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Article: Loss of imprinting of the IGF-II and H19 genes in epithelial ovarian cancer

TitleLoss of imprinting of the IGF-II and H19 genes in epithelial ovarian cancer
Authors
Issue Date2000
PublisherAmerican Association for Cancer Research.
Citation
Clinical Cancer Research, 2000, v. 6 n. 2, p. 474-479 How to Cite?
AbstractTo establish a possible role of genomic imprinting in the carcinogenesis of epithelial ovarian cancer, we determined the imprinting status of both IGF-II and H19 genes in 43 ovarian cancers, 7 low malignant potential ovarian tumors, and their matched normal tissues. In ovarian cancer, loss of heterozygosity (LOH) of IGF-II, H19 RsaI, and H19 AluI was found in 4 of 24 (16.7%), 3 of 20 (15%), and 1 of 16 (6.3%) samples, respectively. All patients with tumor specimens exhibiting LOH are of advanced clinical stages. Loss of imprinting (LOI) was found in 5 of 20 (25%) for IGF-II and in 4 of 17 (23.5%) and 1 of 15 (6.7%) for the RsaI and AluI sites of H19 gene with no LOH. However, no LOH was found in low malignant potential tumors, and only one of them showed LOI in H19 AluI site. Overexpression of IGF-II was demonstrated in all five LOI samples with normal expression of H19. Three of the five tumor specimens exhibiting LOI were transcribed from P1 promoter, whereas the remaining two were from the P3 promoter. These results suggested that LOH of both IGF-II and H19 genes was associated with advanced ovarian cancer. LOI of IGF-II and H19 genes may be involved in the development of ovarian cancer. Transcription of IGF-II from the P1 promoter may account for the biallelic expression of the IGF-II gene.
Persistent Identifierhttp://hdl.handle.net/10722/87351
ISSN
2023 Impact Factor: 10.0
2023 SCImago Journal Rankings: 4.623
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, CLen_HK
dc.contributor.authorIp, SMen_HK
dc.contributor.authorCheng, Den_HK
dc.contributor.authorWong, LCen_HK
dc.contributor.authorNgan, HYSen_HK
dc.date.accessioned2010-09-06T09:28:33Z-
dc.date.available2010-09-06T09:28:33Z-
dc.date.issued2000en_HK
dc.identifier.citationClinical Cancer Research, 2000, v. 6 n. 2, p. 474-479en_HK
dc.identifier.issn1078-0432en_HK
dc.identifier.urihttp://hdl.handle.net/10722/87351-
dc.description.abstractTo establish a possible role of genomic imprinting in the carcinogenesis of epithelial ovarian cancer, we determined the imprinting status of both IGF-II and H19 genes in 43 ovarian cancers, 7 low malignant potential ovarian tumors, and their matched normal tissues. In ovarian cancer, loss of heterozygosity (LOH) of IGF-II, H19 RsaI, and H19 AluI was found in 4 of 24 (16.7%), 3 of 20 (15%), and 1 of 16 (6.3%) samples, respectively. All patients with tumor specimens exhibiting LOH are of advanced clinical stages. Loss of imprinting (LOI) was found in 5 of 20 (25%) for IGF-II and in 4 of 17 (23.5%) and 1 of 15 (6.7%) for the RsaI and AluI sites of H19 gene with no LOH. However, no LOH was found in low malignant potential tumors, and only one of them showed LOI in H19 AluI site. Overexpression of IGF-II was demonstrated in all five LOI samples with normal expression of H19. Three of the five tumor specimens exhibiting LOI were transcribed from P1 promoter, whereas the remaining two were from the P3 promoter. These results suggested that LOH of both IGF-II and H19 genes was associated with advanced ovarian cancer. LOI of IGF-II and H19 genes may be involved in the development of ovarian cancer. Transcription of IGF-II from the P1 promoter may account for the biallelic expression of the IGF-II gene.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research.en_HK
dc.relation.ispartofClinical Cancer Researchen_HK
dc.titleLoss of imprinting of the IGF-II and H19 genes in epithelial ovarian canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1078-0432&volume=6&spage=474&epage=479&date=1999&atitle=Loss+of+imprinting+of+the+IGF-II+and+H19+genes+in+epithelial+ovarian+canceren_HK
dc.identifier.emailNgan, HYS:hysngan@hkucc.hku.hken_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid10690526-
dc.identifier.scopuseid_2-s2.0-0033955676en_HK
dc.identifier.hkuros48042en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033955676&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume6en_HK
dc.identifier.issue2en_HK
dc.identifier.spage474en_HK
dc.identifier.epage479en_HK
dc.identifier.isiWOS:000085502600022-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChen, CL=7501960426en_HK
dc.identifier.scopusauthoridIp, SM=55041321600en_HK
dc.identifier.scopusauthoridCheng, D=7402806161en_HK
dc.identifier.scopusauthoridWong, LC=7402092003en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK
dc.identifier.issnl1078-0432-

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