LOSS OF HETEROZYGOSITY AT MICROSATELLITE MARKER SITES FOR TUMOR-SUPPRESSOR GENES IN ESOPHAGEAL ADENOCARCINOMA

Aims. Loss of cell cycle control is an important step in the developme nt of human tumours. A number of tumour suppressor genes are involved in cell cycle control, including p16, p53 and Rb. The aim of this stud y was to seek evidence of deletions of these genes in oesophageal aden ocarcinoma. Methods. Paired (tumour and normal squamous epithelium) fr ozen tissue samples from 12 patients were analysed by polymerase chain reaction (PCR) for loss of heterozygosity (LoH) at five microsatellit e marker sites (two each for p16 and Rb, one for p53). Aneuploid tumou r cell populations were sorted by flow cytometry prier to PCR, to elim inate stromal cell contamination. Results. Of the 12 tumours, 11 (92%) had LoH at one or more loci. LoH at the p53 locus occurred in nine of 12 tumours, at one or both p16 loci in seven of 11 tumours, and at on e or both Rb loci in eight of 12 tumours. Five tumours had LoH at two tumour suppressor gene loci, and a further four tumours had LoH at loc i for all three genes. Conclusions. Allelic deletions of p53, p16 and Rb are common in oesophageal adenocarcinoma, and may be important in t he development of this disease.