Molecular markers in lung cancer: prognostic role and relationship to smoking
Molecular markers in lung cancer: prognostic role and relationship to smoking
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DOI：
10.1590/s1806-37132006000100012
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发表时间：
2006-02-01
影响因子：
2.7
通讯作者：
Paschoal, Marcos Eduardo Machado
中科院分区：
文献类型：
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作者：
Duarte, Ricardo Luiz de Menezes;Paschoal, Marcos Eduardo Machado
流行病学研究已证明吸烟与肺癌之间有因果关系。虽然大多数肺癌病例与吸烟有关，但只有少数重度吸烟者会患肺癌，这导致了遗传因素影响个体易感性的概念。肺癌中的主要分子变化见于肿瘤抑制基因、原癌基因、生长因子、端粒酶活性和启动子甲基化状态。众所周知的药剂包括血管生成刺激因子（如血管内皮生长因子），以及与肿瘤细胞增殖和凋亡相关的因子（表皮生长因子受体、p53、K-ras、视网膜母细胞瘤和BCL-2）。这些遗传因素中的几个已经被研究，但没有一个单一的参数尚未提出足够的选择性预后价值或治疗效果。治愈肺癌的治疗策略应该集中在这些早期遗传病变上，以促进它们的修复或消除这些肺癌细胞。
Epidemiological studies have demonstrated a causal relationship between smoking and lung cancer. Although most lung cancer cases are linked to smoking, only a minority of heavy smokers develop lung cancer, leading to the notion that genetic factors affect individual susceptibility. The principal molecular changes in lung cancer are seen in tumor suppressor genes, proto-oncogenes, growth factors, telomerase activity, and methylation status of promoters. Well-known agents include angiogenesis-stimulating factors (such as vascular endothelial growth factor), as well as factors related to tumor cell proliferation and apoptosis (epidermal growth factor receptor, p53, K-ras, retinoblastoma and BCL-2). Several of these genetic factors have already been investigated, but no single parameter has yet presented sufficient selectivity regarding prognostic value or therapeutic efficacy. Treatment strategies to cure lung cancer should focus on these early genetic lesions in order to promote their repair or to eliminate these lung cancer cells.