Department of Pathology, Yamagata University, Yamagata 990-9585, Japan.
Anticancer Res. 2011 Apr;31(4):1211-4.
Epidemiological studies have demonstrated a causal link between tobacco smoking and lung cancer. However, lung adenocarcinoma (AC) is also frequently found in non-smokers compared with other non-small cell lung carcinoma (NSCLC) subtypes.
Mutations of both epithelial growth factor receptor (EGFR) and KRAS, and the methylation status of 10 tumor suppressor or tumor-related genes were examined in 62 ACs, and the relationship with smoking status, and the relationship between the genetic alterations and epigenetic alterations were investigated.
The frequency of EGFR mutation was strongly correlated with smoking status, and the frequency of KRAS mutation, and methylation of retinoic acid receptor beta (RAR-β), p16, FHIT and RASSF1A were weakly related with smoking status. Inverse correlation was found between EGFR mutation and FHIT, RASSF1A and RUNX3 methylation.
Tobacco smoking is correlated with the frequencies of EGFR and KRAS mutations as to pathogenesis of ACs.
流行病学研究已经证明吸烟与肺癌之间存在因果关系。然而，与其他非小细胞肺癌（NSCLC）亚型相比，腺癌（AC）在不吸烟者中也经常发现。
在 62 例 AC 中检查了表皮生长因子受体（EGFR）和 KRAS 的突变，以及 10 个肿瘤抑制或肿瘤相关基因的甲基化状态，并研究了与吸烟状况的关系，以及遗传改变与表观遗传改变之间的关系。
EGFR 突变的频率与吸烟状况密切相关，KRAS 突变的频率以及维甲酸受体β（RAR-β）、p16、FHIT 和 RASSF1A 的甲基化与吸烟状况呈弱相关。在 EGFR 突变与 FHIT、RASSF1A 和 RUNX3 甲基化之间发现了负相关。
吸烟与 AC 发病机制中的 EGFR 和 KRAS 突变频率有关。
