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Article: Overexpression and point mutations of p53 tumor suppressor gene in hepatocellular carcinomas in Hong Kong Chinese people

TitleOverexpression and point mutations of p53 tumor suppressor gene in hepatocellular carcinomas in Hong Kong Chinese people
Authors
KeywordsChinese people
Hepatocellular carcinoma
Mutations
Overexpression
p53 gene
Issue Date1994
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741
Citation
Cancer, 1994, v. 74 n. 1, p. 30-37 How to Cite?
AbstractBackground. Gene deletion, point mutations, and abnormalities in expression of the tumor suppressor gene p53 in hepatocellular carcinoma have been reported to occur with varying frequency in different geographic regions. Methods. To assess the expression and point mutation of the p53 gene, 31 patients with hepatocellular carcinomas were examined using Northern blotting, immunohistochemical methods, and DNA sequencing. All patients were Chinese, and 90.3% were positive for hepatitis B surface antigen (HBsAg). Results. p53 transcript or protein was found in 14 (48.4%) of the 31 patients. Detectable p53 mRNA transcripts were found in 10 patients, and p53 protein was detected in 8 patients. In most cases of patients who had detectable p53 mRNA transcripts, the transcripts in the tumors were exhibited at a higher level than they were in the corresponding nontumorous livers. No p53 protein was detected in the nontumorous livers in all 31 patients. Six (23.1%) of the 26 tumors sequenced showed point mutation scattered in exons 5-9. Of these, only two were at codon-249, and the nature of these two mutations was G-to-T transversions. All but one of the six patients with point mutations had overexpression of the gene. Conclusions. Our results show that scattered point mutations are not uncommon in hepatocellular carcinomas in patients from Hong Kong. The distribution pattern of the mutations seems to have no particular correlation with HBsAg status despite a high prevalence rate of HBsAg positivity in our patients. Consistent with a low aflatoxin exposure, aflatoxin-related specific mutation at codon-249 is much less related to the pathogenesis of hepatocellular carcinoma in Hong Kong Chinese people than in other regions with a high-aflatoxin exposure.
Persistent Identifierhttp://hdl.handle.net/10722/148017
ISSN
2015 Impact Factor: 5.649
2015 SCImago Journal Rankings: 3.188
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorNg, IOLen_US
dc.contributor.authorSrivastava, Gen_US
dc.contributor.authorChung, LPen_US
dc.contributor.authorTsang, SWYen_US
dc.contributor.authorNg, MMTen_US
dc.date.accessioned2012-05-29T06:10:24Z-
dc.date.available2012-05-29T06:10:24Z-
dc.date.issued1994en_US
dc.identifier.citationCancer, 1994, v. 74 n. 1, p. 30-37en_US
dc.identifier.issn0008-543Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/148017-
dc.description.abstractBackground. Gene deletion, point mutations, and abnormalities in expression of the tumor suppressor gene p53 in hepatocellular carcinoma have been reported to occur with varying frequency in different geographic regions. Methods. To assess the expression and point mutation of the p53 gene, 31 patients with hepatocellular carcinomas were examined using Northern blotting, immunohistochemical methods, and DNA sequencing. All patients were Chinese, and 90.3% were positive for hepatitis B surface antigen (HBsAg). Results. p53 transcript or protein was found in 14 (48.4%) of the 31 patients. Detectable p53 mRNA transcripts were found in 10 patients, and p53 protein was detected in 8 patients. In most cases of patients who had detectable p53 mRNA transcripts, the transcripts in the tumors were exhibited at a higher level than they were in the corresponding nontumorous livers. No p53 protein was detected in the nontumorous livers in all 31 patients. Six (23.1%) of the 26 tumors sequenced showed point mutation scattered in exons 5-9. Of these, only two were at codon-249, and the nature of these two mutations was G-to-T transversions. All but one of the six patients with point mutations had overexpression of the gene. Conclusions. Our results show that scattered point mutations are not uncommon in hepatocellular carcinomas in patients from Hong Kong. The distribution pattern of the mutations seems to have no particular correlation with HBsAg status despite a high prevalence rate of HBsAg positivity in our patients. Consistent with a low aflatoxin exposure, aflatoxin-related specific mutation at codon-249 is much less related to the pathogenesis of hepatocellular carcinoma in Hong Kong Chinese people than in other regions with a high-aflatoxin exposure.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741en_US
dc.relation.ispartofCanceren_US
dc.rightsCancer. Copyright © John Wiley & Sons, Inc.-
dc.subjectChinese people-
dc.subjectHepatocellular carcinoma-
dc.subjectMutations-
dc.subjectOverexpression-
dc.subjectp53 gene-
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshBlotting, Northernen_US
dc.subject.meshCarcinoma, Hepatocellular - Complications - Ethnology - Geneticsen_US
dc.subject.meshChina - Ethnologyen_US
dc.subject.meshDna Mutational Analysisen_US
dc.subject.meshDna, Neoplasm - Analysisen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expressionen_US
dc.subject.meshGenes, P53 - Geneticsen_US
dc.subject.meshHepatitis B - Complicationsen_US
dc.subject.meshHong Kongen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshIn Situ Hybridizationen_US
dc.subject.meshLiver Neoplasms - Complications - Ethnology - Geneticsen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPoint Mutationen_US
dc.subject.meshRna, Messenger - Analysisen_US
dc.subject.meshTumor Suppressor Protein P53 - Analysis - Geneticsen_US
dc.titleOverexpression and point mutations of p53 tumor suppressor gene in hepatocellular carcinomas in Hong Kong Chinese peopleen_US
dc.typeArticleen_US
dc.identifier.emailNg, IOL:iolng@hkucc.hku.hken_US
dc.identifier.emailSrivastava, G:gopesh@pathology.hku.hken_US
dc.identifier.emailChung, LP:lpchung@hkucc.hku.hken_US
dc.identifier.authorityNg, IOL=rp00335en_US
dc.identifier.authoritySrivastava, G=rp00365en_US
dc.identifier.authorityChung, LP=rp00249en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/1097-0142(19940701)74:1<30::AID-CNCR2820740107>3.0.CO;2-4en_US
dc.identifier.pmid8004579-
dc.identifier.scopuseid_2-s2.0-0028226101en_US
dc.identifier.hkuros5244-
dc.identifier.volume74en_US
dc.identifier.issue1en_US
dc.identifier.spage30en_US
dc.identifier.epage37en_US
dc.identifier.isiWOS:A1994NT71500006-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridNg, IOL=7102753722-
dc.identifier.scopusauthoridSrivastava, G=7202242238-
dc.identifier.scopusauthoridChung, LP=24315879100-
dc.identifier.scopusauthoridTsang, SWY=36838809000-
dc.identifier.scopusauthoridNg, MMT=7202076310-

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