Background-Patients with inflammatory bowel disease (IBD) are at increased risk of developing colorectal cancer. Aberrant microRNA (miRs) expression has been linked to carcinogenesis, however no reports document a relationship between IBD-related neoplasia (IBDN) and altered miR expression. In the current study we sought to identify specific miR dysregulation along the normal-inflammation-cancer axis.

Background: SodA is an important virulence factor in Borrelia burgdorferi. Results: This SodA requires extraordinarily high intracellular manganese for activity and accumulates as either manganese or apoprotein, but not iron-bound. Conclusion: B. burgdorferiSodA is a unique Mn-SOD based on metal requirements and predicted structure. Significance: B. burgdorferi pathogenicity may be controlled by exploiting the unusual properties of SodA.

Background The development of colon cancer represents a major complication in patients with inflammatory bowel disease (IBD). The importance of microRNAs (miRs) in carcinogenesis is becoming clearer, as miRs have been implicated in the regulation of cancer-related cellular processes to include apoptosis, differentiation, cell cycle progression, and immune function. In the current study, we sought to identify miR dysregulation specific to progression along the normal-inflammation-cancer axis in colonic specimens from IBD patients. Methods MiR microarrays and quantitative RT-PCR were used to detect and confirm dysregulated miRs. Receiver-operating characteristic curve analysis was applied to evaluate the potential utility of miR-224 as a neoplastic disease marker in IBD. For miR-224 target mRNA identification, mRNA microarrays were employed in combination with bioinformatic analyses, Western blotting, and luciferase activity measurements. Results We identified 30 miRs that were differentially expressed between chronically inflamed mucosae and cancers arising in IBD. MiR-224 levels increased successively at each stage of IBD progression and accurately discriminated cancers from normal or chronically inflamed IBD tissues. Moreover, mRNA arrays combined with bioinformatic analyses suggested participation of miR-224 in cell cycle regulation. Subsequently, cell cycle experiments indicated that miR-224 regulates the G1/S checkpoint. Finally, in silico prediction analyses, confirmed by Western blotting and luciferase assays, identified p21 as a specific direct mRNA target of miR-224. Conclusions These findings reveal miR dysregulation specific to IBD-associated colorectal carcinoma. MiR-224 is overexpressed in IBD-cancers and targets p21, a key cell cycle regulator. Moreover, these results establish the participation of miR-224 in IBD-carcinogenesis.

Overall, 12% of ulcerative colitis patients have a family history of inflammatory bowel disease, and were more likely to have a family history of ulcerative colitis than Crohn's disease. Pediatric-onset ulcerative colitis patients were more likely to have a family history of inflammatory bowel disease.