"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 |
|---|
| 1995 | 0 | 1 | 1 |
| 2001 | 1 | 0 | 1 |
| 2002 | 1 | 1 | 2 |
| 2003 | 1 | 0 | 1 |
| 2004 | 1 | 0 | 1 |
| 2005 | 2 | 0 | 2 |
| 2006 | 3 | 0 | 3 |
| 2007 | 1 | 2 | 3 |
| 2008 | 3 | 1 | 4 |
| 2009 | 0 | 2 | 2 |
| 2010 | 1 | 0 | 1 |
| 2011 | 1 | 1 | 2 |
| 2013 | 1 | 0 | 1 |
| 2014 | 1 | 1 | 2 |
| 2017 | 1 | 0 | 1 |
| 2018 | 1 | 0 | 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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Pulte ED, Chen H, Price LSL, Gudi R, Li H, Okusanya OO, Ma L, Rodriguez L, Vallejo J, Norsworthy KJ, de Claro RA, Theoret MR, Pazdur R. FDA Approval Summary: Revised Indication and Dosing Regimen for Ponatinib Based on the Results of the OPTIC Trial. Oncologist. 2022 03 04; 27(2):149-157.
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Srutova K, Curik N, Burda P, Savvulidi F, Silvestri G, Trotta R, Klamova H, Pecherkova P, Sovova Z, Koblihova J, Stopka T, Perrotti D, Polakova KM. BCR-ABL1 mediated miR-150 downregulation through MYC contributed to myeloid differentiation block and drug resistance in chronic myeloid leukemia. Haematologica. 2018 12; 103(12):2016-2025.
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Perrotti D, Silvestri G, Stramucci L, Yu J, Trotta R. Cellular and Molecular Networks in Chronic Myeloid Leukemia: The Leukemic Stem, Progenitor and Stromal Cell Interplay. Curr Drug Targets. 2017; 18(4):377-388.
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Frederick L, Beardell F, Viswanatha DS. Novel BCR-ABL1 fusion identified by targeted next-generation sequencing in a patient with an atypical myeloproliferative neoplasm. Hum Pathol. 2014 Aug; 45(8):1784-9.
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Agarwal A, MacKenzie RJ, Pippa R, Eide CA, Oddo J, Tyner JW, Sears R, Vitek MP, Odero MD, Christensen DJ, Druker BJ. Antagonism of SET using OP449 enhances the efficacy of tyrosine kinase inhibitors and overcomes drug resistance in myeloid leukemia. Clin Cancer Res. 2014 Apr 15; 20(8):2092-103.
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Singh H, Shelat AA, Singh A, Boulos N, Williams RT, Guy RK. A screening-based approach to circumvent tumor microenvironment-driven intrinsic resistance to BCR-ABL+ inhibitors in Ph+ acute lymphoblastic leukemia. J Biomol Screen. 2014 Jan; 19(1):158-67.
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Sbenghe MM, Florea AD, Mather P, Gitelson E. Chronic myeloid leukemia following heart transplantation and immunosuppression with tacrolimus. Clin Adv Hematol Oncol. 2011 Aug; 9(8):623-7.
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Calabretta B, Salomoni P. Inhibition of autophagy: a new strategy to enhance sensitivity of chronic myeloid leukemia stem cells to tyrosine kinase inhibitors. Leuk Lymphoma. 2011 Feb; 52 Suppl 1:54-9.
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Lidonnici MR, Audia A, Soliera AR, Prisco M, Ferrari-Amorotti G, Waldron T, Donato N, Zhang Y, Martinez RV, Holyoake TL, Calabretta B. Expression of the transcriptional repressor Gfi-1 is regulated by C/EBP{alpha} and is involved in its proliferation and colony formation-inhibitory effects in p210BCR/ABL-expressing cells. Cancer Res. 2010 Oct 15; 70(20):7949-59.
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Salomoni P, Calabretta B. Targeted therapies and autophagy: new insights from chronic myeloid leukemia. Autophagy. 2009 Oct; 5(7):1050-1.