Roel Bogie

Chapter 1

that LSTs have a typical morphology because of specific molecular alterations that could go hand in hand with an accelerated adenoma-carcinoma sequence. So, LSTs have the potential to become invasive and share features with PCCRCs. However, direct evidence is lacking and it remains unclear to what extent LSTs contribute to development of PCCRCs.

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Often proximal location

Often proximal location

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Di cult endoscopic resection

Residue/ recurrence

Incomplete resection

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Subtle appearence

Missed lesions

Newly developed CRC

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Patient at higher risk

More CRNs

Speci c modular pro les

Speci c modular pro les

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Flat appearance

Often at appearance

Figure 1.3: Hypothetical links between LSTs and PCCRCs.

Link with inflammatory bowel disease Patients with inflammatory bowel disease (IBD) have an increased risk of developing CRC. 39 Instead of the classic adenoma-carcinoma sequence, the chronic effect of cytokines an chemokines caused by inflammation leads to dysplasia which could eventually turn into carcinoma. PCCRCs are also more common among IBD patients, reporting 15.1% of all CRCs in Crohn disease patients and 15.8% in ulcerative colitis patients within a hospital population. 40 More recent data on IBD related CRC risk from the general population are lacking. Besides IBD associated CRC, IBD patients are also at risk of common CRC but are excluded from the national screening programs. Patients are therefore dependent on IBD specific surveillance that starts 8 years after onset of IBD. 41 The risk of PCCRCs may be increased by difficult detection of IBD associated dysplasia, higher prevalence of flat lesions and a shortened duration of the carcinogenic process induced by inflammation. 39

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