Mismatch Repair and Colon Cancer: Mechanisms and Therapies Explored

被引：142

作者：

Li, Stephen K. H. ^{[1
]}

Martin, Alberto ^{[1
]}

机构：

[1] Univ Toronto, Dept Immunol, Toronto, ON, Canada

来源：

TRENDS IN MOLECULAR MEDICINE | 2016年 / 22卷 / 04期

关键词：

MOLECULAR PATHOLOGICAL EPIDEMIOLOGY; INTESTINAL EPITHELIAL-CELLS; COLORECTAL-CANCER; LYNCH-SYNDROME; MICROSATELLITE INSTABILITY; FUSOBACTERIUM-NUCLEATUM; GUT MICROBIOTA; SOMATIC MUTATIONS; MUTS HOMOLOG; BETA-CATENIN;

D O I：

10.1016/j.molmed.2016.02.003

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Colorectal cancer (CRC) remains one of the most prevalent cancers worldwide. In sporadic CRC, mutations frequently occur in the DNA mismatch repair (MMR) pathway. In addition, germline MMR mutations have been linked to Lynch syndrome, the most common form of hereditary CRC. Although genetic mutations, diet, inflammation, and the gut microbiota can influence CRC, it is unclear how MMR deficiency relates to these factors to modulate disease. In this review, the association of MMR to the etiology of CRC is examined, particularly in the context of microRNAs (miRNAs), inflammation, and the microbiome. We also discuss the most current targeted therapies, methods of prevention, and molecular biomarkers against MMR-deficient CRC, all of which are encouraging advancements in the field.

引用

页码：274 / 289

页数：16

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