Who takes the lead in the development of ulcerative colitis–associated colorectal cancers: mutator, suppressor, or methylator pathway?

Combined α-methylacyl coenzyme A racemase/p53 analysis to identify dysplasia in inflammatory bowel disease

“…Furthermore, it cannot be excluded that some morphologically unidentified early neoplastic lesions were also revealed by our p53 immunostaining. The high rate of p53-positive dysplasia in this study may possibly reflect a particularly important role of the p53 pathway in IBD-associated cancers as previously suggested by multiple studies [13,21,23,24,[28][29][30]. This hypothesis is also supported by findings in our own patient cohort where significant differences in the p53 immunostaining between sporadic and colitis-associated cancers were seen after using the same experimental conditions as for this study (unpublished data).…”

Relative role of methylator and tumor suppressor pathways in ulcerative colitis-associated colon cancer

“…Some studies suggest that UC oncogenesis is the effect of an acceleration of age-related epigenetic methylation, 3 while others suggest that the oncogenesis is due to inactivation of tumor suppressors such as APC. [4][5][6] Sporadic colorectal cancers are biologically heterogeneous and arise via at least three distinct molecular pathways. The classic tumor suppressor (chromosomal instability) pathway involves mutations and loss of heterozygosity of oncogenes and tumor suppressor genes such as APC, KRAS, and p53, as normal mucosa transforms to carcinoma via adenomatous polyps.…”

Associations between markers of colorectal cancer stem cells, mutation, microRNA and the clinical features of ulcerative colitis

“…Alterations of this pathway are mostly caused by inactivation of the APC gene, which is a frequent and early genetic event in sporadic colorectal carcinogenesis. Studies of UC-associated dysplasia and cancer have reported various degrees of loss of function of APC [22][23][24][25][26]. The reported frequency of APC mutations in UC-related neoplasia varied from 0% to 6% in one study [27] and up to 50% [23] in several small studies.…”