Analysis of the tumor suppressor p16INK4a and p19ARF gene in esophageal cancer.

2001 Fiscal Year Final Research Report Summary

• Project/Area Number: 12671247
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Digestive surgery
• Research Institution: Nagoya City University
• Principal Investigator: KUWABARA Yoshiyuki Nagoya City University Medical School, Assistant Professor, 医学部, 講師 (90225326)
• Co-Investigator(Kenkyū-buntansha): FUJII Yoshitaka Nagoya City University Medical School, Professor, 医学部, 教授 (40156831)
• Project Period (FY): 2000 – 2001
• Keywords: esophageal cancer / p16INK4a / p19ARF / p53 / pRB

Research Abstract

Although p16INK4a which is the tumor suppressor, and p19ARF consist of common exon2 and 3 and exon1, respectively, they consist of the completely different protein. p161NK4a inhibits the phosphorylation of pRB and stops a cell cycle at G1-/S phase. p19ARF induces apoptosis and carries out a cell cycle stop through p53. We predicted that the importance of the course of the apoptosis through p53 in esophagus cancer generating became clear by searching the abnormalities of p19ARF and considering relation with the variation of p53. This research examined how two cancer control proteins (p16INK4a and p19ARF) by which the code was carried out to the same gene sear CDKN2 would be discovered in an esophagus cancer. RNA was extracted from 43 esophagus cancer cases. In the analysis in semi-quantitative RT-PCR, expression of p16INK4a decreased in 19 cases, and p19ARF decreased in 8 cases. The relation between p16NK4a, p19ARF, and a clinical pathological factor was not significant. In the analysis of immunohistology using the antibody against pRB and p53, pRB, decreased in ten cases (23.3%), and p53 increased in 20 cases (46.5%). However, significant correlation was not detected between p16INK4a, pRB and p19ARF, and p53.