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- Publisher Website: 10.1016/S0046-8177(03)00175-8
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- PMID: 12874766
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Article: Allelic alterations in nontumorous liver tissues and corresponding hepatocellular carcinomas from chinese patients
Title | Allelic alterations in nontumorous liver tissues and corresponding hepatocellular carcinomas from chinese patients |
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Authors | |
Keywords | Allelic imbalance Hepatocellular carcinoma Nontumorous liver Normal DNA |
Issue Date | 2003 |
Publisher | WB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/humpath |
Citation | Human Pathology, 2003, v. 34 n. 7, p. 699-705 How to Cite? |
Abstract | Allelic imbalance may play an important in tumor progression in hepatocarcinogenesis, but the genetic background of the corresponding nontumorous liver in hepatocellular carcinoma (HCC) is not well defined. We studied the incidence of loss of heterozygosity (LOH) and microsatellite instability (MSI) by microsatellite analysis in both nontumorous livers and the corresponding tumors, by comparing them with the normal DNA from Chinese patients with resected primary HCCs. We also evaluated the pathologic significance of the alterations. We used 18 highly polymorphic microsatellite markers on chromosomes 1, 3, 4, 7, 8, 9, 13, 16, 17, and 18. Our results showed that 70.6% (24 of 34) of the HCCs exhibited LOH at 1 or more loci, and that the overall fractional allelic loss (FAL) was 0.169. MSI was observed in only 1 tumor. In contrast, the nontumorous livers of the HCCs showed a very low incidence of LOH, with only a single LOH detected in 1 of 34 (2.9%) of the nontumorous livers, with an overall FAL index of 0.005. Tumors with LOH at I or more loci had significantly more frequent venous invasion (P = 0.019). Allelic loss at locus D9S199 (9p23) was seen more frequently in larger tumors (P = 0.031), and, less significantly, allelic loss at locus D16S516 (16q24.1) was seen more frequently in larger tumors (P = 0.059). LOH was common in predominantly hepatitis B virus-associated HCCs from Chinese patients. However, LOH or MSI in the corresponding cirrhotic or noncirrhotic livers was uncommon. © 2003 Elsevier Inc. All rights reserved. |
Persistent Identifier | http://hdl.handle.net/10722/88322 |
ISSN | 2023 Impact Factor: 2.7 2023 SCImago Journal Rankings: 0.936 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Ho, MKS | en_HK |
dc.contributor.author | Lee, JMF | en_HK |
dc.contributor.author | Chan, CKL | en_HK |
dc.contributor.author | Ng, IOL | en_HK |
dc.date.accessioned | 2010-09-06T09:41:51Z | - |
dc.date.available | 2010-09-06T09:41:51Z | - |
dc.date.issued | 2003 | en_HK |
dc.identifier.citation | Human Pathology, 2003, v. 34 n. 7, p. 699-705 | en_HK |
dc.identifier.issn | 0046-8177 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/88322 | - |
dc.description.abstract | Allelic imbalance may play an important in tumor progression in hepatocarcinogenesis, but the genetic background of the corresponding nontumorous liver in hepatocellular carcinoma (HCC) is not well defined. We studied the incidence of loss of heterozygosity (LOH) and microsatellite instability (MSI) by microsatellite analysis in both nontumorous livers and the corresponding tumors, by comparing them with the normal DNA from Chinese patients with resected primary HCCs. We also evaluated the pathologic significance of the alterations. We used 18 highly polymorphic microsatellite markers on chromosomes 1, 3, 4, 7, 8, 9, 13, 16, 17, and 18. Our results showed that 70.6% (24 of 34) of the HCCs exhibited LOH at 1 or more loci, and that the overall fractional allelic loss (FAL) was 0.169. MSI was observed in only 1 tumor. In contrast, the nontumorous livers of the HCCs showed a very low incidence of LOH, with only a single LOH detected in 1 of 34 (2.9%) of the nontumorous livers, with an overall FAL index of 0.005. Tumors with LOH at I or more loci had significantly more frequent venous invasion (P = 0.019). Allelic loss at locus D9S199 (9p23) was seen more frequently in larger tumors (P = 0.031), and, less significantly, allelic loss at locus D16S516 (16q24.1) was seen more frequently in larger tumors (P = 0.059). LOH was common in predominantly hepatitis B virus-associated HCCs from Chinese patients. However, LOH or MSI in the corresponding cirrhotic or noncirrhotic livers was uncommon. © 2003 Elsevier Inc. All rights reserved. | en_HK |
dc.language | eng | en_HK |
dc.publisher | WB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/humpath | en_HK |
dc.relation.ispartof | Human Pathology | en_HK |
dc.subject | Allelic imbalance | - |
dc.subject | Hepatocellular carcinoma | - |
dc.subject | Nontumorous liver | - |
dc.subject | Normal DNA | - |
dc.subject.mesh | Adult | en_HK |
dc.subject.mesh | Aged | en_HK |
dc.subject.mesh | Aged, 80 and over | en_HK |
dc.subject.mesh | Asian Continental Ancestry Group | en_HK |
dc.subject.mesh | Carcinoma, Hepatocellular - genetics - pathology - surgery | en_HK |
dc.subject.mesh | China - ethnology | en_HK |
dc.subject.mesh | DNA, Neoplasm - analysis | en_HK |
dc.subject.mesh | Female | en_HK |
dc.subject.mesh | Hepatitis B, Chronic - genetics - pathology | en_HK |
dc.subject.mesh | Hong Kong - epidemiology | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.subject.mesh | Liver - pathology | en_HK |
dc.subject.mesh | Liver Cirrhosis - genetics - pathology | en_HK |
dc.subject.mesh | Liver Neoplasms - genetics - pathology - surgery | en_HK |
dc.subject.mesh | Loss of Heterozygosity | en_HK |
dc.subject.mesh | Male | en_HK |
dc.subject.mesh | Microsatellite Repeats | en_HK |
dc.subject.mesh | Middle Aged | en_HK |
dc.title | Allelic alterations in nontumorous liver tissues and corresponding hepatocellular carcinomas from chinese patients | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0046-8177&volume=34&issue=7&spage=699&epage=705 &date=2003&atitle=Allelic+alterations+in+nontumorous+liver+tissues+and+corresponding+hepatocellular+carcinomas+from+Chinese+patients | en_HK |
dc.identifier.email | Ng, IOL:iolng@hkucc.hku.hk | en_HK |
dc.identifier.authority | Ng, IOL=rp00335 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1016/S0046-8177(03)00175-8 | en_HK |
dc.identifier.pmid | 12874766 | - |
dc.identifier.scopus | eid_2-s2.0-0038721494 | en_HK |
dc.identifier.hkuros | 86100 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0038721494&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 34 | en_HK |
dc.identifier.issue | 7 | en_HK |
dc.identifier.spage | 699 | en_HK |
dc.identifier.epage | 705 | en_HK |
dc.identifier.isi | WOS:000184249100010 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.issnl | 0046-8177 | - |