Colorectal cancer carcinogenesis: a review of mechanisms

Kanwal Tariq, Kulsoom Ghias


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


Colorectal cancer; chromosomal instability; microsatellite instability; non-coding RNA mismatch repair

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