Article Figures & Data
Figures
- Figure 1.
Key alterations within the colitis-associated colorectal cancer dysplasia–carcinoma sequence. COX-2, cyclooxygenase-2; ECM, extra-cellular matrix; LPS, lipopolysaccharide; MMR, mismatch repair mutation; TNF, tumor necrosis factor; VEGF, vascular endolethial growth factor.
- Figure 2.
Clinical approach to endoscopic dysplasia surveillance and management based on the SCENIC consensus, ref. 99.
Tables
- Table 1.
Clinical risk factors for colitis-associated colorectal cancer
Age of Onset Increased risk among those diagnosed with IBD at a younger age (≤ 15 years) Disease Extent Crohn's disease: Increased risk when more than 30%–50% of colonic mucosa involved Ulcerative colitis: 10- to 15-fold increased risk with pancolitis throughout disease duration, followed by 2-fold increased risk with left-sided colitis (distal to splenic flexure) until the fourth decade of disease when estimates mirror those of pancolitis, and no risk with proctitis (rectum) Disease Duration and Severity Risk increases with increasing disease severity (endoscopic and histology) and becomes most apparent after 7–10 y with a linear increase thereafter Inflammatory Complications Foreshortened colon, strictures, inflammatory pseudopolyps PSC Predominately right-sided lesions and increased risk present at time of diagnosis as compared with non-PSC IBD patients where risk is apparent after 7–10 y of disease duration. Increased CRC risk remains even after liver transplant and proctocolectomy (i.e., cancer of the pouch). Personal and Family History Additional risk of CRC in IBD patients with a family history of CRC similar to general population. Personal history of dysplasia confers increased risk of synchronous or metachronous CRC Abbreviation: CRC, colorectal cancer.
- Table 2.
Surveillance intervals and strategies
High risk (annually) Intermediate risk (every 3 y) Low risk (every 5 y) Risk-stratified intervals NICE, ECCO, and BSG (85–87) Pancolitis with moderate to severe inflammation; strictures or dysplasia within past 5 y (±surgery), PSC, or family history of CRC in first degree relative > 50 y Pancolitis with active inflammation (endoscopic or histologic); presence of pseudopolyps or family history of CRC in first-degree relative > 50 y Pancolitis without inflammation (endoscopic or histology); left-sided UC or CD of similar extent (i.e., <50% mucosa involved)a Nonstratified intervals ASGE, ACG, and AGA (78, 88, 89) Active inflammation (any severity), anatomic abnormalities (foreshortened colons, strictures or pseudopolyps), history of dysplasia, PSC, or family history of CRC in first-degree relative (irrespective of age) Extension to 1 to 3 years considered after 2 consecutive negative surveillance colonoscopies and no inflammation (no specification on how to lengthen interval) No recommendation to extend to 5-y intervals Abbreviations: ACG, American College of Gastroenterology; AGA: American Gastroenterology Association; ASGE, American Society of Gastrointestinal Endoscopy; BSG, British Society of Gastroenterology; CD, Crohn disease; CRC, colorectal cancer; ECCO, European Crohn's and Colitis Organization; NICE, National Institute of Health and Clinical Excellence; UC, ulcerative colitis.
↵aECCO guidelines do not have specific low-risk criteria. Low risk is those without high or intermediate risk.
- Table 3.
Unanswered questions and future research
Epidemiology and Risk Factors Population level incidence, prevalence, and trends using accurate classification and selection
Incidence and risk for dysplasia and colitis-associated CRC with strictures and identifying strictures associated with an increased risk for harboring dysplasia or colitis-associated CRC
Incremental impact of having multiple risk factors present at baseline or over time
Molecular Basis and Targets of Carcinogenesis Whole-exome sequencing of early dysplasia to understand sequence of genetic alterations
Predictive and prognostic importance of genetic alterations for progression to CRC
Targeted chemoprevention and personalized treatment of early dysplastic lesions with a particular emphasis on NF-κB inhibition, anti-interleukin, and anti-cytokine biologics
Surveillance and Endoscopic Management Risk-stratified surveillance techniques and impact on disease outcomes
Noninvasive surveillance techniques (stool- or blood-based DNA testing)
Comparative effectiveness of enhanced visualization techniques
Volume 9, Issue 12
