Abstract

Colorectal cancer (CRC) is a major cause for morbidity and mortality worldwide; it is the fourth most common cancer in men and the third most common cancer in women. CRC is divided into three categories: hereditary, nonhereditary and familial. Approximately 15% of CRC cases are considered as a hereditary form which most common contains: Familial adenomatous polyposis (FAP) and hereditary non polyposis colorectal cancer (HNPCC) and MYHAssociated polyposis (MAP). CRC develops through multiple pathways leading to different phenotypes.

Highlights

  • Colorectal cancer (CRC) is a major cause for morbidity and mortality worldwide; it is the fourth most common cancer in men and the third most common cancer in women [1]

  • 15% of CRC cases are considered as a hereditary form which most common contains: Familial adenomatous polyposis (FAP) and hereditary non polyposis colorectal cancer (HNPCC) and MYHAssociated polyposis (MAP) [4,5]

  • CIN, or classic adenoma-to-carcinoma pathway, account 65-70% of sporadic CRC, is characterized by an imbalance in chromosome number, chromosomal genomic amplLficatLons, and a high frequency of LOH, which has been determined through a series of mutations in tumor suppressor genes or oncogenes, in some pathways including: WNT/APC/B-CAT, RAS, P53, PI3KCA pathway. 18q LOH where the genes Smad2, Smad4 and DCC are located and loss of 8p and 5q allele correlated with CIN pathway [7,8,9,10]

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Summary

Introduction

Colorectal cancer (CRC) is a major cause for morbidity and mortality worldwide; it is the fourth most common cancer in men and the third most common cancer in women [1]. 15% of CRC cases are considered as a hereditary form which most common contains: Familial adenomatous polyposis (FAP) and hereditary non polyposis colorectal cancer (HNPCC) and MYHAssociated polyposis (MAP) [4,5]. CRC develops through multiple pathways leading to dL‫ٴو‬erent phenotypes. Нese pathways may be defined on molecular features: 1) chromosomal instability (CIN), Microsatellite instability (MSI) and CpG island methylator phenotype (CIMP) [6].

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Conclusion

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