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Cited by 300

The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.

The multiple roles of autophagy in cancer

Open access
Rosenfeldt, M. T., Ryan, K. M.·2011·Carcinogenesis

Abstract

Autophagy is an evolutionarily conserved, catabolic process that involves the entrapment of cytoplasmic components within characteristic vesicles for their delivery to and degradation within lysosomes. Autophagy is regulated via a group of genes called AuTophaGy-related genes and is executed at basal levels in virtually all cells as a homeostatic mechanism for maintaining cellular integrity. The levels and cargos of autophagy can be modulated in response to a variety of intra- and extracellular cues to bring about specific and selective events. Autophagy is a multifaceted process and alterations in autophagic signalling pathways are frequently found in cancer and many other diseases. During tumour development and in cancer therapy, autophagy has paradoxically been reported to have roles in promoting both cell survival and cell death. In addition, autophagy has been reported to control other processes relevant to the aetiology of malignant disease, including oxidative stress, inflammation and both innate and acquired immunity. It is the aim of this review to describe the molecular basis and the signalling events that control autophagy in mammalian cells and to summarize the cellular functions that contribute to tumourigenesis when autophagy is perturbed.

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Crossref · 10.1093/carcin/bgr031

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Metadata

Authors
Rosenfeldt, M. T., & Ryan, K. M.
Venue
Carcinogenesis
Published
2011-02-11
Volume
32
Issue
7
Pages
955-963
ISSN
  • 0143-3334 (ISSN-L)
  • 1460-2180
OpenAlex
W2144715185
Cited by
300
References
41
FWCI
23.12
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: The multiple roles of autophagy in cancer. https://app.cochat.ai/papers/10.1093/carcin/bgr031
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Rosenfeldt, M. T., & Ryan, K. M. (2011). The multiple roles of autophagy in cancer. Carcinogenesis. https://doi.org/10.1093/carcin/bgr031

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