Abstract

Autophagy is a cellular degradation pathway for the clearance of damaged or superfluous proteins and organelles. The recycling of these intracellular constituents also serves as an alternative energy source during periods of metabolic stress to maintain homeostasis and viability. In tumour cells with defects in apoptosis, autophagy allows prolonged survival. Paradoxically, autophagy defects are associated with increased tumorigenesis, but the mechanism behind this has not been determined. Recent evidence suggests that autophagy provides a protective function to limit tumour necrosis and inflammation, and to mitigate genome damage in tumour cells in response to metabolic stress.

Author affiliations

1. Robin Mathew and Eileen White are at the University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA.
2. Vassiliki Karantza-Wadsworth is at the Division of Medical Oncology, Department of Medicine, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA.
3. Vassiliki Karantza-Wadsworth and Eileen White are at The Cancer Institute of New Jersey, New Brunswick, New Jersey 08901, USA.
4. Eileen White is also at the Center for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, New Jersey, USA; and the Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, New Jersey 08854, USA.

Correspondence to: Eileen White^1,3,4 Email: ewhite@cabm.rutgers.edu

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