver tumors or hepatic tumors, are abnormal growths of tissue in the liver. These growths can be benign (non-cancerous) or malignant (cancerous). Malignant liver tumors can be primary, meaning they originate in the liver, or metastatic, meaning they spread to the liver from another part of the body.
There are several types of liver neoplasms, including:
1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and arises from the main cells of the liver (hepatocytes). HCC is often associated with cirrhosis and can be caused by viral hepatitis or alcohol abuse.
2. Cholangiocarcinoma: This type of cancer arises from the cells lining the bile ducts within the liver (cholangiocytes). Cholangiocarcinoma is rare and often diagnosed at an advanced stage.
3. Hemangiosarcoma: This is a rare type of cancer that originates in the blood vessels of the liver. It is most commonly seen in dogs but can also occur in humans.
4. Fibromas: These are benign tumors that arise from the connective tissue of the liver (fibrocytes). Fibromas are usually small and do not spread to other parts of the body.
5. Adenomas: These are benign tumors that arise from the glandular cells of the liver (hepatocytes). Adenomas are usually small and do not spread to other parts of the body.
The symptoms of liver neoplasms vary depending on their size, location, and whether they are benign or malignant. Common symptoms include abdominal pain, fatigue, weight loss, and jaundice (yellowing of the skin and eyes). Diagnosis is typically made through a combination of imaging tests such as CT scans, MRI scans, and ultrasound, and a biopsy to confirm the presence of cancer cells.
Treatment options for liver neoplasms depend on the type, size, location, and stage of the tumor, as well as the patient's overall health. Surgery may be an option for some patients with small, localized tumors, while others may require chemotherapy or radiation therapy to shrink the tumor before surgery can be performed. In some cases, liver transplantation may be necessary.
Prognosis for liver neoplasms varies depending on the type and stage of the cancer. In general, early detection and treatment improve the prognosis, while advanced-stage disease is associated with a poorer prognosis.
The symptoms of hepatitis B can range from mild to severe and may include fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, pale stools, joint pain, and jaundice (yellowing of the skin and eyes). In some cases, hepatitis B can be asymptomatic, meaning that individuals may not experience any symptoms at all.
Hepatitis B is diagnosed through blood tests that detect the presence of HBV antigens or antibodies in the body. Treatment for acute hepatitis B typically involves rest, hydration, and medication to manage symptoms, while chronic hepatitis B may require ongoing therapy with antiviral drugs to suppress the virus and prevent liver damage.
Preventive measures for hepatitis B include vaccination, which is recommended for individuals at high risk of infection, such as healthcare workers, sexually active individuals, and those traveling to areas where HBV is common. In addition, safe sex practices, avoiding sharing of needles or other bodily fluids, and proper sterilization of medical equipment can help reduce the risk of transmission.
Overall, hepatitis B is a serious infection that can have long-term consequences for liver health, and it is important to take preventive measures and seek medical attention if symptoms persist or worsen over time.
A persistent infection with the hepatitis B virus (HBV) that can lead to liver cirrhosis and hepatocellular carcinoma. HBV is a bloodborne pathogen and can be spread through contact with infected blood, sexual contact, or vertical transmission from mother to child during childbirth.
Chronic hepatitis B is characterized by the presence of HBsAg in the blood for more than 6 months, indicating that the virus is still present in the liver. The disease can be asymptomatic or symptomatic, with symptoms such as fatigue, malaise, loss of appetite, nausea, vomiting, joint pain, and jaundice.
Chronic hepatitis B is diagnosed through serological tests such as HBsAg, anti-HBc, and HBV DNA. Treatment options include interferon alpha and nucleos(t)ide analogues, which can slow the progression of the disease but do not cure it.
Prevention strategies for chronic hepatitis B include vaccination with hepatitis B vaccine, which is effective in preventing acute and chronic HBV infection, as well as avoidance of risky behaviors such as unprotected sex and sharing of needles.
https://www.medicinenet.com › Medical Dictionary › G
A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.
Genetic Translocation | Definition & Facts | Britannica
https://www.britannica.com › science › Genetic-tr...
Genetic translocation, also called chromosomal translocation, a type of chromosomal aberration in which a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material. Genetic translocations are often found in cancer cells and may play a role in the development and progression of cancer.
Translocation, Genetic | health Encyclopedia - UPMC
https://www.upmc.com › health-library › gene...
A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.
Genetic Translocation | Genetics Home Reference - NIH
https://ghr.nlm.nih.gov › condition › ge...
A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.
In conclusion, Genetic Translocation is an abnormality in the number or arrangement of chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome, resulting in a gain or loss of genetic material that can have significant effects on the individual.
There are several subtypes of lymphoma, B-cell, including:
1. Diffuse large B-cell lymphoma (DLBCL): This is the most common type of B-cell lymphoma and typically affects older adults.
2. Follicular lymphoma: This type of lymphoma grows slowly and often does not require treatment for several years.
3. Marginal zone lymphoma: This type of lymphoma develops in the marginal zone of the spleen or other lymphoid tissues.
4. Hodgkin lymphoma: This is a type of B-cell lymphoma that is characterized by the presence of Reed-Sternberg cells, which are abnormal cells that can be identified under a microscope.
The symptoms of lymphoma, B-cell can vary depending on the subtype and the location of the tumor. Common symptoms include swollen lymph nodes, fatigue, fever, night sweats, and weight loss.
Treatment for lymphoma, B-cell usually involves chemotherapy, which is a type of cancer treatment that uses drugs to kill cancer cells. Radiation therapy may also be used in some cases. In some cases, bone marrow or stem cell transplantation may be recommended.
Prognosis for lymphoma, B-cell depends on the subtype and the stage of the disease at the time of diagnosis. In general, the prognosis is good for patients with early-stage disease, but the cancer can be more difficult to treat if it has spread to other parts of the body.
Prevention of lymphoma, B-cell is not possible, as the exact cause of the disease is not known. However, avoiding exposure to certain risk factors, such as viral infections and pesticides, may help reduce the risk of developing the disease. Early detection and treatment can also improve outcomes for patients with lymphoma, B-cell.
Lymphoma, B-cell is a type of cancer that affects the immune system and can be treated with chemotherapy and other therapies. The prognosis varies depending on the subtype and stage of the disease at diagnosis. Prevention is not possible, but early detection and treatment can improve outcomes for patients with this condition.
People with Fragile X syndrome may have intellectual disability, developmental delays, and various physical characteristics such as large ears, long face, and joint hypermobility. They may also experience behavioral problems such as anxiety, hyperactivity, and sensory sensitivities. In addition, they are at increased risk for seizures, sleep disturbances, and other health issues.
Fragile X syndrome is usually diagnosed through a combination of clinical evaluation, genetic testing, and molecular analysis. There is no cure for the condition, but various interventions such as behavioral therapy, speech and language therapy, occupational therapy, and medications can help manage its symptoms.
Prevention of Fragile X syndrome is not possible, as it is a genetic disorder caused by an expansion of CGG repeats in the FMR1 gene. However, early identification and intervention can improve outcomes for individuals with the condition.
Overall, Fragile X syndrome is a complex and multifaceted condition that requires comprehensive and individualized care to help individuals with the condition reach their full potential.
DLBCL is characterized by the rapid growth of malignant B cells in the lymph nodes, spleen, bone marrow, and other organs. These cells can also spread to other parts of the body through the bloodstream or lymphatic system. The disease is often aggressive and can progress quickly without treatment.
The symptoms of DLBCL vary depending on the location and extent of the disease, but they may include:
* Swollen lymph nodes in the neck, underarm, or groin
* Fever
* Fatigue
* Night sweats
* Weight loss
* Abdominal pain or discomfort
* Itching
The diagnosis of DLBCL is based on a combination of physical examination findings, imaging studies (such as CT scans or PET scans), and biopsy results. Treatment typically involves a combination of chemotherapy, radiation therapy, and in some cases, immunotherapy or targeted therapy. The prognosis for DLBCL has improved significantly over the past few decades, with overall survival rates ranging from 60% to 80%, depending on the stage and other factors.
Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.
Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.
In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.
It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.
See also: Cancer, Tumor
Word count: 190
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
Source: National Cancer Institute (www.cancer.gov)
The above definition is given by the National Cancer Institute, which is an authoritative source of information on cancer and lymphoma. It provides a concise overview of follicular lymphoma, including its characteristics, diagnosis, treatment options, and prognosis. The definition includes key terms such as "slow-growing," "B cells," "lymph nodes," and "five-year survival rate," which are important to understand when discussing this type of cancer.
Symptoms of this type of cancer can include swelling of the lymph nodes, fatigue, fever, night sweats, and weight loss. Treatment options for marginal zone B-cell lymphoma depend on the stage and location of the cancer and may involve a combination of chemotherapy, immunotherapy, and/or targeted therapy.
The prognosis for this type of cancer is generally good if it is diagnosed early and treated appropriately. However, in some cases, it can be more aggressive and difficult to treat, and the prognosis may be poorer.
There are several subtypes of B-cell leukemia, including:
1. Chronic lymphocytic leukemia (CLL): This is the most common type of B-cell leukemia, and it typically affects older adults. CLL is a slow-growing cancer that can progress over time.
2. Acute lymphoblastic leukemia (ALL): This is a fast-growing and aggressive form of B-cell leukemia that can affect people of all ages. ALL is often treated with chemotherapy and sometimes with bone marrow transplantation.
3. Burkitt lymphoma: This is an aggressive form of B-cell leukemia that typically affects older adults in Africa and Asia. Burkitt lymphoma can be treated with chemotherapy and sometimes with bone marrow transplantation.
4. Hairy cell leukemia: This is a rare type of B-cell leukemia that is characterized by the presence of hair-like projections on the surface of cancer cells. Hairy cell leukemia can be treated with chemotherapy and sometimes with bone marrow transplantation.
The diagnosis of B-cell leukemia is based on a combination of physical examination, medical history, laboratory tests, and biopsies. Treatment options for B-cell leukemia include chemotherapy, bone marrow transplantation, and in some cases, targeted therapy with drugs that specifically target cancer cells. The prognosis for B-cell leukemia varies depending on the subtype of the disease and the patient's overall health.
The term "reticulocytosis" is derived from the Latin words "reticulum," meaning net-like, and "cytosis," meaning the condition of cells. This refers to the characteristic net-like appearance of reticulocytes under a microscope.
There are several possible causes of reticulocytosis, including:
1. Inherited disorders such as hereditary elliptocytosis, hereditary spherocytosis, and pyruvate kinase (PK) deficiency.
2. Acquired disorders such as hemolytic anemia, thalassemia, and sickle cell disease.
3. Infections such as malaria, dengue fever, and babesiosis.
4. Medications such as antibiotics, chemotherapy drugs, and anti-inflammatory medications.
5. Other conditions such as chronic kidney disease, liver disease, and autoimmune disorders.
Reticulocytosis can be diagnosed through a blood test called a complete blood count (CBC) or a reticulocyte count. Treatment depends on the underlying cause of the condition. In some cases, no treatment may be necessary, while in other cases, medication or blood transfusions may be required.
In LLCB, the B cells undergo a mutation that causes them to become cancerous and multiply rapidly. This can lead to an overproduction of these cells in the bone marrow, causing the bone marrow to become crowded and unable to produce healthy red blood cells, platelets, and white blood cells.
LLCB is typically a slow-growing cancer, and it can take years for symptoms to develop. However, as the cancer progresses, it can lead to a range of symptoms including fatigue, weakness, weight loss, fever, night sweats, and swollen lymph nodes.
LLCB is typically diagnosed through a combination of physical examination, blood tests, bone marrow biopsy, and imaging studies such as X-rays or CT scans. Treatment options for LLCB include chemotherapy, radiation therapy, and in some cases, stem cell transplantation.
Overall, while LLCB is a serious condition, it is typically slow-growing and can be managed with appropriate treatment. With current treatments, many people with LLCB can achieve long-term remission and a good quality of life.
When a chromosome breaks, it can lead to genetic instability and potentially contribute to the development of diseases such as cancer. Chromosome breakage can also result in the loss or gain of genetic material, which can further disrupt normal cellular function and increase the risk of disease.
There are several types of chromosome breakage, including:
1. Chromosomal aberrations: These occur when there is a change in the number or structure of the chromosomes, such as an extra copy of a chromosome (aneuploidy) or a break in a chromosome.
2. Genomic instability: This refers to the presence of errors in the genetic material that can lead to changes in the function of cells and tissues.
3. Chromosomal fragile sites: These are specific regions of the chromosomes that are more prone to breakage than other regions.
4. Telomere shortening: Telomeres are the protective caps at the ends of the chromosomes, and their shortening can lead to chromosome breakage and genetic instability.
Chromosome breakage can be detected through cytogenetic analysis, which involves staining the cells with dyes to visualize the chromosomes and look for any abnormalities. The detection of chromosome breakage can help diagnose certain diseases, such as cancer, and can also provide information about the risk of disease progression.
In summary, chromosome breakage is a type of genetic alteration that can occur as a result of various factors, including exposure to radiation or chemicals, errors during cell division, or aging. It can lead to genetic instability and increase the risk of diseases such as cancer. Detection of chromosome breakage through cytogenetic analysis can help diagnose certain diseases and provide information about the risk of disease progression.
Factor X deficiency can be inherited or acquired, and it can have mild to severe effects on the body. People with factor X deficiency may experience prolonged bleeding after an injury or surgery, easy bruising, and frequent nosebleeds. In severe cases, factor X deficiency can lead to spontaneous bleeding, especially in the joints and internal organs.
There are two types of factor X deficiency:
1. Classic factor X deficiency: This is the most common type of factor X deficiency and is caused by a mutation in the gene that codes for factor X. It is usually inherited in an autosomal recessive pattern, which means that the child must inherit two copies of the mutated gene, one from each parent, to develop the condition.
2. Acquired factor X deficiency: This type of factor X deficiency can occur due to certain medical conditions, such as liver disease, vitamin K deficiency, or exposure to certain medications. It can also occur in people who have a high risk of bleeding, such as those with hemophilia.
Treatment for factor X deficiency typically involves replacing the missing clotting factor through infusions of factor X concentrate. In some cases, medications that help the body produce more factor X may also be used. People with factor X deficiency may need to receive regular infusions to maintain adequate levels of factor X in their blood.
Overall, factor X deficiency is a rare but potentially serious condition that can affect the body's ability to form blood clots and stop bleeding. With proper diagnosis and treatment, however, most people with factor X deficiency can lead normal lives.
There are several types of lymphoma, including:
1. Hodgkin lymphoma: This is a type of lymphoma that originates in the white blood cells called Reed-Sternberg cells. It is characterized by the presence of giant cells with multiple nucleoli.
2. Non-Hodgkin lymphoma (NHL): This is a type of lymphoma that does not meet the criteria for Hodgkin lymphoma. There are many subtypes of NHL, each with its own unique characteristics and behaviors.
3. Cutaneous lymphoma: This type of lymphoma affects the skin and can take several forms, including cutaneous B-cell lymphoma and cutaneous T-cell lymphoma.
4. Primary central nervous system (CNS) lymphoma: This is a rare type of lymphoma that develops in the brain or spinal cord.
5. Post-transplantation lymphoproliferative disorder (PTLD): This is a type of lymphoma that develops in people who have undergone an organ transplant, often as a result of immunosuppressive therapy.
The symptoms of lymphoma can vary depending on the type and location of the cancer. Some common symptoms include:
* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss
* Night sweats
* Itching
Lymphoma is diagnosed through a combination of physical examination, imaging tests (such as CT scans or PET scans), and biopsies. Treatment options for lymphoma depend on the type and stage of the cancer, and may include chemotherapy, radiation therapy, immunotherapy, or stem cell transplantation.
Overall, lymphoma is a complex and diverse group of cancers that can affect people of all ages and backgrounds. While it can be challenging to diagnose and treat, advances in medical technology and research have improved the outlook for many patients with lymphoma.
There are several subtypes of NHL, including:
1. B-cell lymphomas (such as diffuse large B-cell lymphoma and follicular lymphoma)
2. T-cell lymphomas (such as peripheral T-cell lymphoma and mycosis fungoides)
3. Natural killer cell lymphomas (such as nasal NK/T-cell lymphoma)
4. Histiocyte-rich B-cell lymphoma
5. Primary mediastinal B-cell lymphoma
6. Mantle cell lymphoma
7. Waldenström macroglobulinemia
8. Lymphoplasmacytoid lymphoma
9. Myelodysplastic syndrome/myeloproliferative neoplasms (MDS/MPN) related lymphoma
These subtypes can be further divided into other categories based on the specific characteristics of the cancer cells.
Symptoms of NHL can vary depending on the location and size of the tumor, but may include:
* Swollen lymph nodes in the neck, underarm, or groin
* Fever
* Fatigue
* Weight loss
* Night sweats
* Itching
* Abdominal pain
* Swollen spleen
Treatment for NHL typically involves a combination of chemotherapy, radiation therapy, and in some cases, targeted therapy or immunotherapy. The specific treatment plan will depend on the subtype of NHL, the stage of the cancer, and other individual factors.
Overall, NHL is a complex and diverse group of cancers that require specialized care from a team of medical professionals, including hematologists, oncologists, radiation therapists, and other support staff. With advances in technology and treatment options, many people with NHL can achieve long-term remission or a cure.
T-ALL typically occurs in children and young adults, although it can also occur in older adults. The symptoms of T-ALL can include fever, fatigue, loss of appetite, weight loss, swollen lymph nodes, and an enlarged spleen. If left untreated, T-ALL can progress rapidly and lead to life-threatening complications such as infection, bleeding, and organ failure.
The exact cause of T-ALL is not known, but it is believed to be linked to genetic mutations that occur in the T cells. The diagnosis of T-ALL typically involves a combination of physical examination, blood tests, bone marrow biopsy, and imaging studies such as CT scans or PET scans.
Treatment for T-ALL usually involves a combination of chemotherapy and/or radiation therapy to kill the abnormal T cells. In some cases, bone marrow transplantation may also be recommended. The prognosis for T-ALL depends on several factors, including the age of the patient, the severity of the disease, and the response to treatment. Overall, the survival rate for T-ALL is relatively low, but with intensive treatment, many patients can achieve long-term remission.
Some common types of nervous system neoplasms include:
1. Brain tumors: These are abnormal growths that develop in the brain, including gliomas (such as glioblastoma), meningiomas, and acoustic neuromas.
2. Spinal cord tumors: These are abnormal growths that develop in the spinal cord, including astrocytomas, oligodendrogliomas, and metastatic tumors.
3. Nerve sheath tumors: These are abnormal growths that develop in the covering of nerves, such as neurofibromas and schwannomas.
4. Pineal gland tumors: These are abnormal growths that develop in the pineal gland, a small endocrine gland located in the brain.
Symptoms of nervous system neoplasms can vary depending on their location and size, but may include headaches, seizures, weakness or numbness in the arms or legs, and changes in vision, speech, or balance. Diagnosis is typically made through a combination of imaging studies (such as MRI or CT scans) and tissue biopsy. Treatment options vary depending on the type and location of the tumor, but may include surgery, radiation therapy, and chemotherapy.
In summary, nervous system neoplasms are abnormal growths that can develop in the brain, spinal cord, and nerves, and can have a significant impact on the body. Diagnosis and treatment require a comprehensive approach, involving a team of medical professionals with expertise in neurology, neurosurgery, radiation oncology, and other related specialties.
Also known as Burkitt's Lymphoma.
There are several different types of leukemia, including:
1. Acute Lymphoblastic Leukemia (ALL): This is the most common type of leukemia in children, but it can also occur in adults. It is characterized by an overproduction of immature white blood cells called lymphoblasts.
2. Acute Myeloid Leukemia (AML): This type of leukemia affects the bone marrow's ability to produce red blood cells, platelets, and other white blood cells. It can occur at any age but is most common in adults.
3. Chronic Lymphocytic Leukemia (CLL): This type of leukemia affects older adults and is characterized by the slow growth of abnormal white blood cells called lymphocytes.
4. Chronic Myeloid Leukemia (CML): This type of leukemia is caused by a genetic mutation in a gene called BCR-ABL. It can occur at any age but is most common in adults.
5. Hairy Cell Leukemia: This is a rare type of leukemia that affects older adults and is characterized by the presence of abnormal white blood cells called hairy cells.
6. Myelodysplastic Syndrome (MDS): This is a group of disorders that occur when the bone marrow is unable to produce healthy blood cells. It can lead to leukemia if left untreated.
Treatment for leukemia depends on the type and severity of the disease, but may include chemotherapy, radiation therapy, targeted therapy, or stem cell transplantation.
The most common types of hemoglobinopathies include:
1. Sickle cell disease: This is caused by a point mutation in the HBB gene that codes for the beta-globin subunit of hemoglobin. It results in the production of sickle-shaped red blood cells, which can cause anemia, infections, and other complications.
2. Thalassemia: This is a group of genetic disorders that affect the production of hemoglobin and can result in anemia, fatigue, and other complications.
3. Hemophilia A: This is caused by a defect in the F8 gene that codes for coagulation factor VIII, which is essential for blood clotting. It can cause bleeding episodes, especially in males.
4. Glucose-6-phosphate dehydrogenase (G6PD) deficiency: This is caused by a point mutation in the G6PD gene that codes for an enzyme involved in red blood cell production. It can cause hemolytic anemia, especially in individuals who consume certain foods or medications.
5. Hereditary spherocytosis: This is caused by point mutations in the ANK1 or SPTA1 genes that code for proteins involved in red blood cell membrane structure. It can cause hemolytic anemia and other complications.
Hemoglobinopathies can be diagnosed through genetic testing, such as DNA sequencing or molecular genetic analysis. Treatment options vary depending on the specific disorder but may include blood transfusions, medications, and in some cases, bone marrow transplantation.
* Peripheral T-cell lymphoma (PTCL): This is a rare type of T-cell lymphoma that can develop in the skin, lymph nodes, or other organs.
* Cutaneous T-cell lymphoma (CTCL): This is a type of PTCL that affects the skin and can cause lesions, rashes, and other skin changes.
* Anaplastic large cell lymphoma (ALCL): This is a rare subtype of PTCL that can develop in the lymph nodes, spleen, or bone marrow.
* Adult T-cell leukemia/lymphoma (ATLL): This is a rare and aggressive subtype of PTCL that is caused by the human T-lymphotropic virus type 1 (HTLV-1).
Symptoms of T-cell lymphoma can include:
* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss
* Night sweats
* Skin lesions or rashes
Treatment options for T-cell lymphoma depend on the subtype and stage of the cancer, but may include:
* Chemotherapy
* Radiation therapy
* Immunotherapy
* Targeted therapy
Prognosis for T-cell lymphoma varies depending on the subtype and stage of the cancer, but in general, the prognosis for PTCL is poorer than for other types of non-Hodgkin lymphoma. However, with prompt and appropriate treatment, many people with T-cell lymphoma can achieve long-term remission or even be cured.
There are different types of Breast Neoplasms such as:
1. Fibroadenomas: These are benign tumors that are made up of glandular and fibrous tissues. They are usually small and round, with a smooth surface, and can be moved easily under the skin.
2. Cysts: These are fluid-filled sacs that can develop in both breast tissue and milk ducts. They are usually benign and can disappear on their own or be drained surgically.
3. Ductal Carcinoma In Situ (DCIS): This is a precancerous condition where abnormal cells grow inside the milk ducts. If left untreated, it can progress to invasive breast cancer.
4. Invasive Ductal Carcinoma (IDC): This is the most common type of breast cancer and starts in the milk ducts but grows out of them and invades surrounding tissue.
5. Invasive Lobular Carcinoma (ILC): It originates in the milk-producing glands (lobules) and grows out of them, invading nearby tissue.
Breast Neoplasms can cause various symptoms such as a lump or thickening in the breast or underarm area, skin changes like redness or dimpling, change in size or shape of one or both breasts, discharge from the nipple, and changes in the texture or color of the skin.
Treatment options for Breast Neoplasms may include surgery such as lumpectomy, mastectomy, or breast-conserving surgery, radiation therapy which uses high-energy beams to kill cancer cells, chemotherapy using drugs to kill cancer cells, targeted therapy which uses drugs or other substances to identify and attack cancer cells while minimizing harm to normal cells, hormone therapy, immunotherapy, and clinical trials.
It is important to note that not all Breast Neoplasms are cancerous; some are benign (non-cancerous) tumors that do not spread or grow.
Bcl-2-like protein 1
Bcl-2-associated X protein
Bcl-2
Bcl-2 family
Bcl-2 homologous antagonist killer
Bcl-2-interacting killer
Sexually dimorphic nucleus
Phycocyanin
Bcl-xL
C-Raf
Venetoclax
Presenilin-1
MTCH2
Jerry Adams
Bcl-2-associated death promoter
Obatoclax
Apoptosis
Mitochondrial ribosomal protein L41
Hypothermia therapy for neonatal encephalopathy
BNIP3
Apoptosome
Protein kinase B
RRAS
HRK (gene)
AI-10-49
Mitochondrial outer membrane permeabilization
BNIP2
MCL1
SNCAIP
Mitochondrial apoptosis-induced channel
Caspase-activated DNase
PIR (gene)
BMF (gene)
Galectin-9
GLI2
Erinna Lee
Waldenström macroglobulinemia
MIR195
BCL2L13
Prostate cancer
AP-1 transcription factor
Index of biochemistry articles
Methylsulfonylmethane
Belimumab
Nuclear receptor 4A1
STAT6
Steven J. Burakoff
Calcineurin
Histone H2A.Z
PPP1CA
Neprilysin
Anticancer gene
Unfolded protein response
CLPTM1L
Cyclin-dependent kinase 1
Chronic lymphocytic leukemia
Gapmer
S100 protein
Minimal residual disease
MicroRNA 148a
Vaccinia virus lacking the Bcl-2-like protein N1 induces a stronger natural killer cell response to infection
Bcl-2 protein in 518A2 melanoma cells in vivo and in vitro<...
Anti-Apoptotic and Pro-Apoptotic Bcl-2 Family Proteins in Peri-Implant Diseases. | Clin Oral Implants Res;34(6): 582-590, 2023...
Langerhans Cell Histiocytosis: Background, Pathophysiology, Etiology
Caspase cleavage of the amyloid precursor protein is prevented after overexpression of bcl-2 in a triple transgenic mouse model...
The discovery from the TRAIL protein and its own death receptors - New dimension in therapeutic targeting of BCL-2 family
Supplementary MaterialsAdditional file 1: Table S1 A-C HLA-A2 binding peptides derived from apoptotic cell-associated proteins ...
Becn1 beclin 1, autophagy related [Mus musculus (house mouse)] - Gene - NCBI
Potent, p53-independent induction of NOXA sensitizes MLL-rearranged B-cell acute lymphoblastic leukemia cells to venetoclax |...
FDA Approves Three New Treatments for AML | AACR Blog
Figure 3 - Immune Cell Apoptosis Prevention as Potential Therapy for Severe Infections - Volume 13, Number 2-February 2007 -...
Plus it
FITC anti-Bcl-2 Antibody anti-Bcl-2 - BCL/10C4
Ultrasonic Nanoemulsification of Cuminum cyminum Essential Oil and Its | IJN
Targeted therapy for the most common leukemia | MD Anderson Cancer Center
New compound shows promise in treating multiple human cancers | WEHI
bcl-x Antibody [Unconjugated] (AF800): Novus Biologicals
Pathology Research Laboratories | Pathology
NIOSHTIC-2 Search Results - Full View
Quercetin is Probably Not a Useful Senolytic - Fight Aging!
HL-60 Cells | Broad Institute
Expression and bioactivity identification of soluble MG7 scFv
Bcl-XL antibody (10783-1-AP) | Proteintech
Exploring the anti-cancer and anti-inflammatory properties of isothiocyanates, News, University of Otago, Christchurch,...
Dose-Dependent Variation in Anticancer Activity of Hexane and Chloroform Extracts of Field Horsetail Plant on Human...
cell death<...
Epigenetic Mechanisms in Autism Spectrum Disorders | IntechOpen
regulation of protein localization Antibodies | Invitrogen
...
IJMS | Free Full-Text | Protective Role of St. John's Wort and Its Components Hyperforin and Hypericin against Diabetes through...
Apoptosis11
- The vaccinia virus (VACV) N1 protein is an intracellular virulence factor that has a Bcl-2-like structure and inhibits both apoptosis and signalling from the interleukin 1 receptor, leading to nuclear factor kappa B activation. (nih.gov)
- Likewise, the induction of apoptosis by G3139 was entirely Bcl-2 independent. (elsevier.com)
- Intrinsic apoptosis , which is regulated by Bcl-2 family proteins , has an important role in chronic inflammatory diseases . (bvsalud.org)
- Presently, inhibitors from the apoptosis protein, mobile FLICE-like R935788 inhibitory proteins (c-FLIP) and inhibitors of apoptosis proteins (IAPs, including XIAP) are believed to lead to cellular Path resistance. (colinsbraincancer.com)
- BCL-2 is a protein that promotes cell survival by preventing cells from undergoing a natural self-destruct process called apoptosis. (aacr.org)
- By blocking BCL-2, venetoclax triggers the leukemia cells to die by apoptosis. (aacr.org)
- Decreased apoptosis caused by overexpression of Bcl-2 protein in a mouse model of plague. (cdc.gov)
- Apoptosis regulator proteins, Bcl-2 family, BH1-4 domains. (biolegend.com)
- 3 Besides, drug resistance due to suppression of apoptosis and expressive levels of anti-apoptotic proteins has intensified in cancer treatment. (dovepress.com)
- One of the isothiocyanates was able to trigger apoptosis in cells overexpressing Bcl-2, a protein that is present at high levels in many cancers. (otago.ac.nz)
- Bak protein interacts with TUMOR SUPPRESSOR PROTEIN P53 and promotes APOPTOSIS. (bvsalud.org)
Anti-apoptotic protein2
- A recent study demonstrated the lack of beta-amyloid (Aβ) plaque formation and accumulation of the amyloid precursor protein (APP) in a triple transgenic mouse model of Alzheimer's disease (3xTg-AD) following overexpression of the anti-apoptotic protein, Bcl-2 (Rohn et al. (uthscsa.edu)
- Inhibition of anti-apoptotic protein BCL-2 with venetoclax emerged as a promising strategy for this subtype of BCP-ALL, however, lack of sufficient responses in preclinical models and the possibility of developing resistance exclude using venetoclax as monotherapy. (nature.com)
Antibodies2
- Lately, several stage 2 clinical research based on the usage of recombinant human being Path or R935788 agonistic monoclonal antibodies against DR4/5 possess failed to display clinical efficacy, even though coupled with traditional chemotherapy (9,10). (colinsbraincancer.com)
- Of many epithelial, neuronal, and glial markers, we found that calcium-binding protein antibodies recognizing calretinin, calmodulin, or parvalbumin labeled immature hair cells in rat vestibular end organs. (jneurosci.org)
Intracellular2
- C57BL/6 splenocytes intracellular stained with BCL/10C4 FITC. (biolegend.com)
- Identification of biphenyl-based hybrid molecules able to decrease the intracellular level of Bcl-2 protein in Bcl-2 overexpressing leukemia cells. (broadinstitute.org)
Transgenic mouse1
- Note the decrease in apoptotic cells in the thymus of the Bcl-2 transgenic mouse (magnification ×400). (cdc.gov)
Antibody4
- The antibody solution should be stored undiluted between 2°C and 8°C, and protected from prolonged exposure to light. (biolegend.com)
- Various lysates were subjected to SDS PAGE followed by western blot with 10783-1-AP (Bcl-XL antibody) at dilution of 1:8000 incubated at room temperature for 1.5 hours. (ptglab.com)
- WB result of Bcl-XL antibody (10783-1-AP, 1:800) with si-Control and si-Bcl-XL transfected HeLa cells. (ptglab.com)
- NIH/3T3 cells were subjected to SDS PAGE followed by western blot with 10783-1-AP (Bcl-XL antibody at dilution of 1:1000 incubated at room temperature for 1.5 hours. (ptglab.com)
Kinase2
- This protein is modified by ASK1/JNK1, PKC, ERKs, and stress-activated kinase phosphorylation and can be ubiquitinated. (biolegend.com)
- In addition, activation of antiapoptotic factors including phospho-Akt (protein kinase B) and Bcl-2 was detected. (cdc.gov)
Mitochondrial membrane3
- Bcl-2 is distributed in the outer mitochondrial membrane, the nuclear envelope, and the endoplasmic reticulum. (biolegend.com)
- This protein blocks apoptotic death by controlling mitochondrial membrane permeability. (biolegend.com)
- A multi-domain mitochondrial membrane protein and member of the bcl-2 Protein family. (bvsalud.org)
Venetoclax3
- Using RNA-seq, we observed that long-term exposure to venetoclax in vivo in a patient-derived xenograft model leads to downregulation of several tumor protein 53 ( TP53 )-related genes. (nature.com)
- Venetoclax is a molecularly targeted therapeutic directed against the protein BCL-2. (aacr.org)
- Venetoclax is in a class of medications called B-cell lymphoma-2 (BCL-2) inhibitors. (medlineplus.gov)
Apoptotic cell1
- Synergistic activity of these drugs resulted from auranofin-mediated upregulation of NOXA pro-apoptotic protein and potent induction of apoptotic cell death. (nature.com)
Cells16
- To help resolve this question, we have permanently and stably down-regulated Bcl-2 protein and mRNA expression in 518A2 cells by two different technologies and evaluated the resulting clones both in vitro and in vivo. (elsevier.com)
- Experimental Design: 518A2 melanoma cells were transfected with plasmids engineered to produce either a single-stranded antisense oligonucleotide targeted to the initiation codon region of the Bcl-2 mRNA or a short hairpin RNA also targeted to the Bcl-2 mRNA. (elsevier.com)
- However, when xenografted into severe combined immunodeficient mice, cells with silenced Bcl-2, using either technology, either failed to grow at all or grew to tumors of low volume and then completely regressed. (elsevier.com)
- In contrast, control cells with "normal" levels of Bcl-2 protein expression expanded to be large, necrotic tumors. (elsevier.com)
- Conclusions: The presence of Bcl-2 protein profoundly affects the ability of 518A2 melanoma cells to grow as human tumor xenografts in severe combined immunodeficient mice. (elsevier.com)
- The in vivo role of Bcl-2 in melanoma cells thus differs significantly from its in vitro role, and these experiments further suggest that Bcl-2 may be an important therapeutic target even in tumors that do not contain the t14:18 translocation. (elsevier.com)
- The discovery from the TRAIL protein and its own death receptors DR4/5 changed the horizon of cancer research because TRAIL specifically kills cancer cells. (colinsbraincancer.com)
- Elevated levels of BCL-2 have been seen in several types of leukemia cells, including AML cells and chronic lymphocytic leukemia (CLL) cells. (aacr.org)
- The Servier compound - S63845 - targets a protein of the BCL2 family, called MCL1, which is essential for the sustained survival of these cancer cells. (edu.au)
- MCL1 is important for many cancers because it is a pro-survival protein that allows the cancerous cells to evade the process of programmed cell death that normally removes cancer cells from the body," Associate Professor Lessene said. (edu.au)
- Walter and Eliza Hall Institute researchers revealed the role of BCL-2 in cancer more than 28 years ago and the essential role of MCL1 for the survival of malignant cells four years ago. (edu.au)
- Western blot shows lysates of A431 human epithelial carcinoma cell line (5 x 104 cells, lane 1 and 2.5 x 104 cells, lane 2) and NIH‑3T3 mouse embryonic fibroblast cell line. (novusbio.com)
- Western-blot analysis showed an activation of proapoptotic factors including Fas (CD95), Fas-associated protein with death domain (FADD), caspase-8, death receptor 3 (DR3) and BID in apoptotic cells induced by metallic nickel particles. (cdc.gov)
- The isothiocyanate had a greater effect on mitochondrial function in cells with Bcl-2, suggesting a mechanism for how it bypasses Bcl-2 action. (otago.ac.nz)
- We have reported that many insults can trigger cells to activate a cellular death pathway (Nature, 361:739-742, 1993), that several viruses encode proteins to block attempted cell suicide (Proc. (hopkinsmedicine.org)
- It works by blocking the action of a certain protein in the body that helps cancer cells survive. (medlineplus.gov)
Therapeutic1
- Glasdegib is a molecularly targeted therapeutic directed against a protein called Smoothened. (aacr.org)
Caspases1
- We have shown that anti-apoptotic Bcl-2 family proteins can be converted into killer molecules (Science 278:1966-8, 1997), that Bcl-2 family proteins interact with regulators of caspases and regulators of cell cycle check point activation (Molecular Cell 6:31-40, 2000). (hopkinsmedicine.org)
Amino acids1
- The peptide corresponds to amino acids 49-68 of human and mouse, long and short forms of Bcl-x. (novusbio.com)
Cleavage1
- Cleavage of Bcl-2 can convert to pro-apoptotic (by cleavage of BH4 domain). (biolegend.com)
Infections2
- Of particular interest to our group are the mechanisms by which Bcl-2 family proteins and other factors regulate programmed cell death , particularly in the nervous system, in cancer and in virus infections. (hopkinsmedicine.org)
- PEM in children is frequently associated with an increased incidence of bacterial, Patients fungal and viral infections [ 2 ] and is the The current study was performed on 42 in- most common cause of secondary immu- fants recruited from the Children's Hospital, nodeficiency [ 3-5 ]. (who.int)
Differs significantly1
- The sequence used for immunization differs significantly from the sequences of the corresponding region of other members of the Bcl-2 family. (novusbio.com)
Regulate1
- Bcl-2 has been reported to regulate cell cycle progression via ROS. (biolegend.com)
Assay1
- Results: Using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, we found that metallic nickel nanoparticle s exhibited higher cytotoxicity than fine particles. (cdc.gov)
Malnutrition4
- Flow cytometric estimation of the apoptotic marker CD95 in peripheral neutrophils, lymphocytes and monocytes was done for 18 infants with non-oedematous protein energy malnutrition (PEM) and 12 oedematous ones, on hospital admission and after supervised nutritional rehabilitation, and compared with 12 matched controls. (who.int)
- RÉSUMÉ La malnutrition continue de faire peser un lourd fardeau sanitaire sur les pays en développement. (who.int)
- Malnutrition, both protein-energy mal-nutrition (PEM) and micronutrient deficiencies, continues to be a major health burden in developing countries. (who.int)
- Malnutrition, both protein-energy mal- aimed to assess the use of CD95 expression nutrition (PEM) and micronutrient defi- as a marker for following up these patients ciencies, continues to be a major health during their nutritional rehabilitation and burden in developing countries. (who.int)
Clone1
- Clone BCL/10C4 has been shown to be useful for Western blotting, immunoprecipitation, and immunofluorescence of the mouse and rat Bcl-2 protein. (biolegend.com)
Mice1
- Wild-type mice (A) and mice that overexpressed Bcl-2 in lymphocytes (B) were injected intranasally with Yersinia pestis . (cdc.gov)
Compound3
- This compound has recently completed phase III global clinical evaluation, but the function of Bcl-2 as a target in melanoma has not been completely clarified. (elsevier.com)
- A new compound, discovered jointly by international pharmaceutical company Servier , headquartered in France, and Vernalis (R&D) , a company based in the UK, has been shown by researchers at the Walter and Eliza Hall Institute and Servier to block a protein that is essential for the sustained growth of up to a quarter of all cancers. (edu.au)
- A new compound has been shown to block a protein essential for the growth of many cancers. (edu.au)
Tissue2
- The aim of the study was to identify the tissue levels and ratios of anti- and pro-apoptotic Bcl-2 family proteins in peri-implant diseases . (bvsalud.org)
- The tissue levels of Bcl-2 family pro-apoptotic (Bak, Bax, active caspase-3 ) and anti-apoptotic (Bcl-2, Bcl-xL, Mcl-1) proteins were determined by multiplex immunoassay method . (bvsalud.org)
Mouse1
- Detects human and mouse Bcl‑x in Western blots. (novusbio.com)
Significantly higher1
- Bak, Bax and anti-apoptotic proteins Bcl-2, Bcl-xL, Mcl-1 were detected significantly higher in controls compared with patients with peri-implant mucositis and peri-implantitis (p (bvsalud.org)
Mechanism1
- The Kyriakides Laboratory is focused on elucidating the mechanism through which the endogenous inhibitor of angiogenesis TSP-2 limits angiogenesis and arteriogenesis. (yale.edu)
Activation2
- More recently, histiocytic diseases have been reclassified into five groups: (1) Langerhans-related, (2) cutaneous and mucocutaneous, (3) malignant histiocytosis, (4) Rosai-Dorfman disease, and (5) hemophagocytic lymphohistiocytosis and macrophage activation syndrome. (medscape.com)
- Activation of Akt and Bcl-2 may play an important role in preventing cytochrome c release from mitochondria to the cytoplasm and may also be important in the carcinogenicity of metallic nickel particles. (cdc.gov)
Family members1
- The Bcl-2 protein forms homo- or hetero-dimers with other Bcl-2 family members. (biolegend.com)
Cellular2
- Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. (fightaging.org)
- Molecular and cellular biochemistry 2012 Feb 361 (1-2): 189-95. (cdc.gov)
Addition2
- In addition, the G3139-induced release from isolated mitochondria was also relatively independent of Bcl-2 expression. (elsevier.com)
- In addition, Bcl-2 family proteins have normal physiological roles in regulating mitochondrial fission/fusion and mitochondrial energetics to facilitate neuronal activity in healthy brains. (hopkinsmedicine.org)
Cancer1
- Cancer is one of the most dreadful diseases globally, and it appears to be due to extreme free radical damage, which eventually causes damage to the DNA, lipids, and protein. (hindawi.com)
Results1
- Results: In vitro, down-regulation of Bcl-2 expression by either method produced no change either in the rate of growth or in sensitivity to standard cytotoxic chemotherapeutic agents. (elsevier.com)
Disorders1
- The working group of the Histiocyte Society divided histocytic disorders into three groups: (1) dendritic cell histiocytosis, (2) macrophage-related disorders, and (3) malignant histiocytosis. (medscape.com)
Exposure1
- Different Roles of Beclin1 in the Interaction Between Glia and Neurons after Exposure to Morphine and the HIV- Trans-Activator of Transcription (Tat) Protein. (nih.gov)
Death1
- MCL1 is a member of this protein family, and inhibiting it activates the process of programmed cell death. (edu.au)
Domain1
- An isoform of Bak protein containing only the N-terminal BH3 domain. (bvsalud.org)
Urine1
- Aromatic hydrocarbons in this size range are well absorbed from the 14 gut when administered at low doses: 80-90% of ingested 2-methylnaphthalene and isopropylbenzene was recovered in the urine (ATSDR 1999). (cdc.gov)
Factors1
- 1 , 2 In spite of these advantages, factors associated with gastric residence time and instability can affect the efficacy of these bioactives. (dovepress.com)