| Project/Area Number |
12671782
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Morphological basic dentistry
|
|---|
| Research Institution | Showa University |
|---|
Principal Investigator |
TACHIKAWA Tetsuhiko Showa University, School of Dentistry, Professor, 歯学部, 教授 (10085772)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
AIDA Tadateru Showa University, School of Dentistry, Assistant, 歯学部, 助手 (10307051)
IRIE Taro Showa University, School of Dentistry, Assistant Professor, 歯学部, 講師 (00317570)
|
|---|
| Project Period (FY) |
2000 – 2001
|
| Project Status |
Completed (Fiscal Year 2001)
|
| Budget Amount *help |
¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2001: ¥500,000 (Direct Cost: ¥500,000)
|
|---|
| Keywords | squamous cell carcinoma / keratinocvte / progression / carcinogenesis / doc-1 / apoptosis / dysplasia / cvclin / P21doc-1 / 癌浸潤 |
|---|
| Research Abstract |
Disruption of the homeostatic balance between proliferation and apoptosis is widely believed to contribute to human oral carcinogenesis. Recently, p12doc-1 is a growth suppressor that negatively regulates cyclin-dependent kinase 2 (CDK 2) activities. Expression of p2ldoc-l is reduced and /or lost in tumor tissue.
Using the Syrian hamster oral cancer model, we examined normal, hyperplastic, dysplastic and malignant oral epithelium for the fraction of apoptotic, proliferating and p21doc-1 expressing keratinocytes using TUNEL assay, as well as PCNA and p21doc-1 immunostaing, respectively. The percentage of TUNEL positive cells progressively increased from normal to dysplastic cells increased progressively through hamster oral malignant progression. The overall ratio of apoptotic to proliferating keratinocyte remains similar until the transition between dysplastic and malignant epithelium, where the ratio is markedly reduced. P21doc-1 labeling demonstrated a similar expression pattern. This study demonstrates that the apoptosis, proliferation and expression of p21doc-1 reflect alterations reported during human oral carcinogenesis.
|
