| Literature DB >> 30323273 |
Michele Carbone1, Ivano Amelio2, El Bachir Affar3, James Brugarolas4, Lisa A Cannon-Albright5,6, Lewis C Cantley7, Webster K Cavenee8, Zhijian Chen9, Carlo M Croce10, Alan D' Andrea11, David Gandara12, Carlotta Giorgi13, Wei Jia14, Qing Lan15, Tak Wah Mak16, James L Manley17, Katsuhiko Mikoshiba18, Jose N Onuchic19, Harvey I Pass20, Paolo Pinton13, Carol Prives21, Nathaniel Rothman15, Said M Sebti22, James Turkson14, Xifeng Wu23, Haining Yang14, Herbert Yu14, Gerry Melino24,25.
Abstract
The relative contribution of intrinsic genetic factors and extrinsic environmental ones to cancer aetiology and natural history is a lengthy and debated issue. Gene-environment interactions (G x E) arise when the combined presence of both a germline genetic variant and a known environmental factor modulates the risk of disease more than either one alone. A panel of experts discussed our current understanding of cancer aetiology, known examples of G × E interactions in cancer, and the expanded concept of G × E interactions to include somatic cancer mutations and iatrogenic environmental factors such as anti-cancer treatment. Specific genetic polymorphisms and genetic mutations increase susceptibility to certain carcinogens and may be targeted in the near future for prevention and treatment of cancer patients with novel molecularly based therapies. There was general consensus that a better understanding of the complexity and numerosity of G × E interactions, supported by adequate technological, epidemiological, modelling and statistical resources, will further promote our understanding of cancer and lead to novel preventive and therapeutic approaches.Entities:
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Year: 2018 PMID： 30323273 PMCID： PMC6219489 DOI： 10.1038/s41418-018-0213-5
Source DB: PubMed Journal: Cell Death Differ ISSN： 1350-9047 Impact factor: 15.828