Risk factors and distinguishing features of cancer in IBD

Ekbom, Anders

doi:10.1002/ibd.3780040308

Cited by 8 publications

(5 citation statements)

References 78 publications

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“…In our study, consistent with previous studies 1–4, colorectal cancer or dysplasia occurred at a significantly younger age in patients with long‐standing and extensive disease. Similar to others, we found a predominance of poorly differentiated, mucinous and rectal tumours 9–11, all characteristics associated with a more aggressive disease phenotype in the sporadic CRC setting.…”

Section: Discussionsupporting

confidence: 93%

“…Ulcerative colitis (UC) and Crohn's colitis (CC) are associated with an increased risk of colonic epithelial dysplasia with progression to invasive colon cancer 1–4. Disease extent, young age at onset, and extended duration of active disease (>8 years) are considered major risk factors for colorectal cancer (CRC) in chronic colitis 1–5. Additional risk factors may include coexistent primary sclerosing cholangitis (PSC), first‐degree family history of sporadic CRC, and severity of colonic inflammation 6–8.…”

Section: Introductionmentioning

confidence: 99%

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Characterization of tumour‐infiltrating lymphocytes and apoptosis in colitis‐associated neoplasia: comparison with sporadic colorectal cancer

Michael-Robinson

Pandeya

Walsh

et al. 2005

The Journal of Pathology

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The development of colorectal cancer is a major complication for patients with chronic idiopathic colitis. Colitis-associated tumours tend to occur at a younger age and be more aggressive than sporadic colorectal cancers. While we have previously associated the presence of tumour-infiltrating lymphocytes (TILs) and increased apoptosis in sporadic colorectal cancer with high-level microsatellite instability and improved prognosis, little is known of the relationship between these variables in colitis-associated colorectal cancer. The aim of this study was to correlate TILs and tumour cell apoptosis in colitis-associated neoplasms stratified according to microsatellite instability. Twenty tumour and 11 dysplastic samples resected from 21 patients with long-standing colitis were analysed for microsatellite instability at 10 microsatellite markers. TIL distribution (CD3, CD8) and function (granzyme B) were quantified by immunohistochemistry. Neoplastic cell apoptosis was assessed using the M30 CytoDEATH antibody. These findings were compared with 40 microsatellite stable (MSS) sporadic colorectal cancers previously evaluated for TILs and neoplastic apoptosis. Low-level microsatellite instability was found in 1/20 colitis-associated tumours. All other colitis-associated lesions were designated MSS. CD3(+) and CD8(+) TIL counts were significantly higher in colitis-associated lesions compared with MSS sporadic colorectal cancer (p < 0.0001, p = 0.001 respectively). Despite their higher TIL density, colitis-associated tumours were more likely to present late (Dukes' stage C or D) (p = 0.02). Functionally, colitis-associated TILs demonstrated significantly less granzyme B expression compared to sporadic cancers (p = 0.002). The level of tumour cell apoptosis was similar between the two groups (sporadic, 1.53%; colitis cancers, 1.45%). In conclusion, MSS colitis-associated tumours have a higher prevalence of CD3(+)/CD8(+) TILs but no associated increase in tumour cell killing by apoptosis. Unlike cytotoxic T cells in sporadic colorectal cancer, TILs do not appear to enhance the prognosis of colitis-associated colorectal cancer. This may be related to an impairment of granzyme B expression within these lesions.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Characterization of tumour‐infiltrating lymphocytes and apoptosis in colitis‐associated neoplasia: comparison with sporadic colorectal cancer

Michael-Robinson

Pandeya

Walsh

et al. 2005

The Journal of Pathology

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“…Accordingly, there is evidence for a non-redundant regulatory role of this molecule in inflammation involving the gastrointestinal mucosa [32]. Colitis-associated cancer is a colorectal illness that arises in patients suffering from chronic inflammatory bowel disease, in particular, ulcerative colitis [33]. In a mouse model of intestinal inflammation in response to dextran sulfate sodium salt (DSS) administration, Tir8-deficient mice exhibited a dramatic susceptibility to inflammation in terms of weight loss, intestinal bleeding and mortality, and showed increased susceptibility to colitis-associated cancer in response to azoxymethane and DSS ( Figure 1).…”

Section: Importance Of Negative Regulation: Tir8/sigirrmentioning

confidence: 99%

Pathways connecting inflammation and cancer

Allavena

Garlanda

Borrello

et al. 2008

Current Opinion in Genetics & Development

384

264

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“…Studies on IBDRC, performed in the last 40 years and with an observation period of up to 25 years, reported a 0.9–1.5% prevalence for CRC and a 1.7–5.4% prevalence for extra-intestinal cancer [1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16]. …”

Section: Discussionmentioning

confidence: 99%

“…Several papers have reported a prevalence of colorectal cancer (CRC) in IBD from 0.6 to 17% [1,2,3,4,5,6,7,8,9,10]. In a recent meta-analysis on the occurrence of CRC and small bowel cancers in population-based studies, a significant increase was found with odds ratios of 2.7 for CRC and 17.5 for ileal cancer [11].…”

Section: Introductionmentioning

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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Risk factors and distinguishing features of cancer in IBD

Cited by 8 publications

References 78 publications

Characterization of tumour‐infiltrating lymphocytes and apoptosis in colitis‐associated neoplasia: comparison with sporadic colorectal cancer

Characterization of tumour‐infiltrating lymphocytes and apoptosis in colitis‐associated neoplasia: comparison with sporadic colorectal cancer

Pathways connecting inflammation and cancer

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

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