De Santis, S and Liso, M and Vacca, M and Verna, G and Cavalcanti, E and Coletta, S and Calabrese, FM and Eri, R and Lippolis, A and Armentano, R and Mastronardi, M and De Angelis, M and Chieppa, M, Dysbiosis triggers ACF development in genetically predisposed subjects, Cancers, 13, (2) pp. 1-21. ISSN 2072-6694 (2021) [Refereed Article]
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Background: Colorectal cancer (CRC) is the third most common cancer worldwide, characterized by a multifactorial etiology including genetics, lifestyle, and environmental factors including microbiota composition. To address the role of microbial modulation in CRC, we used our recently established mouse model (the Winnie-APCMin/+) combining inflammation and genetics.
Methods: Gut microbiota profiling was performed on 8-week-old Winnie-APCMin/+ mice and their littermates by 16S rDNA gene amplicon sequencing. Moreover, to study the impact of dysbiosis induced by the mother's genetics in ACF development, the large intestines of APCMin/+ mice born from wild type mice were investigated by histological analysis at 8 weeks.
Results: ACF development in 8-week-old Winnie-APCMin/+mice was triggered by dysbiosis. Specifically, the onset of ACF in genetically predisposed mice may result from dysbiotic signatures in the gastrointestinal tract of the breeders. Additionally, fecal transplant from Winnie donors to APCMin/+ hosts leads to an increased rate of ACF development.
Conclusions: The characterization of microbiota profiling supporting CRC development in genetically predisposed mice could help to design therapeutic strategies to prevent dysbiosis. The application of these strategies in mothers during pregnancy and lactation could also reduce the CRC risk in the offspring.
|Item Type:||Refereed Article|
|Keywords:||colorectal cancer, microbiota, dysbiosis, ulcerative colitis, murine model|
|Research Division:||Biological Sciences|
|Research Field:||Genetic immunology|
|Objective Group:||Clinical health|
|Objective Field:||Clinical health not elsewhere classified|
|UTAS Author:||Eri, R (Associate Professor Raj Eri)|
|Web of Science® Times Cited:||2|
|Deposited By:||Health Sciences|
|Downloads:||2 View Download Statistics|
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