{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T12:16:12Z","timestamp":1791029772516,"version":"4.1.0"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":6028,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1999,3]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>This study evaluated whether the codon 72 <jats:italic toggle=\"yes\">p53<\/jats:italic> polymorphism was related to hepatocellular carcinoma (HCC). Genotypes of <jats:italic toggle=\"yes\">p53<\/jats:italic> were determined in 80 incident cases of HCC and 328 controls nested in a cohort study of 4,841 male chronic hepatitis B carriers. No overall increase in HCC risk with the <jats:italic toggle=\"yes\">Pro<\/jats:italic> variant allele of the <jats:italic toggle=\"yes\">p53<\/jats:italic> polymorphism was apparent. However, there were synergistic effects on HCC development for the <jats:italic toggle=\"yes\">Pro<\/jats:italic> allele with chronic liver disease and family history of HCC in first\u2013degree relatives. Compared with subjects without the <jats:italic toggle=\"yes\">Pro<\/jats:italic> allele and chronic liver disease, the increase in HCC risk associated with chronic liver disease among those without the <jats:italic toggle=\"yes\">Pro<\/jats:italic> allele was only threefold. Subjects with both chronic liver disease and the <jats:italic toggle=\"yes\">Pro<\/jats:italic> allele were at an increased risk of 7.60 (95% CI = 2.28\u201325.31). When subjects without family history of HCC and the <jats:italic toggle=\"yes\">Pro<\/jats:italic> allele were considered as the reference group, there was no apparent increased risk of HCC for those without the <jats:italic toggle=\"yes\">Pro<\/jats:italic> allele who had family history of HCC. Among those with both factors, there was a significantly increased risk of 3.29 (95% CI = 1.10\u20139.85). Both cigarette smoking and glutathione <jats:italic toggle=\"yes\">S<\/jats:italic>\u2013transferase <jats:italic toggle=\"yes\">M1<\/jats:italic> genotype modified the risk of HCC associated with the <jats:italic toggle=\"yes\">p53<\/jats:italic> polymorphism. Significantly increased risk associated with the <jats:italic toggle=\"yes\">p53<\/jats:italic> genotype was observed only among smokers who were glutathione <jats:italic toggle=\"yes\">S<\/jats:italic>\u2013transferase-null (<jats:italic toggle=\"yes\">Pro\/Pro<\/jats:italic> vs. <jats:italic toggle=\"yes\">Arg\/Arg<\/jats:italic>: odds ratio = 6.46; 95% CI = 1.55\u201326.94). The <jats:italic toggle=\"yes\">p53<\/jats:italic> polymorphism also interacted with the cytochrome P450 <jats:italic toggle=\"yes\">1A1<\/jats:italic> and carotenoid levels in smoking\u2013related hepatocarcinogenesis.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.510290330","type":"journal-article","created":{"date-parts":[[2004,7,28]],"date-time":"2004-07-28T07:25:38Z","timestamp":1090999538000},"page":"697-702","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":97,"title":["A P53 Genetic Polymorphism As A Modulator of Hepatocellular Carcinoma Risk in Relation to Chronic Liver Disease, Familial Tendency, and Cigarette Smoking in Hepatitis B Carriers"],"prefix":"10.1097","volume":"29","author":[{"given":"Ming-Whei","family":"Yu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shi-Yi","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yueh-Hsia","family":"Chiu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi-Ching","family":"Chiang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yun-Fan","family":"Liaw","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chien-Jen","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"BIB1","doi-asserted-by":"crossref","first-page":"71","DOI":"10.1016\/1040-8428(94)90020-5","volume":"17","author":"Yu","year":"1994","journal-title":"Crit Rev Oncol Hematol"},{"key":"BIB2","doi-asserted-by":"crossref","first-page":"1942","DOI":"10.1002\/1097-0142(19880515)61:10<1942::AID-CNCR2820611003>3.0.CO;2-J","volume":"61","author":"Beasley","year":"1988","journal-title":"Cancer"},{"key":"BIB3","first-page":"5621","volume":"51","author":"Yu","year":"1991","journal-title":"Cancer Res"},{"key":"BIB4","first-page":"128","volume":"59","author":"Chen","year":"1996","journal-title":"Am J Hum Genet"},{"key":"BIB5","doi-asserted-by":"crossref","first-page":"320","DOI":"10.1016\/S0168-8278(97)80178-X","volume":"27","author":"Yu","year":"1997","journal-title":"J Hepatol"},{"key":"BIB6","doi-asserted-by":"crossref","first-page":"398","DOI":"10.1002\/hep.1840130303","volume":"13","author":"Chen","year":"1991","journal-title":"Hepatology"},{"key":"BIB7","doi-asserted-by":"crossref","first-page":"1820","DOI":"10.1093\/jnci\/83.24.1820","volume":"83","author":"Yu","year":"1991","journal-title":"J Natl Cancer Inst"},{"key":"BIB8","first-page":"1301","volume":"55","author":"Yu","year":"1995","journal-title":"Cancer Res"},{"key":"BIB9","doi-asserted-by":"crossref","first-page":"1266","DOI":"10.1016\/0016-5085(95)90587-1","volume":"109","author":"Yu","year":"1995","journal-title":"Gastroenterology"},{"key":"BIB10","author":"Yu","unstructured":"et al. 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