Common pathogenic mechanisms and pathways in the development of COPD and lung cancer

被引：98

作者：

Yang, Ian A. ^{[1
,2
]}

Relan, Vandana ^{[1
,2
]}

Wright, Casey M. ^{[1
,2
]}

Davidson, Morgan R. ^{[1
,2
]}

Sriram, Krishna B. ^{[1
,2
]}

Francis, Santiyagu M. Savarimuthu ^{[1
,2
]}

Clarke, Belinda E. ^{[3
]}

Duhig, Edwina E. ^{[3
]}

Bowman, Rayleen V. ^{[1
,2
]}

Fong, Kwun M. ^{[1
,2
]}

机构：

[1] Prince Charles Hosp, Dept Thorac Med, Thorac Res Lab, Brisbane, Qld 4032, Australia

[2] Univ Queensland, UQ Thorac Res Ctr, Sch Med, Brisbane, Qld, Australia

[3] Prince Charles Hosp, Dept Anat Pathol, Brisbane, Qld 4032, Australia

来源：

EXPERT OPINION ON THERAPEUTIC TARGETS | 2011年 / 15卷 / 04期

基金：

英国医学研究理事会;

关键词：

chronic obstructive; genomics; lung neoplasms; pathogenesis; pulmonary disease; OBSTRUCTIVE PULMONARY-DISEASE; COMPARATIVE GENOMIC HYBRIDIZATION; NICOTINIC ACETYLCHOLINE-RECEPTORS; BRONCHIAL EPITHELIAL-CELLS; AIR-FLOW OBSTRUCTION; GENE-EXPRESSION; SUSCEPTIBILITY LOCUS; PROMOTER METHYLATION; SIGNALING PATHWAYS; DNA METHYLATION;

D O I：

10.1517/14728222.2011.555400

中图分类号：

R9 [药学];

学科分类号：

100702 [药剂学];

摘要：

Areas covered: This review discusses the common mechanisms for susceptibility to lung cancer and COPD, which in addition to cigarette smoke, may involve inflammation, epithelial--mesenchymal transition, abnormal repair, oxidative stress, and cell proliferation. Furthermore, we discuss the underlying genomic and epigenomic changes (single nucleotide polymorphisms (SNPs), copy number variation, promoter hypermethylation and microRNAs) that are likely to alter biological pathways, leading to susceptibility to lung cancer and COPD (e.g., altered nicotine receptor biology). Expert opinion: Strategies to study genomics, epigenomics and gene-environment interaction will yield greater insight into the shared pathogenesis of lung cancer and COPD, leading to new diagnostic and therapeutic modalities.

引用

收藏

页码：439 / 456

页数：18

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