KMID : 0982820020010010055
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Journal of Lung Cancer 2002 Volume.1 No. 1 p.55 ~ p.59
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K-ras Gene Mutation in Non-Small Cell Lung Cancer
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Yoon Hyo-Joong
Ju Jin-Young Cho Gye-Jung Kim Eun-Joung Park Kyung-Hwa Kim Kyu-Sik Ko Young-Choon Lim Sung-Chul Kim Young-Chul Park Jong-Tae
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Abstract
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Purpose: Point mutation of the K-ras gene causes irreversible binding of GTP to the P21-ras protein, which induces nuclear transcription factors and enhances cellular proliferation. Point mutation of the K-ras gene is known to be a poor prognostic marker of an adenocarcinoma of the lung. As about 30% of adenocarcinomas harbor the K-ras mutation, studies are being undertaken trying to use the K-ras mutation as a marker for the early detection of lung cancer. In Korea, squamous cell carcinomas are more prevalent than adenocarcinomas, but the incidence of the K-ras mutation has not been properly investigated.
Materials and Methods: Using 25 surgically resected lung cancer specimens (10 squamous cell lung carcinomas, 10 adenocarcinomas and 5 non-small cell lung cancers), 25 pairs of DNA were extracted from cancerous and normal lung tissues. After PCR, with two sets of primers flanking codons 12¡13 and 61 of the K-ras gene, the mutation was screened using single strand conformational polymorphism (SSCP). To verify the SSCP findings, automatic sequencing was also performed for all DNA¡¯s from the tumor and normal lung tissues.
Results: No samples with a band shift in SSCP were observed. In the sequencing of the 25 pairs of DNA, there were no mutations in codons 12, 13 or 61 of the K-ras gene.
Conclusion: As there were no mutations in the K-ras codons 12, 13 and 61 in this study, the incidence of the K-ras mutation, in Korean lung cancer, may well be very low. However, further investigations on a larger population will be required, as we only studied 25 non-small cell lung cancer specimens, with only 10 adenocarcinomas.
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KEYWORD
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Non-small cell lung cancer, K-ras, Mutation, SSCP, Sequencing
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