Hypermethylation of CCND2 May Reflect a Smoking-Induced Precancerous Change in the Lung
| Autor: | C. Diana Jordan, Hiep Lu, Stephen E. Hawes, Alexander Salskov, Janet S. Rasey, Qinghua Feng, Hubert Vesselle, Linda Wiens, Nancy B. Kiviat, Joshua E. Stern |
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| Jazyk: | angličtina |
| Rok vydání: | 2011 |
| Předmět: |
Pathology
medicine.medical_specialty Article Subject IGFBP3 medicine.disease_cause lcsh:RC254-282 Tobacco smoke CDH1 03 medical and health sciences 0302 clinical medicine CDKN2A CDKN2B Medicine 030304 developmental biology 0303 health sciences biology business.industry Cancer lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens medicine.disease 3. Good health respiratory tract diseases Oncology 030220 oncology & carcinogenesis DNA methylation Cancer research biology.protein business Carcinogenesis Research Article |
| Zdroj: | Journal of Oncology Journal of Oncology, Vol 2011 (2011) |
| ISSN: | 1687-8469 1687-8450 |
| Popis: | It remains unknown whether tobacco smoke induces DNA hypermethylation as an early event in carcinogenesis or as a late event, specific to overt cancer tissue. Using MethyLight assays, we analyzed 316 lung tissue samples from 151 cancer-free subjects (121 ever-smokers and 30 never-smokers) for hypermethylation of 19 genes previously observed to be hypermethylated in nonsmall cell lung cancers. Only APC (39%), CCND2 (21%), CDH1 (7%), and RARB (4%) were hypermethylated in >2% of these cancer-free subjects. CCND2 was hypermethylated more frequently in ever-smokers (26%) than in never-smokers (3%). CCND2 hypermethylation was also associated with increased age and upper lobe sample location. APC was frequently hypermethylated in both ever-smokers (41%) and never-smokers (30%). BVES, CDH13, CDKN2A (p16), CDKN2B, DAPK1, IGFBP3, IGSF4, KCNH5, KCNH8, MGMT, OPCML, PCSK6, RASSF1, RUNX, and TMS1 were rarely hypermethylated ( |
| Databáze: | OpenAIRE |
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