Molecular Origins of Cancer: Molecular Basis of Colorectal Cancer.

被引：1432

作者：

Markowitz, Sanford D. ^{[1
,2
,3
,4
]}

Bertagnolli, Monica M. ^{[5
]}

机构：

[1] Case Western Reserve Univ, Sch Med, Dept Med, Div Hematol Oncol, Cleveland, OH 44106 USA

[2] Case Western Reserve Univ, Sch Med, Ireland Canc Ctr, Cleveland, OH 44106 USA

[3] Case Med Ctr, Cleveland, OH USA

[4] Howard Hughes Med Inst, Chevy Chase, MD USA

[5] Brigham & Womens Hosp, Boston, MA 02115 USA

来源：

NEW ENGLAND JOURNAL OF MEDICINE | 2009年 / 361卷 / 25期

关键词：

GENOME-WIDE ASSOCIATION; ISLAND METHYLATOR PHENOTYPE; SPORADIC COLON-CANCER; FACTOR-BETA RECEPTOR; FECAL OCCULT BLOOD; P53; GENE-MUTATIONS; MICROSATELLITE-INSTABILITY; ADJUVANT CHEMOTHERAPY; GERMLINE MUTATIONS; 15-HYDROXYPROSTAGLANDIN DEHYDROGENASE;

D O I：

10.1056/NEJMra0804588

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

This review gives an account of recent advances in our knowledge of the molecular mechanisms in colorectal cancer. Genetic changes in the germ line, combined with somatic mutations, occur in familial syndromes of colorectal cancer, whereas somatic mutations are the outstanding feature of sporadic colorectal cancer. Genetic changes drive the progression from adenoma to carcinoma and probably influence individual susceptibility and response to treatment. Copyright © 2009 Massachusetts Medical Society.

引用

页码：2449 / 2460

页数：12

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