LOSS OF HETEROZYGOSITY ON CHROMOSOME-8 IN SQUAMOUS-CELL CARCINOMAS OFTHE HEAD AND NECK

Citation
H. Kiaris et al., LOSS OF HETEROZYGOSITY ON CHROMOSOME-8 IN SQUAMOUS-CELL CARCINOMAS OFTHE HEAD AND NECK, International journal of oncology, 5(6), 1994, pp. 1243-1248
Citations number
26
Categorie Soggetti
Oncology
ISSN journal
10196439
Volume
5
Issue
6
Year of publication
1994
Pages
1243 - 1248
Database
ISI
SICI code
1019-6439(1994)5:6<1243:LOHOCI>2.0.ZU;2-C
Abstract
LOH studies provide evidence for the implication of novel TSGs in huma n tumours. The p arm of chromosome 8 has been reported to harbour tumo ur 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, ha s been found to be overexpressed in SCCHN. In the present study we hav e investigated the incidence of loss of heterozygosity (LOH) in chromo some 8 in 37 tumour specimens of squamous cell carcinomas of the head and neck (SCCHN), using a bank of 11 polymorphic microsatellite marker s. The aim of this work was to assess whether there was an 8p TSG(s) i n SCCHN, as reported in other tumours and also to investigate whether other areas of chromosome 8 exhibit a high LOH. A relatively high inci dence of LOH was found for the markers D8S87 (29%) on 8p12 and ANK1 (2 0%) 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 invest igated 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.