Moloney murine leukemia virus
Leukemia Virus, Murine
Leukemia, Experimental
AKR murine leukemia virus
Friend murine leukemia virus
Moloney murine sarcoma virus
RNA-Directed DNA Polymerase
Abelson murine leukemia virus
Retroviridae
Sarcoma Viruses, Murine
Preleukemia
Gene Products, gag
Leukemia Virus, Feline
Proviruses
Virus Replication
3T3 Cells
Mink Cell Focus-Inducing Viruses
Virus Integration
Base Sequence
Rauscher Virus
Molecular Sequence Data
Ribonuclease H
Repetitive Sequences, Nucleic Acid
Genetic Vectors
Leukemia Virus, Bovine
Gammaretrovirus
Tumor Virus Infections
Genes, gag
Virion
Receptors, Virus
Gene Products, env
Viral Envelope Proteins
Retroviridae Proteins, Oncogenic
Leukemia
Defective Viruses
Integrases
Cell Transformation, Viral
Mice, Inbred Strains
Retroviridae Proteins
Genes, pol
Helper Viruses
Amino Acid Sequence
Genes, env
Recombination, Genetic
Virus Assembly
Nucleic Acid Hybridization
Cloning, Molecular
Transfection
DNA, Recombinant
Transcription, Genetic
Mutation
Terminal Repeat Sequences
Enhancer Elements, Genetic
Transduction, Genetic
Hylobates
Leukemia, Myeloid, Acute
Paralysis
Mink
Thymoma
RNA, Transfer, Pro
Leukemia Virus, Gibbon Ape
Gene Expression Regulation, Viral
Lymphoma, T-Cell
DNA Restriction Enzymes
Plasmids
Proto-Oncogene Proteins c-pim-1
Cell Transformation, Neoplastic
Blotting, Southern
Oncogenes
Human T-lymphotropic virus 1
HIV-1
Giant Cells
Cells, Cultured
Restriction Mapping
Fusion Proteins, gag-pol
Species Specificity
DNA Nucleotidyltransferases
NIH 3T3 Cells
DNA Primers
Proto-Oncogenes
Leukemia, Erythroblastic, Acute
Viral Plaque Assay
Templates, Genetic
Binding Sites
Polymerase Chain Reaction
T-Lymphocytes
Temperature
Gene Transfer Techniques
Cell Fusion
Xenotropic murine leukemia virus-related virus
Recombinant Fusion Proteins
Nucleic Acid Conformation
Oligonucleotides
Leukemia, Lymphocytic, Chronic, B-Cell
Mutagenesis
Clone Cells
Leukemia, Lymphoid
Muridae
Mutagenesis, Insertional
Cell Line, Transformed
Promoter Regions, Genetic
Simian virus 40
Lentivirus
Radiation Leukemia Virus
Genes
Murine Acquired Immunodeficiency Syndrome
Gene Products, tax
Vesicular stomatitis Indiana virus
Sarcoma, Experimental
Glycoproteins
Tumor Cells, Cultured
Oligodeoxyribonucleotides
Membrane Fusion
RNA, Messenger
Avian Sarcoma Viruses
Bone Marrow
Thymus Gland
Gene Products, pol
DNA
Gene Expression Regulation
Genetic Therapy
Viral Core Proteins
RNA, Transfer
Protein Processing, Post-Translational
DNA-Binding Proteins
Cricetinae
Endoribonucleases
Cats
Viral Interference
Teratoma
Kanamycin Kinase
HeLa Cells
Mutagenesis, Site-Directed
DNA, Circular
Vaccinia virus
Sequence Homology, Nucleic Acid
Oncogene Proteins v-abl
Structure-Activity Relationship
Chromosome Mapping
Enzootic Bovine Leukosis
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Zinc Fingers
Fibroblasts
Nucleic Acid Heteroduplexes
RNA
Gene Expression
Avian leukosis virus
Lymphocytes
Transcription Factors
Deoxyribonucleotides
Microscopy, Electron
Cell-Free System
RNA Splicing
Sodium-Phosphate Cotransporter Proteins, Type III
Genes, Regulator
Chloramphenicol O-Acetyltransferase
Leukemia, Radiation-Induced
Antiviral Agents
Nucleic Acid Denaturation
Codon
Suppression of Moloney sarcoma virus immunity following sensitization with attenuated virus. (1/1467)
Murine sarcoma virus (Moloney strain) (MSV-M)-induced tumors are unusual in that they regularly appear less than 2 weeks after virus inoculation, progress for 1 to 2 weeks, and are rejected by normal adult BALB/c mice. Rejectio leaves the animals immune to tumor induction. In the present study, presensitization of normal adult BALB/c mice with attenuated MSV-M resulted in an altered pattern of tumor immunity. Injection of active MSV-M into the presensitized animals resulted in tumor induction and rejection similar to that observed in normal animals, but rejection failed to produce protection against the secondary inoculation with MSV-M. After the second inoculation with active MSV-M, tumors appeared and progressed but ultimately were rejected. Over 80% of the mice died, 25% after the primary challenge and the remainder after the secondary challenge. At death, all mice had histological evidence of leukemia which was the probable cause of death. The animals that died following the secondary challenge also had evidence of disseminated MSV-M. Solid tumor nodules were found in skeletal muscle distant from the original site of inoculation, and active MSV-M was isolated from spleen and lungs. The possibility that the results were produced by specific suppression of MSV-Moloney leukemia virus immunity is discussed. (+info)Inhibition of the rous sarcoma virus long terminal repeat-driven transcription by in vitro methylation: different sensitivity in permissive chicken cells versus mammalian cells. (2/1467)
Rous sarcoma virus (RSV) enhancer sequences in the long terminal repeat (LTR) have previously been shown to be sensitive to CpG methylation. We report further that the high density methylation of the RSV LTR-driven chloramphenicol acetyltransferase reporter is needed for full transcriptional inhibition in chicken embryo fibroblasts and for suppression of tumorigenicity of the RSV proviral DNA in chickens. In nonpermissive mammalian cells, however, the low density methylation is sufficient for full inhibition. The time course of inhibition differs strikingly in avian and mammalian cells: although immediately inhibited in mammalian cells, the methylated RSV LTR-driven reporter is fully inhibited with a significant delay after transfection in avian cells. Moreover, transcriptional inhibition can be overridden by transfection with a high dose of the methylated reporter plasmid in chicken cells but not in hamster cells. The LTR, v-src, LTR proviral DNA is easily capable of inducing sarcomas in chickens but not in hamsters. In contrast, Moloney murine leukemia virus LTR-driven v-src induces sarcomas in hamsters with high incidence. Therefore, the repression of integrated RSV proviruses in rodent cells is directed against the LTR. (+info)Gene transfer of cytokine inhibitors into human synovial fibroblasts in the SCID mouse model. (3/1467)
OBJECTIVE: To investigate the effects of retrovirus-based gene delivery of inhibitory cytokines and cytokine inhibitors into human synovial fibroblasts in the SCID mouse model of rheumatoid arthritis (RA). METHODS: The MFG vector was used for gene delivery of tumor necrosis factor alpha receptor (TNFalphaR) p55, viral interleukin-10 (IL-10), and murine IL-10 into RA synovial fibroblasts. The effect on invasion of these cells into human articular cartilage and on perichondrocytic cartilage degradation was examined after 60 days of coimplantation into the SCID mouse. RESULTS: TNFalphaR p55 gene transfer showed only a limited effect on inhibition of RA synovial fibroblast invasiveness and cartilage degradation. In contrast, invasion of the RA synovial fibroblasts into the coimplanted cartilage was strongly inhibited by both viral and murine IL-10. Perichondrocytic cartilage degradation was not affected by either form of IL-10. CONCLUSION: The data show that cytokines can be successfully inserted into the genome of human RA synovial fibroblasts using a retroviral vector delivery system, and that the SCID mouse model of human RA is a valuable tool for examining the effects of gene transfer. In addition, inhibition of more than one cytokine pathway may be required to inhibit both synovial- and chondrocyte-mediated cartilage destruction in RA. (+info)Development of viral vectors for gene therapy of beta-chain hemoglobinopathies: optimization of a gamma-globin gene expression cassette. (4/1467)
Progress toward gene therapy of beta-chain hemoglobinopathies has been limited in part by poor expression of globin genes in virus vectors. To derive an optimal expression cassette, we systematically analyzed the sequence requirements and relative strengths of the Agamma- and beta-globin promoters, the activities of various erythroid-specific enhancers, and the importance of flanking and intronic sequences. Expression was analyzed by RNase protection after stable plasmid transfection of the murine erythroleukemia cell line, MEL585. Promoter truncation studies showed that the Agamma-globin promoter could be deleted to -159 without affecting expression, while deleting the beta-globin promoter to -127 actually increased expression compared with longer fragments. Expression from the optimal beta-globin gene promoter was consistently higher than that from the optimal Agamma-globin promoter, regardless of the enhancer used. Enhancers tested included a 2.5-kb composite of the beta-globin locus control region (termed a muLCR), a combination of the HS2 and HS3 core elements of the LCR, and the HS-40 core element of the alpha-globin locus. All three enhancers increased expression from the beta-globin gene to roughly the same extent, while the HS-40 element was notably less effective with the Agamma-globin gene. However, the HS-40 element was able to efficiently enhance expression of a Agamma-globin gene linked to the beta-globin promoter. Inclusion of extended 3' sequences from either the beta-globin or the Agamma-globin genes had no significant effect on expression. A 714-bp internal deletion of Agamma-globin intron 2 unexpectedly increased expression more than twofold. With the combination of a -127 beta-globin promoter, an Agamma-globin gene with the internal deletion of intron 2, and a single copy of the HS-40 enhancer, gamma-globin expression averaged 166% of murine alpha-globin mRNA per copy in six pools and 105% in nine clones. When placed in a retrovirus vector, this cassette was also expressed at high levels in MEL585 cells (averaging 75% of murine alpha-globin mRNA per copy) without reducing virus titers. However, recombined provirus or aberrant splicing was observed in 5 of 12 clones, indicating a significant degree of genetic instability. Taken together, these data demonstrate the development of an optimal expression cassette for gamma-globin capable of efficient expression in a retrovirus vector and form the basis for further refinement of vectors containing this cassette. (+info)One-day ex vivo culture allows effective gene transfer into human nonobese diabetic/severe combined immune-deficient repopulating cells using high-titer vesicular stomatitis virus G protein pseudotyped retrovirus. (5/1467)
Retrovirus-mediated gene transfer into long-lived human pluripotent hematopoietic stem cells (HSCs) is a widely sought but elusive goal. A major problem is the quiescent nature of most HSCs, with the perceived requirement for ex vivo prestimulation in cytokines to induce stem cell cycling and allow stable gene integration. However, ex vivo culture may impair stem cell function, and could explain the disappointing clinical results in many current gene transfer trials. To address this possibility, we examined the ex vivo survival of nonobese diabetic/severe combined immune-deficient (NOD/SCID) repopulating cells (SRCs) over 3 days. After 1 day of culture, the SRC number and proliferation declined twofold, and was further reduced by day 3; self-renewal was only detectable in noncultured cells. To determine if the period of ex vivo culture could be shortened, we used a vesicular stomatitis virus G protein (VSV-G) pseudotyped retrovirus vector that was concentrated to high titer. The results showed that gene transfer rates were similar without or with 48 hours prestimulation. Thus, the use of high-titer VSV-G pseudotyped retrovirus may minimize the loss of HSCs during culture, because efficient gene transfer can be obtained without the need for extended ex vivo culture. (+info)Gene transfer to human pancreatic endocrine cells using viral vectors. (6/1467)
We have studied the factors that influence the efficiency of infection of human fetal and adult pancreatic endocrine cells with adenovirus, murine retrovirus, and lentivirus vectors all expressing the green fluorescent protein (Ad-GFP, MLV-GFP, and Lenti-GFP, respectively). Adenoviral but not retroviral vectors efficiently infected intact pancreatic islets and fetal islet-like cell clusters (ICCs) in suspension. When islets and ICCs were plated in monolayer culture, infection efficiency with all three viral vectors increased. Ad-GFP infected 90-95% of the cells, whereas infection with MLV-GFP and Lenti-GFP increased only slightly. Both exposure to hepatocyte growth factor/scatter factor (HGF/SF) and dispersion of the cells by removal from the culture dish and replating had substantial positive effects on the efficiency of infection with retroviral vectors. Studies of virus entry and cell replication revealed that cell dispersion and stimulation by HGF/SF may be acting through both mechanisms to increase the efficiency of retrovirus-mediated gene transfer. Although HGF/SF and cell dispersion increased the efficiency of infection with MLV-GFP, only rare cells with weak staining for insulin were infected, whereas approximately 25% of beta-cells were infected with Lenti-GFP. We conclude that adenovirus is the most potent vector for ex vivo overexpression of foreign genes in adult endocrine pancreatic cells and is the best vector for applications where high-level but transient expression is desired. Under the optimal conditions of cell dispersion plus HGF/SF, infection with MLV and lentiviral vectors is reasonably efficient and stable, but only lentiviral vectors efficiently infect pancreatic beta-cells. (+info)Transplantation of transduced nonhuman primate CD34+ cells using a gibbon ape leukemia virus vector: restricted expression of the gibbon ape leukemia virus receptor to a subset of CD34+ cells. (7/1467)
The transduction efficiencies of immunoselected rhesus macaque (Macaca mulatta) CD34+ cells and colony-forming progenitor cells based on polymerase chain reaction (PCR) analysis were comparable for an amphotropic Moloney murine leukemia virus (MLV) retroviral vector and a retroviral vector derived from the gibbon ape leukemia virus (GaLV) packaging cell line, PG13. On performing autologous transplantation studies using immunoselected CD34+ cells transduced with the GaLV envelope (env) retroviral vector, less than 1% of peripheral blood (PB) contained provirus. This was true whether bone marrow (BM) or cytokine-mobilized PB immunoselected CD34+ cells were reinfused. This level of marking was evident in two animals whose platelet counts never fell below 50,000/microliter and whose leukocyte counts had recovered by days 8 and 10 after having received 1.7 x 10(7) or greater of cytokine-mobilized CD34+ PB cells/kg. Reverse transcriptase(RT)-PCR analysis of CD34+ subsets for both the GaLV and amphotropic receptor were performed. The expression of the GaLV receptor was determined to be restricted to CD34+ Thy-1+ cells, and both CD34+ CD38+ and CD34+ CD38dim cells, while the amphotropic receptor was present on all CD34+ cell subsets examined. Our findings suggest that, in rhesus macaques, PG13-derived retroviral vectors may only be able to transduce a subset of CD34+ cells as only CD34+ Thy-1+ cells express the GaLV receptor. (+info)Retrovirus integration site Mintb encoding the mouse homolog of hnRNP U. (8/1467)
Retroviral genes are not usually expressed in mouse embryonal carcinoma (EC) cells, but they are readily expressed upon differentiation of these cells. We previously reported the isolation of EC cell lines that express a neomycin resistance (neo) gene introduced by a recombinant transducing Moloney murine leukemia virus from specific integration sites, Minta, Mintb, Mintc, or Mintd. In some of these clones, the entire 5' long terminal repeat (LTR) was deleted, and the neo gene was expressed by read-through transcription from upstream cellular promoters in a "promoter-trap" fashion. One such promoter ("promoter B" at the Mintb locus) was found in a CpG island, associated with an upstream enhancer ("enhancer B"). Although enhancer B caused expression of the neo gene in the transductant EC cell line, no endogenous transcription from promoter B was detected in the parental EC or NIH3T3 cells. In contrast, we found a strong counter-flow endogenous transcription unit ("R" for reverse), which apparently interfered with transcription from promoter B. Promoter R turned out to have a bidirectional activity in transfection assays. In normal tissues, promoter R activates gene R, which encodes an 800-residue protein that is highly homologous to the rat and human heterogeneous nuclear ribonucleoprotein U (hnRNP U). Northern and in situ hybridization analyses revealed that gene R was abundantly expressed in the testis, especially in the pachytene spermatocytes and round spermatids. (+info)Examples of experimental leukemias include:
1. X-linked agammaglobulinemia (XLA): A rare inherited disorder that leads to a lack of antibody production and an increased risk of infections.
2. Diamond-Blackfan anemia (DBA): A rare inherited disorder characterized by a failure of red blood cells to mature in the bone marrow.
3. Fanconi anemia: A rare inherited disorder that leads to a defect in DNA repair and an increased risk of cancer, particularly leukemia.
4. Ataxia-telangiectasia (AT): A rare inherited disorder characterized by progressive loss of coordination, balance, and speech, as well as an increased risk of cancer, particularly lymphoma.
5. Down syndrome: A genetic disorder caused by an extra copy of chromosome 21, which increases the risk of developing leukemia, particularly acute myeloid leukemia (AML).
These experimental leukemias are often used in research studies to better understand the biology of leukemia and to develop new treatments.
1. HIV (Human Immunodeficiency Virus): This is a virus that attacks the body's immune system, making it difficult to fight off infections and diseases. HIV is a type of retrovirus that can lead to AIDS (Acquired Immunodeficiency Syndrome).
2. HTLV-1 (Human T-lymphotropic virus type 1): This is a virus that affects the immune system and can lead to diseases such as adult T-cell leukemia/lymphoma and myelopathy.
3. HBV (Hepatitis B Virus): This is a virus that attacks the liver and can cause inflammation, scarring, and cirrhosis.
4. HCV (Hepatitis C Virus): This is a virus that attacks the liver and can cause inflammation, scarring, and cirrhosis.
5. FeLV (Feline Leukemia Virus): This is a virus that affects cats and can cause a variety of diseases, including leukemia and lymphoma.
6. FIV (Feline Immunodeficiency Virus): This is a virus that affects cats and can weaken their immune system, making them more susceptible to other infections and diseases.
7. Bovine Immunodeficiency Virus (BIV): This is a virus that affects cattle and can cause a variety of diseases, including leukemia and lymphoma.
8. Equine Infectious Anemia Virus (EIAV): This is a virus that affects horses and can cause a variety of diseases, including anemia and swelling of the lymph nodes.
Retroviridae infections are typically diagnosed through blood tests that detect the presence of antibodies or genetic material from the virus. Treatment options vary depending on the specific virus and the severity of the infection, but may include antiretroviral medications, immune-suppressive drugs, and supportive care such as blood transfusions or antibiotics for secondary infections.
It is important to note that retroviruses can be transmitted through contact with infected bodily fluids, such as blood, semen, and breast milk. Therefore, it is important to take precautions such as using condoms, gloves, and other protective measures when dealing with infected individuals or animals. Additionally, it is important to maintain good hygiene practices, such as washing hands regularly, to reduce the risk of transmission.
There are several different types of preleukemia, including:
1. Myelodysplastic syndrome (MDS): A condition where there is a defect in the development of immature blood cells in the bone marrow, leading to an overproduction of blasts and a decrease in the number of healthy red blood cells, white blood cells, and platelets.
2. Myeloproliferative neoplasms (MPNs): A group of conditions characterized by an overproduction of one or more types of blood cells, including red blood cells, white blood cells, and platelets. MPNs can progress to leukemia over time.
3. Chronic myelogenous leukemia (CML): A type of leukemia that develops from a preleukemic condition called chronic myeloid leukemia. CML is characterized by the presence of a genetic abnormality known as the Philadelphia chromosome, which leads to an overproduction of white blood cells.
4. Acute myeloid leukemia (AML): A type of leukemia that can develop from preleukemic conditions such as MDS and MPNs. AML is characterized by the rapid growth of immature white blood cells in the bone marrow, which can crowd out healthy cells and lead to a decrease in the number of normal red blood cells, white blood cells, and platelets.
Preleukemia can be difficult to diagnose, as it often does not have clear symptoms in its early stages. However, doctors may use a variety of tests, including blood tests and bone marrow biopsies, to detect abnormalities in the blood or bone marrow that could indicate preleukemia.
Treatment for preleukemia depends on the specific type of condition and its severity. Some common treatments include:
1. Chemotherapy: A type of cancer treatment that uses drugs to kill cancer cells. Chemotherapy may be used to treat preleukemia, particularly in cases where there are abnormalities in the blood or bone marrow.
2. Blood transfusions: Transfusions of healthy red blood cells, platelets, or plasma may be given to patients with preleukemia who have low levels of these cells.
3. Supportive care: Patients with preleukemia may require supportive care, such as antibiotics or other medications, to manage symptoms and prevent complications.
4. Stem cell transplantation: In some cases, stem cell transplantation may be recommended for patients with preleukemia who have a high risk of developing acute leukemia. This involves replacing the patient's defective bone marrow stem cells with healthy ones from a donor.
Overall, early detection and treatment of preleukemia can improve outcomes and reduce the risk of developing acute leukemia. If you have been diagnosed with preleukemia or are experiencing symptoms that may indicate preleukemia, it is important to discuss your treatment options with your healthcare provider.
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.
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.
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.
A thymus neoplasm is a type of cancer that originates in the thymus gland, which is located in the chest behind the sternum and is responsible for the development and maturation of T-lymphocytes (T-cells) of the immune system.
Types of Thymus Neoplasms
There are several types of thymus neoplasms, including:
1. Thymoma: A slow-growing tumor that is usually benign but can sometimes be malignant.
2. Thymic carcinoma: A more aggressive type of cancer that is less common than thymoma.
3. Thymic lymphoma: A type of cancer that arises from the T-cells in the thymus gland and can be either B-cell or T-cell derived.
Symptoms of Thymus Neoplasms
The symptoms of thymus neoplasms can vary depending on the location and size of the tumor, but they may include:
1. Chest pain or discomfort
2. Coughing or shortness of breath
3. Fatigue or fever
4. Swelling in the neck or face
5. Weight loss or loss of appetite
Diagnosis of Thymus Neoplasms
The diagnosis of a thymus neoplasm typically involves a combination of imaging tests such as chest X-rays, computed tomography (CT) scans, and positron emission tomography (PET) scans, as well as a biopsy to confirm the presence of cancer cells.
Treatment of Thymus Neoplasms
The treatment of thymus neoplasms depends on the type and stage of the cancer, but may include:
1. Surgery to remove the tumor
2. Radiation therapy to kill any remaining cancer cells
3. Chemotherapy to destroy cancer cells
4. Targeted therapy to specific molecules involved in the growth and progression of the cancer.
Prognosis of Thymus Neoplasms
The prognosis for thymus neoplasms depends on the type and stage of the cancer at the time of diagnosis. In general, the earlier the cancer is detected and treated, the better the prognosis.
Prevention of Thymus Neoplasms
There is no known way to prevent thymus neoplasms, as they are rare and can occur in people of all ages. However, early detection and treatment of the cancer can improve the chances of a successful outcome.
Current Research on Thymus Neoplasms
Researchers are currently studying new treatments for thymus neoplasms, such as targeted therapies and immunotherapy, which use the body's own immune system to fight cancer. Additionally, researchers are working to develop better diagnostic tests to detect thymus neoplasms at an earlier stage, when they are more treatable.
Conclusion
Thymus neoplasms are rare and complex cancers that require specialized care and treatment. While the prognosis for these cancers can be challenging, advances in diagnosis and treatment have improved outcomes for many patients. Researchers continue to study new treatments and diagnostic tools to improve the chances of a successful outcome for those affected by thymus neoplasms.
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.
AML is a fast-growing and aggressive form of leukemia that can spread to other parts of the body through the bloodstream. It is most commonly seen in adults over the age of 60, but it can also occur in children.
There are several subtypes of AML, including:
1. Acute promyelocytic leukemia (APL): This is a subtype of AML that is characterized by the presence of a specific genetic abnormality called the PML-RARA fusion gene. It is usually responsive to treatment with chemotherapy and has a good prognosis.
2. Acute myeloid leukemia, not otherwise specified (NOS): This is the most common subtype of AML and does not have any specific genetic abnormalities. It can be more difficult to treat and has a poorer prognosis than other subtypes.
3. Chronic myelomonocytic leukemia (CMML): This is a subtype of AML that is characterized by the presence of too many immature white blood cells called monocytes in the blood and bone marrow. It can progress slowly over time and may require ongoing treatment.
4. Juvenile myeloid leukemia (JMML): This is a rare subtype of AML that occurs in children under the age of 18. It is characterized by the presence of too many immature white blood cells called blasts in the blood and bone marrow.
The symptoms of AML can vary depending on the subtype and the severity of the disease, but they may include:
* Fatigue
* Weakness
* Shortness of breath
* Pale skin
* Easy bruising or bleeding
* Swollen lymph nodes, liver, or spleen
* Bone pain
* Headache
* Confusion or seizures
AML is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as:
1. Complete blood count (CBC): This test measures the number and types of cells in the blood, including red blood cells, white blood cells, and platelets.
2. Bone marrow biopsy: This test involves removing a small sample of bone marrow tissue from the hipbone or breastbone to examine under a microscope for signs of leukemia cells.
3. Genetic testing: This test can help identify specific genetic abnormalities that are associated with AML.
4. Immunophenotyping: This test uses antibodies to identify the surface proteins on leukemia cells, which can help diagnose the subtype of AML.
5. Cytogenetics: This test involves staining the bone marrow cells with dyes to look for specific changes in the chromosomes that are associated with AML.
Treatment for AML typically involves a combination of chemotherapy, targeted therapy, and in some cases, bone marrow transplantation. The specific treatment plan will depend on the subtype of AML, the patient's age and overall health, and other factors. Some common treatments for AML include:
1. Chemotherapy: This involves using drugs to kill cancer cells. The most commonly used chemotherapy drugs for AML are cytarabine (Ara-C) and anthracyclines such as daunorubicin (DaunoXome) and idarubicin (Idamycin).
2. Targeted therapy: This involves using drugs that specifically target the genetic abnormalities that are causing the cancer. Examples of targeted therapies used for AML include midostaurin (Rydapt) and gilteritinib (Xospata).
3. Bone marrow transplantation: This involves replacing the diseased bone marrow with healthy bone marrow from a donor. This is typically done after high-dose chemotherapy to destroy the cancer cells.
4. Supportive care: This includes treatments to manage symptoms and side effects of the disease and its treatment, such as anemia, infection, and bleeding. Examples of supportive care for AML include blood transfusions, antibiotics, and platelet transfusions.
5. Clinical trials: These are research studies that involve testing new treatments for AML. Participating in a clinical trial may give patients access to innovative therapies that are not yet widely available.
It's important to note that the treatment plan for AML is highly individualized, and the specific treatments used will depend on the patient's age, overall health, and other factors. Patients should work closely with their healthcare team to determine the best course of treatment for their specific needs.
1. Complete paralysis: When there is no movement or sensation in a particular area of the body.
2. Incomplete paralysis: When there is some movement or sensation in a particular area of the body.
3. Localized paralysis: When paralysis affects only a specific part of the body, such as a limb or a facial muscle.
4. Generalized paralysis: When paralysis affects multiple parts of the body.
5. Flaccid paralysis: When there is a loss of muscle tone and the affected limbs feel floppy.
6. Spastic paralysis: When there is an increase in muscle tone and the affected limbs feel stiff and rigid.
7. Paralysis due to nerve damage: This can be caused by injuries, diseases such as multiple sclerosis, or birth defects such as spina bifida.
8. Paralysis due to muscle damage: This can be caused by injuries, such as muscular dystrophy, or diseases such as muscular sarcopenia.
9. Paralysis due to brain damage: This can be caused by head injuries, stroke, or other conditions that affect the brain such as cerebral palsy.
10. Paralysis due to spinal cord injury: This can be caused by trauma, such as a car accident, or diseases such as polio.
Paralysis can have a significant impact on an individual's quality of life, affecting their ability to perform daily activities, work, and participate in social and recreational activities. Treatment options for paralysis depend on the underlying cause and may include physical therapy, medications, surgery, or assistive technologies such as wheelchairs or prosthetic devices.
Thymoma can be broadly classified into two main types:
1. Benign thymoma: This type of thymoma is non-cancerous and does not spread to other parts of the body. It is usually small in size and may not cause any symptoms.
2. Malignant thymoma: This type of thymoma is cancerous and can spread to other parts of the body, including the lungs, liver, and bone marrow. Malignant thymomas are more aggressive than benign thymomas and can be life-threatening if not treated promptly.
The exact cause of thymoma is not known, but it is believed to arise from abnormal cell growth in the thymus gland. Some risk factors that may increase the likelihood of developing thymoma include:
1. Genetic mutations: Certain genetic mutations, such as those affecting the TREX1 gene, can increase the risk of developing thymoma.
2. Radiation exposure: Exposure to radiation, such as from radiation therapy, may increase the risk of developing thymoma.
3. Thymic hyperplasia: Enlargement of the thymus gland, known as thymic hyperplasia, may increase the risk of developing thymoma.
The symptoms of thymoma can vary depending on the size and location of the tumor. Some common symptoms include:
1. Chest pain or discomfort
2. Shortness of breath
3. Coughing
4. Fatigue
5. Weight loss
6. Fever
7. Night sweats
8. Pain in the arm or shoulder
Thymoma is diagnosed through a combination of imaging tests, such as computed tomography (CT) scans and magnetic resonance imaging (MRI), and biopsy, which involves removing a sample of tissue from the thymus gland for examination under a microscope. Treatment options for thymoma depend on the stage and aggressiveness of the tumor, and may include:
1. Surgery: Removing the tumor through surgery is often the first line of treatment for thymoma.
2. Radiation therapy: High-energy beams can be used to kill cancer cells and shrink the tumor.
3. Chemotherapy: Drugs can be used to kill cancer cells and shrink the tumor.
4. Targeted therapy: Drugs that target specific molecules involved in the growth and spread of cancer cells can be used to treat thymoma.
5. Immunotherapy: Treatments that use the body's immune system to fight cancer, such as checkpoint inhibitors, can be effective for some people with thymoma.
Overall, the prognosis for thymoma is generally good, with a 5-year survival rate of about 70% for people with localized disease. However, the prognosis can vary depending on the stage and aggressiveness of the tumor, as well as the effectiveness of treatment.
* 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.
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
Erythroleukemia typically affects adults in their 50s and 60s, although it can occur at any age. Symptoms may include fever, night sweats, weight loss, and fatigue. The cancer cells can spread to other parts of the body, including the spleen, liver, and lymph nodes.
Erythroleukemia is diagnosed through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment typically involves chemotherapy and/or radiation therapy to kill cancer cells and restore normal blood cell production. In some cases, a bone marrow transplant may be necessary. The prognosis for erythroleukemia is generally poor, with a five-year survival rate of about 20%.
Erythroleukemia is classified as an acute leukemia, meaning it progresses rapidly and can lead to life-threatening complications if left untreated. It is important for patients to receive prompt and appropriate treatment to improve their chances of survival and quality of life.
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.
The two main types of lymphoid leukemia are:
1. Acute Lymphoblastic Leukemia (ALL): This type of leukemia is most commonly seen in children, but it can also occur in adults. It is characterized by a rapid increase in the number of immature white blood cells in the blood and bone marrow.
2. Chronic Lymphocytic Leukemia (CLL): This type of leukemia usually affects older adults and is characterized by the gradual buildup of abnormal white blood cells in the blood, bone marrow, and lymph nodes.
Symptoms of lymphoid leukemia include fatigue, fever, night sweats, weight loss, and swollen lymph nodes. Treatment options for lymphoid leukemia can vary depending on the type of cancer and the severity of symptoms, but may include chemotherapy, radiation therapy, or bone marrow transplantation.
The term "Murine" refers to the fact that the condition occurs in mice and other rodents. "Acquired Immunodeficiency Syndrome" (AIDS) is a similar condition in humans caused by HIV. The similarity between MAIDS and AIDS lies in their shared origins as retroviral infections, but there are significant differences in the viruses themselves and the symptoms they cause.
Example sentence: The patient was diagnosed with experimental sarcoma and underwent a novel chemotherapy regimen that included a targeted therapy drug.
Some common effects of chromosomal deletions include:
1. Genetic disorders: Chromosomal deletions can lead to a variety of genetic disorders, such as Down syndrome, which is caused by a deletion of a portion of chromosome 21. Other examples include Prader-Willi syndrome (deletion of chromosome 15), and Williams syndrome (deletion of chromosome 7).
2. Birth defects: Chromosomal deletions can increase the risk of birth defects, such as heart defects, cleft palate, and limb abnormalities.
3. Developmental delays: Children with chromosomal deletions may experience developmental delays, learning disabilities, and intellectual disability.
4. Increased cancer risk: Some chromosomal deletions can increase the risk of developing certain types of cancer, such as chronic myelogenous leukemia (CML) and breast cancer.
5. Reproductive problems: Chromosomal deletions can lead to reproductive problems, such as infertility or recurrent miscarriage.
Chromosomal deletions can be diagnosed through a variety of techniques, including karyotyping (examination of the chromosomes), fluorescence in situ hybridization (FISH), and microarray analysis. Treatment options for chromosomal deletions depend on the specific effects of the deletion and may include medication, surgery, or other forms of therapy.
There are several types of teratomas, including:
1. Mature teratoma: This type of teratoma is made up of well-differentiated tissues that resemble normal tissues. It can contain structures such as hair follicles, sweat glands, and sebaceous glands.
2. Immature teratoma: This type of teratoma is made up of poorly differentiated cells that do not resemble normal tissues. It can contain structures such as cartilage, bone, and nervous tissue.
3. Teratoid mesodermal tumor: This type of teratoma arises from the mesoderm, which is one of the three primary layers of cells in the embryo. It can contain structures such as muscle, bone, and connective tissue.
4. Teratoid endodermal tumor: This type of teratoma arises from the endoderm, which is another primary layer of cells in the embryo. It can contain structures such as glandular tissue and epithelial tissue.
Teratomas are usually benign, but they can sometimes be malignant. Malignant teratomas can spread to other parts of the body and cause serious complications. The treatment of teratomas depends on their type, size, and location, as well as the patient's overall health. Treatment options can include surgery, chemotherapy, and radiation therapy.
In summary, a teratoma is a type of tumor that contains abnormal cells that grow and multiply in an uncontrolled manner, often forming masses or lumps. There are several types of teratomas, and they can occur in various parts of the body. Treatment options depend on the type, size, location, and patient's overall health.
Symptoms of EBL can vary widely and may include:
* Swollen lymph nodes
* Chronic diarrhea
* Weight loss
* Anemia
* Lethargy
* Enlarged spleen and liver
* Neoplastic diseases such as lymphosarcoma, leukemia, or other types of cancer.
EBL is usually diagnosed through a combination of physical examination, blood tests, and biopsies. There is no cure for EBL, and treatment is primarily focused on managing symptoms and preventing the spread of the disease.
Prevention of EBL includes:
* Testing herds for BLV regularly
* Avoiding close contact between animals
* Practicing good hygiene and sanitation
* Implementing strict biosecurity measures
* Eliminating infected animals from the herd
It is important to note that EBL is not a reportable disease in all countries, and testing for BLV may not be mandatory in all regions. However, it is still important for farmers and veterinarians to be aware of the risk of EBL and take appropriate measures to prevent its spread.
The BCR-ABL gene is a fusion gene that is present in the majority of cases of CML. It is created by the translocation of two genes, called BCR and ABL, which leads to the production of a constitutively active tyrosine kinase protein that promotes the growth and proliferation of abnormal white blood cells.
There are three main phases of CML, each with distinct clinical and laboratory features:
1. Chronic phase: This is the earliest phase of CML, where patients may be asymptomatic or have mild symptoms such as fatigue, night sweats, and splenomegaly (enlargement of the spleen). The peripheral blood count typically shows a high number of blasts in the blood, but the bone marrow is still functional.
2. Accelerated phase: In this phase, the disease progresses to a higher number of blasts in the blood and bone marrow, with evidence of more aggressive disease. Patients may experience symptoms such as fever, weight loss, and pain in the joints or abdomen.
3. Blast phase: This is the most advanced phase of CML, where there is a high number of blasts in the blood and bone marrow, with significant loss of function of the bone marrow. Patients are often symptomatic and may have evidence of spread of the disease to other organs, such as the liver or spleen.
Treatment for CML typically involves targeted therapy with drugs that inhibit the activity of the BCR-ABL protein, such as imatinib (Gleevec), dasatinib (Sprycel), or nilotinib (Tasigna). These drugs can slow or stop the progression of the disease, and may also produce a complete cytogenetic response, which is defined as the absence of all Ph+ metaphases in the bone marrow. However, these drugs are not curative and may have significant side effects. Allogenic hematopoietic stem cell transplantation (HSCT) is also a potential treatment option for CML, but it carries significant risks and is usually reserved for patients who are in the blast phase of the disease or have failed other treatments.
In summary, the clinical course of CML can be divided into three phases based on the number of blasts in the blood and bone marrow, and treatment options vary depending on the phase of the disease. It is important for patients with CML to receive regular monitoring and follow-up care to assess their response to treatment and detect any signs of disease progression.
The symptoms of T-cell leukemia can vary depending on the severity of the disease, but they may include:
* Fatigue
* Weakness
* Frequent infections
* Easy bruising or bleeding
* Swollen lymph nodes
* Pain in the bones or joints
* Headaches
* Confusion or seizures (in severe cases)
T-cell leukemia is diagnosed through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment typically involves chemotherapy and/or radiation therapy to kill cancer cells and restore the body's normal production of blood cells. In some cases, bone marrow transplantation may be recommended.
The prognosis for T-cell leukemia varies depending on the patient's age and overall health, as well as the aggressiveness of the disease. However, with current treatments, the 5-year survival rate is around 70% for children and adolescents, and around 40% for adults.
It's important to note that T-cell leukemia is relatively rare compared to other types of leukemia, such as acute myeloid leukemia (AML) or chronic lymphocytic leukemia (CLL). However, it can be a very aggressive and difficult-to-treat form of cancer, and patients with T-cell leukemia often require intensive treatment and close follow-up care.
Radiation-induced leukemia is a rare but potentially fatal condition that occurs when a person is exposed to high levels of ionizing radiation, such as from nuclear fallout or radiation therapy. The radiation damages the DNA in the stem cells of the bone marrow, leading to mutations that can cause the development of cancer.
There are two main types of radiation-induced leukemia: acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). AML is the more common type and typically occurs within 1-5 years after exposure to high levels of radiation. CML can take up to 10 years or more to develop.
Symptoms of radiation-induced leukemia can include fatigue, fever, night sweats, weight loss, and easy bruising or bleeding. Treatment typically involves chemotherapy and/or bone marrow transplantation. The prognosis for radiation-induced leukemia is generally poor, with a 5-year survival rate of less than 50%.
Prevention is key to avoiding radiation-induced leukemia. People who work with or are exposed to high levels of radiation, such as nuclear power plant workers, should take precautions to minimize their exposure and undergo regular medical checkups to monitor their health. Additionally, people who have undergone radiation therapy for cancer should be closely monitored by their healthcare providers for any signs of leukemia or other radiation-related side effects.
Aloxistatin
Retroviral ribonuclease H
William A. Haseltine
Murine leukemia virus
Gammaretrovirus core encapsidation signal
PIM2 (gene)
Andrew G. Campbell
Retroviral matrix protein
Abelson murine leukemia virus
Prime editing
RUNX1
Gammaretrovirus
Viral vector
Env (gene)
BOSC23
Reverse transcriptase
Gibbon ape leukemia virus
Myricetin
Complementary DNA
Ubiquitin C
PIM1
Ubiquitin D
BMI1
List of MeSH codes (B04)
Ribonuclease H
Retrovirus
Natural killer cell
Moloney murine leukemia virus retroviral vector pLXSHD, complete seque - Nucleotide - NCBI
Human genetics and its impact on cardiovascular disease - Argentine Bioethics Association
Publications - Robert Craigie, Ph.D. - NIDDK
Publication Detail
Biomarkers Search
Conditionally immortalised leukaemia initiating cells co-expressing Hoxa9/Meis1 demonstrate microenvironmental adaptation...
Subject: Retroviruses--Genetics | Search Results | Academic Commons
PCR Amplification | An Introduction to PCR Methods | Promega
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WikiGenes - ECs3002 - exonuclease
JCI -
Mice generated by in vitro fertilization exhibit vascular dysfunction and shortened life span
Analysis of genetic mutations in the 7a7b open reading frame of coronavirus of cheetahs (Acinonyx jubatus) in: American Journal...
WebmedCentral.com :: Aging Editor - Dr. Pankaj Kumar
Manaker, Robert 1995 - Office of NIH History and Stetten Museum
Publications - Salk Institute for Biological Studies
Response to Staphylococcus aureus requires CD36-mediated phagocytosis triggered by the COOH-terminal cytoplasmic domain |...
MMLV-RT | Meridian Bioscience
Selected Publications - Judith Levin Lab | NICHD - Eunice Kennedy Shriver National Institute of Child Health and Human...
The IFITM proteins mediate cellular resistance to influenza A H1N1 virus, West Nile virus, and dengue virus - PubMed
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PDB 1WWF | Chain NMR STRUCTURE DETERMINED FOR MLV NC COMPLEX WITH RNA SEQUENCE CCUCCGU | 1WWF A | 3D Structure | canSARS
3-BrPA eliminates human bladder cancer cells with highly oncogenic signatures via engagement of specific death programs and...
Pesquisa | Biblioteca Virtual em Saúde - BRASIL
Circular Moloney murine leuke1
- By screening a library of unintegrated, circular Moloney murine leukemia virus (M-MuLV) DNA cloned in lambda phage, we found that approximately 20% of the M-MuLV DNA inserts contained internal sequence deletions or inversions. (nih.gov)
MMLV3
- MMLV (Moloney Murine Leukemia Virus) enzyme which allows fast cDNA synthesis due to its exceptionally strong strand-displacement activity. (medica-tradefair.com)
- Moloney Murine Leukemia Virus Reverse Transcriptase (MMLV RT) is an RNA-dependent DNA polymerase that can be used for cDNA synthesis and subsequent PCR or qPCR in one-step or two-step RT-PCR or RT-qPCR assays. (meridianbioscience.com)
- Most investigators employ either avian myeloblastosis virus (AMV) RT or Moloney murine leukemia virus (MMLV) RT to accomplish this. (nih.gov)
Proviral integration5
- 9. Recurring proviral integration suggests a role for proto-oncogene activation in thymomas induced with Mo-MuLV-rescued BCR/ABL virus. (nih.gov)
- 1. Insights into the Interaction Mechanisms of the Proviral Integration Site of Moloney Murine Leukemia Virus (Pim) Kinases with Pan-Pim Inhibitors PIM447 and AZD1208: A Molecular Dynamics Simulation and MM/GBSA Calculation Study. (nih.gov)
- 13. Integrating molecular dynamics simulation and molecular mechanics/generalized Born surface area calculation into pharmacophore modeling: a case study on the proviral integration site for Moloney murine leukemia virus (Pim)-1 kinase inhibitors. (nih.gov)
- We identified the proviral integration site for Moloney murine leukemia virus 1 (PIM1) and its target nuclear factor of activated T cells-1 (NFATc1) as putative drivers of the sustained profibrotic gene signatures in injured aged fibroblasts. (jci.org)
- The Pim kinase family is a group of three serine/threonine kinases encoded by genes that were identified as hotspots for proviral integration of Moloney murine leukemia virus (Pim) in retrovirus-induced lymphomas [ 5 ]. (oncotarget.com)
Lymphomas3
- 2. Activation of multiple genes by provirus integration in the Mlvi-4 locus in T-cell lymphomas induced by Moloney murine leukemia virus. (nih.gov)
- 3. Activation of the Mlvi-1/mis1/pvt-1 locus in Moloney murine leukemia virus-induced T-cell lymphomas. (nih.gov)
- 12. Tumor progression in murine leukemia virus-induced T-cell lymphomas: monitoring clonal selections with viral and cellular probes. (nih.gov)
Locus1
- 5. Human homologue of Moloney leukemia virus integration-4 locus (MLVI-4), located 20 kilobases 3' of the myc gene, is rearranged in multiple myelomas. (nih.gov)
Enzyme1
- Evaluation of influenza virus detection by Direct enzyme immunoassay (EIA) and conventional methods in asthmatic patients. (webmedcentral.com)
Isolate1
- 1963 and hepatitis A in 1973, but many of the blood varies according to the isolate and genotype of the samples taken for post transfusion illness tested virus from 3008 to 3037 amino acids (6). (who.int)
Retroviruses3
- The need to understand these and other aspects of retroviruses has become more urgent with the dis- covery that AIDS is caused by a retrovirus, the hu- man immunodeficiency virus (HIV). (nih.gov)
- Although we continue to perform most of these studies with avian and murine retroviruses, we are giving increasing attention to HIV. (nih.gov)
- The remarkable specificity of virus-host interactions has been known for over twenty years from studies of the polymorphic envelope proteins of avian retroviruses, yet little biochemical information is available about the receptors or about the nature of their interactions with viral envelope glycoproteins. (nih.gov)
Integration2
- Assembly of prototype foamy virus strand transfer complexes on product DNA bypassing catalysis of integration. (nih.gov)
- Scientists found that B-cell-specific Moloney murine leukemia virus integration site 1 ( Bmi-1 ) mRNA levels were elevated in nasopharyngeal carcinoma cell lines. (stemcellsciencenews.com)
Avian2
20022
- Nile virus (WNV) isolates collected during the summer and years, the virus has traversed North America, presumably fall of 2001 and 2002 indicated genetic variation among from New York City, where it was first isolated during the strains circulating in geographically distinct regions of the summer of 1999 (4-7). (cdc.gov)
- These results show the geographic clustering of genetically similar WNV iso- deaths attributed to WNV in humans, equines, and birds lates and the possible emergence of a dominant variant cir- documented since the discovery of the virus in North culating across much of the United States during 2002. (cdc.gov)
Kinase4
- 7. AZD1208, a potent and selective pan-Pim kinase inhibitor, demonstrates efficacy in preclinical models of acute myeloid leukemia. (nih.gov)
- 10. Identification of N-(4-((1R,3S,5S)-3-Amino-5-methylcyclohexyl)pyridin-3-yl)-6-(2,6-difluorophenyl)-5-fluoropicolinamide (PIM447), a Potent and Selective Proviral Insertion Site of Moloney Murine Leukemia (PIM) 1, 2, and 3 Kinase Inhibitor in Clinical Trials for Hematological Malignancies. (nih.gov)
- 12. Protein profiling identifies mTOR pathway modulation and cytostatic effects of Pim kinase inhibitor, AZD1208, in acute myeloid leukemia. (nih.gov)
- Researchers performed a comprehensive evaluation of metabolic adaptation to tyrosine kinase inhibitor treatment and its role in chronic myelogenous leukemia hematopoietic stem and progenitor cell persistence. (stemcellsciencenews.com)
Protein1
- Recently, the receptor for ecotropic murine leukemia virus (MLV) was shown to be a very different type of protein, with about fourteen transmembrane domains. (nih.gov)
Proviruses1
- The results obtained from the autointegrated clones were supported by nucleotide sequencing of the host-virus junction of two cloned M-MuLV integrated proviruses obtained from infected rat cells. (nih.gov)
Strain1
- A strain of Murine leukemia virus ( LEUKEMIA VIRUS, MURINE ) arising during the propagation of S37 mouse sarcoma, and causing lymphoid leukemia in mice. (nih.gov)
20011
- America from 1999 through 2001 set the stage for the Texas shared the following differences from WN-NY99: five rapid and widespread movement of the virus across the nucleotide mutations and one amino acid substitution. (cdc.gov)
Acute8
- The kit Ampli set PML-RARa identifies the translocation t(15;17) associated with acute promyelocytic leukemia (APL). (medica-tradefair.com)
- be used to reliably and rapidly diagnose Acute Myeloid Leukemia (AML). (medica-tradefair.com)
- Clonit, Innovation and Passion to serve Acute myeloid leukemia (AML) diagnosis and monitoring. (medica-tradefair.com)
- significant sensitivity in the detection of the translocations or chromosomal abnormalities in patients with Acute myeloid leukemia (AML). (medica-tradefair.com)
- 5. The novel combination of dual mTOR inhibitor AZD2014 and pan-PIM inhibitor AZD1208 inhibits growth in acute myeloid leukemia via HSF pathway suppression. (nih.gov)
- Search, retrieve and analyze Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) sequences in NCBI Virus . (nih.gov)
- Scientists demonstrated for the first time that ZDHHC21 palmitoyltransferase served as a key regulator of oxidative phosphorylation hyperactivity in acute myeloid leukemia (AML) cells. (stemcellsciencenews.com)
- The authors characterized stem cell-related gene expression and identified stemness biomarker genes in acute myeloid leukemia. (stemcellsciencenews.com)
Nucleotide1
- geographic distribution of the virus was limited to Africa, Phylogenetic comparisons of partial and complete the Middle East, India, and western and central Asia with nucleotide sequences from isolates collected in the north- occasional epidemics in Europe (1,2). (cdc.gov)
Reverse3
- Moloney murine leukemia virus integrase and reverse transcriptase interact with PML proteins. (nbrp.jp)
- Pull-down assay and co-immunoprecipitation of cell extracts in which the integrase or reverse transcriptase of Moloney murine leukemia virus was transiently expressed showed that both enzymes interacted with PML proteins. (nbrp.jp)
- M-MuLV-RH is a genetically modified Moloney Murine Leukemia Virus reverse transcriptase (M-MuLV). (geneon.net)
Influenza3
- 5. PANKAJ KUMAR, Madhu Khanna, Yogesh tyagi, G Pal, Raj HG, (2005) Effect of Quercetin supplementation on alterations in antioxidant defenses in lung after experimental influenza virus infection. (webmedcentral.com)
- Effect of Quercetin on lipid peroxidation and changes in lung morphology in experimental influenza virus infection. (webmedcentral.com)
- Then Groupé, at that time, was interested in the usual influenza viruses, the PR8 virus and such stuff, and this is the reason we had a lot of chicken eggs around. (nih.gov)
Translocation1
- 16. Robertsonian translocation studies on the significance of trisomy 15 in murine T-cell leukemia. (nih.gov)
Variant1
- 20. Leukaemogenesis by the delta Mo + SV Moloney murine leukaemia virus (M-MuLV) variant in E mu pim-1 transgenic mice: high frequency of recombination with a solo endogenous M-MuLV LTR in vivo. (nih.gov)
Genes1
- and 5) the regulation of viral gene expression displays many features characteristic of cellular genes and some thus far unique to viruses. (nih.gov)
Hepatitis6
- Justification: Hepatitis C virus (HCV) continues to be a major disease burden on the world and Man is the only known natural host of Hepatitis C virus (Chivaliez and Pawlotsky, 2007). (who.int)
- Results: of the 259 plasma specimens screened for Hepatitis C virus in this study, 20(7.7%) were positive for anti HCV antibodies by ELISA and 16(6.2%) of the antibodies positive specimen were positive for HCV RNA. (who.int)
- Hepatitis C virus genotype 1b was found in the entire HCV RNA positive sample. (who.int)
- Conclusions: The findings of 6.2% prevalence of HCV infection based on HCV RNA test confirmed that there is Hepatitis C virus in Kaduna State with genotype 1b as the predominant genotype found in all the three senatorial zones. (who.int)
- identified the virus to be Hepatitis C virus (2). (who.int)
- Hepatitis C virus (HCV) is a member of or genome fragment sequencing, genotype specific the family Flaviviridae, placed in a new monotypic amplification of a genomic region or PCR genus Hepacivirus (4, 5). (who.int)
Herpes2
- PMID- 214407 TI - Antibodies to Herpes simplex virus types 1 and 2 in patients with squamous-cell carcinoma of uterine cervix in India. (nih.gov)
- AB - Antibody activity to Herpes simplex virus type-1 (HSV-1) and type-2 (HSV-2) was measured by the indirect hemagglutination (IHA) test in sera from 124 women with squamous-cell carcinoma of the uterine cervix, 46 women with non-cervical cancer and 116 matched normal women. (nih.gov)
19951
- This is an interview of Dr. Robert Manaker, who was Deputy Director of the Viruses Cancer Program, taken on March 9, 1995. (nih.gov)
Chronic1
- chronic myelogenic leukemia (CML). (medica-tradefair.com)
Sequences1
- See all publicly available virus sequences in newly designed interface at NCBI Virus and send us your feedback! (nih.gov)
Term2
- PMID- 214405 TI - Long-term T-cell-mediated immunity to Epstein-Barr virus in man. (nih.gov)
- The results strongly suggest that the regression phenomenon is an in vitro expression of long-term T-cell-mediated immunity to EB virus which the large majority, if not all, infected individuals possess. (nih.gov)
Antibody1
- Hybridoma cell line 500 expresses monoclonal antibody specific for Moloney murine leukemia virus (MuLV) gp80. (nih.gov)
Mouse1
- 15. Differential disease restriction of Moloney and Friend murine leukemia viruses by the mouse Rmcf gene is governed by the viral long terminal repeat. (nih.gov)
Evaluation1
- Virus mutation evaluation additional revealed the presence of HPV16 and HPV58 sublineages related to probably excessive oncogenicity. (aabioetica.org)
Cell5
- 1. Rearrangement of c-myc, pim-1 and Mlvi-1 and trisomy of chromosome 15 in MCF- and Moloney-MuLV-induced murine T-cell leukemias. (nih.gov)
- 14. Is trisomy cause or consequence of murine T cell leukemia development? (nih.gov)
- 19. Trisomy 15 and other nonrandom chromosome changes in Rauscher murine leukemia virus-induced leukemia cell lines. (nih.gov)
- Host Cell Cathepsins Potentiate Moloney Murine Leukemia Virus Infection. (webmedcentral.com)
- AB - Peripheral blood mononuclear cells from donors of known serological status with respect to EB virus were exposed to the virus in vitro and then cultured at various cell concentrations. (nih.gov)
PMID1
- PMID- 214400 TI - Transmission of Japanese encephalitis virus by Culex bitaeniorhynchus Giles. (nih.gov)
Assembly1
- and virus assembly. (nih.gov)
Complete1
- I. Complete regression of virus-induced transformation in cultures of seropositive donor leukocytes. (nih.gov)