| Literature DB >> 33923068 |
Chiara Alquati1,2, Anna Prossomariti1,2, Giulia Piazzi1,2, Francesco Buttitta1, Franco Bazzoli1, Luigi Laghi3,4, Luigi Ricciardiello1,2.
Abstract
Colorectal cancer (CRC) develops through a multi-step process characterized by the acquisition of multiple somatic mutations in oncogenes and tumor-suppressor genes, epigenetic alterations and genomic instability. These events lead to the progression from precancerous lesions to advanced carcinomas. This process requires several years in a sporadic setting, while occurring at an early age and or faster in patients affected by hereditary CRC-predisposing syndromes. Since advanced CRC is largely untreatable or unresponsive to standard or targeted therapies, the endoscopic treatment of colonic lesions remains the most efficient CRC-preventive strategy. In this review, we discuss recent studies that have assessed the genetic alterations in early colorectal lesions in both hereditary and sporadic settings. Establishing the genetic profile of early colorectal lesions is a critical goal in the development of risk-based preventive strategies.Entities:
Keywords: colorectal cancer; conventional colorectal adenomas; familial adenomatous polyposis; lynch syndrome; serrated colorectal adenomas
Year: 2021 PMID: 33923068 DOI: 10.3390/cancers13092081
Source DB: PubMed Journal: Cancers (Basel) ISSN: 2072-6694 Impact factor: 6.639