| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1992: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1991: ¥1,500,000 (Direct Cost: ¥1,500,000)
|
|---|
| Research Abstract |
The deletion and mutation of tumor suppressor gene have been implicated to be an important step of carcinogenesis. In this study, we investigated these changes in tumor suppressor genes in skin cancer.
The incidence of basal cell carcinoma (BCC) is rapidly increasing, but the molecular mechanism of the tumorigenesis remains unknown. In a wide variety of cancers, the inactivation of tumor suppressor gene p53 is suggested to play a part in carcinogenesis. We examined the mutations of p53 exons in 11 cases of BCC by PCR-SSCP. However, no aberrant band was detected in the amplified DNA, suggesting that p53 gene is not a target gene in BCC. Recently, the high frequency of detections of chromosome 9q has been shown in BCCs of Gorlin syndrome (basal cell nevus syndrome) (Gailani, M. R., et al. Cell 69, 111-117, 1992). Therefore, we also examined the loss of heterozygosity of the loci in our cases of BCC using the marker probes of D9S28 and D9S29 for the loci on 9q31-34 and 9q31, respectively. By Southern hybridization, the loss of heterozygosities in 2 of 5 informative cases on these loci were detected. From the result, we suggests that the region of chromosome 9q is closely associated with the pathogenesis of BCC.
|
