T Su1, H Liu, S Lu. 1. Cancer Institute (Hospital), Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing.
Abstract
OBJECTIVE: To search new genes related to human esophageal cancer (EC) for revealing carcinogenesis mechanism and genetic susceptibility of EC. METHODS: Three normal esophageal epithelia (including 1 tumor-adjacent tissue) and two primary squamous cell carcinomas collected from high incidence family in Lin-xian county were studied using technique of mRNA differential display. The differential fragments were sequenced and identified by RT-PCR assay. RESULTS: (1) Eighteen differential fragments were isolated and identified, 13 of which were expressed in normal esophageal epithelia but not in EC(assigned as normal esophageal gene, NEG), while 5 were expressed in EC but not in normal esophageal epithelia(assigned as mutated esophageal gene, MEG). (2) Four NEG fragments were not homologous to the known sequences in the public database of GenBank (of NLM in USA). These 4 fragments were assigned as esophageal cancer related gene (ECRG) 1 to 4. (3)The remaining 14 fragments were homologues to 12 known genes or gene fragment. Their role in EC remains unclear. (4) Using RT-PCR technique, the expression of ECRG between normal epithelia and EC was significantly different. (5) All 4 ECRG genes were expressed in cDNA libraries derived from normal fetal brain, adult brain, liver, kidney, testis, bone marrow and skeletal muscle. (6) In the 20 cancerous and tumor-adjacent tissues obtained from the liver, lung, breast, colo-rectum and endometria, ECRG1 and ECRG2 was not detected by RT-PCR, while ECRG3 was highly expressed. For the ECRG4 the expression was much stronger in tumor-adjacent tissues than in cancerous tissues. CONCLUSION: ECRG 1 and ECRG2 may contribute to the causation and progression of the EC in Lin-xian, and may be candidates of tumor suppressor genes.
OBJECTIVE: To search new genes related to humanesophageal cancer (EC) for revealing carcinogenesis mechanism and genetic susceptibility of EC. METHODS: Three normal esophageal epithelia (including 1 tumor-adjacent tissue) and two primary squamous cell carcinomas collected from high incidence family in Lin-xian county were studied using technique of mRNA differential display. The differential fragments were sequenced and identified by RT-PCR assay. RESULTS: (1) Eighteen differential fragments were isolated and identified, 13 of which were expressed in normal esophageal epithelia but not in EC(assigned as normal esophageal gene, NEG), while 5 were expressed in EC but not in normal esophageal epithelia(assigned as mutated esophageal gene, MEG). (2) Four NEG fragments were not homologous to the known sequences in the public database of GenBank (of NLM in USA). These 4 fragments were assigned as esophageal cancer related gene (ECRG) 1 to 4. (3)The remaining 14 fragments were homologues to 12 known genes or gene fragment. Their role in EC remains unclear. (4) Using RT-PCR technique, the expression of ECRG between normal epithelia and EC was significantly different. (5) All 4 ECRG genes were expressed in cDNA libraries derived from normal fetal brain, adult brain, liver, kidney, testis, bone marrow and skeletal muscle. (6) In the 20 cancerous and tumor-adjacent tissues obtained from the liver, lung, breast, colo-rectum and endometria, ECRG1 and ECRG2 was not detected by RT-PCR, while ECRG3 was highly expressed. For the ECRG4 the expression was much stronger in tumor-adjacent tissues than in cancerous tissues. CONCLUSION:ECRG 1 and ECRG2 may contribute to the causation and progression of the EC in Lin-xian, and may be candidates of tumor suppressor genes.