Abstract

Sporadic fundic gland polyps (FGPs) are ubiquitous benign lesions with no potential for malignant transformation. Familial adenomatous polyposis (FAP) is associated with the development of FGPs that are morphologically identical to but genetically distinct from those seen in sporadic cases. The shared aetiology involves disruption of the WNT signalling pathway, however FAP associated cases are predominantly driven by germline APC gene mutations rather than the somatic CTNNB1 gene mutations prevalent in sporadic lesions.

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