Distribution of Dysplasia in Ulcerative Colitis

Mh, Vatn; Elgjo, Kjell; Bergan, A.

doi:10.1080/00365521.1984.12005827

Cited by 13 publications

(3 citation statements)

References 12 publications

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“…In our experiment, DMH and DSS induced colitis-related tumors dominant in the distal part of colon followed by in the middle part. In human UC, dysplasia was found in two or more segments in 42-75% of the cases and the incidence of mutiple synchronous cancers was reported to vary from 22-50% [20][21][22] . In the current study, the result also showed that dysplasia was present in two or more segment in 60% of the animals and the incidence of synchronous cancers was 33.3%.…”

Section: Discussionmentioning

confidence: 99%

A novel mouse model for colitis-associated colon carcinogenesis induced by 1,2-dimethylhydrazine and dextran sulfate sodium

Wang

Wang²,

Lv³

et al. 2004

WJG

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AIM:To develop an efficient animal colitis-associated carcinogenesis model and to detect the expression of β-catenin and p53 in this new model. METHODS:Dysplasia and cancer were investigated in mice pretreated with a single intraperitoneal injection of 20 mg/kg body mass of 1,2-dimethylhydrazine prior to three repetitive oral administrations of 30 g/L dextran sulfate sodium to give conditions similar to the clinically observed active and remission phases. Immunohistochemical staining of β-catenin and p53 was performed on paraffin-imbedded specimens of animals with cancer and/or dysplasia, those without dysplasia and the normal control animals. RESULTS:At wk 11, four early-invasive adenocarcinomas and 36 dysplasia were found in 10 (90.9%) of the 11 mice that underwent 1,2-dimethylhydrazine-pretreatment with 3 cycles of 30 g/L dextran sulfate sodium-exposure. Dysplasia and/or cancer occurred as flat lesions or as dysplasia-associated lesion or mass (DALM) as observed in humans. Colorectal carcinogenesis occurred primarily on the distal portion of the large intestine. No dysplasia and/or cancer lesion was observed in the control groups with 1,2-dimethylhydrazine pretreatment or 3 cycles of 30 g/L dextran sulfate sodium exposure alone. Immunohistochemical investigation revealed that β-catenin was translocated from cell membrane to cytoplasm and/or nucleus in 100% of cases with dysplasia and neoplasm, while normal membrane staining was observed in cases without dysplasia and the normal control animals. Nuclear expression of p53 was not detected in specimens. CONCLUSION:A single dose of procarcinogen followed by induction of chronic ulcerative colitis results in a high incidence of colorectal dysplasia and cancer. Abnormal expression of β-catenin occurs frequently in dysplasia and cancer. This novel mouse model may provide an excellent vehicle for studying colitis-related colon carcinogenesis.Wang JG, Wang DF, Lv BJ, Si JM. A novel mouse model for colitis-associated colon carcinogenesis induced by 1,2-dimethylhydrazine and dextran sulfate sodium. World J Gastroenterol

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Section: Discussionmentioning

confidence: 99%

A novel mouse model for colitis-associated colon carcinogenesis induced by 1,2-dimethylhydrazine and dextran sulfate sodium

Wang

Wang²,

Lv³

et al. 2004

WJG

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“…An underestimation of the real prevalence of dysplasia due to a ‘loss of dysplasia data’ could be an option in our study despite the fact that colectomy rates and post-surgery specimen pathology was available [47]. Our patients have been followed up for 10 years from diagnosis, so our study has probably limited value for assessing dysplasia as a marker for cancer risk.…”

Section: Discussionmentioning

confidence: 99%

Dysplasia and Cancer in Inflammatory Bowel Disease 10 Years after Diagnosis: Results of a Population-Based European Collaborative Follow-Up Study

et al. 2007

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Objective: To determine dysplasia and cancer in the 1991–2004 European Collaborative Inflammatory Bowel Disease (EC-IBD) Study Group cohort. Patients and Methods: A patient questionnaire and a physician per patient form were completed for each of the 1,141 inflammatory bowel disease patients (776 ulcerative colitis/365 Crohn’s disease) from 9 centers (7 countries) derived from the EC-IBD cohort. Rates of detection of intestinal cancer and dysplasia as well as extra-intestinal neoplasms were computed. Results: Patient follow-up time was 10.3 ± 0.8 (range 9.4–11) years. The mean age of the whole group of IBD patients was 37.8 ± 11.3 (range 16–76) years. Thirty-eight patients (3.3%; 26 with ulcerative colitis/12 with Crohn’s disease, 21 males/17 females, aged 61.3 ± 13.4, range 33–77 years), were diagnosed with 42 cancers. Cancers occurred 5.4 ± 3.3 (range 0–11) years after inflammatory bowel disease diagnosis. Colorectal cancer was diagnosed in 8 (1 Crohn’s disease and 7 ulcerative colitis patients – 0.3 and 0.9% of the Crohn’s disease and ulcerative colitis cohort, respectively) of 38 patients and 30 cancers were extra-intestinal. Four of 38 patients (10.5%) were diagnosed as having 2 cancers and they were younger compared to patients with one cancer (p = 0.0008). There was a trend for a higher prevalence of intestinal cancer in the northern centers (0.9%) compared to southern centers (0.3%, p = NS). Southern centers had more cases of extra-intestinal cancer compared to northern centers (2 vs. 3.8%, p = 0.08). Ten patients (0.9%; 8 with ulcerative colitis/2 with Crohn’s disease, 8 males, aged 62.3 ± 14.1 years) had colorectal dysplasia. Conclusions: In the first decade of the EC-IBD Study Group cohort follow-up study, the prevalence of cancer was as expected with most patients having a single neoplasm and an extra-intestinal neoplasm. In northern centers there was a trend for more intestinal cancers, while in southern centers there was a trend for more extra-intestinal cancers compared to northern centers.

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“…The overall incidence of carcinoma in patients with ulcerative colitis is approximately 5 % (McDougall 1964; Gozzetti et al 1987). Patients with ulcerative colitis, when compared with those without colitis, develop color ectal cancer at a younger age, often at multiple sites in the colon and frequently present at sites other than the rectum or sigmoid colon (Greenstein et al 1979;Vatn 1984). There appears to be a higher incidence of synchronous cancers in ulcerative colitis than in a control population, and also the cancers in ulcerative colitis tend to be less well differentiated.…”

Section: Kumarmentioning

confidence: 99%

Crohn’s Disease and Ulcerative Colitis

Kumar¹,

Alexander-Williams²

1993

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Cover illustration: Ch. 12, Fig. 12. A long strictureplasty in Crohn's disease. The incised gut is bent over in a loop and the posterior wall is sutured with a continuous seromuscular stitch. Ch. 23, Fig. 16. The steps in pouch construction. The beginning of the suture line for the anterior layer of a pouch; a small hole is made in the proximal limb of the pouch; completed pouch-anal stapled anastomosis.

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Distribution of Dysplasia in Ulcerative Colitis

Cited by 13 publications

References 12 publications

A novel mouse model for colitis-associated colon carcinogenesis induced by 1,2-dimethylhydrazine and dextran sulfate sodium

A novel mouse model for colitis-associated colon carcinogenesis induced by 1,2-dimethylhydrazine and dextran sulfate sodium

Dysplasia and Cancer in Inflammatory Bowel Disease 10 Years after Diagnosis: Results of a Population-Based European Collaborative Follow-Up Study

Crohn’s Disease and Ulcerative Colitis

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