Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2005: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2004: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2003: ¥1,400,000 (Direct Cost: ¥1,400,000)
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Research Abstract |
In the analysis of COX-2 expression with proliferaive activity in 200 oral squamous carcinoma (OSCC), COX-2 was guided on the occasion of metastasis early, and found that there were poor prognosis in patients in overexpression (74% of high-expression). In addition, COX-2 extremely high expressed in the top of an invasive foci in OSCC patients with poor outcome. Therefore, it was considered that the COX-2 related to tumor invasiveness, and was suggested that the COX-2 expression become a possible indicator in the outcome in patients with OSCC. We investigated p53-Rb pathway related to COX-2 expression and a trend of cell cycle regulator gene group to the subject next. Among of this analysis, HPV16 type was detected to 78%, and HPV18 type to 69% among COX-2 expression 45 examples again by p53 related to COX-2 expression and Brigati labelled in situ hybridization method for HPV16 type in 82 OSCC, COX-2 expression and 18 type about expected HPV-E6,E7 gene expression to each gene of Rb when
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we performed it. As a result of having examined the above generally, linked a high level of Topoll alpha LI in all both positive examples, overexpression of Rb protein, and p21/p53, cyclinB, D1,E overexpression were revealed, but the expression of p27 protein was not shown. As the result, cell cycle rapidly progress by failure of a regulator gene with COX-2 overexpression in a p53-Rb pathway through COX-2 pathway and raised an increase in OSCC than the above, but, in the example that HPV16/18 type was detected with COX-2 underexpression, possibility we restored p27 gene abnormality, and to evade was suggested by participation of an E6, E7 gene. Progress of OSCC accelerated, in COX-2 overexpression, it was considered that we participated in convalescence defectiveness by linking a significant expression lack of p27 protein. On the other hand, overexpression of HPV16/18 type and a p27 protein level were comparatively stable and, in COX-2 underexpression example, stopped an increase of cancer in a limited part, and possibility to keep convalescence comparatively well was suggested. From the above mentioned research results, COX-2 linked abnormality of a regulator gene in various cell cycles and was related to permeation of OSCC and metastasis and invasiveness, and it was thought that it could be it with a prognostic factor. Furthermore, it was recognized, and COX-2 received various oncogene abnormality, and mutual expression of COX-2 and Laminin-5 gamma 2 expression in 73% when we examined COX-2 and laminin-5 gamma 2, relevance of Integrin alpha expression with tumor invasiveness and metastasis, and possibility to acquisition of invasive activity and promotion of metastatic character was thought about. We want to go ahead through investigation about the role of invasiveness and metastasis of OSCC, identification of a COX-2 instruction factor, participation in COX-2 pathway in future. Less
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