Colorectal cancer carcinogenesis: a review of mechanisms

Kanwal Tariq, Kulsoom Ghias

Research output: Contribution to journalReview articlepeer-review

201 Citations (Scopus)

Abstract

Colorectal cancer (CRC) is the second most common cancer in women and the third most common in men globally. CRC arises from one or a combination of chromosomal instability, CpG island methylator phenotype, and microsatellite instability. Genetic instability is usually caused by aneuploidy and loss of heterozygosity. Mutations in the tumor suppressor or cell cycle genes may also lead to cellular transformation. Similarly, epigenetic and/or genetic alterations resulting in impaired cellular pathways, such as DNA repair mechanism, may lead to microsatellite instability and mutator phenotype. Non-coding RNAs, more importantly microRNAs and long non-coding RNAs have also been implicated at various CRC stages. Understanding the specific mechanisms of tumorigenesis and the underlying genetic and epigenetic traits is critical in comprehending the disease phenotype. This paper reviews these mechanisms along with the roles of various non-coding RNAs in CRCs.

Original languageEnglish
Pages (from-to)120-135
Number of pages16
JournalCancer Biology and Medicine
Volume13
Issue number1
DOIs
Publication statusPublished - 1 Mar 2016

Keywords

  • Chromosomal instability
  • Colorectal cancer
  • Microsatellite instability
  • Non-coding RNA mismatch repair

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