Molecular profiling of ulcerative colitis-associated neoplastic progression

The Actin-Cytoskeleton Pathway and Its Potential Role in Inflammatory Bowel Disease-Associated Human Colorectal Cancer

“…To minimize variability between multiple comparisons, chips that did not include Affymetrix control probes, expressed sequence tags, and probes were excluded. The remaining 8089 probe sets were each fitted using a repeated-measure design across tissue type and analyzed using the comparatively new Proc Mixed procedure (SAS, v 9.0; SAS Institute, Cary, NC), as previously described (Colliver et al, 2006). For data analysis, we utilized the Ingenuity Pathway Analysis (IPA) Program version 7.6 ª (Redwood, CA).…”

The pattern of CD44 and matrix metalloproteinase 9 expression is a useful predictor of ulcerative colitis–associated dysplasia and neoplasia

“…Ulcerative colitis-associated carcinoma is preceded by and coexists with dysplastic precursors; thus, it is possible to detect the cancer precursors through biomarkers to improve cancer surveillance [4]. Dysplasia often arises multifocal and is difficult to be recognized by colonoscopic biopsies because those lesions are sometimes cannot be differentiated from regenerative changes of the epithelium [5].…”

Reduced mucin sulfonation and impaired intestinal barrier function in the hyposulfataemic NaS1 null mouse

“…In addition to the importance of mucin sulfonation, the strong expression of NaS1 in the ileum and its role in intestinal sulfate absorption makes the ileum an appropriate tissue to investigate the effects of a disrupted NaS1 gene ( Slc13a1 ) on the ileal transcriptional profile. Gene arrays are a valuable tool for investigating the intestinal transcriptome and have provided important insights into genes that are involved in ulcerative colitis, inflammatory bowel disease and the inflammatory response to bacterial gut pathogens, such as Campylobacter jejuni 29 – 31. Studies of the Nas1 −/− mouse can provide valuable insights into the physiological consequences of altered sulfate homeostasis and function of the NaS1 gene, which are yet to be characterised in human disease.…”