Cancer surveillance in ulcerative colitis

Chambers, William; Warren, Bryan F.; Jewell, D P; Mortensen, N. J. McC.

doi:10.1002/bjs.5106

Cited by 83 publications

(44 citation statements)

References 73 publications

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“…Previous studies in Western countries have reported that UC-CRC often presents as a mucinous or of signet-ring cell type, and it is multiple and more uniformly distributed throughout the colon than sporadic CRC. 37,38 Consistent with these findings, the present study showed that mucinous or signet ring cell type cancer accounted for 17% of the UC-CRCs, which was almost four times higher than among the sporadic CRCs. Furthermore, in 11% of the UC-CRC cases there were multiple lesions, a rate that was almost twice as high as among the sporadic CRC cases.…”

Section: Discussionsupporting

confidence: 93%

Ulcerative colitis-associated colorectal cancer shows a poorer survival than sporadic colorectal cancer: A nationwide Japanese study

Watanabe

Konishi

Kishimoto

et al. 2011

Inflammatory Bowel Diseases

192

139

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Section: Discussionsupporting

confidence: 93%

Ulcerative colitis-associated colorectal cancer shows a poorer survival than sporadic colorectal cancer: A nationwide Japanese study

Watanabe

Konishi

Kishimoto

et al. 2011

Inflammatory Bowel Diseases

192

139

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“…Chronic inflammation and cancer have been linked since the 1850s and current thought has it as a major contributor to cancer pathogenesis. For example, inflammatory bowel diseases such as ulcerative colitis and Crohn's diseases are associated with an increased risk of colorectal cancer [34,35]. Individuals with ulcerative colitis have a 10-fold greater risk of developing colorectal cancer compared to the risk defined for the general population [36][37][38].…”

Section: C1 the Immune System Is Linked To Tumor Development And Prmentioning

confidence: 99%

Tumor immunoediting and immunosculpting pathways to cancer progression

Reiman

Kmieciak

Manjili

et al. 2007

Seminars in Cancer Biology

171

130

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Recent studies have suggested that a natural function of the immune system is to respond and destroy aberrant, dysfunctional cells by a process called immunosurveillance. These studies also suggest that the tumors that arise despite immunosurveillance have been immunosculpted by the immune system. The purported abilities of tumors to induce immune tolerance and suppression, the increased pathogenic behavior of the tumor cells following exposure to immune effectors and the loss of immunogenicity (i.e. immunoediting) often observed in advanced stage tumors could be the result of immunosculpting. In some cases, these immunosculpting features may be permanent and irreversible. However, in other cases, reversible epigenetic mechanisms may underlie the immune resistant tumor phenotype. Regardless, these immune-induced alterations could contribute to cancer pathogenesis. Understanding the mechanisms by which tumors evade immunity will be important for disease prevention and therapeutics.

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“…Colorectal cancer is one of the most serious complications of inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease. The relative risk of colorectal cancer in patient with colitis is two to eight times that of the general population (1). Although it is clear that chronic inflammation is a risk factor of colorectal cancer, the pathogenesis of colitis-associated cancer (CAC) is still uncertain.…”

Section: Introductionmentioning

confidence: 99%

SPINK1 Status in Colorectal Cancer, Impact on Proliferation, and Role in Colitis-Associated Cancer

Ida

Ozaki

Araki

et al. 2015

Molecular Cancer Research

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Colorectal cancer is a major cause of deaths due to cancer; therefore, research into its etiology is urgently needed. Although it is clear that chronic inflammation is a risk factor for colorectal cancer, the details remain uncertain. Serine protease inhibitor, Kazal type 1 (SPINK1) is mainly produced in pancreatic acinar cells. However, SPINK1 is expressed in various cancers and in inflammatory states, such as colon cancer and inflammatory bowel disease. There are structural similarities between SPINK1 and epidermal growth factor (EGF). Hence, it was hypothesized that SPINK1 functions as a growth factor for tissue repair in inflammatory states, and if prolonged, acts as a promoter for cell proliferation in cancerous tissues. Here, immunohistochemical staining for SPINK1 was observed in a high percentage of colorectal cancer patient specimens and SPINK1 induced proliferation of human colon cancer cell lines. To clarify its role in colon cancer in vivo, a mouse model exposed to the colon carcinogen azoxymethane and nongenotoxic carcinogen dextran sodium sulfate revealed that Spink3 (mouse homolog of SPINK1) is overexpressed in cancerous tissues. In Spink3 heterozygous mice, tumor multiplicity and tumor volume were significantly decreased compared with wild-type mice. These results suggest that SPINK1/Spink3 stimulates the proliferation of colon cancer cells and is involved in colorectal cancer progression.Implications: Evidence suggests that SPINK1 is an important growth factor that connects chronic inflammation and cancer.

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Cancer surveillance in ulcerative colitis

Abstract: Rates of detection of dysplasia can be improved by chromoendoscopy. Molecular genetics has the potential to identify patients most at risk of cancer and can differentiate between different types of lesion.

Cited by 83 publications

References 73 publications

Ulcerative colitis-associated colorectal cancer shows a poorer survival than sporadic colorectal cancer: A nationwide Japanese study

Ulcerative colitis-associated colorectal cancer shows a poorer survival than sporadic colorectal cancer: A nationwide Japanese study

Tumor immunoediting and immunosculpting pathways to cancer progression

SPINK1 Status in Colorectal Cancer, Impact on Proliferation, and Role in Colitis-Associated Cancer

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