Cancer risk in patients with inflammatory bowel disease

Bernstein, Çharles N.; Blanchard, James; Kliewer, Erich V.; Wajda, André

doi:10.1002/1097-0142(20010215)91:4<854::aid-cncr1073>3.0.co;2-z

Cited by 1,078 publications

(679 citation statements)

References 47 publications

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“…Typically histological features of UC are different from CrD and include mononuclear inflammation in the lamina propria, crypt distortion, and goblet cell (mucin) depletion. The relative risk for colorectal cancer is increased in patients with CrD and UC compared to the non-IBD population and is associated with the anatomic expanse of inflammation, duration of disease, and presence of additional risk factors (e.g., primary sclerosing cholangitis) [8,9]. Patients with CrD have also an increased risk for small bowel cancer [10].…”

Section: Autoimmunity In Crohn's Diseasementioning

confidence: 99%

Crohn’s disease specific pancreatic antibodies: clinical and pathophysiological challenges

Roggenbuck¹,

Reinhold

Schierack

et al. 2014

Clinical Chemistry and Laboratory Medicine

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Crohn's disease (CrD) and ulcerative colitis (UC) are the main inflammatory bowel diseases (IBD). IBDspecific humoral markers of autoimmunity in the form of autoantibodies have been reported first in the late 1950s by demonstrating the occurrence of autoimmunity in UC, while humoral autoimmunity in CrD can be traced back to the 1970s. Ever since, the pathophysiological role of autoimmune responses in IBDs has remained poorly understood. Notwithstanding, autoreactive responses play a major role in inflammation leading to overt IBD. In CrD, approximately 40% of patients and < 20% of patients with UC demonstrate loss of tolerance to antigens of the exocrine pancreas. Glycoprotein 2 (GP2) has been identified as a major autoantigenic target of the so-called pancreatic antibodies. The previously unsolved contradiction of pancreatic autoreactivity and intestinal inflammation in IBD was elucidated by demonstrating the expression of GP2 at the site thereof. Intriguingly, GP2 has been reported to be a receptor on microfold cells of intestinal Peyer's patches, which are believed to represent the origin of CrD inflammation. The development of immunoassays for the detection of antibodies to GP2 has paved the way to investigate the association of such antibodies with the clinical phenotype in CrD. Given the recently discovered immunomodulating role of GP2 in innate and adaptive intestinal immunity, this association can shed further light on the pathophysiology of IBD. In this context, the association of anti-GP2 autoantibodies as novel CrD-specific markers with the clinical phenotype in CrD will be discussed in this review.

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Section: Autoimmunity In Crohn's Diseasementioning

confidence: 99%

Crohn’s disease specific pancreatic antibodies: clinical and pathophysiological challenges

Roggenbuck¹,

Reinhold

Schierack

et al. 2014

Clinical Chemistry and Laboratory Medicine

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“…This approach has been developed in an attempt to prevent death from colorectal cancer in patients with chronic ulcerative colitis. A similar approach is also employed in Crohn's disease of the colon, where the risk of colorectal cancer is less well-described but appears to be similar to ulcerative colitis [1,2]. In ulcerative colitis, the risk of colorectal cancer is associated with longer duration of disease, greater extent of colonic involvement, presence of primary sclerosing cholangitis, and a family history of colorectal cancer [3].…”

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confidence: 99%

Surveillance of Dysplasia in Inflammatory Bowel Disease: The Gastroenterologist-Pathologist Partnership

Rubin

Turner

2006

Clinical Gastroenterology and Hepatology

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Cancer prevention in inflammatory bowel disease depends on the detection of precancerous dysplasia during scheduled screening and surveillance colonoscopy, but the detection and diagnosis of dysplasia remains challenging. In this article, we review the risks of cancer and dysplasia in ulcerative colitis, the current prevention recommendations and, through a sample case, demonstrate an approach that involves an active partnership between the gastroenterologist or surgeon and pathologist. We address the challenge of management of polypoid lesions and incorporate new information about degree of inflammation as an additional risk of neoplasia in these patients. Keywords ulcerative colitis; surveillance; dysplasia; colorectal cancer Case PresentationA 45 year-old man with left-sided ulcerative colitis diagnosed at age 21 is seen in your office as a new patient and inquires about colorectal cancer prevention. He has undergone periodic surveillance colonoscopy since he was in his early 30s and his last examination was performed 2 years ago and revealed no dysplasia. After discussing current guidelines, you recommend an endoscopic examination with surveillance biopsies. Colonoscopy reveals vascular blunting and minimal touch friability diffusely from the rectum to the hepatic flexure, and an endoscopically normal ascending colon and cecum. This also a 2 cm polypoid lesion with exudate on its surface (Figure 1), but no masses or strictures. You obtain numerous surveillance biopsies throughout the colon and perform snare polypectomy of the polyp, with additional biopsies of the flat mucosa surrounding it. You submit these to the Pathology Department along with a report of the patient's history and these endoscopic findings. Your pathologist calls to report that all of the biopsies show mild active inflammation and architectural distortion, typical of mildlyactive chronic ulcerative colitis, and the polyp appears inflammatory in nature (Figure 2). However, there are also two separate biopsies from non-polypoid areas that include low grade dysplasia. A second gastrointestinal pathologist was consulted and concurs with the diagnosis of mulitfocal low grade dysplasia. You inform the patient and recommend proctocolectomy and ileo-pouch anal anastomosis, to which he agrees. The colectomy specimen reveals several Address correspondence to: David T. Rubin, MD 5841 S. Maryland Ave. MC 4076 Chicago, IL 60637 drubin@uchicago.edu 773-702-2950. Dr. Rubin and Dr. Turner have no conflicts of interest related to this publication Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errorsmaybe discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Acce...

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“…Indeed, p53 mutations are seen at frequencies similar to those in cancers in chronic inflammatory diseases such as rheumatoid arthritis and inflammatory bowel disease 37. The strongest association of chronic inflammation with cancers is in colon and liver carcinogenesis arising in individuals with inflammatory bowel diseases 38. Some specific cancers such as colon, liver, pancreas, breast, prostate, hematology, head and neck and skin cancers where the inflammatory process is a cofactor in carcinogenesis 34, 35, 39, 40, 41, 42, 43.…”

Section: Discussionmentioning

confidence: 99%

Recurrent aphthous stomatitis may be a precursor or risk factor for specific cancers: A case‐control frequency‐matched study

et al. 2018

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BackgroundRecurrent aphthous stomatitis (RAS) is considered a prophase symptom in patients with specific cancers. This study assessed the association between RAS and subsequent onset of cancer based on a nationwide population‐based database in Taiwan.Materials and MethodsWe selected study participants from the National Health Insurance Research Database from January 2000 to December 2008. Patients in the non‐RAS cohort were matched to case study patients at a 1:1 ratio through frequency matching. All participants were followed up for at least 5 years, and those who received cancer diagnoses during follow‐up were identified.ResultsAmong 52 307 patients with and 52 304 patients without RAS, the combined hazard ratio (HR) of all subsequent cancer cases was 1.3 (95% confidence interval [CI]: 1.25‐1.35, P = 0). RAS diagnosis was associated with risk for cancers of the head and neck (aHR = 2, 95% CI: 1.8‐2.3), colon (aHR = 1.2, 95% CI: 1.1‐1.4), liver (aHR = 1.1, 95% CI: 1‐1.3), pancreas (aHR = 1.4, 95% CI: 1.1‐1.7), skin (aHR = 1.4, 95% CI: 1.2‐1.7), breast (aHR = 1.2, 95% CI: 1.1‐1.4), and prostate (aHR = 1.5, 95% CI: 1.3‐1.8), as well as hematologic cancers (aHR = 1.6, 95% CI: 1.3‐1.9). A higher risk was observed for male patients (aHR = 1.35, 95% CI: 1.28‐1.42) than for female patients (aHR = 1.25, 95% CI: 1.18‐1.31) with RAS.Conclusions RAS was associated with specific cancers. Susceptible RAS patients should be screened for specific cancers.

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Cancer risk in patients with inflammatory bowel disease

Cited by 1,078 publications

References 47 publications

Crohn’s disease specific pancreatic antibodies: clinical and pathophysiological challenges

Crohn’s disease specific pancreatic antibodies: clinical and pathophysiological challenges

Surveillance of Dysplasia in Inflammatory Bowel Disease: The Gastroenterologist-Pathologist Partnership

Recurrent aphthous stomatitis may be a precursor or risk factor for specific cancers: A case‐control frequency‐matched study

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