作者: Carmen J. Marsit , Duk‐Hwan Kim , Mei Liu , Philip W. Hinds , John K. Wiencke
DOI: 10.1002/IJC.20714
关键词: Internal medicine 、 Risk factor 、 Medicine 、 Adenocarcinoma 、 Immunology 、 Carcinogen 、 Carcinoma 、 Tobacco smoke 、 Tumor suppressor gene 、 Oncology 、 Lung cancer 、 DNA methylation
摘要: The putative tumor suppressors RASSF1A and BLU are mapped adjacent to one another on chromosome 3p21.3, a region frequently deleted in lung cancer. These genes often inactivated by promoter hypermethylation, but the association of this inactivation with clinical features disease or carcinogen exposure has been poorly studied. Early age starting smoking hypothesized as an independent risk factor for cancer, mechanistically, adolescence may constitute critical period tobacco exposure. To study relationship smoke hypermethylation BLU, methylation-specific PCR was performed case series incident, surgically resected non-small cell cancer (NSCLC), prevalence alteration examined relation information collected patients. Hypermethylation occurred 47% (83/178) 43% (68/160) NSCLC tumors examined. There no significant between methylation these 2 genes, either tended occur more adenocarcinoma (AC) histology compared squamous carcinoma (SCC). Controlling pack-years smoked, age, gender histology, under 18 significantly related [prevalence ratio (PR) = 1.6, 95% confidence interval [CI] 1.1-2.3]. results indicate that is thus identifying molecular epidemiologic effect teenage risk.