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Chemically induced colitis-associated cancer models in rodents for pharmacological modulation: a systematic review

2022-05Journal article Open access
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dc.contributor.authorModesto, Rita
dc.contributor.authorEstarreja, João
dc.contributor.authorSilva, Inês
dc.contributor.authorRocha, João
dc.contributor.authorPinto, Rui
dc.contributor.authorMateus, Vanessa
dc.date.accessioned2022-05-23T12:11:42Z
dc.date.available2022-05-23T12:11:42Z
dc.date.issued2022-05
dc.descriptionProject IPL/2021/PharmCAC_ESTeSL.pt_PT
dc.descriptionFCT_UIDB/05608/2020. FCT_UIDP/05608/2020.pt_PT
dc.description.abstractAnimal models for colitis-associated colorectal cancer (CACC) represent an important tool to explore the mechanistic basis of cancer-related inflammation, providing important evidence that several inflammatory mediators play specific roles in the initiation and perpetuation of colitis and CACC. Although several original articles have been published describing the CACC model in rodents, there is no consensus about the induction method. This review aims to identify, summarize, compare, and discuss the chemical methods for the induction of CACC through the PRISMA methodology. Methods: We searched MEDLINE via the Pubmed platform for studies published through March 2021, using a highly sensitive search expression. The inclusion criteria were only original articles, articles where a chemically-induced animal model of CACC is described, preclinical studies in vivo with rodents, and articles published in English. Results: Chemically inducible models typically begin with the administration of a carcinogenic compound (as azoxymethane (AOM) or 1,2-dimethylhydrazine (DMH)), and inflammation is caused by repeated cycles of colitis-inducing agents (such as 2,4,6-trinitrobenzenesulfonic acid (TNBS) or dextran sulfate sodium (DSS)). The strains mostly used are C57BL/6 and Balb/c with 5–6 weeks. To characterize the preclinical model, the parameters more used include body weight, stool consistency, and morbidity, inflammatory biomarkers such as tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β, angiogenesis markers such as proliferating cell nuclear antigen (PCNA), a marker of proliferation Ki-67, and caspase 3, the presence of ulcers, thickness or hyperemia in the colon, and histological evaluation of inflammation. Conclusion: The AOM administration seems to be important to the CACC induction method since the carcinogenic effect is achieved with just one administration. DSS has been the more used inflammatory agent; however, the TNBS contribution should be more studied, since it allows a reliable, robust, and highly reproducible animal model of intestinal inflammation.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationModesto R, Estarreja J, Silva IJ, Rocha J, Pinto R, Mateus V. Chemically induced colitis-associated cancer models in rodents for pharmacological modulation: a systematic review. J Clin Med. 2022;11(10):2739.pt_PT
dc.identifier.doi10.3390/jcm11102739pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.21/14656
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.relationIPL/2021/ PharmCAC_ESTeSLpt_PT
dc.relation.publisherversionhttps://www.mdpi.com/2077-0383/11/10/2739pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/pt_PT
dc.subjectColitispt_PT
dc.subjectColorectal cancerpt_PT
dc.subjectPreclinical studiespt_PT
dc.subjectDisease animal modelspt_PT
dc.subjectAnimal experimentationpt_PT
dc.subjectIPL/2021/ PharmCAC_ESTeSLpt_PT
dc.subjectFCT_UIDB/05608/2020pt_PT
dc.subjectFCT_UIDP/05608/2020pt_PT
dc.titleChemically induced colitis-associated cancer models in rodents for pharmacological modulation: a systematic reviewpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.issue10pt_PT
oaire.citation.startPage2739pt_PT
oaire.citation.titleJournal of Clinical Medicinept_PT
oaire.citation.volume11pt_PT
person.familyNameEstarreja
person.familyNameda Silva
person.familyNamePinho Mateus
person.givenNameJoão
person.givenNameInês Filipa Janeiro da Silva
person.givenNameVanessa Alexandra
person.identifier.ciencia-idEB19-EDA2-704B
person.identifier.ciencia-idC010-323F-3266
person.identifier.ciencia-id5A12-571D-AD6A
person.identifier.orcid0000-0002-8283-3174
person.identifier.orcid0000-0001-7049-2512
person.identifier.orcid0000-0002-3204-3772
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublicationd16a20d0-ac73-4989-b83d-abeab53139f7
relation.isAuthorOfPublication995e1831-ff5b-49e7-a6e3-8bc692212204
relation.isAuthorOfPublication406041a5-682c-4f94-a4e2-ddbfc541313c
relation.isAuthorOfPublication.latestForDiscoveryd16a20d0-ac73-4989-b83d-abeab53139f7

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