Abstract
Autophagy is an evolutionarily conserved catabolic process, which is used by the cells for cytoplasmic quality control. This process is induced following different kinds of stresses e.g., metabolic, environmental, or therapeutic, and acts, in this framework, as a cell survival mechanism. However, under certain circumstances, autophagy has been associated with cell death. This duality has been extensively reported in solid and hematological cancers, and has been observed during both tumor development and cancer therapy. As autophagy plays a critical role at the crossroads between cell survival and cell death, its involvement and therapeutic modulation (either activation or inhibition) are currently intensively studied in cancer biology, to improve treatments and patient outcomes. Over the last few years, studies have demonstrated the occurrence of autophagy in different Anaplastic Lymphoma Kinase (ALK)-associated cancers, notably ALK-positive anaplastic large cell lymphoma (ALCL), non-small cell lung carcinoma (NSCLC), Neuroblastoma (NB), and Rhabdomyosarcoma (RMS). In this review, we will first briefly describe the autophagic process and how it can lead to opposite outcomes in anti-cancer therapies, and we will then focus on what is currently known regarding autophagy in ALK-associated cancers.
Highlights
The Anaplastic Lymphoma Kinase (ALK) is physiologically expressed in a specific subset of neuronal cells during the embryonic life [1]
Over the past ten years, and driven by the impulsion of the success of breakpoint cluster region-abelson (BCR-ABL) tyrosine kinase targeted therapies that are developed for Chronic Myelogenous Leukemia patients [5,6], researchers and clinicians have worked in concert for the development of specific ALK tyrosine kinase targeted therapies
Autophagy has been shown to be induced upon therapies in different kinds of ALK-associated cancers
Summary
The Anaplastic Lymphoma Kinase (ALK) is physiologically expressed in a specific subset of neuronal cells during the embryonic life [1]. Cancers 2017, 9, 161 to evolve and to develop resistance mechanisms against those TKIs [13,14,15,16] To counteract these resistances, the combination of ALK TKIs, with other drugs, targeting the survival pathways that are involved in the acquisition of resistance, appeared logically as an appealing approach to eradicate cancer cells [17,18]. The combination of ALK TKIs, with other drugs, targeting the survival pathways that are involved in the acquisition of resistance, appeared logically as an appealing approach to eradicate cancer cells [17,18] In this framework, autophagy has had a burst of interest over the past ten years, especially in the cancer research field [19].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
