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Loss of heterozygosity on chromosome-8 in squamous-cell carcinomas of the head and neck
Authors:Kiaris H  Jones A  Spandidos D  Vaughan E  Field J
Affiliation:UNIV LIVERPOOL,DEPT CLIN DENT SCI,MOLEC ONCOL GRP,LIVERPOOL L69 3BX,MERSEYSIDE,ENGLAND. UNIV CRETE,SCH MED,IRAKLION,GREECE. UNIV LIVERPOOL,DEPT OTORHINOLARYNGOL,LIVERPOOL L69 3BX,MERSEYSIDE,ENGLAND. NATL HELLEN RES FDN,GR-11635 ATHENS,GREECE. WALTON HOSP,MAXILLOFACIAL UNIT,LIVERPOOL L9 1AE,MERSEYSIDE,ENGLAND.
Abstract:LOH studies provide evidence for the implication of novel TSGs in human tumours. The p arm of chromosome 8 has been reported to harbour tumour suppressor genes (TSGs) which are very likely to be involved in the development of colon, lung, bladder and hepatocellular carcinomas. In addition, the c-myc proto-oncogene which is located on the 8q arm, has been found to be overexpressed in SCCHN. In the present study we have investigated the incidence of loss of heterozygosity (LOH) in chromosome 8 in 37 tumour specimens of squamous cell carcinomas of the head and neck (SCCHN), using a bank of 11 polymorphic microsatellite markers. The aim of this work was to assess whether there was an 8p TSG(s) in SCCHN, as reported in other tumours and also to investigate whether other areas of chromosome 8 exhibit a high LOH. A relatively high incidence of LOH was found for the markers D8S87 (29%) on 8p12 and ANK1 (20%) on 8p21.2-p11. These two markers are located in the area in which TSG(s) for other cancers have been previously described. When the data on D8S87 and ANK1 were analyzed together it was found that 13/35 (37%) of the SCCHN specimens had a loss at one or other of these markers, thus indicating that a putative TSG(s) in this region may play a role in the development of the SCCHN. No correlation was found between the LOH data and any of the clinicopathological parameters. We also investigated the incidence of c-myc amplification in 144 SCCHN specimens but only 4% were found to have an amplified c-myc allele, thus indicating that the overexpression of c-myc in SCCHN was not the result of gene amplification.
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