肺癌
特发性肺纤维化
表观遗传学
医学
癌变
肺纤维化
癌症研究
Wnt信号通路
病理
肺
DNA甲基化
癌症
免疫学
生物
纤维化
信号转导
内科学
基因表达
遗传学
基因
作者
Αrgyris Τzouvelekis,Georgia Gomatou,Evangelos Bouros,Rodoula Trigidou,Vasilios Tzilas
出处
期刊:Chest
[Elsevier]
日期:2019-08-01
卷期号:156 (2): 383-391
被引量:83
标识
DOI:10.1016/j.chest.2019.04.114
摘要
Abundant epidemiologic evidence supports an association between idiopathic pulmonary fibrosis (IPF) and lung cancer. Lung tumors in patients with IPF develop preferentially in the periphery immediately adjacent to fibrotic areas, with different histologic distribution and immunohistochemical features compared with non-IPF-associated lung tumors. In this context, evidence indicates that IPF and lung cancer share many pathogenic similarities including genetic and epigenetic markers. It has been suggested that specific germline mutations predispose toward both IPF and lung cancer, leading to imbalance between oncogenes and tumor suppressor genes and ultimately carcinogenesis within fibrotic lungs. Aberrant epigenetic regulation due to methylation, histone modifications, and mainly deregulation of common noncoding RNAs represents a possible pathogenic link between the two disease paradigms. Genetic and epigenetic alterations lead to abnormal activation of common transduction pathways, including Wnt/β-catenin and phosphoinositide 3-kinase/protein kinase B, mediating metaplasia and hyperproliferation in alveolar type II epithelial cells. Cellular transformations in the mesenchymal phenotype represent a common link between lung fibrosis and carcinogenesis. In this review we summarize current data on common cellular and molecular pathogenic mechanisms between IPF and lung cancer and highlight promising therapeutic targets for this disease combination.
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