Loss of multi-sites allde heterozygosity on chromosome 9 in esophageal carcinoma / 肿瘤研究与临床

ABSTRACT

Objective To investigate the gene variation and the dependability and to evaluate the possible tumor suppressor genes on chromosome 9 in the development and progression of EC. Methods LOH was detected in normal esophageal mucosa, high-grade squamous dysplasia and esophageal squamous cell carcinoma by microdissection, polymerase chain reaction, denaturing polyacrylamide gel eleetrophoresis and silver nitrate staining technology. The changes of LOH at six microsatellite markers and the relationship between LOH rate were analyzed. Results In the informative cases, total frequency of LOH was 17.2 % in high-grade squamous dysplasia and 24.9 % in esophageal squamous cell carcinoma. In high grade squamous dysplasia and squamous cell carcinoma, LOH was detected at marker D9S162 (20.8 %, 36.7 %), D9S171 (33.3 %, 36 %), D9S753(34.8 %, 46.2 %), D9S1748(4.2 %, 13.8 %), D9S242(14.3 %, 21.2 %), D9S43(0, 0). The frequency of LOH showed significant difference among the six microsatellite markers (X2=17.26, P< 0.005; X2=22.66,P<0.005). Conclusion The progression from normal squamous epithelium to high-grade Squamous dysplasia and subsequently to squamous cell carcinoma of the esophagus is associated with accumulation of chromosomal change. The situs of D9S171, D9S162, D9S242, D9S753 exist higher LOH and all exceed 20 %. Possible tumor suppressor genes at or near D9S171, D9S162, D9S242, D9S753 may be related to the progression of esophageal squamous cell carcinoma.