1. Diagnosis and management of dysplasia in patients with inflammatory bowel diseases 
Steven H Itzkowitz, Noam Harpaz 
Gastroenterology 
Volume 126, Issue 6, Pages (May 2004)
DOI: /j.gastro

2. Figure 1
Macroscopic classification of dysplasia illustrated in a hypothetical case of ulcerative colitis with partial colonic involvement. Dysplasia is shown in black, normal colon in yellow, diseased colon in red.
Gastroenterology  , DOI: ( /j.gastro )

3. Figure 2
Example of chromoendoscopy identifying an area of flat LGD (within the arrows). The lesion was not visible prior to dye spraying the mucosa with methylene blue (Photo courtesy of Dr. Jerome Waye, Mount Sinai School of Medicine, New York).
Gastroenterology  , DOI: ( /j.gastro )

4. Figure 3
Regenerative mucosa from the colectomy specimen of a young patient with a brief history of fulminant ulcerative colitis. The crowded crypts show a distinct maturation gradient with transformation of atypical epithelial cells at the crypt base to mature goblet and columnar cells with small bland nuclei in the upper crypt zone.
Gastroenterology  , DOI: ( /j.gastro )

5. Figure 4
Low-grade dysplasia. (A ) Grossly unremarkable mucosa from the colectomy specimen of a patient with long-standing ulcerative colitis who underwent surgery for an indication of flat low-grade dysplasia in a surveillance biopsy. The crypts are lined by columnar epithelium with inappropriately crowded, hyperchromatic nuclei, most located in the basal half of the cells. Note the absence of a maturation gradient. (B) Mucosa from an irregularly shaped, slightly elevated lesion in the transverse colon of a 45-year-old woman with inactive Crohn’s colitis of 15 years duration. The crypts are lined throughout by tall columnar cells with reduced cytoplasmic mucin and crowded, enlarged, “picket fence” nuclei. The histology is identical to that of typical sporadic adenomatous polyps.
Gastroenterology  , DOI: ( /j.gastro )

6. Figure 5
(A ) High-grade dysplasia in a rectal biopsy of an elderly patient with long-standing ulcerative colitis. The crypt is lined by crowded columnar cells with marked nuclear stratification that are beginning to assume a cribriform, or gland-within-gland, configuration in the basal zone. (B) Flat high-grade dysplasia in the colectomy specimen of a patient with long-standing ulcerative colitis who is undergoing surgery for an indication of a DALM. The epithelium lining most of the crypts contains irregularly shaped, overlapping, and stratified nuclei (inset).
Gastroenterology  , DOI: ( /j.gastro )

7. Figure 6
The course of 7 patients who developed colorectal cancer following the initial detection of flat LGD. None of the patients had a history of polypoid dysplasia prior to the diagnosis of flat LGD. Symbols above each line represent the worst pathology detected at interval colonoscopic examinations. Patients 1 and 2 had Dukes’ A cancers diagnosed within 6 months of the first detection of LGD. Except for patient 1, no other patient endoscopically progressed to HGD prior to the diagnosis of cancer. Of note, patients 6 and 7 had no dysplasia on their last colonoscopy prior to the diagnosis of node-positive colon cancer. (Adapted from Ullman et al., Gastroenterology 2003;195:1311–1319.)
Gastroenterology  , DOI: ( /j.gastro )

8. Figure 7
Progression to advanced neoplasia (HGD or cancer) in 46 patients after initial detection of flat LGD (solid line). The overall 5-year progression rate was 53% (95% confidence interval 0.29–0.77). There was no difference in rate of progression between patients who only had flat LGD detected in only 1 biopsy (unifocal; n = 39) (dashed line) compared with those with fLGD in more than 1 biopsy (multifocal; n = 7) (dotted line). (Adapted from Ullman et al., Gastroenterology 2003;195:1311–1319.)
Gastroenterology  , DOI: ( /j.gastro )

9. Figure 8
Summary of molecular genetic alterations that contribute to the development of sporadic colon cancer (top) and colitis-associated colon cancer (bottom). Note that, loss of function of APC is an early event, in sporadic colon carcinogenesis, whereas loss of p53 occurs later. In colitis-associated carcinogenesis, p53 alterations occur quite early, even before dysplasia has developed, whereas APC mutations or loss tend to occur later.
Gastroenterology  , DOI: ( /j.gastro )

10. Figure 9
Suggested surveillance strategy. See Recommended Surveillance Strategy section in text for explanation. ∗Duration of short-term surveillance has not been determined.
Gastroenterology  , DOI: ( /j.gastro )