CCND2 高甲基化可能反映了肺部吸烟诱导的癌前变化。
Hypermethylation of CCND2 May Reflect a Smoking-Induced Precancerous Change in the Lung.
机构信息
Division of Nuclear Medicine, Department of Radiology, Box 357115, School of Medicine, University of Washington, Seattle, WA 98195-7115, USA.
出版信息
J Oncol. 2011;2011:950140. doi: 10.1155/2011/950140. Epub 2011 Mar 28.
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 (<2%) in all subjects. Hypermethylation of CCND2 may reflect a smoking-induced precancerous change in the lung.
目前尚不清楚烟草烟雾是否会诱导 DNA 超甲基化，是作为致癌作用的早期事件，还是作为特定于明显癌组织的晚期事件。我们使用 MethyLight 分析了 151 例无癌症受试者（121 例曾吸烟者和 30 例从不吸烟者）的 316 个肺组织样本，以分析 19 个先前在非小细胞肺癌中观察到超甲基化的基因的超甲基化。这些无癌症受试者中，仅有 APC（39%）、CCND2（21%）、CDH1（7%）和 RARB（4%）的超甲基化发生率超过 2%。CCND2 在曾吸烟者（26%）中的超甲基化频率高于从不吸烟者（3%）。CCND2 的超甲基化也与年龄增加和上叶样本位置有关。APC 在曾吸烟者（41%）和从不吸烟者（30%）中均频繁超甲基化。BVES、CDH13、CDKN2A（p16）、CDKN2B、DAPK1、IGFBP3、IGSF4、KCNH5、KCNH8、MGMT、OPCML、PCSK6、RASSF1、RUNX 和 TMS1 在所有受试者中的超甲基化发生率均较低（<2%）。CCND2 的超甲基化可能反映了吸烟引起的肺部癌前变化。
Zotero 插件