"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
|
| 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 |
|---|
| 1993 | 1 | 0 | 1 |
| 1994 | 1 | 0 | 1 |
| 1995 | 3 | 0 | 3 |
| 1996 | 4 | 0 | 4 |
| 1997 | 3 | 1 | 4 |
| 1998 | 3 | 0 | 3 |
| 1999 | 1 | 0 | 1 |
| 2000 | 2 | 2 | 4 |
| 2002 | 1 | 2 | 3 |
| 2003 | 0 | 3 | 3 |
| 2004 | 1 | 0 | 1 |
| 2005 | 0 | 1 | 1 |
| 2006 | 2 | 1 | 3 |
| 2007 | 1 | 3 | 4 |
| 2008 | 2 | 2 | 4 |
| 2009 | 1 | 3 | 4 |
| 2010 | 2 | 5 | 7 |
| 2011 | 3 | 0 | 3 |
| 2012 | 0 | 1 | 1 |
| 2013 | 3 | 3 | 6 |
| 2014 | 1 | 0 | 1 |
| 2015 | 2 | 3 | 5 |
| 2016 | 0 | 3 | 3 |
| 2017 | 1 | 1 | 2 |
| 2018 | 1 | 2 | 3 |
| 2020 | 1 | 1 | 2 |
| 2021 | 1 | 0 | 1 |
| 2022 | 0 | 2 | 2 |
| 2023 | 0 | 2 | 2 |
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Below are the most recent publications written about "Fusion Proteins, bcr-abl" by people in Profiles.
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Molecular response in newly diagnosed chronic-phase chronic myeloid leukemia: prediction modeling and pathway analysis. Haematologica. 2023 06 01; 108(6):1567-1578.
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Preclinical pharmacokinetic and pharmacodynamic evaluation of dasatinib and ponatinib for the treatment of T-cell acute lymphoblastic leukemia. Leukemia. 2023 06; 37(6):1194-1203.
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Asciminib monotherapy for newly diagnosed chronic myeloid leukemia in chronic phase: the ASC4FIRST phase III trial. Future Oncol. 2022 Dec; 18(38):4161-4170.
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MUC4 expression by immunohistochemistry is a specific marker for BCR-ABL1+ and BCR-ABL1-like B-lymphoblastic leukemia. Leuk Lymphoma. 2022 06; 63(6):1436-1444.
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Assessment of Outcomes After Stopping Tyrosine Kinase Inhibitors Among Patients With Chronic Myeloid Leukemia: A Nonrandomized Clinical Trial. JAMA Oncol. 2021 Jan 01; 7(1):42-50.
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"All Our Wisdom is Stored in the Trees" - Degrading BCR-ABL with Berberis Vulgaris. Clin Cancer Res. 2020 08 01; 26(15):3899-3900.
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European LeukemiaNet 2020 recommendations for treating chronic myeloid leukemia. Leukemia. 2020 04; 34(4):966-984.
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Imatinib is still recommended for frontline therapy for CML. Blood Adv. 2018 12 26; 2(24):3648-3652.
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Design and rationale for the life after stopping tyrosine kinase inhibitors (LAST) study, a prospective, single-group longitudinal study in patients with chronic myeloid leukemia. BMC Cancer. 2018 04 02; 18(1):359.
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Myeloproliferative neoplasms with concurrent BCR-ABL1 translocation and JAK2 V617F mutation: a multi-institutional study from the bone marrow pathology group. Mod Pathol. 2018 05; 31(5):690-704.