1997 Fiscal Year Final Research Report Summary
Molecular pathological study on development, progression and prognosis of oral squamous cell carcinoma
| Project/Area Number |
07457429
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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 |
Morphological basic dentistry
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
NIKAI Hiromasa Hiroshima University School of Dentistry, Professor, 歯学部, 教授 (60028735)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAUCHI Mutsumi Hiroshima University School of Dentistry, Research Associate, 歯学部, 助手 (50169265)
ITO Hiroshi Hiroshima University School of Dentistry, Research Associate, 歯学部, 助手 (20184682)
OGAWA Ikuko Hiroshima University Dental Hospital, Assistant Professor, 歯学部・附属病院, 講師 (70136092)
TAKATA Takashi Hiroshima University School of Dentistry, Associate Professor, 歯学部, 助教授 (10154783)
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| Project Period (FY) |
1995 – 1997
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| Keywords | Oral squamous cell carcinoma / Molecular pathology / IL-1alpha / p53 / p27 / bc1-2 protein / cytokeratin / CD44 |
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| Research Abstract |
1. Interleukin-1alpha (IL-1alpha) acts as autocrine growth stimulator for OSCC in vitro and its interaction with EGF/TGF-alpha/receptor system may play a role in this enhanced growth by IL-1alpha.
2. The accumulation of p53 protein, which may reflect mutations of this gene, possibly occurs in an important early step, being maintained during multistep process for the development of OSCC.
3. The reduced expression of p27, one of the cyclin-dependent kinase inhibitor, may correlate with the development and progression of OSCC and can be an indicator of malignant behavior of this neoplasm. In addition, increased proteasome-mediated degradation may play an important role in the reduction of p27 protein expression.
4. With CAM5.2 staining, which reflects the expression of low-molecular weight cyto-keratins (CKs), the OSCC cases showing survival period less than 2 years exhibited significantly higher proportion of intensely positive cases, suggesting that CKs reacting with CAM 5.2 may relate to some prognostic factors such as aggressiveness of cancer cells.
5. The accumulation of p53 and bcl-2 proteins was related to the resistance of cancer cells to radiation therapy. Apoptosis of the cancer cells induced by irradiation may partly be inhibited by these proteins in OSCC.
6. The reduced expression of CD44v9 was frequently observed in OSCC and it was significantly related to lymph node metastasis and worse prognosis. The alteration of CD 44 expression may have some role in metastasis in OSCC.
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