title: Breakpoint cluster region-c-abl oncogene 1, non-receptor tyrosine kinase signaling: current patterns of the versatile regulator revisited.
abstract: Increasing sophisticated information suggests that cancer cells express constitutively active oncogenic kinases such as breakpoint cluster region- c-abl oncogene 1, non-receptor tyrosine kinase (BCR-ABL1) that promote carcinogenesis independent of extrinsic growth factors. It is a well-established fact that through the aberrant activation of BCR-ABL1 signal transduction cascade, the perception of cellular growth signals becomes disconnected from the processes promoting cell growth, and this underlies the pathophysiology of leukemia. In this particular review we discuss the oncogenes and tumor suppressors comprising the regulatory network upstream and downstream of BCR-ABL1 and dismantle how derailed BCR-ABL1 signaling provides cell a selective growth advantage. Besides, we discuss why activation of BCR-ABL1, as an outcome of distinct oncogenic events, results in miscellaneous clinical outcomes, and how the intricacy of the BCR-ABL1 signaling network might dictate therapeutic approaches. In this review, our current comprehension of BCR-ABL1 signaling will be summarized.
authors.affiliation: National Institute for Genomics and Advanced Biotechnology, NIGAB, 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: Bibi
authors.initials: B
authors.lastname: Sabiha
authors.forename: Shazia
authors.initials: S
authors.lastname: Malik
authors.forename: Asma M
authors.initials: AM
authors.lastname: Riaz
authors.forename: Ammad A
authors.initials: AA
authors.lastname: Farooqi
mesh_terms: D001343:Autophagy; D016044:Fusion Proteins, bcr-abl / Q000235:genetics* / Q000378:metabolism*; D006801:Humans; D042541:Intracellular Space / Q000378:metabolism; D007938:Leukemia / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism; D021381:Protein Transport; D015398:Signal Transduction
chemical_list: C581634:BCR-ABL1 fusion protein, human; D016044:Fusion Proteins, bcr-abl