{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,14]],"date-time":"2026-02-14T12:40:49Z","timestamp":1771072849171,"version":"3.50.1"},"reference-count":38,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2001,12,21]],"date-time":"2001-12-21T00:00:00Z","timestamp":1008892800000},"content-version":"vor","delay-in-days":203,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Gastro and Hepatol"],"published-print":{"date-parts":[[2001,6]]},"abstract":"<jats:sec><jats:title>Abstract<\/jats:title><\/jats:sec><jats:sec><jats:title>Background:<\/jats:title><jats:p>Several etiologic factors including hepatitis viruses, alcohol and aflatoxin have been implicated in the pathogenesis of hepatocellular carcinoma (HCC). There is, however, limited information from the Indian subcontinent.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods:<\/jats:title><jats:p>Seventy\u2010four consecutive cases of HCC were studied. A detailed history, tests for hepatitis B virus (HBV; HBsAg, HBeAg, anti\u2010HBe, IgG anti\u2010HBc, anti\u2010HBs and HBV\u2010DNA), hepatitis C virus (HCV; anti\u2010HCV and HCV\u2010RNA) infection, liver histopathology and HBV\u2010DNA integration by using Southern blot hybridization were studied. A p53 gene mutation was also studied by using PCR and single\u2010strand conformation polymorphism.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results:<\/jats:title><jats:p>Hepatocellular carcinoma patients were predominantly males (mean age 49.5 \u00b1 14.0 years). Portal hypertension and cirrhosis were seen in 56 (76%) patients, more often (<jats:italic>P<\/jats:italic> &lt; 0.05) in viral marker positive cases. Forty\u2010five percent of patients had features of hepatic decompensation at presentation. Evidence of HBV infection was present in 53 (71%) patients. Twenty\u2010six (49%) of these patients had either HBeAg + ve, HBV\u2010DNA + ve (<jats:italic>n<\/jats:italic> = 12), or HBsAg \u2013 ve, HBV\u2010DNA + ve (<jats:italic>n<\/jats:italic> = 14) forms of HBV infection. Hepatitis B virus DNA integration in the liver tissue was seen in 10 of 17 (59%) patients. Infection with HCV alone was detected in three (4%) and dual HBV and HCV infection in six (8%) patients. A majority (78.5%) of the chronic alcoholics had associated viral infection. The etiology of HCC remained undetermined in 15 (20%) patients. The p53 gene mutations were detected only in three of 21 (14%) liver tissues. Aflatoxin toxicity, oral contraceptive use or metabolic disorder were not seen.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions:<\/jats:title><jats:p>In India: (i) HBV infection is the predominant factor for the development of HCC, often related to mutant forms of HBV; (ii) a majority of the HCC patients have overt cirrhosis of the liver; and (iii) HCV and alcohol per se are uncommonly associated.<\/jats:p><\/jats:sec>","DOI":"10.1046\/j.1440-1746.2001.02476.x","type":"journal-article","created":{"date-parts":[[2003,3,12]],"date-time":"2003-03-12T05:20:00Z","timestamp":1047446400000},"page":"666-673","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":56,"title":["Profile of hepatocellular carcinoma in India: An insight into the possible etiologic associations"],"prefix":"10.1111","volume":"16","author":[{"given":"Shiv Kumar","family":"Sarin","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Varsha","family":"Thakur","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rajkumar C","family":"Guptan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sanjeev","family":"Saigal","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Veena","family":"Malhotra","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sadras P","family":"Thyagarajan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bhudev C","family":"Das","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2001,12,21]]},"reference":[{"key":"e_1_2_5_2_2","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-108-3-390"},{"key":"e_1_2_5_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(89)90770-8"},{"key":"e_1_2_5_4_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2893.1998.00116.x"},{"key":"e_1_2_5_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2893.1996.tb00001.x"},{"key":"e_1_2_5_6_2","first-page":"1141","article-title":"Hepatitis B virus antigen in the pathogenesis of chronic infections and the development of hepatocellular carcinoma.","volume":"150","author":"Feitelson MA","year":"1997","journal-title":"Am. 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