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RISS 인기검색어
- 검색키워드
- 저자 : Gujuluva, Chandrasekhar N. (검색결과 2 건)
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Gujuluva, Chandrasekhar N.,Park, No-Hee Korean Academy of Oral Biology and the UCLA Dental 1999 International Journal of Oral Biology Vol.24 No.4
Human oral keratinocytes immortalized with cloned "high risk" human papillomavirus DNA can readily convert to tumorigenic cells when exposed to chemical carcinogens. Tumorigenic conversion of immortalized cells may, in part, be due to their lack of DNA repair responses to genotoxic stress. To study this possibility, we determined the nucleotide excision repair (NER) capacities and the level of proteins associated with DNA damage/DNA repair (p53, p21^WAF1/CIP1, gadd45 and PCNA)from primary normal human oral keratinocytes (NHOK), normal human skin epidermal keratinocytes (NHEK), HPV-immortalized human oral keratinocytes, and several human oral cancer cell lines before and after genotoxic exposure. Genotoxic exposure significantly increased the levels of cellular p53, p21^WAF1/CIP1, and gadd45 proteins and the NER activity in NHOK and NHEK, whereas it did not alter the protein levels and the NER activities of eht HPV-immortalized oral keratinocytes and oral cancer cells. These data indicate that normal epithelial cells lining the human oral cavity can increase the DNS repair function when challenged by genotoxic stress, and in doing so may protect themselves from transformation or cell death. Infection of these cells with "high risk" human papillomaviruses seems to abrogate this protection mechanism.
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Li, Sheng-Lin,Baek, Jeong-Hwa,Zhang, Kui-Hua,Min, Byung-Moo,Gujuluva, Chandrasekhar N.,Bertolami, Charles N.,Park, No-Hee Korean Academy of Oral Biology and the UCLA Dental 1996 International Journal of Oral Biology Vol.21 No.1
Aberrant expression and mutation in the p53 and MTS1/CDK41 genes were determined from 11 normal, 8 preneoplastic and 25 neoplastic oral tissues obtained from Beijing, China, using immunostaining, single strand conformational polymorphism analysis, and nucleotide sequencing. Normal tissue showed a negligible amount of p53 immunostaining, while 3 (38%) of 8 preneoplastic, and 16 (64%) of 25 cancer tissues demonstrated moderate to strong p53 immunostaining. Point mutations within exons 5 to 8 were not detected in normal tissue specimens, but were detected in 2 (25%) preneoplastic tissues and in 15 (60%) cancer specimens. OF the tissues with mutations, 2 (100%) preneoplatic and 14 (93%) cancer tissues contained a CGT to CAT mutation at codon 273 of p53 gene. One cancer tissue showed a silent mutation (CGC to CTC) at codon 283. Three cancer specimens containing a point mutation at codon 273 also showed additional silent mutations at codons 156, 157, or 275. These data indicate that p53 mutation is highly prevalent in tested preneoplastic and neoplastic oral tissues and that the codon 273 is the "hot-spot" for point mutations. The enhanced p53 immunostaining was, in general, closely associated with point mutations, but 1 (13%) preneoplastic sample and 5 (20%) neoplastic oral tissues not containing point mutations within exons 5 to 8 demonstrated enhanced immunostaining. Over 62% of preneoplastic and 80% of neoplastic oral tissues contained mutations in MTS1/CDK4I gene, but, unlike p53 mutations, the mutation pattern of MTS1/CDK4I gene was not specific. Two preneoplastic (25%) and 12 neoplastic (48%) tissues contained mutations in both p53 and MTS1/CDK4I genes, and 2 preneoplastic (25%) and 3 neoplastic (12%) tissues contained mutations neither in p53 nor in MTS1/CDK4I genes.
RISS
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