GENETIC ALTERATIONS ON CHROMOSOME-3 AND CHROMOSOME-9 OF ESOPHAGEAL CANCER TISSUES FROM CHINA

In previous studies, we had demonstrated that allelic losses in esopha geal cancer (EC) tissues are frequently involved in chromosomes 3 and 9 acid that EC patients and their blood relatives have low capacity to repair damaged DNA and showed genetic instability. To better define t he deleted chromosomal loci and understand the genetic instability in EC tissues, we selected 12 microsatellite markers (D3S1232, D3S1238, D 3S1289, D3S1480, D3S647, D3S966, D3S1317, D3S659, D9S156, D9S171, D9S1 76 and GSN) to examine 36 paired EC tissues for loss of heterozygosity (LOH) and microsatellite instability (MIN) on chromosomes 3 and 9. Th e frequent LOH was found at D9S156(9p21), D3S647(3p23) and D3S1480(3p1 4.2), implying the possible existence of tumor suppressor genes near t he deleted loci. Higher LOH incidence at D9S156 (9/18) and D3S1480 (8/ 19) was observed in EC tissues from Beijing, a low EC area. More frequ ent LOH at D3S647 (6/14) was found in EC tissues from Yangquan, a high EC area, This geographic difference of LOH occurrence was indicative of genetic heterogeneity in the etiology of EC. 24 of 36 (66.7%) EC ti ssues showed MIN at one or more chromosomal loci. The putative EC supp ressor genes on chromosomes 3 and 9 and the molecular basis of the gen etic instability associated with EC remain to be elucidated.