| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1997: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1995: ¥900,000 (Direct Cost: ¥900,000)
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| Research Abstract |
Deletion or point mutation of p15, p16 and p53 genes was frequently observed in the tumor cells of malignant neoplasm. However, deletion or point mutation of these genes could not be detected on malignant melanoma and cutaneous lymphomas by PCR method or PCR-SSCP method. On the other hand, over expression of P53-gene-product was detected on squamous cell carcinoma (SCC) and actinic keratosis by immunohistochemistry. In other word, mutation of P53-gene-product was detected on actinic keratosis, precancerous stage of SCC.In fact, two patients with actinic keratosis, having over expression of P53-gene-product, progressed to SCC and a prognosis of these patients was poor. These results suggest patients with actinic keratosis, over expression of P53-gene-product, could be required a prudent treatment.
Through developments in biotechnology, several kinds of biological reponse modifiers (BRMs), such as interferons (IFNs)-alpha, beta and gamma, interleukin-2 (IL2) and tumor necrosis factors (TNFs), have been used to treat advanced-stage malignant melanoma. The growth of melanoma cell lines was inhibited by nIFN-beta. ^3H-TdR-incorporation and ^3H-UdR-incorporation were also inhibited by nIFN-beta in a dose dependent manner. These growth inhibition activity of nIFN-beta on melanoma cell lines was caused by an activation of IRF-1 and p21 genes but not by p53 and p16 genes. Furthermore, apoptosis was evidenced in melanoma cell lines cocultured with nIFN-beta by the TUNEL method. Results showed that nIFN-beta had direct killer activity on melanoma cell lines though the activation of IRF-1 AND p21 genes. The growth inhibition activity of nIFN-beta on melanoma cell lines was enhanced by betamethasone
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