{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,14]],"date-time":"2025-10-14T14:45:20Z","timestamp":1760453120886,"version":"build-2065373602"},"reference-count":130,"publisher":"MDPI AG","issue":"10","license":[{"start":{"date-parts":[[2021,9,23]],"date-time":"2021-09-23T00:00:00Z","timestamp":1632355200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"European Union\u2019s Horizon 2020 research and innovative Programme under the Marie Sklodowska-Curie grant","award":["Grant agreement No 675712"],"award-info":[{"award-number":["Grant agreement No 675712"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>Autophagy has been described as harboring a dual role in cancer development and therapy. Depending on the context, it can exert either pro-survival or pro-death functions. Here, we review what is known about autophagy in crizotinib-treated ALK+ ALCL. We first present our main findings on the role and regulation of autophagy in these cells. Then, we provide literature-driven hypotheses that could explain mechanistically the pro-survival properties of autophagy in crizotinib-treated bulk and stem-like ALK+ ALCL cells. Finally, we discuss how the potentiation of autophagy, which occurs with combined therapies (ALK and BCL2 or ALK and RAF1 co-inhibition), could convert it from a survival mechanism to a pro-death process.<\/jats:p>","DOI":"10.3390\/cells10102517","type":"journal-article","created":{"date-parts":[[2021,9,23]],"date-time":"2021-09-23T09:59:15Z","timestamp":1632391155000},"page":"2517","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["The Dual Role of Autophagy in Crizotinib-Treated ALK+ ALCL: From the Lymphoma Cells Drug Resistance to Their Demise"],"prefix":"10.3390","volume":"10","author":[{"given":"Estelle","family":"Espinos","sequence":"first","affiliation":[{"name":"CRCT, Inserm UMR1037\u2014Universit\u00e9 Toulouse III-Paul Sabatier\u2014CNRS ERL5294, F-31037 Toulouse, France"},{"name":"European Research Initiative on ALK-Related Malignancies (ERIA), Cambridge CB2 0QQ, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6963-2407","authenticated-orcid":false,"given":"Raymond","family":"Lai","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB T6G 2E1, Canada"},{"name":"Department of Oncology, University of Alberta, Edmonton, AB T6G 2R7, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3274-3397","authenticated-orcid":false,"given":"Sylvie","family":"Giuriato","sequence":"additional","affiliation":[{"name":"CRCT, Inserm UMR1037\u2014Universit\u00e9 Toulouse III-Paul Sabatier\u2014CNRS ERL5294, F-31037 Toulouse, France"},{"name":"European Research Initiative on ALK-Related Malignancies (ERIA), Cambridge CB2 0QQ, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2021,9,23]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Turner, S.D., Lamant, L., Kenner, L., and Brugi\u00e8res, L. 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