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With improved survival into mid\u2010 and late adulthood, aided by newborn screening, optimised nutrition and the advent of highly effective CF transmembrane conductance regulator (CFTR) modulators, implementation of colonoscopic surveillance has highlighted a several\u2010fold increase in early\u2010onset colorectal cancer (CRC) and a broader spectrum of intestinal pathology. In parallel, work in mouse models, human tissue and patient\u2010derived intestinal organoids now places the CFTR at the centre of a complex epithelial compartment that integrates ion and pH homeostasis, mucus biology, microbiota, redox balance and immune\/stromal function. In this review, we advance the hypothesis that CF may be conceptualised as a niche\u2010centric hereditary CRC predisposition syndrome, in which germline CFTR dysfunction chronically destabilises epithelial identity in addition to increasing mutational burden. We synthesise evidence that CFTR loss remodels stem cell regulation, promotes hypoxia and oxidative stress, perturbs microbial ecosystems, drives chronic immune activation and stromal remodelling, and induces epithelial\u2013mesenchymal plasticity (EMP) and DNA\u2010damage vulnerability, collectively creating a pre\u2010neoplastic intestinal ecosystem. We situate this model within contemporary CRC frameworks that emphasise cell\u2010state transitions, hybrid epithelial\u2013mesenchymal (E\/M) states and specialised stromal niches, and we distinguish it from oncofoetal reprogramming, an\n                    <jats:italic>APC<\/jats:italic>\n                    \u2010driven programme that CF does not clearly recapitulate. We propose that CF may provide a naturally occurring human context in which chronic epithelial stress sustains EMP\u2010like pressure, a concept that requires direct validation in human CF intestinal tissue. Finally, we consider how CFTR modulators, microbiome\u2010directed therapies and redox\u2010targeted interventions might re\u2010programme the CF intestinal niche and outline experimental and clinical strategies needed to determine whether early, ecosystem\u2010level correction can prevent GI cancers in this high\u2010risk population.\n                  <\/jats:p>","DOI":"10.1111\/cpr.70272","type":"journal-article","created":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T04:15:19Z","timestamp":1786940119000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Cystic Fibrosis and Colorectal Cancer Risk: Reprogramming of the Intestinal Epithelial Niche and Cell\u2010State Plasticity in the\n                    <scp>CFTR<\/scp>\n                    Modulator Era"],"prefix":"10.1111","volume":"59","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0796-5273","authenticated-orcid":false,"given":"Bala","family":"Umashankar","sequence":"first","affiliation":[{"name":"School of Biomedical Sciences, Faculty of Medicine and Health UNSW Sydney  Sydney New South Wales Australia"},{"name":"Molecular and Integrative Cystic Fibrosis (miCF) Research Centre UNSW Sydney  Sydney New South Wales Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ines","family":"Pankonien","sequence":"additional","affiliation":[{"name":"BioISI\u2014Biosystems &amp; Integrative Sciences Institute, Faculty of Sciences University of Lisbon  Lisbon Portugal"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0828-8630","authenticated-orcid":false,"given":"Margarida","family":"Amaral","sequence":"additional","affiliation":[{"name":"BioISI\u2014Biosystems &amp; Integrative Sciences Institute, Faculty of Sciences 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