"Fusion Proteins, bcr-abl" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
Translation products of a fusion gene derived from CHROMOSOMAL TRANSLOCATION of C-ABL GENES to the genetic locus of the breakpoint cluster region gene on chromosome 22. Several different variants of the bcr-abl fusion proteins occur depending upon the precise location of the chromosomal breakpoint. These variants can be associated with distinct subtypes of leukemias such as PRECURSOR CELL LYMPHOBLASTIC LEUKEMIA-LYMPHOMA; LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE; and NEUTROPHILIC LEUKEMIA, CHRONIC.
Descriptor ID |
D016044
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MeSH Number(s) |
D08.811.913.696.620.682.725.500.500 D12.776.602.500.500.100 D12.776.624.664.500.100 D12.776.624.664.700.171.500
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Concept/Terms |
Fusion Proteins, bcr-abl- Fusion Proteins, bcr-abl
- Fusion Proteins, bcr abl
- bcr-abl Fusion Proteins
- bcr abl Fusion Proteins
- Bcr-Abl Tyrosine Kinase
- Bcr Abl Tyrosine Kinase
- Kinase, Bcr-Abl Tyrosine
- Tyrosine Kinase, Bcr-Abl
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Below are MeSH descriptors whose meaning is more general than "Fusion Proteins, bcr-abl".
Below are MeSH descriptors whose meaning is more specific than "Fusion Proteins, bcr-abl".
This graph shows the total number of publications written about "Fusion Proteins, bcr-abl" by people in this website by year, and whether "Fusion Proteins, bcr-abl" was a major or minor topic of these publications.
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Year | Major Topic | Minor Topic | Total |
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1995 | 0 | 1 | 1 |
1996 | 1 | 0 | 1 |
2004 | 0 | 1 | 1 |
2006 | 0 | 1 | 1 |
2015 | 1 | 0 | 1 |
2018 | 1 | 1 | 2 |
2019 | 1 | 2 | 3 |
2020 | 2 | 0 | 2 |
2023 | 0 | 1 | 1 |
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Below are the most recent publications written about "Fusion Proteins, bcr-abl" by people in Profiles.
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Mast cell deficiency prevents BCR::ABL1 induced splenomegaly and cytokine elevation in a CML mouse model. Leukemia. 2023 07; 37(7):1474-1484.
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BCR-ABL tyrosine kinase inhibitors promote pathological changes in dilator phenotype in the human microvasculature. Microcirculation. 2020 10; 27(7):e12625.
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Therapeutic inhibition of Fc?RIIb signaling targets leukemic stem cells in chronic myeloid leukemia. Leukemia. 2020 10; 34(10):2635-2647.
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Infliximab therapy together with tyrosine kinase inhibition targets leukemic stem cells in chronic myeloid leukemia. BMC Cancer. 2019 Jul 04; 19(1):658.
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Differential roles of STAT1 and STAT2 in the sensitivity of JAK2V617F- vs. BCR-ABL-positive cells to interferon alpha. J Hematol Oncol. 2019 04 02; 12(1):36.
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Stem cell persistence in CML is mediated by extrinsically activated JAK1-STAT3 signaling. Leukemia. 2019 08; 33(8):1964-1977.
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Targeting HSP90 dimerization via the C terminus is effective in imatinib-resistant CML and lacks the heat shock response. Blood. 2018 07 19; 132(3):307-320.
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Loss of Pax5 Exploits Sca1-BCR-ABLp190 Susceptibility to Confer the Metabolic Shift Essential for pB-ALL. Cancer Res. 2018 05 15; 78(10):2669-2679.
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Mtss1 is a critical epigenetically regulated tumor suppressor in CML. Leukemia. 2016 Apr; 30(4):823-32.
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Deregulated Syk inhibits differentiation and induces growth factor-independent proliferation of pre-B cells. J Exp Med. 2006 Dec 25; 203(13):2829-40.