title: BCR-ABL1 in leukemia: disguise master outplays riding shotgun.
abstract: Leukemia is a many-sided molecular disorder that arises because of over expression of oncogenes, suppression of tumor suppressor genes, and chromosomal translocations. These chromosomal rearrangements are nonetheless among the many determinants that underlie transformation of cells from normal to a cancerous phenotype and predispose cells to refractoriness against interventions by reduced drug influx and substantial drug efflux. This review unfolds current understanding of BCR-ABL1 (break point cluster region-c-abl oncogene 1, non-receptor tyrosine kinase) signaling with a focus on apoptotic suppressive mechanisms and alternative approaches to chronic myeloid leukemia therapy.
authors.affiliation: National Institute for Genomics and Advanced Biotechnology, NARC, Islamabad.
authors.forename: Aamir
authors.initials: A
authors.lastname: Rana
authors.forename: Ghulam M
authors.initials: GM
authors.lastname: Ali
authors.forename: Shaukat
authors.initials: S
authors.lastname: Ali
authors.forename: Ammara
authors.initials: A
authors.lastname: Khan
authors.forename: Sajid
authors.initials: S
authors.lastname: Mansoor
authors.forename: Shazia
authors.initials: S
authors.lastname: Malik
authors.forename: Ammad A
authors.initials: AA
authors.lastname: Farooqi
mesh_terms: D018450:Disease Progression; D019008:Drug Resistance, Neoplasm / Q000235:genetics; D016044:Fusion Proteins, bcr-abl / Q000235:genetics* / Q000378:metabolism*; D006801:Humans; D007938:Leukemia / Q000188:drug therapy / Q000235:genetics* / Q000378:metabolism*; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction
chemical_list: C581634:BCR-ABL1 fusion protein, human; D016044:Fusion Proteins, bcr-abl