The tumor genetics study found that human renal cell carcinoma (RCC) tissue often short arm of chromosome 3 (3p) loss of heterozygosity (Loss of heterozygosity, LOH), especially concentrated in 3p14, 3p21 and 3p25 [1]. Following the tumor suppressor gene VHL (located at 3p25) found, Ohta equal to 3 p 14.2 FHIT (Fragile histidine triad) gene was successfully cloned in 1996 and found that the human esophagus, head and neck cancer, lung cancer, stomach cancer, breast cancer, abnormal cervical cancer and cell lines, there is a higher frequency of FHIT fragile histidine triad gene transcripts [2 ~ 5]. FHIT gene protein-coding exon deletion or mutation in this experiment, using PCR and Southern blot hybridization to detect RCC tissue, and compared with the corresponding peritumoral and normal kidney organizers of clear RCC FHIT fragile histidine triad gene abnormalities characteristic, the FHIT gene a development relationship with the RCC. 

Purpose: the detection of renal cell carcinoma (RCC) organization FHIT fragile histidine triad gene protein encoded outside exon abnormal situation, understand the RCC in the FHIT gene abnormalities characteristic, explore the relationship of the FHIT gene with RCC. Methods: RCC and the corresponding peritumoral kidney tissue samples 22 and 16 were extracted tissue DNA. DIG-labeled FHIT full-length cDNA probe. PCR amplification the FHIT fragile histidine triad gene E5 ~ E9, product line Southern blot hybridization. Results: 15 (68.2%) of cancer tissue samples, 6 (37.5%) peritumoral kidney tissue of protein coding exons of the FHIT gene deletion or mutation, of which 10 were at the same time there are two exons abnormal changes. Cancer tissue and peritumoral kidney tissue the E5 abnormalities (including missing, an exception) rates were 40.9% (9/22) and 25.0% (4/16). CONCLUSION:   FHIT fragile histidine triad gene abnormalities may be an early event in the process occurs in RCC.