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REVIEW ARTICLE
Year : 2013  |  Volume : 9  |  Issue : 1  |  Page : 3-5

Breakpoint cluster region-c-abl oncogene 1, non-receptor tyrosine kinase signaling: Current patterns of the versatile regulator revisited


1 National Institute for Genomics and Advanced Biotechnology (NIGAB), NARC, Islamabad; Attaur Rahman School of Applied Biosciences (ASAB), National University of Science and Technology, Islamabad, Pakistan
2 National Institute for Genomics and Advanced Biotechnology (NIGAB), NARC, Islamabad, Pakistan
3 Attaur Rahman School of Applied Biosciences (ASAB), National University of Science and Technology, Islamabad, Pakistan
4 Punjab Medical College, Faisalabad, Pakistan
5 Institute of Molecular Biology and Biotechnology (IMBB), University of Lahore, Lahore, Pakistan
6 Lab for Translational Oncology and Personalized Medicine, Rashid Latif Medical College (RLMC), Ferozepur Road, Lahore, Pakistan

Correspondence Address:
Aamir Rana
National Institute for Genomics and Advanced Biotechnology (NIGAB), NARC, Islamabad, Atta ur Rahman School of Applied Biosciences (ASAB), National University of Science and Technology, Islamabad
Pakistan
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-1482.110338

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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.


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