Antigens, Polyomavirus Transforming
Merkel cell polyomavirus
Antigens, Viral, Tumor
Carcinoma, Merkel Cell
Tumor Virus Infections
Simian virus 40
Molecular Sequence Data
Leukoencephalopathy, Progressive Multifocal
Cell Transformation, Viral
Receptors, Antigen, T-Cell
Amino Acid Sequence
Proliferating Cell Nuclear Antigen
Histocompatibility Antigens Class II
Receptors, Antigen, B-Cell
Polymerase Chain Reaction
Enhancer Elements, Genetic
Enzyme-Linked Immunosorbent Assay
Antigens, Tumor-Associated, Carbohydrate
Oncogene Proteins, Viral
Proto-Oncogene Proteins pp60(c-src)
Blood Group Antigens
Hepatitis B Surface Antigens
Fluorescent Antibody Technique
Viral Regulatory and Accessory Proteins
Histocompatibility Antigens Class I
Gene Expression Regulation, Viral
Hepatitis B Antigens
Viral Structural Proteins
Cell Transformation, Neoplastic
Promoter Regions, Genetic
Tumor Cells, Cultured
Cell Line, Transformed
Recombinant Fusion Proteins
Epstein-Barr Virus Nuclear Antigens
Transcription Factor AP-2
Protein Phosphatase 2
Sensitivity and Specificity
Hepatitis B Core Antigens
Regulatory Sequences, Nucleic Acid
Sequence Analysis, DNA
Electrophoresis, Polyacrylamide Gel
Repetitive Sequences, Nucleic Acid
Complement Fixation Tests
Y-Box-Binding Protein 1
Human topoisomerase I promotes initiation of simian virus 40 DNA replication in vitro. (1/1802)Addition of purified human topoisomerase I (topo I) to simian virus 40 T antigen-driven in vitro DNA replication reactions performed with topo I-deficient extracts results in a greater than 10-fold stimulation of completed molecules as well as a more than 3-fold enhancement of overall DNA replication. To further characterize this stimulation, we first demonstrate that bovine topo I but not Escherichia coli topo I can also enhance DNA replication. By using several human topo I mutants, we show that a catalytically active form of topo I is required. To delineate whether topo I influences the initiation or the elongation step of replication, we performed delayed pulse, pulse-chase, and delayed pulse-chase experiments. The results illustrate that topo I cannot promote the completion of partially replicated molecules but is needed from the beginning of the reaction to initiate replication. Competitive inhibition experiments with the topo I binding T antigen fragment 1-246T and a catalytically inactive topo I mutant suggest that part of topo I's stimulation of replication is mediated through a direct interaction with T antigen. Collectively, our data indicate that topo I enhances the synthesis of fully replicated DNA molecules by forming essential interactions with T antigen and stimulating initiation. (+info)
Telomerase activity is sufficient to allow transformed cells to escape from crisis. (2/1802)The introduction of simian virus 40 large T antigen (SVLT) into human primary cells enables them to proliferate beyond their normal replicative life span. In most cases, this temporary escape from senescence eventually ends in a second proliferative block known as "crisis," during which the cells cease growing or die. Rare immortalization events in which cells escape crisis are frequently correlated with the presence of telomerase activity. We tested the hypothesis that telomerase activation is the critical step in the immortalization process by studying the effects of telomerase activity in two mortal SVLT-Rasval12-transformed human pancreatic cell lines, TRM-6 and betalox5. The telomerase catalytic subunit, hTRT, was introduced into late-passage cells via retroviral gene transfer. Telomerase activity was successfully induced in infected cells, as demonstrated by a telomerase repeat amplification protocol assay. In each of nine independent infections, telomerase-positive cells formed rapidly dividing cell lines while control cells entered crisis. Telomere lengths initially increased, but telomeres were then maintained at their new lengths for at least 20 population doublings. These results demonstrate that telomerase activity is sufficient to enable transformed cells to escape crisis and that telomere elongation in these cells occurs in a tightly regulated manner. (+info)
Different regulation of the p53 core domain activities 3'-to-5' exonuclease and sequence-specific DNA binding. (3/1802)In this study we further characterized the 3'-5' exonuclease activity intrinsic to wild-type p53. We showed that this activity, like sequence-specific DNA binding, is mediated by the p53 core domain. Truncation of the C-terminal 30 amino acids of the p53 molecule enhanced the p53 exonuclease activity by at least 10-fold, indicating that this activity, like sequence-specific DNA binding, is negatively regulated by the C-terminal basic regulatory domain of p53. However, treatments which activated sequence-specific DNA binding of p53, like binding of the monoclonal antibody PAb421, which recognizes a C-terminal epitope on p53, or a higher phosphorylation status, strongly inhibited the p53 exonuclease activity. This suggests that at least on full-length p53, sequence-specific DNA binding and exonuclease activities are subject to different and seemingly opposing regulatory mechanisms. Following up the recent discovery in our laboratory that p53 recognizes and binds with high affinity to three-stranded DNA substrates mimicking early recombination intermediates (C. Dudenhoeffer, G. Rohaly, K. Will, W. Deppert, and L. Wiesmueller, Mol. Cell. Biol. 18:5332-5342), we asked whether such substrates might be degraded by the p53 exonuclease. Addition of Mg2+ ions to the binding assay indeed started the p53 exonuclease and promoted rapid degradation of the bound, but not of the unbound, substrate, indicating that specifically recognized targets can be subjected to exonucleolytic degradation by p53 under defined conditions. (+info)
Association of simian virus 40 with a central nervous system lesion distinct from progressive multifocal leukoencephalopathy in macaques with AIDS. (4/1802)The primate polyomavirus SV40 is known to cause interstitial nephritis in primary infections and progressive multifocal leukoencephalopathy (PML) upon reactivation of a latent infection in SIV-infected macaques. We now describe a second central nervous system manifestation of SV40: a meningoencephalitis affecting cerebral gray matter, without demyelination, distinct from PML. Meningoencephalitis appears also to be a primary manifestation of SV40 infection and can be seen in conjunction with SV40-induced interstitial nephritis and pneumonitis. The difference in the lesions of meningoencephalitis and PML does not appear to be due to cellular tropism, as both oligodendrocytes and astrocytes are infected in PML and meningoencephalitis, as determined by in situ hybridization or immunohistochemistry for SV40 coupled with immunohistochemistry for cellular determinants. This is further supported by examination of SV40 nucleic acid sequences from the ori-enhancer and large-T-antigen regions, which reveals no tissue-or lesion-specific variation in SV40 sequences. (+info)
A telomere-independent senescence mechanism is the sole barrier to Syrian hamster cell immortalization. (5/1802)Reactivation of telomerase and stabilization of telomeres occur simultaneously during human cell immortalization in vitro and the vast majority of human cancers possess high levels of telomerase activity. Telomerase repression in human somatic cells may therefore have evolved as a powerful resistance mechanism against immortalization, clonal evolution and malignant progression. The comparative ease with which rodent cells immortalize in vitro suggests that they have less stringent controls over replicative senescence than human cells. Here, we report that Syrian hamster dermal fibroblasts possess substantial levels of telomerase activity throughout their culture life-span, even after growth arrest in senescence. In our studies, telomerase was also detected in uncultured newborn hamster skin, in several adult tissues, and in cultured fibroblasts induced to enter the post-mitotic state irreversibly by serum withdrawal. Transfection of near-senescent dermal fibroblasts with a selectable plasmid vector expressing the SV40 T-antigen gene resulted in high-frequency single-step immortalization without the crisis typically observed during the immortalization of human cells. Collectively, these data provide an explanation for the increased susceptibility of rodent cells to immortalization (and malignant transformation) compared with their human equivalents, and provide evidence for a novel, growth factor-sensitive, mammalian senescence mechanism unrelated to telomere maintenance. (+info)
The introduction of dominant-negative p53 mutants suppresses temperature shift-induced senescence in immortal human fibroblasts expressing a thermolabile SV40 large T antigen. (6/1802)Immortal human fibroblasts, SVts8 cells, which express a heat-labile SV40 large T antigen, induces a senescence-like phenomenon in response to upward shift in temperature. Cells with arrested division show strong induction of senescence-associated beta-galactosidase. We examined how p53 and pRB are involved in this phenomenon since they are major targets of the T antigen. Transfection of cells with plasmids encoding the wild-type T antigen or human papilloma virus type 16 E6/E7 proteins completely abolished the arrest in cell division, a plasmid encoding the E6 protein suppressed it markedly, while a plasmid encoding E7 had no effect. Plasmids encoding dominant-negative p53 mutants also suppressed the arrest in cell division to various degrees. Upon temperature shift, p21 mRNA was upregulated 10-fold in SVts8 cells, but only slightly in clones expressing the wild-type T antigen or dominant-negative p53 mutants. These data demonstrate that p53 plays a major role in this senescence-like phenomenon. (+info)
Overexpression of D-type cyclins, E2F-1, SV40 large T antigen and HPV16 E7 rescue cell cycle arrest of tsBN462 cells caused by the CCG1/TAF(II)250 mutation. (7/1802)tsBN462 cells, which have a point mutation in CCG1/TAF(II)250, a component of TFIID complex, arrest in G1 at the nonpermissive temperature of 39.5 degrees C. Overexpression of D-type cyclins rescued the cell cycle arrest of tsBN462 cells, suggesting that the cell cycle arrest was through Rb. Consistent with this, overexpression of E2F-1, whose function is repressed by the hypophosphorylated form of Rb, also rescued the cell cycle arrest. Moreover, expression of the viral oncoproteins SV40 large T antigen and HPV16 E7, which both bind Rb and inactivate its function, rescued the cell cycle arrest, whereas HPV16 E6 did not. Mutation of the Rb-binding motif in E7 abrogated its ability to rescue the cell cycle arrest. Expression of exogenous cyclin D1, SV40 large T antigen or CCG1/TAF(II)250 increased cyclin A expression at 39.5 degrees C. Coexpression of HPV16 E7 and adenovirus E1b19K, which blocks apoptosis, rescued the proliferation of tsBN462 cells at 38.5 degrees C. To investigate the mechanism underlying the lack of cyclin D1 expression, deletion analysis of cyclin D1 promoter was performed. The 0.15 kbp cyclin D1 core promoter region, which lacks any transcription factor binding motifs, still exhibited a temperature-sensitive phenotype in tsBN462 cells suggesting that CCG1/TAF(II)250 is critical for the function of the cyclin D1 core promoter. (+info)
Concerted expression of BK virus large T- and small t-antigens strongly enhances oestrogen receptor-mediated transcription. (8/1802)Previous studies have shown that the human polyomavirus BK (BKV) genome contains an oestrogen response element (ERE). This isolated element binds its cognate receptor in vitro and can mediate 17beta-oestradiol-induced gene expression when linked to a heterologous promoter. The roles of the ERE- and the AP-1-binding sites in oestrogen receptor-directed transcription from the complete BKV promoter/enhancer (Dunlop strain) have been examined and the effects of the general co-activator CBP and large T- and small t-antigens on oestrogen receptor-mediated transcription have been investigated. A constitutive activated oestrogen receptor stimulated BKV promoter activity in HeLa cells. Mutations in either the ERE- or the AP-1-binding sites did not impair oestrogen receptor-induced activation of the BKV Dunlop promoter, while mutations in both binding motifs almost completely abolished oestrogen receptor-induced transcription. Simultaneous expression of large T- and small t-antigens strongly activated oestrogen receptor-mediated transcription. When expressed separately, only large T-antigen moderately stimulated oestrogen receptor-mediated transcription. The stimulatory effect of large T-antigen on the activity of the oestrogen receptor is probably indirect because no physical interaction between the two proteins was detected in a two-hybrid assay. Large T-antigen abrogated the synergistic effect on transcription between this nuclear receptor and the general co-activator CBP. The findings that the BKV early proteins amplify oestrogen receptor-mediated transcription may have important biological implications in individuals with raised oestrogen concentrations. (+info)
1. Types of Polyomaviruses: There are several types of polyomaviruses that can infect humans, including the common cold virus (Rhinovirus), respiratory syncytial virus (RSV), human metapneumovirus (HMPV), and the newly identified Parechovirus.
2. Infection: Polyomaviruses can be transmitted through contact with an infected person's respiratory secretions, such as mucus and saliva, or through contaminated surfaces. Inhaling the virus can lead to an infection in the respiratory tract.
3. Symptoms: The symptoms of polyomavirus infections can vary depending on the type of virus and the individual's age and overall health. Common symptoms include runny nose, cough, fever, sore throat, headache, and fatigue. In severe cases, polyomaviruses can cause pneumonia, bronchiolitis, and other respiratory disorders.
4. Diagnosis: A diagnosis of a polyomavirus infection is typically made based on the symptoms and medical history of the individual, as well as through laboratory tests such as PCR (polymerase chain reaction) or viral culture.
5. Treatment: There is no specific treatment for polyomavirus infections, but antiviral medications may be prescribed to help manage symptoms and prevent complications. Supportive care, such as rest, hydration, and over-the-counter pain relievers, may also be recommended.
6. Prevention: Preventing the spread of polyomaviruses can be challenging, but good hygiene practices such as frequent handwashing, avoiding close contact with people who are sick, and disinfecting surfaces can help reduce the risk of transmission. Vaccines are also being developed to protect against certain types of polyomaviruses.
7. Prognosis: In most cases, polyomavirus infections are mild and self-limiting, with symptoms resolving on their own within a few days to a week. However, severe infections can be life-threatening, particularly in individuals with weakened immune systems or underlying medical conditions.
8. Epidemiology: Polyomaviruses are common and widespread, with the majority of individuals worldwide being infected at some point in their lives. Outbreaks of polyomavirus infections can occur in settings such as hospitals, long-term care facilities, and daycare centers, where individuals with weakened immune systems are more susceptible to infection.
9. Research: Research on polyomaviruses is ongoing to better understand the viruses, their transmission, and their clinical impact. This includes development of vaccines and antiviral medications, as well as studies to identify risk factors for severe infections and to improve diagnostic tests.
10. Public health: Polyomaviruses are a public health concern, particularly in settings where individuals with weakened immune systems are more susceptible to infection. Prevention strategies include practicing good hygiene, such as frequent handwashing, and avoiding close contact with individuals who are sick.
Overall, polyomaviruses are a diverse group of viruses that can cause a range of diseases, from mild and self-limiting to severe and life-threatening. Understanding the clinical features, diagnosis, treatment, prognosis, epidemiology, research, and public health implications of polyomavirus infections is essential for providing appropriate care and preventing outbreaks.
MCC typically affects older adults, with most cases occurring in people over the age of 60. The disease is more common in fair-skinned individuals, especially those who have had prolonged exposure to the sun. MCC can occur anywhere on the body, but it is most commonly found on the face, neck, and arms.
The symptoms of MCC can vary depending on the location and size of the tumor, but they may include:
* A firm, shiny nodule or lump on the skin
* Painless lumps or swelling in the affected area
* Redness, scaliness, or oozing of the skin around the nodule
* Itching or burning sensations in the affected area
If MCC is suspected, a biopsy will be performed to confirm the diagnosis. Treatment for MCC typically involves surgery to remove the tumor and any affected tissue. In some cases, radiation therapy or chemotherapy may also be recommended to kill any remaining cancer cells.
The prognosis for MCC is generally poor, as it tends to be an aggressive disease that can spread quickly to other parts of the body. However, early detection and treatment can improve the chances of a successful outcome.
There are several different types of tumor viruses, including:
1. Human papillomavirus (HPV): This virus is responsible for causing cervical cancer and other types of cancer, such as anal, vulvar, vaginal, and penile cancer.
2. Hepatitis B virus (HBV): This virus can cause liver cancer, known as hepatocellular carcinoma (HCC).
3. Human immunodeficiency virus (HIV): This virus can increase the risk of developing certain types of cancer, such as Kaposi's sarcoma and lymphoma.
4. Epstein-Barr virus (EBV): This virus has been linked to the development of Burkitt lymphoma and Hodgkin's lymphoma.
5. Merkel cell polyomavirus (MCPyV): This virus is responsible for causing Merkel cell carcinoma, a rare type of skin cancer.
6. Human T-lymphotropic virus (HTLV-1): This virus has been linked to the development of adult T-cell leukemia/lymphoma (ATLL).
Tumor virus infections can be diagnosed through a variety of methods, including blood tests, imaging studies, and biopsies. Treatment for these infections often involves antiviral medications, chemotherapy, and surgery. In some cases, tumors may also be removed through radiation therapy.
It's important to note that not all tumors or cancers are caused by viruses, and that many other factors, such as genetics and environmental exposures, can also play a role in the development of cancer. However, for those tumor virus infections that are caused by a specific virus, early diagnosis and treatment can improve outcomes and reduce the risk of complications.
Overall, tumor virus infections are a complex and diverse group of conditions, and further research is needed to better understand their causes and develop effective treatments.
The term "leukoencephalopathy" refers to any disease or condition that affects the white matter of the brain, which is composed of nerve fibers covered in a fatty insulating substance called myelin. In LEPM, this degeneration occurs in multiple areas of the brain and spinal cord, leading to a multifocal pattern of damage.
The symptoms of LEPM usually become apparent in early childhood and may include:
* Vision loss or blurred vision
* Difficulty with movement and balance
* Cognitive decline
* Speech difficulties
As the disease progresses, patients may experience increasing disability and loss of motor function, leading to difficulties with walking, speaking, and performing everyday activities. The exact progression of LEPM is highly variable, and some individuals may experience more rapid decline than others.
The cause of LEPM is a genetic mutation in the PLP1 gene, which codes for a protein called proteolipid protein (PLP). This protein plays a critical role in the maintenance of myelin sheaths around nerve fibers, and mutations in the PLP1 gene lead to degeneration of these sheaths and the loss of axons.
There is currently no cure for LEPM, and treatment is focused on managing symptoms and slowing disease progression. This may include medications to control seizures, physical therapy to maintain muscle strength and flexibility, and vision aids to improve visual function. In some cases, bone marrow transplantation may be considered as a potential treatment option.
Overall, LEPM is a severe and debilitating disorder that can significantly impact the quality of life of affected individuals and their families. While there is currently no cure, ongoing research into the genetics and pathophysiology of this disease may lead to new treatment options in the future.
1. Activation of oncogenes: Some viruses contain genes that code for proteins that can activate existing oncogenes in the host cell, leading to uncontrolled cell growth.
2. Inactivation of tumor suppressor genes: Other viruses may contain genes that inhibit the expression of tumor suppressor genes, allowing cells to grow and divide uncontrollably.
3. Insertional mutagenesis: Some viruses can insert their own DNA into the host cell's genome, leading to disruptions in normal cellular function and potentially causing cancer.
4. Epigenetic changes: Viral infection can also cause epigenetic changes, such as DNA methylation or histone modification, that can lead to the silencing of tumor suppressor genes and the activation of oncogenes.
Viral cell transformation is a key factor in the development of many types of cancer, including cervical cancer caused by human papillomavirus (HPV), and liver cancer caused by hepatitis B virus (HBV). In addition, some viruses are specifically known to cause cancer, such as Kaposi's sarcoma-associated herpesvirus (KSHV) and Merkel cell polyomavirus (MCV).
Early detection and treatment of viral infections can help prevent the development of cancer. Vaccines are also available for some viruses that are known to cause cancer, such as HPV and hepatitis B. Additionally, antiviral therapy can be used to treat existing infections and may help reduce the risk of cancer development.
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
There are several types of skin neoplasms, including:
1. Basal cell carcinoma (BCC): This is the most common type of skin cancer, and it usually appears as a small, fleshy bump or a flat, scaly patch. BCC is highly treatable, but if left untreated, it can grow and invade surrounding tissue.
2. Squamous cell carcinoma (SCC): This type of skin cancer is less common than BCC but more aggressive. It typically appears as a firm, flat, or raised bump on sun-exposed areas. SCC can spread to other parts of the body if left untreated.
3. Melanoma: This is the most serious type of skin cancer, accounting for only 1% of all skin neoplasms but responsible for the majority of skin cancer deaths. Melanoma can appear as a new or changing mole, and it's essential to recognize the ABCDE signs (Asymmetry, Border irregularity, Color variation, Diameter >6mm, Evolving size, shape, or color) to detect it early.
4. Sebaceous gland carcinoma: This rare type of skin cancer originates in the oil-producing glands of the skin and can appear as a firm, painless nodule on the forehead, nose, or other oily areas.
5. Merkel cell carcinoma: This is a rare and aggressive skin cancer that typically appears as a firm, shiny bump on the skin. It's more common in older adults and those with a history of sun exposure.
6. Cutaneous lymphoma: This type of cancer affects the immune system and can appear as a rash, nodules, or tumors on the skin.
7. Kaposi sarcoma: This is a rare type of skin cancer that affects people with weakened immune systems, such as those with HIV/AIDS. It typically appears as a flat, red or purple lesion on the skin.
While skin cancers are generally curable when detected early, it's important to be aware of your skin and notice any changes or unusual spots, especially if you have a history of sun exposure or other risk factors. If you suspect anything suspicious, see a dermatologist for an evaluation and potential biopsy. Remember, prevention is key to avoiding the harmful effects of UV radiation and reducing your risk of developing skin cancer.
Types of Kidney Diseases:
1. Acute Kidney Injury (AKI): A sudden and reversible loss of kidney function that can be caused by a variety of factors, such as injury, infection, or medication.
2. Chronic Kidney Disease (CKD): A gradual and irreversible loss of kidney function that can lead to end-stage renal disease (ESRD).
3. End-Stage Renal Disease (ESRD): A severe and irreversible form of CKD that requires dialysis or a kidney transplant.
4. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste products.
5. Interstitial Nephritis: An inflammation of the tissue between the tubules and blood vessels in the kidneys.
6. Kidney Stone Disease: A condition where small, hard mineral deposits form in the kidneys and can cause pain, bleeding, and other complications.
7. Pyelonephritis: An infection of the kidneys that can cause inflammation, damage to the tissues, and scarring.
8. Renal Cell Carcinoma: A type of cancer that originates in the cells of the kidney.
9. Hemolytic Uremic Syndrome (HUS): A condition where the immune system attacks the platelets and red blood cells, leading to anemia, low platelet count, and damage to the kidneys.
Symptoms of Kidney Diseases:
1. Blood in urine or hematuria
2. Proteinuria (excess protein in urine)
3. Reduced kidney function or renal insufficiency
4. Swelling in the legs, ankles, and feet (edema)
5. Fatigue and weakness
6. Nausea and vomiting
7. Abdominal pain
8. Frequent urination or polyuria
9. Increased thirst and drinking (polydipsia)
10. Weight loss
Diagnosis of Kidney Diseases:
1. Physical examination
2. Medical history
3. Urinalysis (test of urine)
4. Blood tests (e.g., creatinine, urea, electrolytes)
5. Imaging studies (e.g., X-rays, CT scans, ultrasound)
6. Kidney biopsy
7. Other specialized tests (e.g., 24-hour urinary protein collection, kidney function tests)
Treatment of Kidney Diseases:
1. Medications (e.g., diuretics, blood pressure medication, antibiotics)
2. Diet and lifestyle changes (e.g., low salt intake, increased water intake, physical activity)
3. Dialysis (filtering waste products from the blood when the kidneys are not functioning properly)
4. Kidney transplantation ( replacing a diseased kidney with a healthy one)
5. Other specialized treatments (e.g., plasmapheresis, hemodialysis)
Prevention of Kidney Diseases:
1. Maintaining a healthy diet and lifestyle
2. Monitoring blood pressure and blood sugar levels
3. Avoiding harmful substances (e.g., tobacco, excessive alcohol consumption)
4. Managing underlying medical conditions (e.g., diabetes, high blood pressure)
5. Getting regular check-ups and screenings
Early detection and treatment of kidney diseases can help prevent or slow the progression of the disease, reducing the risk of complications and improving quality of life. It is important to be aware of the signs and symptoms of kidney diseases and seek medical attention if they are present.
SV40 large T antigen
Middle tumor antigen
Merkel cell polyomavirus
Index of biochemistry articles
List of MeSH codes (D12.776)
List of MeSH codes (D23)
Small tumor antigen
Large tumor antigen
Eugene O. Major
Kimberly W. Anderson
Tumor antigens recognized by T lymphocytes
Mouse models of breast cancer metastasis
Janet S. Butel
Digital polymerase chain reaction
Antigens, Polyomavirus Transforming | Profiles RNS
Isolation and characterization of NIH 3T3 cells expressing polyomavirus small T antigen - PubMed
Establishment of a line of human fetal glial cells that supports JC virus multiplication - PubMed
OPUS Würzburg | Search
JCI - Human glial chimeric mice reveal astrocytic dependence of JC virus infection
Antigens cd137. Medical search
Cancer resistance in the blind mole rat is mediated by concerted necrotic cell death mechanism - Fingerprint - University...
Yu-Guang He - Research output - University of Texas Southwestern Medical Center
DeCS 2018 - July 31, 2018 version
Pesquisa | Prevenção e Controle de Câncer
Frontiers | Generation and Characterization of Immortalized Mouse Cortical Astrocytes From Wildtype and Connexin43 Knockout Mice
NDF-RT Code NDF-RT Name
Novel Polyomavirus associated with Brain Tumors in Free-Ranging Raccoons, Western United States - Volume 19, Number 1-January...
ABORTIFACIENT AGENTS ABORTIFACIENT AGENTS
The immune response to sporadic colorectal cancer in a novel mouse model. - Radcliffe Department of Medicine
1st February, 1973
Chickens | Scholars@Duke
Merkel Cell Carcinoma and Rare Appendageal Tumors: Overview, Tumors of the Epidermis, Tumorlike Lesions of Fibrous or Elastic...
Beeman, Edward S. 2004 - Office of NIH History and Stetten Museum
- The large T antigen is necessary for the initiation of viral DNA synthesis, repression of transcription of the early region and is responsible in conjunction with the middle T antigen for the transformation of primary cells. (uchicago.edu)
- the expression of viral T antigens is crucial for growth of virus-positive tumor cells. (uni-wuerzburg.de)
- Our results uncover the mechanism of a host stress response regulating human polyomavirus genome maintenance in viral persistency, which may lead to targeted intervention for MCC. (bvsalud.org)
- We were excited to find that middle T antigen became phosphorylated in immunoprecipitates, and by the middle of 1979, we had shown through the use of viral mutants that the presence of this protein kinase activity correlated well with the ability of middle T antigen to transform mammalian cells. (nih.gov)
- Furthermore, transgenic mice harboring the viral-encoded large T-antigen (LT-Ag) alone develop tumors of neuroectodermal origin, including malignant peripheral nerve sheath tumors (MPNSTs) and glioblastomas. (cdc.gov)
- Other studies reported that SV40 T-antigen, a viral protein, binds to Please note that this is not a comprehensive list of all SV40-associated cancers or all medical/scientific articles written about the detection of SV40 in cancer. (netlify.app)
- This heritability of virus-transformed phenotype, even in the absence of viral replication [ 9 ], led Howard Temin to postulate that in the infected cell, the RSV genome made a DNA copy which then integrated into host chromosomal DNA [ 10 ]. (biomedcentral.com)
- The piggyBac transposon-mediated expression of SV40 T antigen efficiently immortalizes mouse embryonic fibroblasts (MEFs). (uchicago.edu)
- Studies have reported differing frequencies of detection of polyomavirus simian virus 40 (SV40) in association with human lymphomas. (nih.gov)
- This time I have included an SV40 transformed BHK as a control as well as ST6. (nih.gov)
- Virus förmåga att framkalla cancer är en följd av att Minst fyra satser vaccin smittat med ett virus kallat SV40 släpptes uppges ha visat att apviruset var en möjlig orsak till cancer hos människor. (netlify.app)
- Kinetics of Senescence-associated Changes of Gene Expression in an Epithelial, Temperature-sensitive SV40 Large T Antigen Model. (netlify.app)
- Read Cancer from the story Kost & kunskap by Nikki_Jansson (Nikki Janzon) SV40- viruset spreds förstås som en löpeld och vi kan hitta den i mängder av Start studying Virologi 9 - Virus och Cancer. (netlify.app)
- Svarta, homosexuella och handikappade barn har ingått Mellan 56-61 så fann man att en form av oralt poliovaccin hade kontaminerats av SV40, även om SV40 tekniskt sett ger tumörer och inte cancer. (netlify.app)
- The phosphorylation of tyrosine residues in proteins was discovered in 1979 during our analysis of the protein kinase activity that phosphorylates the middle T antigen of polyoma virus in vitro. (nih.gov)
- Other retroviral transforming proteins were soon found to be tyrosine kinases, and the epidermal growth factor (EGF) receptor was shown to have tyrosine kinase activity that is stimulated by EGF binding. (nih.gov)
- This finding was quickly followed by the demonstration by others that the v-Fps and v-Abl retroviral transforming proteins are tyrosine kinases, and that the EGF receptor also has tyrosine kinase activity that is stimulated by EGF binding. (nih.gov)
- Cytokine -- Non-antibody immune system proteins released by one type of cell in response to a specific antigen. (nih.gov)
- Here, we show that MCPyV large T (LT) antigen expression in human skin fibroblasts causes a novel nucleolar stress response, followed by p21-dependent senescence and senescence-associated secretory phenotypes (SASPs), which are required for MCPyV genome maintenance. (bvsalud.org)
- ALV replicates in chick embryo fibroblasts but does not transform them. (biomedcentral.com)
- Rous sarcoma virus (RSV) is closely related but carries the src oncogene and transforms fibroblasts. (biomedcentral.com)
- Localization of Merkel cell polyomavirus (MCPyV) RNA was confirmed by RNAScope in situ hybridization. (bvsalud.org)
- Based on Merkel cell polyomavirus (MCPyV) status and morphology, MCCs are often divided into several distinct subsets: pure MCPyV-positive, pure MCPyV-negative, and combined MCC. (bvsalud.org)
- Merkel cell carcinoma (MCC) is an aggressive skin cancer induced by a life-long human infection of Merkel cell polyomavirus (MCPyV). (bvsalud.org)
- Recent advances have been made by an accumulation of studies on Merkel cell polyomavirus (MCPyV), which is highly associated and integrated in most Merkel cell carcinomas ( 5 ). (cdc.gov)
- Merkel cell polyomavirus (MCV) is known to be a human carcinogen based on sufficient evidence from studies in humans. (nih.gov)
Middle T antigen5
- These include a syngeneic model using E0771 mammary tumor cells as well as the Polyoma Middle T antigen (PyMT) transgenic model. (nih.gov)
- The presence of phosphotyrosine in the middle T antigen was the first indication that tyrosine could be a target for phosphorylation by a protein kinase. (nih.gov)
- As soon as Marc Collett and Ray Erikson, then at University of Colorado in Denver, reported in 1978 that the RSV-transforming protein, v-Src, had protein-kinase activity when assayed in an immunoprecipitate, we began to test whether polyoma virus middle T antigen also had such activity. (nih.gov)
- In the course of analyzing by acid hydrolysis which amino acid was phosphorylated in middle T antigen, we discovered that the phosphate was not linked to serine or threonine but to another amino acid. (nih.gov)
- We guessed that this might be tyrosine, quickly made some phosphotyrosine, and showed that the product of acid hydrolysis of phosphorylated middle T antigen co-migrated with the synthetic phosphotyrosine. (nih.gov)
- Two transgenic mouse models with spontaneous tumor development were generated, directing the expression of SV40T antigen (Tag) either constitutively (Vil-Cre × LoxP-Tag-transgenic mice) or stochastically (Vil-Cre-ER(T2) × LoxP-Tag-transgenic mice) into the putative stem cell region of the crypt of Lieberkühn. (ox.ac.uk)
- CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. (lookformedical.com)
- Costimulatory T-LYMPHOCYTE receptors that have specificity for CD80 ANTIGEN and CD86 ANTIGEN. (lookformedical.com)
- Differentiation antigens residing on mammalian leukocytes. (lookformedical.com)
- Differentiation antigens found on thymocytes and on cytotoxic and suppressor T-lymphocytes. (lookformedical.com)
- Differentiation antigens expressed on B-lymphocytes and B-cell precursors. (lookformedical.com)
- A membrane glycoprotein and differentiation antigen expressed on the surface of T-cells that binds to CD40 ANTIGENS on B-LYMPHOCYTES and induces their proliferation. (lookformedical.com)
- Differentiation antigens expressed on pluripotential hematopoietic cells, most human thymocytes, and a major subset of peripheral blood T-lymphocytes. (lookformedical.com)
- Complex of at least five membrane-bound polypeptides in mature T-lymphocytes that are non-covalently associated with one another and with the T-cell receptor (RECEPTORS, ANTIGEN, T-CELL). (lookformedical.com)
- The CD3 gamma and delta chains (subunits) are separate from and not related to the gamma/delta chains of the T-cell receptor (RECEPTORS, ANTIGEN, T-CELL, GAMMA-DELTA). (lookformedical.com)
- CD44 antigens are the principle cell surface receptors for hyaluronate and this interaction mediates binding of lymphocytes to high endothelial venules. (lookformedical.com)
- When antigen binds to the T-cell receptor, the CD3 complex transduces the activating signals to the cytoplasm of the T-cell. (lookformedical.com)
- Interest had centered on a single protein called middle T (or tumor) antigen, which is encoded by one of the three alternatively spliced mRNAs generated from the so-called early region of the polyoma virus genome. (nih.gov)
- For instance, a multivalent target binding protein may bind to both a tumor antigen and a cytotoxic agent, and can be used for delivery of radionuclides, drugs, toxins or other cytotoxic agents to tumor cells. (allindianpatents.com)
- This effect was accompanied by reduced large T antigen (LT) expression. (uni-wuerzburg.de)
- The multifunctional nuclear protein large T-antigen was detectable by immunohistochemical analyses in a subset of neoplastic cells. (cdc.gov)
- We will isolate 5 more clones in the ST series (starting from scratch but infecting low serum cells), grow them into large batches and if you are willing and interested will send them to you for testing, as well as to Vittorio Defendi for T-antigen. (nih.gov)
- Interestingly, in one MCC cell line (WaGa), T antigen knockdown rendered cells less sensitive to artesunate, while for two other MCC cell lines, we could not substantiate such a relation. (uni-wuerzburg.de)
- Antigens on surfaces of cells, including infectious or foreign cells or viruses. (lookformedical.com)
- Moreover, we showed that v-Src- transformed cells have elevated levels of phosphotyrosine in protein. (nih.gov)
- The transplantation antigen on ST1 cells is at the moment under test again. (nih.gov)
- On one plate with 4 x 105 cells there were 75 transformed foci on a background of normal cells. (nih.gov)
- [ 7 ] In KAs, cells that stain positive with proliferating-cell nuclear antigen immunostaining are distributed only in the outer edges of the tumor, corresponding to the proliferating squamous epithelial cells. (medscape.com)
- In contrast, cells within an SCC that stain positive with proliferating-cell nuclear antigen immunostaining are more diffusely distributed. (medscape.com)
- The BPV-1 E1 ORF encodes two gene products expressed in BPV transformed cells from the major early promoter, P89. (nih.gov)
- More recent findings, however, indicate that E1-M is not essential for stable plasmid replication in BPV-1 transformed cells (25). (nih.gov)
- Isolated fractions were examined for their capacity to bind [125I]C1q as a measure of immune complex levels, and for their ability to bind soluble tumour-specific antigen as well as to react with antigens expressed at the surface of viable hepatoma cells. (nih.gov)
- However, cells transformed by RSV maintained stable properties through many mitoses. (biomedcentral.com)
- Thus the concept of integration of DNA tumor virus genomes in transformed somatic cells was debated, and was demonstrated in 1968 [ 12 ]. (biomedcentral.com)
- Although of clinical diagnostic and prognostic value, the currently widely used PSA (prostate specific antigen) biomarker does not fulfil the above mentioned requirements, and there is an immense search for new more specific and sensitive biomarkers in order to provide the necessary information regarding screening, classification, prognosis and prediction. (abcdocz.com)
- Adenovector-mediated gene transfer of active transforming growth factor-beta1 induces prolonged severe fibrosis in rat lung. (mcmaster.ca)
- However, natural disease studies of human infection and experimental disease studies suggest that a potential outcome of some polyomavirus (PyV) infections is tumor formation ( 4 - 6 ). (cdc.gov)
- We have identified a candidate etiologic agent, dubbed raccoon polyomavirus, that was present in the tumor tissue of all affected animals but not in tissues from 20 unaffected animals. (cdc.gov)
- Much of what we know about the immune system and its relationship to cancer was discovered by scientists affiliated with the Cancer Research Institute (CRI), which since 1953 has served as the world's leading (and for several decades only) nonprofit organization dedicated exclusively to transforming cancer patient care by advancing immunotherapy and the science behind it. (cancerresearch.org)
- Small T antigen is necessary for the completion of the productive infection cycle. (uchicago.edu)
- This graph shows the total number of publications written about "Antigens, Polyomavirus Transforming" by people in this website by year, and whether "Antigens, Polyomavirus Transforming" was a major or minor topic of these publications. (uchicago.edu)
- CD8 antigens are members of the immunoglobulin supergene family and are associative recognition elements in MHC (Major Histocompatibility Complex) Class I-restricted interactions. (lookformedical.com)