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Alternative Splicing at the Crossroad of Inflammatory Bowel Diseases and Colitis-Associated Colon Cancer

datacite.subject.fosCiências Médicas::Ciências da Saúde
datacite.subject.sdg03:Saúde de Qualidade
dc.contributor.authorMatos, Paulo
dc.contributor.authorJordan, Peter
dc.date.accessioned2025-11-11T13:51:18Z
dc.date.available2025-11-11T13:51:18Z
dc.date.issued2025-01-11
dc.description(This article belongs to the Special Issue Advances in Molecular Oncology and Therapeutics)
dc.description.abstractSimple Summary: Patients with ulcerative colitis (UC) face a higher risk of developing colorectal cancer (CRC) due to chronic inflammation, a known promoter of tumour growth. Here, we review the molecular differences between colitis-associated cancer (CAC) and sporadic CRC, with a focus on “alternative splicing”, a mechanism by which the same gene can produce various protein forms. We explore how inflammation triggers changes in this process, increasing cancer risk for UC patients. The revised data emphasize that additional research into these molecular changes could help identify new biomarkers (molecules that indicate disease progression) and pave the way for innovative treatments targeting these alterations. Such advances would improve outcomes and quality of life for patients while contributing to cancer prevention and care.por
dc.description.abstractAbstract: The risk of developing colorectal cancer (CRC) is increased in ulcerative colitis patients compared to the general population. This increased risk results from the state of chronic inflammation, a well-known tumour-promoting condition. This review explores the pathologic and molecular characteristics of colitis-associated colon cancer (CAC), emphasizing the distinct features from sporadic CRC. We focus on the key signalling pathways involved in the transition to CAC, highlighting the emerging role of alternative splicing in these processes, namely on how inflammation-induced alternative splicing can significantly contribute to the increased CRC risk observed among UC patients. This review calls for more transcriptomic studies to elucidate the molecular mechanisms through which inflammation-induced alternative splicing drives CAC pathogenesis. A better understanding of these splicing events is crucial as they may reveal novel biomarkers for disease progression and have the potential to target changes in alternative splicing as a therapeutic strategy.por
dc.description.sponsorshipWork in the authors’ laboratory was supported by Fundação para a Ciência e a Tecnologia (FCT), Portugal, through grant doi: 10.54499/UIDB/04046/2020 to Research Unit BioISI—Biosystems & Integrative Sciences Institute, Faculty of Sciences, University of Lisbon, Portugal
dc.identifier.citationCancers (Basel). 2025 Jan 11;17(2):219. doi: 10.3390/cancers1702021
dc.identifier.doi10.3390/cancers17020219
dc.identifier.eissn2072-6694
dc.identifier.pmid39858001
dc.identifier.urihttp://hdl.handle.net/10400.18/10589
dc.language.isoeng
dc.peerreviewedyes
dc.publisherMDPI
dc.relationBiosystems and Integrative Sciences Institute
dc.relation.hasversionhttps://www.mdpi.com/2072-6694/17/2/219
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectAlternative Splicing
dc.subjectColitis-associated Cancer
dc.subjectInterleukin
dc.subjectSignalling Pathway
dc.subjectSplicing Factor
dc.subjectVias de Transdução de Sinal
dc.titleAlternative Splicing at the Crossroad of Inflammatory Bowel Diseases and Colitis-Associated Colon Cancereng
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleBiosystems and Integrative Sciences Institute
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/6817 - DCRRNI ID/UIDB%2F04046%2F2020/PT
oaire.citation.issue2
oaire.citation.startPage219
oaire.citation.titleCancers
oaire.citation.volume17
oaire.fundingStream6817 - DCRRNI ID
oaire.versionhttp://purl.org/coar/version/c_970fb48d4fbd8a85
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
relation.isProjectOfPublicationdc433369-36fd-4935-bd52-c56aa49c72e1
relation.isProjectOfPublication.latestForDiscoverydc433369-36fd-4935-bd52-c56aa49c72e1

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