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Andrea Weckman Division of Neurosurgery, Division of Pathology, Department of Neurosurgery, Department of Surgery

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Fabio Rotondo Division of Neurosurgery, Division of Pathology, Department of Neurosurgery, Department of Surgery

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Antonio Di Ieva Division of Neurosurgery, Division of Pathology, Department of Neurosurgery, Department of Surgery

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Luis V Syro Division of Neurosurgery, Division of Pathology, Department of Neurosurgery, Department of Surgery

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Henriett Butz Division of Neurosurgery, Division of Pathology, Department of Neurosurgery, Department of Surgery

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Michael D Cusimano Division of Neurosurgery, Division of Pathology, Department of Neurosurgery, Department of Surgery

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Kalman Kovacs Division of Neurosurgery, Division of Pathology, Department of Neurosurgery, Department of Surgery

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Autophagy is an important intracellular process involving the degradation of cytoplasmic components. It is involved in both physiological and pathological conditions, including cancer. The role of autophagy in cancer is described as a ‘double-edged sword,’ a term that reflects its known participation in tumor suppression, tumor survival and tumor cell proliferation. Available research regarding autophagy in endocrine cancer supports this concept. Autophagy shows promise as a novel therapeutic target in different types of endocrine cancer, inhibiting or increasing treatment efficacy in a context- and cell-type-dependent manner. At present, however, there is very little research concerning autophagy in endocrine tumors. No research was reported connecting autophagy to some of the tumors of the endocrine glands such as the pancreas and ovary. This review aims to elucidate the roles of autophagy in different types of endocrine cancer and highlight the need for increased research in the field.

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Michael Solarski Division of Neurosurgery, Department of Surgery, St. Michael’s Hospital, Toronto, Ontario, Canada

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Fabio Rotondo Division of Pathology, Department of Laboratory Medicine, St. Michael’s Hospital, Toronto, Ontario, Canada

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William D Foulkes Department of Human Genetics, Medicine and Oncology, McGill University, Montreal, Quebec, Canada
Lady Davis Institute, Jewish General Hospital and Research Institute, McGill University Health Centre, Montreal, Quebec, Canada

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John R Priest Department of Medicine, Minneapolis, Minnesota, USA

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Luis V Syro Department of Neurosurgery, Hospital Pablo Tobon Uribe and Clinica Medellin, Medellin, Colombia

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Henriett Butz Molecular Medicine Research Group, Hungarian Academy of Sciences, Semmelweis University, Budapest, Hungary

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Michael D Cusimano Division of Neurosurgery, Department of Surgery, St. Michael’s Hospital, Toronto, Ontario, Canada

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Kalman Kovacs Division of Pathology, Department of Laboratory Medicine, St. Michael’s Hospital, Toronto, Ontario, Canada

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In this review, the importance of the DICER1 gene in the function of endocrine cells is discussed. There is conclusive evidence that DICER1 mutations play a crucial role in the development, progression, cell proliferation, therapeutic responsiveness and behavior of several endocrine tumors. We review the literature of DICER1 gene mutations in thyroid, parathyroid, pituitary, pineal gland, endocrine pancreas, paragangliomas, medullary, adrenocortical, ovarian and testicular tumors. Although significant progress has been made during the last few years, much more work is needed to fully understand the significance of DICER1 mutations.

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