FHIT alterations in human esophageal, gastric and colorectal carcinomas

Abstract

OBJECTIVE: To assay alterations in the fragile histidine triad (FHIT) gene in human esophageal, gastric and colorectal carcinomas.METHODS: Carcinomatous tissues from 93 patients with digestive tract carcinoma (including 21 esophageal, 43 gastric and 32 colorectal carcinomas) and neighboring non‐carcinomatous tissues were examined in addition to 18 normal tissue samples. From the above tissue samples, RNA was extracted using guanidinium thiocyanate−phenol−chloroform. FHIT gene transcripts were amplified by using nested reverse transcription−polymerase chain reaction (RT‐PCR).RESULTS: Only wild‐type transcripts of the FHIT gene were found in the 18 normal tissue samples. Wild‐type FHIT gene transcripts were found in most carcinoma tissues, with the exception of seven cases (including two esophageal cancers, three gastric carcinomas and two colorectal carcinomas). In addition, abnormal FHIT transcripts were obtained from 33.3% of esophageal carcinomas, 51.7% of gastric carcinomas and 31.3% of colorectal carcinomas. Abnormal FHIT transcripts were obtained from neighboring tissue from 4.8, 20.9 and 9.4% of esophageal, gastric and colorectal carcinomas, respectively. The proportion of abnormal FHIT transcripts in carcinomatous tissues was significantly higher (P < 0.05) than that in neighboring non‐carcinomatous tissues and normal tissues.CONCLUSION: The proportion of abnormal FHIT cDNA in carcinomatous tissue is greater than that in non‐carcinomatous tissues, which suggests that transcripts of abnormal FHIT genes are related to the occurrence and development of carcinomas in the digestive tract.