Document Detail


Role of the hybrid Bcr/Abl kinase in the pathogenesis of chronic myeloid leukemia lacking C-Abl and CXCR4 proteins.
MedLine Citation:
PMID:  25265345     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Philadelphia chromosome is a result of chromosomal rearrangement that leads to the appearing of the hybrid gene bcr/abl. A hybrid mRNA transcribes from bcr-promoter and many copies of hybrid molecules of Bcr/Abl protein are formed as a result of bcr/abl gene expression. It is supposed that a hybrid Abl molecule, replacing the normal one, in majority of cases functions abnormally or does not function at all. Also it is possible that Abl moiety of Bcr/Abl protein which is possibly recognized by some hypothetical cell control system interpreted by cell as an overproduction of c-abl. This, probably, leads to blocking the normal C-Abl molecules production from the normal c-abl gene transcribed from the second non-aberrant chromosome 9. Based on C-Abl physiological functions in conjunction with the most important proteins of which functions directly depend on its activity we tried to outline the research directions that might explain disruptions of the processes at chronic myeloleukosis such as cell migration due to CXCL12/CXCR4 axis activation, reparation, apoptosis, control for mitochondria state, and to propose new perspective therapeutic approaches based on all this knowledge.
Authors:
L A Polishchuk; G D Telegeev
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Experimental oncology     Volume:  36     ISSN:  1812-9269     ISO Abbreviation:  Exp. Oncol.     Publication Date:  2014 Sep 
Date Detail:
Created Date:  2014-09-30     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101230541     Medline TA:  Exp Oncol     Country:  Ukraine    
Other Details:
Languages:  eng     Pagination:  138-43     Citation Subset:  IM    
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