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Article: p53 gene mutation spectrum in hepatocellular carcinomas in Hong Kong Chinese

Titlep53 gene mutation spectrum in hepatocellular carcinomas in Hong Kong Chinese
Authors
Issue Date1994
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
Citation
Oncogene, 1994, v. 9 n. 3, p. 985-990 How to Cite?
AbstractTo examine the significance of mutation of the p53 tumour suppressor gene in the development of human hepatocellular carcinoma in a high-prevalence area for hepatitis B viral infection but a low-exposure area for aflatoxin B1, the spectrum of p53 gene mutations was examined in 21 tumour samples from Hong Kong Chinese patients, all of whom were HBsAg positive. DNA sequencing covering exons 5 to 9 of the p53 gene and Hae III restriction enzyme digestion for preliminary assessment of mutation at codon 249 were performed. Immunohistochemical staining with anti-p53 monoclonal antibodies was done on both tumour and nontumour liver tissues. Six tumours (28.6%) showed a p53 mutation and all were point mutations. Of the six point mutations, two (9.5%) were at codon 249 and both were G to T transversions (AGG→ATG and AGG→AGT transversions). The remaining point mutations were transversions scattered at codon 172 (exon 5), 214 (exon 6), 273 (exon 8) and 330 (exon 9). Mutated p53 protein was detected in five of these six cases with demonstrable point mutations by DNA sequencing, in contrast to none detected in all of the 15 cases without demonstrable point mutations. The presence of p53 mutations, including those at codon 249, did not show a significant association with tumour size, sex, age, tumour invasiveness in terms of liver invasion, microsatellites and venous permeation, cirrhosis and encapsulation, but tumours with low cellular differentiation tended to have a higher incidence (71%) of point mutations than those with high cellular differentiation (8%). In conclusion, both the overall p53 mutation rate and that at codon 249 in HCC in Hong Kong Chinese are lower than those reported in tumours from China and sub-Saharan Africa. The low mutation rate at codon 249 is compatible with a low aflatoxin exposure. A special type of p53 mutation has not been found to be associated with hepatitis B viral infection. Mutations of p53 gene tends to occur in tumours with low cellular differentiation, suggesting a late occurrence in the event of tumour progression.
Persistent Identifierhttp://hdl.handle.net/10722/148011
ISSN
2015 Impact Factor: 7.932
2015 SCImago Journal Rankings: 4.047
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorNg, IOLen_HK
dc.contributor.authorChung, LPen_HK
dc.contributor.authorTsang, SWYen_HK
dc.contributor.authorLam, CLDen_HK
dc.contributor.authorLai, ECSen_HK
dc.contributor.authorFan, STen_HK
dc.contributor.authorNg, Men_HK
dc.date.accessioned2012-05-29T06:10:22Z-
dc.date.available2012-05-29T06:10:22Z-
dc.date.issued1994en_HK
dc.identifier.citationOncogene, 1994, v. 9 n. 3, p. 985-990en_HK
dc.identifier.issn0950-9232en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148011-
dc.description.abstractTo examine the significance of mutation of the p53 tumour suppressor gene in the development of human hepatocellular carcinoma in a high-prevalence area for hepatitis B viral infection but a low-exposure area for aflatoxin B1, the spectrum of p53 gene mutations was examined in 21 tumour samples from Hong Kong Chinese patients, all of whom were HBsAg positive. DNA sequencing covering exons 5 to 9 of the p53 gene and Hae III restriction enzyme digestion for preliminary assessment of mutation at codon 249 were performed. Immunohistochemical staining with anti-p53 monoclonal antibodies was done on both tumour and nontumour liver tissues. Six tumours (28.6%) showed a p53 mutation and all were point mutations. Of the six point mutations, two (9.5%) were at codon 249 and both were G to T transversions (AGG→ATG and AGG→AGT transversions). The remaining point mutations were transversions scattered at codon 172 (exon 5), 214 (exon 6), 273 (exon 8) and 330 (exon 9). Mutated p53 protein was detected in five of these six cases with demonstrable point mutations by DNA sequencing, in contrast to none detected in all of the 15 cases without demonstrable point mutations. The presence of p53 mutations, including those at codon 249, did not show a significant association with tumour size, sex, age, tumour invasiveness in terms of liver invasion, microsatellites and venous permeation, cirrhosis and encapsulation, but tumours with low cellular differentiation tended to have a higher incidence (71%) of point mutations than those with high cellular differentiation (8%). In conclusion, both the overall p53 mutation rate and that at codon 249 in HCC in Hong Kong Chinese are lower than those reported in tumours from China and sub-Saharan Africa. The low mutation rate at codon 249 is compatible with a low aflatoxin exposure. A special type of p53 mutation has not been found to be associated with hepatitis B viral infection. Mutations of p53 gene tends to occur in tumours with low cellular differentiation, suggesting a late occurrence in the event of tumour progression.en_HK
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/oncen_HK
dc.relation.ispartofOncogeneen_HK
dc.subject.meshCarcinoma, Hepatocellular - Ethnology - Genetics - Pathologyen_US
dc.subject.meshChina - Ethnologyen_US
dc.subject.meshCodonen_US
dc.subject.meshDeoxyribonucleases, Type Ii Site-Specificen_US
dc.subject.meshFemaleen_US
dc.subject.meshGenes, P53en_US
dc.subject.meshHong Kongen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshLiver Neoplasms - Ethnology - Genetics - Pathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPoint Mutationen_US
dc.subject.meshSequence Analysis, Dnaen_US
dc.titlep53 gene mutation spectrum in hepatocellular carcinomas in Hong Kong Chineseen_HK
dc.typeArticleen_HK
dc.identifier.emailNg, IOL: iolng@hku.hken_HK
dc.identifier.emailChung, LP: lpchung@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.identifier.authorityChung, LP=rp00249en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid8108145-
dc.identifier.scopuseid_2-s2.0-0028123801en_HK
dc.identifier.volume9en_HK
dc.identifier.issue3en_HK
dc.identifier.spage985en_HK
dc.identifier.epage990en_HK
dc.identifier.isiWOS:A1994MW55100039-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridNg, IOL=7102753722en_HK
dc.identifier.scopusauthoridChung, LP=24315879100en_HK
dc.identifier.scopusauthoridTsang, SWY=36838809000en_HK
dc.identifier.scopusauthoridLam, CL=7402990922en_HK
dc.identifier.scopusauthoridLai, ECS=55187403900en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.scopusauthoridNg, M=7202076310en_HK

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