Open AccessSignificance of bcr-abl molecular detection in chronic myeloid leukemia patients
Author(s) -
Manzoor Ahmad Malik
Publication year - 2016
Publication title -
journal of medical sciences/journal of medical sciences (srinagar. online)
Language(s) - English
Resource type - Journals
eISSN - 2582-063X
pISSN - 0972-110X
DOI - 10.33883/jms.v19i2.299
Subject(s) - philadelphia chromosome , myeloid leukemia , medicine , breakpoint cluster region , chromosomal translocation , abl , cancer research , leukemia , chromosome , myeloid , fusion gene , chromosome 22 , immunology , gene , genetics , biology , tyrosine kinase , receptor
Important advances in the understanding of the molecular basis of chronic myeloid leukemia have resulted in the development of new therapies and changed the paradigm for managing this myeloproliferative disease. The reciprocal translocation of the abl (Abelson murine leukemia) proto-oncogene on chromosome 9 to the bcr (breakpoint cluster region) gene on chromosome 22 creates a transcriptionally active, chimeric bcr-abl gene and gives rise to the Philadelphia chromosome. 1
The genetic hallmark of chronic myeloid leukemia (CML) is the Philadelphia chromosome (Ph), which occurs in at least 95% of CML cases as well as some cases of acute lymphocytic leukemia (ALL; approximately 5% for children, 20% for adults). It also has been reported in some other hematologic disorders, albeit rarely. 2-4 JMS 2016; 19(2):95-96