1998 Fiscal Year Final Research Report Summary
Expressionand Regulation of Autocrineand Angiogenic Factors produced by Oral Cancer
| Project/Area Number |
09470455
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
OKAMOTO Tetsuji Hiroshima University School of Dentistry, Professor, 歯学部, 教授 (00169153)
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| Co-Investigator(Kenkyū-buntansha) |
TORATANI Shigeaki Hiroshima University Dental Hospital, Associate Prof., 歯学部・附属病院, 講師 (90172220)
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| Project Period (FY) |
1997 – 1998
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| Keywords | Oral Cancer / Salivary Gland Tumor / Gene Therapy / Differentiation / Apoptosis / FGF / FGF Receptor / Caspase |
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| Research Abstract |
Malignant salivary gland adenocarcinoma is devastating neoplasm that is associated with a poor prognosis in the head and neck regions. Although the reasons for aggressiveness of these disorder are not well known, some alternations of oncogenic molecules and the overexpression of growth factors which may give neoplastic cells a growth advantage have been demonstrated. The normal salivary gland is composed of well-defined epithelial and stromal cell components which communicate to maintain normal gland structure, function and differentiation. The epithelial compartment of benign salivary gland tumors usually exhibits some degree of morphological differentiation that distinguishes it from the stromal compartment. In contrast, malignant tumors are undifferentiated and exhibit no apparent relationship between epithelial and stromal cells.
Our previous studies indicated that FGF receptors. underwent parallel changes during malignant progression. FGFR1-IIIc and FGFR4 were overexpressed in malignant salivary gland adenocarcinoma, but absent in normal salivary gland and benign salivary gland tumors which overexpressed FGFR2IIIb (KGFR).
In present study, full-length of wild type KGFR/wtFGFR2-IIIb cDNA was ligated into pcDNA 3.l/zeo mammalian expression vector ; and transfected into malignant salivary gland adenocarcinoma HSY cell. The results clarified that wtFGFR2IIIb inhibit populational growth rate, induce cell differentiation and programmed cell death of malignant salivary gland adenocarcinoma in vitro and in vivo.
Base on present study, FGFR2-IIIb gene transfer ex vivo with gene gun would be available and may be quite efficent for malignant salivary gland adenocarcinoma. FGFR2-IIIb gene transfer ex vivo is expected to .be a brand new gene therapy for malignant salivary gland adenocarcinoma.
In summary, the introduction of wtFGFR2-IIIb into malignant salivary gland adenocarcinoma cells can suppress the growth of the cancer cells and induce apoptosis in vitro and in vivo.
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Research Products
(17 results)
