To study the mechanism of p16,Cyclin D1 and CDK4 and their relationship with pancreatic carcinoma, their expressions were examined by immunchistochemistry methods. Results: overpression of Cyclin D1 and CDK4 was revealed in these samples and p16 was undertectable. There was a negitive correlation between p16 and Cyclin D1 (Ｐ＜0.05), and a positive relation between Cyclin D1 and CDK4 (Ｐ＜0.05). The results indicate that abnormality of p16, Cyclin D1 and CDK4 may be involved in the molecular mechanism of pancreatic carcinoma, p16 lower expression and Cyclin D1 over expression may coexit in the development of pancreatic carcinoma.
Citation：
He jinsong,Lai Huanhui,Jian Lihua,et al.. THE SIGNIFICANCE OF EXPRESSION OF P16、CYCLIN D1 AND CDK4 IN PANCREATIC CARCINOMA. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 1999, 6(6): 337-338. doi:
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- 1. Hunter T, Pines J. Cyclin D1 and caner Ⅱ: Cyclin D1 and CDK inhibitors come of age. Cell, 1994; 79(2)∶573.
- 2. Kamba. Cellcycle regulators and cancer. Trends Genet, 1995; 11(2)∶136.
- 3. Fromowitz FB, Viola MV, Chao S, et al. Ras p21 expression in the progression of breast cancer. Human Pathol, 1987; 18(12)∶1268.
- 4. Caldas C, Hahn SA, DaCosta CT, et al. Frequent somatic mutations and homozygous deletions of the p16 (MTS1) gene in pancreatic adenocarcinoma. Nat Genet, 1994; 8(1)∶27.
- 5. Bartsch D, Shevlin DW, Tung WS, et al. Frequent mutation of CDKN2 in primary pancreatic adenocarcinomas. Genes Chromosomcs Cancer, 1995; 14(3)∶189.
- 6. Khatib ZA， Matsushime H. Coamplification of the CDK4 gene with MDM2 and GLI in human sarcomas. Cancer Res, 1993; 53(20)∶5535.
- 7. Serrano M, Hanon GJ, Beach DA. A new regulatory motif in cellcycle control causing specific inhibition of cyclin D/CDK4. Nature, 1993; 366(3)∶704.
- 8. Yeager T, Studler W, Belair C, et al. Increased p16 levels correlate with pRb alterations in human urothelial cells. Cancer Res, 1995; 55(2)∶493.
