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- Publisher Website: 10.1038/s41418-018-0213-5
- Scopus: eid_2-s2.0-85055056293
- PMID: 30323273
- WOS: WOS:000449400600001
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Article: Consensus report of the 8 and 9th Weinman Symposia on Gene x Environment Interaction in carcinogenesis: novel opportunities for precision medicine
Title | Consensus report of the 8 and 9th Weinman Symposia on Gene x Environment Interaction in carcinogenesis: novel opportunities for precision medicine |
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Authors | Carbone, MicheleAmelio, IvanoAffar, El BachirBrugarolas, JamesCannon-Albright, Lisa A.Cantley, Lewis C.Cavenee, Webster K.Chen, ZhijianCroce, Carlo M.Andrea, Alan D’Gandara, DavidGiorgi, CarlottaJia, WeiLan, QingMak, Tak WahManley, James L.Mikoshiba, KatsuhikoOnuchic, Jose N.Pass, Harvey I.Pinton, PaoloPrives, CarolRothman, NathanielSebti, Said M.Turkson, JamesWu, XifengYang, HainingYu, HerbertMelino, Gerry |
Issue Date | 2018 |
Citation | Cell Death and Differentiation, 2018, v. 25, n. 11, p. 1885-1904 How to Cite? |
Abstract | © 2018, ADMC Associazione Differenziamento e Morte Cellulare. 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. |
Persistent Identifier | http://hdl.handle.net/10722/292085 |
ISSN | 2023 Impact Factor: 13.7 2023 SCImago Journal Rankings: 4.102 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Carbone, Michele | - |
dc.contributor.author | Amelio, Ivano | - |
dc.contributor.author | Affar, El Bachir | - |
dc.contributor.author | Brugarolas, James | - |
dc.contributor.author | Cannon-Albright, Lisa A. | - |
dc.contributor.author | Cantley, Lewis C. | - |
dc.contributor.author | Cavenee, Webster K. | - |
dc.contributor.author | Chen, Zhijian | - |
dc.contributor.author | Croce, Carlo M. | - |
dc.contributor.author | Andrea, Alan D’ | - |
dc.contributor.author | Gandara, David | - |
dc.contributor.author | Giorgi, Carlotta | - |
dc.contributor.author | Jia, Wei | - |
dc.contributor.author | Lan, Qing | - |
dc.contributor.author | Mak, Tak Wah | - |
dc.contributor.author | Manley, James L. | - |
dc.contributor.author | Mikoshiba, Katsuhiko | - |
dc.contributor.author | Onuchic, Jose N. | - |
dc.contributor.author | Pass, Harvey I. | - |
dc.contributor.author | Pinton, Paolo | - |
dc.contributor.author | Prives, Carol | - |
dc.contributor.author | Rothman, Nathaniel | - |
dc.contributor.author | Sebti, Said M. | - |
dc.contributor.author | Turkson, James | - |
dc.contributor.author | Wu, Xifeng | - |
dc.contributor.author | Yang, Haining | - |
dc.contributor.author | Yu, Herbert | - |
dc.contributor.author | Melino, Gerry | - |
dc.date.accessioned | 2020-11-17T14:55:44Z | - |
dc.date.available | 2020-11-17T14:55:44Z | - |
dc.date.issued | 2018 | - |
dc.identifier.citation | Cell Death and Differentiation, 2018, v. 25, n. 11, p. 1885-1904 | - |
dc.identifier.issn | 1350-9047 | - |
dc.identifier.uri | http://hdl.handle.net/10722/292085 | - |
dc.description.abstract | © 2018, ADMC Associazione Differenziamento e Morte Cellulare. 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. | - |
dc.language | eng | - |
dc.relation.ispartof | Cell Death and Differentiation | - |
dc.title | Consensus report of the 8 and 9th Weinman Symposia on Gene x Environment Interaction in carcinogenesis: novel opportunities for precision medicine | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1038/s41418-018-0213-5 | - |
dc.identifier.pmid | 30323273 | - |
dc.identifier.pmcid | PMC6219489 | - |
dc.identifier.scopus | eid_2-s2.0-85055056293 | - |
dc.identifier.volume | 25 | - |
dc.identifier.issue | 11 | - |
dc.identifier.spage | 1885 | - |
dc.identifier.epage | 1904 | - |
dc.identifier.eissn | 1476-5403 | - |
dc.identifier.isi | WOS:000449400600001 | - |
dc.identifier.issnl | 1350-9047 | - |