title: Autophagy: cancer therapy's friend or foe?
abstract: Autophagy is a physiological process that is activated not only in response to stress (e.g., degradation of damaged organelles or nutrient starvation) but also during carcinogenesis and tumor progression. Furthermore, a number of commonly used anticancer drugs activate the autophagic program, a response that, in most cases, suppresses the cytotoxic effects of the drugs, where in some other cases, autophagy promotes drug-induced cell death. Significant progress has been made on delineating the signaling cascades activated during autophagy. A number of known or candidate tumor-suppressor genes that are involved in autophagy have been shown to be activated or inactivated in various cancer types. These genetic perturbations do not only affect carcinogenesis but also the responses of the cancer cells to treatment. The current state-of-the-art with respect to the genes regulating autophagy and the importance of autophagy in the cytotoxic response of cancer treatments will be discussed in this review.
authors.affiliation: Department of Oncology and Pathology, Cancer Centre Karolinska, Karolinska Institutet and Karolinska University Hospital, S-171 76 Stockholm, Sweden.
authors.forename: Dan
authors.initials: D
authors.lastname: Grandér
authors.forename: Theocharis
authors.initials: T
authors.lastname: Panaretakis
mesh_terms: D001343:Autophagy / Q000187:drug effects / Q000235:genetics; D016923:Cell Death / Q000187:drug effects / Q000502:physiology*; D002471:Cell Transformation, Neoplastic / Q000187:drug effects / Q000473:pathology*; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000188:drug therapy / Q000503:physiopathology*; D015388:Organelles / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology