Abelson murine leukemia virus
Leukemia Virus, Murine
Oncogene Proteins v-abl
Moloney murine leukemia virus
Cell Transformation, Viral
Leukemia, Experimental
AKR murine leukemia virus
Friend murine leukemia virus
Genes, abl
Thymoma
Cell Transformation, Neoplastic
Helper Viruses
Oncogenes
Leukemia Virus, Feline
Sarcoma Viruses, Feline
Rauscher Virus
B-Lymphocytes
Mice, Inbred Strains
Leukemia Virus, Bovine
Cell Line, Transformed
Base Sequence
Protein-Tyrosine Kinases
Leukemia
Defective Viruses
Retroviridae
Lymphocytes
Mutation
Virus Replication
Clone Cells
Protein Kinases
Mink Cell Focus-Inducing Viruses
RNA-Directed DNA Polymerase
Receptors, Virus
Molecular Sequence Data
Proviruses
Gene Products, gag
Tumor Virus Infections
Gammaretrovirus
Leukemia, Myeloid, Acute
Virus Integration
Leukemia Virus, Gibbon Ape
3T3 Cells
Nucleic Acid Hybridization
Cloning, Molecular
Viral Envelope Proteins
Mink
Immunoglobulin mu-Chains
Blotting, Southern
DNA Restriction Enzymes
Preleukemia
Human T-lymphotropic virus 1
Gene Rearrangement, B-Lymphocyte, Heavy Chain
Plasmacytoma
Phosphorylation
Gene Products, env
Retroviridae Proteins, Oncogenic
Transfection
Repetitive Sequences, Nucleic Acid
Genetic Vectors
Sarcoma Viruses, Murine
Genes
Amino Acid Sequence
p53 mediates apoptotic crisis in primary Abelson virus-transformed pre-B cells. (1/205)
Transformation of pre-B cells by Abelson murine leukemia virus (Ab-MLV) involves a balance between positive, growth-stimulatory signals from the v-Abl oncoprotein and negative regulatory cues from cellular genes. This phenomenon is reflected by the clonal selection that occurs during Ab-MLV-mediated transformation in vivo and in vitro. About 50% of all Ab-MLV-transformed pre-B cells express mutant forms of p53 as they emerge from this process, suggesting that this protein may play an important role in the transformation process. Consistent with this idea, expression of p19(Arf), a protein whose function depends on the presence of a functional p53, is required for the apoptotic crisis that characterizes primary Ab-MLV transformants. To test the role of p53 in pre-B-cell transformation directly, we examined the response of Trp53(-/-) mice to Ab-MLV. The absence of p53 shortens the latency of Abelson disease induction but does not affect the frequency of cells susceptible to Ab-MLV-induced transformation. However, primary transformants derived from the null animals bypass the apoptotic crisis that characterizes the transition from primary transformant to fully malignant cell line. These effects do not require p21(Cip-1), a major downstream target of p53; however, consistent with a role of p19(Arf), transformants expressing mutant p53 and abundant p19 retain wild-type p19 sequences. (+info)Functional characterization of B lymphocytes generated in vitro from embryonic stem cells. (2/205)
To study molecular events involved in B lymphocyte development and V(D)J rearrangement, we have established an efficient system for the differentiation of embryonic stem (ES) cells into mature Ig-secreting B lymphocytes. Here, we show that B lineage cells generated in vitro from ES cells are functionally analogous to normal fetal liver-derived or bone marrow-derived B lineage cells at three important developmental stages: first, they respond to Flt-3 ligand during an early lymphopoietic progenitor stage; second, they become targets for Abelson murine leukemia virus (A-MuLV) infection at a pre-B cell stage; third, they secrete Ig upon stimulation with lipopolysaccharide at a mature mitogen-responsive stage. Moreover, the ES cell-derived A-MuLV-transformed pre-B (EAB) cells are phenotypically and functionally indistinguishable from standard A-MuLV-transformed pre-B cells derived from infection of mouse fetal liver or bone marrow. Notably, EAB cells possess functional V(D)J recombinase activity. In particular, the generation of A-MuLV transformants from ES cells will provide an advantageous system to investigate genetic modifications that will help to elucidate molecular mechanisms in V(D)J recombination and in A-MuLV-mediated transformation. (+info)Drosophila abelson interacting protein (dAbi) is a positive regulator of abelson tyrosine kinase activity. (3/205)
Human and mouse Abelson interacting proteins (Abi) are SH3-domain containing proteins that bind to the proline-rich motifs of the Abelson protein tyrosine kinase. We report a new member of this gene family, a Drosophila Abi (dAbi) that is a substrate for Abl kinase and that co-immunoprecipitates with Abl if the Abi SH3 domain is intact. We have identified a new function for both dAbi and human Abi-2 (hAbi-2). Both proteins activate the kinase activity of Abl as assayed by phosphorylation of the Drosophila Enabled (Ena) protein. Removal of the dAbi SH3 domain eliminates dAbi's activation of Abl kinase activity. dAbi is an unstable protein in cells and is present at low steady state levels but its protein level is increased coincident with phosphorylation by Abl kinase. Expression of the antisense strand of dAbi reduces dAbi protein levels and abolishes activation of Abl kinase activity. Modulation of Abi protein levels may be an important mechanism for regulating the level of Abl kinase activity in the cell. (+info)Inhibition of v-Abl transformation by p53 and p19ARF. (4/205)
Tumorigenesis is a multistep process that involves the activation of oncogenes and the inactivation of tumor suppressor genes. The transforming activity of the v-Abl oncogene of Abelson murine leukemia virus (A-MuLV) in immortal cell lines has been well studied, while the effects of v-Abl in primary fibroblasts are less clear. Here we show that v-Abl causes cell cycle arrest in primary mouse embryonic fibroblasts (MEFs) and elevated levels of both p53 and the cyclin-dependent kinase inhibitor p21Cip. p53-/- or p19ARF-/- MEFs were resistant to v-Abl-induced cell cycle arrest. Although wild-type MEFs were resistant to v-Abl transforming activity, p53-/- or p19ARF-/- MEFs were susceptible. The results indicate that loss of p19ARF and p53 function plays an important role during the transformation of primary cells by v-Abl. We suggest that although v-Abl is a potent oncogene, its full potential transforming activity cannot be realized until the ARF-, and p53-dependent growth inhibitory pathway is disabled. We also show that p53 is not the mediator of v-Abl toxicity in immortal fibroblasts and does not determine the susceptibility of immortal fibroblasts to v-Abl transformation. (+info)The carboxyl terminus of v-Abl protein can augment SH2 domain function. (5/205)
Abelson murine leukemia virus (Ab-MLV) transforms NIH 3T3 and pre-B cells via expression of the v-Abl tyrosine kinase. Although the enzymatic activity of this molecule is absolutely required for transformation, other regions of the protein are also important for this response. Among these are the SH2 domain, involved in phosphotyrosine-dependent protein-protein interactions, and the long carboxyl terminus, which plays an important role in transformation of hematopoietic cells. Important signals are sent from each of these regions, and transformation is most likely orchestrated by the concerted action of these different parts of the protein. To explore this idea, we compared the ability of the v-Src SH2 domain to substitute for that of v-Abl in the full-length P120 v-Abl protein and in P70 v-Abl, a protein that lacks the carboxyl terminus characteristic of Abl family members. Ab-MLV strains expressing P70/S2 failed to transform NIH 3T3 cells and demonstrated a greatly reduced capacity to mediate signaling events associated with the Ras-dependent mitogen-activated protein (MAP) kinase pathway. In contrast, Ab-MLV strains expressing P120/S2 were indistinguishable from P120 with respect to these features. Analyses of additional mutants demonstrated that the last 162 amino acids of the carboxyl terminus were sufficient to restore transformation. These data demonstrate that an SH2 domain with v-Abl substrate specificity is required for NIH 3T3 transformation in the absence of the carboxyl terminus and suggest that cooperativity between the extreme carboxyl terminus and the SH2 domain facilitates the transmission of transforming signals via the MAP kinase pathway. (+info)Transgenic human lambda 5 rescues the murine lambda 5 nullizygous phenotype. (6/205)
The human lambda 5 (hu lambda 5) gene is the structural homologue of the murine lambda 5 (m lambda 5) gene and is transcriptionally active in pro-B and pre-B lymphocytes. The lambda 5 and VpreB polypeptides together with the Ig mu H chain and the signal-transducing subunits, Ig alpha and Ig beta, comprise the pre-B cell receptor. To further investigate the pro-B/pre-B-specific transcription regulation of hu lambda 5 in an in vivo model, we generated mouse lines that contain a 28-kb genomic fragment encompassing the entire hu lambda 5 gene. High levels of expression of the transgenic hu lambda 5 gene were detected in bone marrow pro-B and pre-B cells at the mRNA and protein levels, suggesting that the 28-kb transgene fragment contains all the transcriptional elements necessary for the stage-specific B progenitor expression of hu lambda 5. Flow cytometric and immunoprecipitation analyses of bone marrow cells and Abelson murine leukemia virus-transformed pre-B cell lines revealed the hu lambda 5 polypeptide on the cell surface and in association with mouse Ig mu and mouse VpreB. Finally, we found that the hu lambda 5 transgene is able to rescue the pre-B lymphocyte block when bred onto the m lambda 5-/- background. Therefore, we conclude that the hu lambda 5 polypeptide can biochemically and functionally substitute for m lambda 5 in vivo in pre-B lymphocyte differentiation and proliferation. These studies on the mouse and human pre-B cell receptor provide a model system to investigate some of the molecular requirements necessary for B cell development. (+info)Activation of V(D)J recombination induces the formation of interlocus joints and hybrid joints in scid pre-B-cell lines. (7/205)
V(D)J recombination is the mechanism by which antigen receptor genes are assembled. The site-specific cleavage mediated by RAG1 and RAG2 proteins generates two types of double-strand DNA breaks: blunt signal ends and covalently sealed hairpin coding ends. Although these DNA breaks are mainly resolved into coding joints and signal joints, they can participate in a nonstandard joining process, forming hybrid and open/shut joints that link coding ends to signal ends. In addition, the broken DNA molecules excised from different receptor gene loci could potentially be joined to generate interlocus joints. The interlocus recombination process may contribute to the translocation between antigen receptor genes and oncogenes, leading to malignant transformation of lymphocytes. To investigate the underlying mechanisms of these nonstandard recombination events, we took advantage of recombination-inducible cell lines derived from scid homozygous (s/s) and scid heterozygous (s/+) mice by transforming B-cell precursors with a temperature-sensitive Abelson murine leukemia virus mutant (ts-Ab-MLV). We can manipulate the level of recombination cleavage and end resolution by altering the cell culture temperature. By analyzing various recombination products in scid and s/+ ts-Ab-MLV transformants, we report in this study that scid cells make higher levels of interlocus and hybrid joints than their normal counterparts. These joints arise concurrently with the formation of intralocus joints, as well as with the appearance of opened coding ends. The junctions of these joining products exhibit excessive nucleotide deletions, a characteristic of scid coding joints. These data suggest that an inability of scid cells to promptly resolve their recombination ends exposes the ends to a random joining process, which can conceivably lead to chromosomal translocations. (+info)Loss of heterozygosity at the Ink4a/Arf locus facilitates Abelson virus transformation of pre-B cells. (8/205)
In many tumor systems, analysis of cells for loss of heterozygosity (LOH) has helped to clarify the role of tumor suppressor genes in oncogenesis. Two important tumor suppressor genes, p53 and the Ink4a/Arf locus, play central roles in the multistep process of Abelson murine leukemia virus (Ab-MLV) transformation. p53 and the p53 regulatory protein, p19Arf, are required for the apoptotic crisis that characterizes the progression of primary transformed pre-B cells to fully malignant cell lines. To search for other tumor suppressor genes which may be involved in the Ab-MLV transformation process, we used endogenous proviral markers and simple-sequence length polymorphism analysis to screen Abelson virus-transformed pre-B cells for evidence of LOH. Our survey reinforces the role of the p53-p19 regulatory pathway in transformation; 6 of 58 cell lines tested had lost sequences on mouse chromosome 4, including the Ink4a/Arf locus. Consistent with this pattern, a high frequency of primary pre-B-cell transformants derived from Ink4a/Arf +/- mice became established cell lines. In addition, half of them retained the single copy of the locus when the transformation process was complete. These data demonstrate that a single copy of the Ink4a/Arf locus is not sufficient to fully mediate the effects of these genes on transformation. (+info)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.
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.
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.
Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.
Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.
In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.
It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.
See also: Cancer, Tumor
Word count: 190
1. 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 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.
There are several types of lymphoma, including:
1. Hodgkin lymphoma: This is a type of lymphoma that originates in the white blood cells called Reed-Sternberg cells. It is characterized by the presence of giant cells with multiple nucleoli.
2. Non-Hodgkin lymphoma (NHL): This is a type of lymphoma that does not meet the criteria for Hodgkin lymphoma. There are many subtypes of NHL, each with its own unique characteristics and behaviors.
3. Cutaneous lymphoma: This type of lymphoma affects the skin and can take several forms, including cutaneous B-cell lymphoma and cutaneous T-cell lymphoma.
4. Primary central nervous system (CNS) lymphoma: This is a rare type of lymphoma that develops in the brain or spinal cord.
5. Post-transplantation lymphoproliferative disorder (PTLD): This is a type of lymphoma that develops in people who have undergone an organ transplant, often as a result of immunosuppressive therapy.
The symptoms of lymphoma can vary depending on the type and location of the cancer. Some common symptoms include:
* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss
* Night sweats
* Itching
Lymphoma is diagnosed through a combination of physical examination, imaging tests (such as CT scans or PET scans), and biopsies. Treatment options for lymphoma depend on the type and stage of the cancer, and may include chemotherapy, radiation therapy, immunotherapy, or stem cell transplantation.
Overall, lymphoma is a complex and diverse group of cancers that can affect people of all ages and backgrounds. While it can be challenging to diagnose and treat, advances in medical technology and research have improved the outlook for many patients with lymphoma.
There are several 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.
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.
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.
Plasmacytoma is a type of plasma cell dyscrasia, which is a group of diseases that affect the production and function of plasma cells. Plasma cells are a type of white blood cell that produces antibodies to fight infections. In plasmacytoma, the abnormal plasma cells grow and multiply out of control, leading to a tumor.
There are several subtypes of plasmacytoma, including:
* solitary plasmacytoma: A single tumor that occurs in one location.
* multiple myeloma: A type of cancer that affects the bones and is characterized by an overgrowth of malignant plasma cells in the bone marrow.
* extramedullary plasmacytoma: A tumor that occurs outside of the bone marrow, such as in soft tissue or organs.
Plasmacytoma is usually diagnosed through a combination of physical examination, imaging tests such as X-rays or CT scans, and biopsy. Treatment typically involves chemotherapy and/or radiation therapy to destroy the abnormal cells. In some cases, surgery may be necessary to remove the tumor.
Plasmacytoma is a relatively rare cancer, but it can be aggressive and potentially life-threatening if left untreated. It is important for patients with symptoms of plasmacytoma to seek medical attention as soon as possible to receive an accurate diagnosis and appropriate treatment.
Abelson murine leukemia virus
Owen Witte
Clifford Tabin
David Baltimore
ABL (gene)
Abelson
Leukemia virus
Murine leukemia virus
List of MeSH codes (B04)
NSG mouse
Philadelphia chromosome
ABL2
Biomarkers Search
![Recombinant Anti-CREBBP + KAT3B / p300 antibody [EPR23495-276] (ab275379)](data:image/png;base64,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)
Recombinant Anti-CREBBP + KAT3B / p300 antibody [EPR23495-276] (ab275379)
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Oncogenesis - Retroviruses - NCBI Bookshelf
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MESH TREE NUMBER CHANGES - 2003 MeSH
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Treatment Study for Older Patients with Acute Lymphoblastic Leukemia | RUSH
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Acute lymphobl2
- Blinatumomab and combination chemotherapy or dasatinib, prednisone, and blinatumomab in treating older patients with acute lymphoblastic leukemia. (rush.edu)
- This phase II trial studies the side effects and how well blinatumomab and combination chemotherapy or dasatinib, prednisone, and blinatumomab work in treating older patients with acute lymphoblastic leukemia. (rush.edu)
Cells2
- Rotter V, Boss MA, Baltimore D (1981) Increased concentration of an apparently identicalcellular protein in cells transformed by either Abelson murine leukemia virus or other trans-forming agents. (bfnionizers.com)
- Invivo study, nanoparticles were evaluated to inspect their cytotoxic activity against SNU-182 (human hepatocellular carcinoma), K562 (human leukemia), and THLE2 (human normal epithelial liver) cells via MTT test. (bvsalud.org)
Study2
- This study was conducted to investigate the effect of magnetite nanoparticles (MNPs) and magnetite folate core shell (MFCS) on leukemic and hepatocarcinoma cell cultures as well as their effect on the animal model of acute myelocytic leukemia (AML). (bvsalud.org)
- Houston, TX - December 17, 2020 - Moleculin Biotech, Inc., (NASDAQ: MBRX) (Moleculin or the Company), a clinical stage pharmaceutical company with a broad portfolio of drug candidates targeting highly resistant tumors and viruses, today announced that the US Food and Drug Administration (FDA) is allowing the company's Investigational New Drug (IND) application to study Annamycin for the treatment of soft tissue sarcoma lung metastases to go into effect. (financialnewsmedia.com)
Drug1
- Moleculin Biotech, Inc. is a clinical stage pharmaceutical company focused on the development of a broad portfolio of oncology drug candidates for the treatment of highly resistant tumors and viruses. (financialnewsmedia.com)
EXPERIMENTAL1
- 11. Droplet digital PCR allows vector copy number assessment and monitoring of experimental CAR T cells in murine xenograft models or approved CD19 CAR T cell-treated patients. (nih.gov)
CORONAVIRUS1
- Search, retrieve and analyze Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) sequences in NCBI Virus . (nih.gov)
Human1
- The human kallikrein DNA constructs were placed under the control of the metallothionein metal response element, the cytomegalovirus promoter/enhancer or the Rous sarcoma virus 3'-LTR. (nih.gov)
