Autophagy in malignant transformation and cancer progression.
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Galluzzi L
Equipe 11 labellisée pas la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France INSERM U1138, Paris, France Gustave Roussy Cancer Campus, Villejuif, France Université Paris Descartes Sorbonne Paris Cité, Paris, France deadoc@vodafone.it.
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Pietrocola F
Equipe 11 labellisée pas la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France INSERM U1138, Paris, France Gustave Roussy Cancer Campus, Villejuif, France.
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Bravo-San Pedro JM
Equipe 11 labellisée pas la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France INSERM U1138, Paris, France Gustave Roussy Cancer Campus, Villejuif, France.
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Amaravadi RK
Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA, USA.
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Baehrecke EH
Department of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, USA.
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Cecconi F
Cell Stress and Survival Unit, Danish Cancer Society Research Center, Copenhagen, Denmark IRCCS Fondazione Santa Lucia and Department of Biology University of Rome Tor Vergata, Rome, Italy.
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Codogno P
Université Paris Descartes Sorbonne Paris Cité, Paris, France Institut Necker Enfants-Malades (INEM), Paris, France INSERM U1151, Paris, France CNRS UMR8253, Paris, France.
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Debnath J
Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, USA.
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Gewirtz DA
Department of Pharmacology, Toxicology and Medicine, Virginia Commonwealth University, Richmond Virginia, VA, USA.
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Karantza V
Merck Research Laboratories, Rahway, NJ, USA.
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Kimmelman A
Division of Genomic Stability and DNA Repair, Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
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Kumar S
Centre for Cancer Biology, University of South Australia, Adelaide, SA, Australia.
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Levine B
Center for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
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Maiuri MC
Equipe 11 labellisée pas la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France INSERM U1138, Paris, France Gustave Roussy Cancer Campus, Villejuif, France.
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Martin SJ
Department of Genetics, Trinity College, The Smurfit Institute, Dublin, Ireland.
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Penninger J
Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria.
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Piacentini M
Department of Biology, University of Rome Tor Vergata, Rome, Italy National Institute for Infectious Diseases IRCCS 'Lazzaro Spallanzani', Rome, Italy.
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Rubinsztein DC
Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK.
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Simon HU
Institute of Pharmacology, University of Bern, Bern, Switzerland.
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Simonsen A
Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
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Thorburn AM
Department of Pharmacology, University of Colorado School of Medicine, Aurora, CO, USA.
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Velasco G
Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University of Madrid, Madrid, Spain Instituto de Investigaciones Sanitarias San Carlos (IdISSC), Madrid, Spain.
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Ryan KM
Cancer Research UK Beatson Institute, Glasgow, UK.
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Kroemer G
Equipe 11 labellisée pas la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France INSERM U1138, Paris, France Université Paris Descartes Sorbonne Paris Cité, Paris, France Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, Paris, France Metabolomics and Cell Biology Platforms, Gustave Roussy Cancer Campus, Villejuif, France.
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English
Autophagy plays a key role in the maintenance of cellular homeostasis. In healthy cells, such a homeostatic activity constitutes a robust barrier against malignant transformation. Accordingly, many oncoproteins inhibit, and several oncosuppressor proteins promote, autophagy. Moreover, autophagy is required for optimal anticancer immunosurveillance. In neoplastic cells, however, autophagic responses constitute a means to cope with intracellular and environmental stress, thus favoring tumor progression. This implies that at least in some cases, oncogenesis proceeds along with a temporary inhibition of autophagy or a gain of molecular functions that antagonize its oncosuppressive activity. Here, we discuss the differential impact of autophagy on distinct phases of tumorigenesis and the implications of this concept for the use of autophagy modulators in cancer therapy.
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Language
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Open access status
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green
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Identifiers
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Persistent URL
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https://folia.unifr.ch/global/documents/89681
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