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Mutational Analysis of JAK1 Exons 10 and 13 in Non-small Cell Lung Cancers
Oh, Ji Eun,Yoon, Hyung Kyu,Woo, In Sook,Kim, Seung Joon,Yoo, Nam Jin,Lee, Sug Hyung 대한폐암연구회 2008 Journal of Lung Cancer Vol.7 No.2
Purpose: JAK kinases play important roles not only in normal cellular processes, but they are also important in tumor development. A recent study identified two somatic mutations of JAK1 in leukemia cells that were detected in exon 10 (p.T478S) and exon 13 (p.V623A). The aim of this study was to see whether the JAK1 mutations in these exons occur in non-small cell lung cancers (NSCLC). Materials and Methods: We analyzed the exons 10 and 13 of JAK1 for detecting somatic mutations in NSCLC by performing polymerase chain reaction (PCR) and single-strand conformation polymorphism (SSCP) assay. Results: The SSCP analysis revealed no evidence of somatic mutation in the DNA sequences of JAK1 exon 10 and exon 13 in the 47 NSCLCs. Conclusion: The data presented here indicate that the JAK1 exons 10 and 13 may not be somatically mutated in human NSCLCs, and this suggests that the JAK1 mutation in exons 10 and 13 may not play an important role in the tumorigenesis of NSCLCs.
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Mutational Analysis of the Tumor Suppressor WTX Gene in Non-small Cell Lung Cancer
Moon, Seok Whan,Chung, Yeun Jun,Yoo, Nam Jin,Kim, Min Sung,Lee, Sug Hyung 대한폐암연구회 2008 Journal of Lung Cancer Vol.7 No.1
Purpose: In a recent study of Wilms' tumors, a new X chromosome gene, Wilms' tumor gene on the X chromosome (WTX), was discovered that was found to harbor small deletions and point mutations. The WTX protein negatively regulates Wnt/β-catenin signaling, and is considered to be a tumor suppressor gene. One of the questions about the WTX gene is whether the genetic alterations of the WTX gene are specific only to Wilms' tumors. The aim of this study was to explore whether the WTX gene mutation is a characteristic of human non-small cell lung cancer (NSCLC). Materials and Methods: In the current study, we analyzed the part of the WTX gene encoding the N-terminal of WTX, where most of the WTX point mutations have been detected in Wilms' tumors. Forty-eight NSCLC tissues were analyzed by a single-strand conformation polymorphism assay and DNA sequencing. Results: SSCP analysis revealed no evidence of somatic mutations in the DNA sequences encoding the N-terminal of the WTX gene in the 48 NSCLC tissues. Conclusion: The data presented here indicate that the WTX gene may not be somatically-mutated in human NSCLCs, and suggest that NSCLCs may not utilize mutational events of the WTX gene in the process of pathogenesis.
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Detection of Serum Free DNA Hypermethylation in Surgically Resected Adenocarcinoma of the Lung
Park, Sun Jung,Kim, Young Tae,Park, Ju-Yeon,Wi, Hyun Cho,Kang, Chang Hyun,Sung, Sook-Whan,Kim, Joo Hyun 대한폐암연구회 2008 Journal of Lung Cancer Vol.7 No.2
Purpose: Aberrant DNA methylation patterns have been commonly associated with human cancers. We have investigated the frequency of DNA hypermethylation in promoter regions from adenocarcinomas of the lung and then attempted to detect the same epigenetic changes from patient serum samples. Materials and Methods: We collected tissues from 72 cases of lung adenocarcinomas. The cancer and normal lung tissues were tested for DNA hypermethylation using methylation-specific PCR (MSP). The genes investigated were DAPK, RARβP2 and p16. We selected 12 patients where promoter hypermethylation was present for all three genes and four patients where hypermethylation was not seen for any of the three genes. Serum-free DNA was extracted and was tested for promoter hypermethylation. The status of serum-free DNA methylation was analyzed; the hypermethylation status was compared to clinical variables and cancer outcomes. Results: DNA hypermethylation was observed in 32% of samples for DAPK, 63% of samples for RARβP2 and 83% of samples for p16 from the cancer tissues. Among the 12 matched serum samples where the primary tumor showed hypermethylation in all three gene promoter regions, we were able to detect five incidences of serum DNA hypermethylation in four patients. The four patients had TNM stage II or higher disease. None of the patients with stage I disease showed serum-free DNA hypermethylation. Conclusion: Aberrant promoter hypermethylation was frequently observed in surgically resected adenocarcinoma of the lung. Concurrent serum-free DNA hypermethylation was detected in 34% of patients where the primary tumor showed hypermethylation in all three gene promoter regions. The findings suggest that the serum-free DNA methylation status might be used as a potential target for the diagnosis of lung cancer. However, the low sensitivity should be improved for use in a clinical application.
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