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Lung India Official publication of Indian Chest Society  
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Year : 2008  |  Volume : 25  |  Issue : 4  |  Page : 148-151

Tumoral tissue specific promoter hypermethylation of distinct tumor suppressor genes in a case with non­-small cell lung carcinoma: A case report

1 Department of Thorax Diseases, Faculty of Medicine, Cumhuriyet University 58140 Sivas, Turkey
2 Department of Medical Genetics, Faculty of Medicine, Cumhuriyet University 58140 Sivas, Turkey
3 Department of Radiology, Faculty of Medicine, Cumhuriyet University 58140 Sivas, Turkey
4 Department of Pathology, Faculty of Medicine, Cumhuriyet University 58140 Sivas, Turkey

Correspondence Address:
Ozturk Ozdemir
Department of Medical Genetics, Faculty of Medicine, Cumhuriyet University 58140, Sivas
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0970-2113.45279

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Objective: Non-small cell lung carcinoma is an aggressive phenomenon and the epigenetical alterations of some tumor supressor genes have been reported for the different tumor types. Case Presentation: It is presented a case report concerning a 43 years old male with NSCLC on the lower segment of the right lung. The patient underwent a diag­nostic excisional thin-needle biopsy and after the histological confirmation. We examined the promoter methylation status of some distinct tumor supressor genes in tumoral and blood tissues of the case after sodium bisulfite conversion and DNA amplification with methylation specific multiplex PCR technique. Both tissues were also searched for G to A transitions in codons 12 and 13 of the K-ras proto-oncogene. Results: Tumor specimen showed fully methyl pattern profiles for the SFRP2, p16, DAPK1 and partially hyper­methylated profile for the p53 and MGMT genes in this case with non-small lung carci­noma. Blood speicemen showed normal hypomethylated profiles for all studied TS genes. The K-ras proto-oncogene was in normal structure both in blood and tumoral spiecemens that examined. Conclusion: Results indicate that genes exhibit tumor suppressor activi­ties in blood, but exhibit epigenetic inactivation in carcinoma cell. These findings strongly support the hypothesis that epigenetic mechanisms may play an important role in the non-small cell lung carcinogenesis in human.

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