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Distribution of common BCR-ABL fusion transcripts and their impact on treatment response in Imatinib treated CML patients: A study from India
Author(s) -
Sudha Sazawal,
Sunita Chhikara,
Kanwaljeet Singh,
Rekha Chaubey,
Manoranjan Mahapatra,
Tulika Seth,
Renu Saxena
Publication year - 2019
Publication title -
indian journal of pathology and microbiology/indian journal of pathology and microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.217
H-Index - 31
eISSN - 0974-5130
pISSN - 0377-4929
DOI - 10.4103/ijpm.ijpm_726_17
Subject(s) - imatinib , fusion transcript , breakpoint cluster region , exon , medicine , chromosomal translocation , imatinib mesylate , fusion gene , oncology , cancer research , biology , gastroenterology , genetics , gene , receptor , myeloid leukemia
Philadelphia chromosome (Ph): Hallmark of CML is caused by reciprocal translocation between chromosomes 9 and 22 resulting in BCR-ABL fusion protein. Most commonly associated breakpoint with CML is M-bcr in exon 13 or exon 14, producing splice variant b2a2 or b3a2 respectively. The distribution of these transcripts and their influence on clinico-hematological parameters is variable. Impact of the fusion transcripts on treatment outcome in Imatinib treated CML patients is still a matter of debate.

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