"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
|
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 |
|---|
| 2007 | 0 | 1 | 1 |
| 2008 | 1 | 0 | 1 |
| 2011 | 1 | 0 | 1 |
| 2013 | 2 | 0 | 2 |
| 2014 | 0 | 1 | 1 |
| 2017 | 4 | 2 | 6 |
| 2018 | 2 | 2 | 4 |
| 2019 | 1 | 0 | 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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Kinase inhibitors developed for treatment of hematologic malignancies: implications for immune modulation in COVID-19. Blood Adv. 2021 02 09; 5(3):913-925.
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Discovery of novel Bcr-AblT315I inhibitors with flexible linker. Part 1: Confirmation optimization of phenyl-1H-indazol-3-amine as hinge binding moiety. Eur J Med Chem. 2019 Sep 15; 178:232-242.
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The impact of introducing tyrosine kinase inhibitors on chronic myeloid leukemia survival: a population-based study. BMC Cancer. 2018 Nov 06; 18(1):1069.
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Aryl hydrocarbon receptor (AHR) is a novel druggable pathway controlling malignant progenitor proliferation in chronic myeloid leukemia (CML). PLoS One. 2018; 13(8):e0200923.
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Discontinuation of tyrosine kinase inhibitor therapy in chronic myeloid leukaemia (EURO-SKI): a prespecified interim analysis of a prospective, multicentre, non-randomised, trial. Lancet Oncol. 2018 06; 19(6):747-757.
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Recent advances in the genomics and therapy of BCR/ABL1-positive and -negative chronic myeloproliferative neoplasms. Leuk Res. 2018 04; 67:67-74.
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Role of flow-cytometric immunophenotyping in prediction of BCR/ABL1 gene rearrangement in adult B-cell acute lymphoblastic leukemia. Cytometry B Clin Cytom. 2018 05; 94(3):468-476.
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Deregulated expression of miR-29a-3p, miR-494-3p and miR-660-5p affects sensitivity to tyrosine kinase inhibitors in CML leukemic stem cells. Oncotarget. 2017 Jul 25; 8(30):49451-49469.
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E14a2 BCR-ABL1 transcript is associated with a higher rate of treatment-free remission in individuals with chronic myeloid leukemia after stopping tyrosine kinase inhibitor therapy. Haematologica. 2017 08; 102(8):e297-e299.
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Clinical characteristics of patients with central nervous system relapse in BCR-ABL1-positive acute lymphoblastic leukemia: the importance of characterizing ABL1 mutations in cerebrospinal fluid. Ann Hematol. 2017 Jul; 96(7):1069-1075.