Molecular approach to genetic and epigenetic pathogenesis of early-onset colorectal cancer

被引:16
|
作者
Tezcan, Gulcin [1 ]
Tunca, Berrin [1 ]
Ak, Secil [1 ]
Cecener, Gulsah [1 ]
Egeli, Unal [1 ]
机构
[1] Uludag Univ, Dept Med Biol, Fac Med, Gorukle Kampusu, TR-16059 Bursa, Turkey
关键词
Early-onset; Colorectal cancer; Epigenetic mechanism; Genetic mechanism; Clinical outcome; PEUTZ-JEGHERS-SYNDROME; FAMILIAL ADENOMATOUS POLYPOSIS; MUTYH-ASSOCIATED-POLYPOSIS; MICROSATELLITE INSTABILITY STATUS; WNT SIGNALING ACTIVATION; LYNCH-SYNDROME; COLON-CANCER; JUVENILE POLYPOSIS; MISMATCH REPAIR; GERMLINE MUTATIONS;
D O I
10.4251/wjgo.v8.i1.83
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Colorectal cancer (CRC) is the third most frequent cancer type and the incidence of this disease is increasing gradually per year in individuals younger than 50 years old. The current knowledge is that early-onset CRC (EOCRC) cases are heterogeneous population that includes both hereditary and sporadic forms of the CRC. Although EOCRC cases have some distinguishing clinical and pathological features than elder age CRC, the molecular mechanism underlying the EOCRC is poorly clarified. Given the significance of CRC in the world of medicine, the present review will focus on the recent knowledge in the molecular basis of genetic and epigenetic mechanism of the hereditary forms of EOCRC, which includes Lynch syndrome, Familial CRC type X, Familial adenomatous polyposis, MutYH-associated polyposis, Juvenile polyposis syndrome, Peutz-Jeghers Syndrome and sporadic forms of EOCRC. Recent findings about molecular genetics and epigenetic basis of EOCRC gave rise to new alternative therapy protocols. Although exact diagnosis of these cases still remains complicated, the present review paves way for better predictions and contributes to more accurate diagnostic and therapeutic strategies into clinical approach.
引用
收藏
页码:83 / 98
页数:16
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