{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,2]],"date-time":"2025-12-02T15:18:17Z","timestamp":1764688697344,"version":"3.44.0"},"reference-count":52,"publisher":"Cambridge University Press (CUP)","issue":"2b","license":[{"start":{"date-parts":[[2007,9,27]],"date-time":"2007-09-27T00:00:00Z","timestamp":1190851200000},"content-version":"unspecified","delay-in-days":2370,"URL":"https:\/\/www.cambridge.org\/core\/terms"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Public Health Nutr."],"published-print":{"date-parts":[[2001,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                    <jats:p>At least six types of gene\u2013environment interactions (GEI) have been\n                        proposed (Kouhry and Wagener, 1993) In the first type, neither the\n                        environmental exposure (EE) nor the genetic risk factor (GRF) have any\n                        effect by themselves, but interaction between them causes disease. This is\n                        the case of phenylalanine exposure and the phenylketonuria genotype. Type 2\n                        is a situation in which the GRF has no effect on disease in the absence of\n                        exposure, but exacerbates the effects of the latter. This is the most\n                        important type of GEI in relation to metabolic susceptibility genes and\n                        human carcinogenesis. The third type is the converse of the second (EE is\n                        ineffective per se, but enhances the effect of GRF). Type 4 occurs when both\n                        EE and GRF increase the risk for disease, but the combination is interactive\n                        or synergistic: an example is the interaction between Xeroderma Pigmentosum\n                        and UV radiation. Types 5 and 6, according to the classification proposed by\n                        Kouhry, refer to cases in which the GRF is protective.<\/jats:p>\n                    <jats:p>The model of GEI that is emerging as the most important in chemical\n                        carcinogenesis refers to metabolic susceptibility genes. The general\n                        population can be divided into subgroups depending on their susceptibility\n                        to the action of carcinogens, based on their ability to metabolize such\n                        compounds to electrophilic, reactive metabolites (which form adducts with\n                        DNA), or, respectively, electrophobic metabolites that are excreted. The\n                        present contribution is a short review of the relevant literature, with\n                        particular emphasis on some polymorphisms involved in dietary exposures. In\n                        addition, the practical implications of genetic testing in this field are\n                        discussed.<\/jats:p>","DOI":"10.1079\/phn2001135","type":"journal-article","created":{"date-parts":[[2008,6,3]],"date-time":"2008-06-03T14:03:09Z","timestamp":1212501789000},"page":"485-491","source":"Crossref","is-referenced-by-count":9,"title":["Diet, genetic susceptibility and carcinogenesis"],"prefix":"10.1017","volume":"4","author":[{"given":"Paolo","family":"Vineis","sequence":"first","affiliation":[{"name":"University of Torino and\n                                    CPO-Piemonte"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"56","published-online":{"date-parts":[[2007,9,27]]},"reference":[{"key":"S1368980001001409_manual_ref-49","doi-asserted-by":"publisher","DOI":"10.1136\/jech.32.4.303"},{"key":"S1368980001001409_manual_ref-36","doi-asserted-by":"publisher","DOI":"10.2307\/3579189"},{"key":"S1368980001001409_manual_ref-48","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/21.2.183"},{"key":"S1368980001001409_manual_ref-6","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/19.12.2129"},{"key":"S1368980001001409_manual_ref-10","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(96)91012-0"},{"key":"S1368980001001409_manual_ref-9","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.94.10.2410"},{"key":"S1368980001001409_manual_ref-25","first-page":"5786","article-title":"Development and field-test validation of an assay for DNA\n                            repair in circulating human lymphocytes","volume":"51","author":"Athas","year":"1991","journal-title":"Cancer Res."},{"key":"S1368980001001409_manual_ref-33","first-page":"99","article-title":"Mutagen sensitivity as a biological marker of lung cancer\n                            risk in African Americans","volume":"4","author":"Spits","year":"1995","journal-title":"Cancer Epidemiol. 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