"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 |
|---|
| 1995 | 0 | 1 | 1 |
| 1996 | 1 | 0 | 1 |
| 1998 | 1 | 1 | 2 |
| 1999 | 2 | 0 | 2 |
| 2000 | 0 | 1 | 1 |
| 2002 | 1 | 0 | 1 |
| 2003 | 0 | 1 | 1 |
| 2006 | 1 | 1 | 2 |
| 2007 | 2 | 1 | 3 |
| 2008 | 2 | 0 | 2 |
| 2009 | 0 | 1 | 1 |
| 2010 | 1 | 2 | 3 |
| 2011 | 1 | 1 | 2 |
| 2013 | 0 | 1 | 1 |
| 2014 | 1 | 0 | 1 |
| 2019 | 0 | 1 | 1 |
| 2020 | 0 | 1 | 1 |
| 2021 | 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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TNK1 is a ubiquitin-binding and 14-3-3-regulated kinase that can be targeted to block tumor growth. Nat Commun. 2021 09 09; 12(1):5337.
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The Current Genomic and Molecular Landscape of Philadelphia-like Acute Lymphoblastic Leukemia. Int J Mol Sci. 2020 Mar 22; 21(6).
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Dynamic anticipation by Cdk2/Cyclin A-bound p27 mediates signal integration in cell cycle regulation. Nat Commun. 2019 04 11; 10(1):1676.
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The Sox4/Tcf7l1 axis promotes progression of BCR-ABL-positive acute lymphoblastic leukemia. Haematologica. 2014 Oct; 99(10):1591-8.
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PP2A-activating drugs selectively eradicate TKI-resistant chronic myeloid leukemic stem cells. J Clin Invest. 2013 Oct; 123(10):4144-57.
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Acquired resistance to drugs targeting receptor tyrosine kinases. Biochem Pharmacol. 2012 Apr 15; 83(8):1041-8.
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Sphingosine kinase-1 and sphingosine 1-phosphate receptor 2 mediate Bcr-Abl1 stability and drug resistance by modulation of protein phosphatase 2A. Blood. 2011 Jun 02; 117(22):5941-52.
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BCR/ABL stimulates WRN to promote survival and genomic instability. Cancer Res. 2011 Feb 01; 71(3):842-51.
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Dasatinib 140 mg once daily versus 70 mg twice daily in patients with Ph-positive acute lymphoblastic leukemia who failed imatinib: Results from a phase 3 study. Am J Hematol. 2010 Mar; 85(3):164-70.
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K562/GM-CSF immunotherapy reduces tumor burden in chronic myeloid leukemia patients with residual disease on imatinib mesylate. Clin Cancer Res. 2010 Jan 01; 16(1):338-47.