"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
|
| 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
|
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 |
|---|
| 1998 | 1 | 0 | 1 |
| 1999 | 1 | 0 | 1 |
| 2001 | 1 | 0 | 1 |
| 2004 | 1 | 0 | 1 |
| 2005 | 1 | 0 | 1 |
| 2007 | 1 | 0 | 1 |
| 2008 | 2 | 1 | 3 |
| 2009 | 1 | 1 | 2 |
| 2010 | 2 | 0 | 2 |
| 2011 | 1 | 1 | 2 |
| 2012 | 1 | 0 | 1 |
| 2014 | 1 | 1 | 2 |
| 2015 | 1 | 0 | 1 |
| 2016 | 1 | 2 | 3 |
| 2017 | 2 | 2 | 4 |
| 2019 | 0 | 1 | 1 |
| 2020 | 0 | 1 | 1 |
| 2022 | 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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Secondary chronic myeloid leukemia in a patient with CALR and ASXL1-mutated primary myelofibrosis. Int J Hematol. 2022 Sep; 116(3):442-445.
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Ultra-accurate Duplex Sequencing for the assessment of pretreatment ABL1 kinase domain mutations in Ph+ ALL. Blood Cancer J. 2020 05 26; 10(5):61.
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A KLF4-DYRK2-mediated pathway regulating self-renewal in CML stem cells. Blood. 2019 11 28; 134(22):1960-1972.
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Engineering and Functional Characterization of Fusion Genes Identifies Novel Oncogenic Drivers of Cancer. Cancer Res. 2017 07 01; 77(13):3502-3512.
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Targetable kinase gene fusions in high-risk B-ALL: a study from the Children's Oncology Group. Blood. 2017 06 22; 129(25):3352-3361.
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Germline mutations in ABL1 cause an autosomal dominant syndrome characterized by congenital heart defects and skeletal malformations. Nat Genet. 2017 Apr; 49(4):613-617.
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Fall of the mutants: T cells targeting BCR-ABL. Blood. 2017 02 02; 129(5):539-540.
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Cytogenetic landscape and impact in blast phase of chronic myeloid leukemia in the era of tyrosine kinase inhibitor therapy. Leukemia. 2017 03; 31(3):585-592.
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Ponatinib versus imatinib for newly diagnosed chronic myeloid leukaemia: an international, randomised, open-label, phase 3 trial. Lancet Oncol. 2016 05; 17(5):612-21.
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The impact of multiple low-level BCR-ABL1 mutations on response to ponatinib. Blood. 2016 Apr 14; 127(15):1870-80.