FREQUENT LOSS OF HETEROZYGOSITY ON CHROMOSOME-17 AT 17Q11.2-Q12 IN BARRETTS ADENOCARCINOMA

Allelic loss on chromosome 17 in 18 Barrett's oesophageal tumours was analysed with 17 polymorphic microsatellite markers. Loss of heterozyg osity (LOH) of one or more markers was seen in 72% (13 of 18) tumours on 17p and 56% (10 of 18) on 17q. The highest 17p losses were found at D17S799 (62%, five of eight) and D17S261 (55%, five of nine), while l oss at the p53 locus was 31% (5 of 16). The highest loss on 17q was fo und at the TCF-2 (17q11.2-q12) locus with 66% (8 of 12) LOH. TCF-2 was the only marker lost in two of the tumour samples; furthermore, TCF-2 was lost in four other tumours which retained heterozygosity at the m arkers on either side of it, D17S261 and D17S740. Six markers were use d to assess LOH at 17q11.2-q12, and five of eight of the tumour specim ens which had LOH at TCF-2 had no other loss on 17q. No statistically significant correlations were found between loss on 179 or 17p and any clinicopathological parameters. We propose from these data that the 1 7q11.2-q12 region contains a novel predisposing gene in Barrett's aden ocarcinomas and may represent the site of a tumour-suppressor gene.