1. Intestinal Inflammation and Cancer
Thomas A. Ullman, Steven H. Itzkowitz 
Gastroenterology 
Volume 140, Issue 6, Pages e1 (May 2011)
DOI: /j.gastro
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2. Figure 1
Histological Activity Index. This figure demonstrates examples of the degree of histological inflammation commonly seen in the mucosa of patients with ulcerative colitis. (A) Inactive colitis: no cryptitis or crypt abscesses. (B) Mildly active colitis: neutrophil infiltration of <50% of sampled crypts or cross sections, no ulcers or erosions. Arrow: crypt with neutrophilic infiltration. (C) Moderately active colitis: neutrophil infiltration of ≥50% of sampled crypts or cross sections, no ulcers or erosions. Arrows: crypt neutrophils. (D) Severely active colitis: erosion or ulceration, irrespective of other features. Here, severely active colitis due to presence of ulceration.
Reprinted from Gastroenterology, vol. 133, Gupta RB et al, Histologic inflammation is a risk factor for progression to colorectal neoplasia in ulcerative colitis: a cohort study, pg 1099–1105, copyright 2007, with permission from Elsevier.6
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3. Figure 2
Molecular pathogenesis of sporadic colon cancer (top) and colitis-associated colorectal cancer (bottom). There are similarities between the pathways, including the development of aneuploidy (chromosomal instability), MSI, DNA methylation, activation of the oncogene k-ras, activation of COX-2, and mutation and eventual loss of heterozygosity of p53, APC, and DCC/DPC4. However, the frequency and sequence of these events differs between the cancers.
Modified from Gastroenterology Clinics of North America, vol. 35, Itzkowitz SH, Molecular biology of dysplasia and cancer in inflammatory bowel disease, pgs 553–571, copyright 2006, with permission from Elsevier.19
Gastroenterology  , e1DOI: ( /j.gastro )
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4. Figure 3
The sequence of events from inflammation to cancer in patients with inflammatory bowel disease. The colitis is triggered in a genetically susceptible individual by an environmental insult (eg, gastrointestinal infection, nonsteroidal anti-inflammatory drug use, other environmental toxins), which then gives rise to overactive innate and adaptive immune responses to certain commensal bacteria, a process that is modified by various environmental factors.40 A simplified model suggests that the innate immune system is responsible for initiating the intestinal inflammation, whereas the adaptive immune response contributes to the establishment and maintenance of chronic inflammation.
Modified from Itzkowitz and Yio,2 used with permission.
Gastroenterology  , e1DOI: ( /j.gastro )
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5. Gastroenterology 2011 140, 1807-1816. e1DOI: (10. 1053/j. gastro. 2011
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6. Gastroenterology 2011 140, 1807-1816. e1DOI: (10. 1053/j. gastro. 2011
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