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Review
. 2024 Apr 17:9:27.
doi: 10.21037/tgh-23-36. eCollection 2024.

From random to precise: updated colon cancer screening and surveillance for inflammatory bowel disease

Affiliations
Review

From random to precise: updated colon cancer screening and surveillance for inflammatory bowel disease

Karina Fatakhova et al. Transl Gastroenterol Hepatol. .

Abstract

Patients with inflammatory bowel disease (IBD) are at increased risk of developing colorectal cancer (CRC). The pathogenesis of CRC in IBD differs from sporadic cancer, with the burden of inflammation being an important contributing factor. Other risk factors for developing CRC in patients with Crohn's disease (CD) or ulcerative colitis (UC) includes a family history of CRC, personal history of dysplasia, history of strictures, or primary sclerosing cholangitis (PSC). Dysplasia is the precursor of cancer and ensuring effective surveillance strategies is vital for early detection and intervention. In the past, dysplasia detection relied on random biopsies, but recent studies have shown that, with the adaptation of high-definition white light endoscopy (HD-WLE), dye sprayed chromoendoscopy (DCE) and virtual chromoendoscopy (VCE), dysplasia detection has improved. While there exists a certain degree of consensus amongst experts regarding the management of dysplasia, it is important to implement a personalized approach to each patient's care. Our review focuses on advancements in the past two decades, specifically highlighting the modifications that have been implemented since the SCENIC guidelines. It also explores future directions, including the potential implementation of stool studies as a non-invasive tool for surveillance and the emerging role of artificial intelligence (AI) in dysplasia detection.

Keywords: Crohn’s disease (CD); Inflammatory bowel disease (IBD); colorectal cancer (CRC); colorectal cancer screening (CRC screening); ulcerative colitis (UC).

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Conflict of interest statement

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://tgh.amegroups.com/article/view/10.21037/tgh-23-36/coif). The series “Controversies and Updates in Inflammatory Bowel Disease” was commissioned by the editorial office without any funding or sponsorship. The authors have no other conflicts of interest to declare.

Figures

Figure 1
Figure 1
Pathogenesis of CRC in IBD. CRC, colorectal cancer; IBD, inflammatory bowel disease.
Figure 2
Figure 2
Molecular pathogenesis of sporadic versus colitis-associated cancer. Permission was obtained to reuse the figure by publisher (23). APC, adenomatous polyposis coli; CRC, colorectal cancer; CAC, colitis-associated cancer; MSI, microsatellite instability; COX2, cyclooxygenase 2; KRAS, Kirsten rat sarcoma viral oncogene homolog; DCC, deleted in colorectal carcinoma; DPC4, deleted in pancreatic carcinoma 4; TP53, tumor suppressor P53; CIN, chromosomal instability; TGF, transforming growth factor.
Figure 3
Figure 3
Pseudopolyps highlighted by dye-sprayed chromoendoscopy using methylene blue.

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