| Co-Investigator(Kenkyū-buntansha) |
ONO Yasuhiro OKAYAMA UNIVERSITY MEDICAL SCHOOL,ASSISTANT, 医学部, 助手 (40294409)
TAMIYA Takashi OKAYAMA UNIVERSITY HOSPITAL,LECTURER, 医学部附属病院, 講師 (50252953)
MATSUMOTO Kengo OKAYAMA UNIVERSITY MEDICAL SCHOOL,ASSOCIATE PROFESSOR, 医学部, 助教授 (10190521)
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| Research Abstract |
Recently, cell cycle regulators and tumor suppressor genes have been shown to be disrupted in human cancers. We therefore investigated homozygous CDKN2/p16 deletions, p53 gene and protein status, and expression of p21, p27^< Kipl> and cyclin E proteins in astrocytomas and compared to the cell cycle or prognosis of patients with astrocytomas.
In astrocytomas grade 3 and 4, Ki-67 labeling indices were significantly higher in tumors with CDKN2/p16 deletions than in those without deletions. These results suggest that homozygous CDKN2/p16 deletions in high-grade astrocytomas may have a more deleterious effect on tumor proliferation than the other aberrations in cell cycle control pathways.
Neither p53 nor p21 status correlated with proliferation indices, as assessed by Ki-67. p53 alterations are thought to be more related to tumor initiation than to tumor malignancy.
High expression of cyclin E and low expression of p27^< Kipl> was related with worse prognosis of patients with astrocytoma.
These findings demonstrate that analyses of cell cycle regulators and tumor suppressor genes, such as p16, p21, p27^< Kipl> and p53, are potentially useful in classifying astrocytomas by histological or biological malignancy and in predicting the prognosis of patients with astrocytomas, and suggest the possibility of gene therapy with adenovirus vectors expressing cell cycle regulators and tumor suppressor genes, such as p16, p21, p27^< Kipl> and p53.
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