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Article: Gut microbiota alterations are distinct for primary colorectal cancer and hepatocellular carcinoma

TitleGut microbiota alterations are distinct for primary colorectal cancer and hepatocellular carcinoma
Authors
Keywordscolorectal cancer
gut microbiota
hepatocellular carcinoma
Issue Date2021
Citation
Protein and Cell, 2021, v. 12, n. 5, p. 374-393 How to Cite?
AbstractColorectal cancer (CRC) and hepatocellular carcinoma (HCC) are the second and third most common causes of death by cancer, respectively. The etiologies of the two cancers are either infectious insult or due to chronic use of alcohol, smoking, diet, obesity and diabetes. Pathological changes in the composition of the gut microbiota that lead to intestinal inflammation are a common factor for both HCC and CRC. However, the gut microbiota of the cancer patient evolves with disease pathogenesis in unique ways that are affected by etiologies and environmental factors. In this review, we examine the changes that occur in the composition of the gut microbiota across the stages of the HCC and CRC. Based on the idea that the gut microbiota are an additional “lifeline” and contribute to the tumor microenvironment, we can observe from previously published literature how the microbiota can cause a shift in the balance from normal → inflammation → diminished inflammation from early to later disease stages. This pattern leads to the hypothesis that tumor survival depends on a less pro-inflammatory tumor microenvironment. The differences observed in the gut microbiota composition between different disease etiologies as well as between HCC and CRC suggest that the tumor microenvironment is unique for each case.
Persistent Identifierhttp://hdl.handle.net/10722/342607
ISSN
2023 Impact Factor: 13.6
2023 SCImago Journal Rankings: 4.412
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorJia, Wei-
dc.contributor.authorRajani, Cynthia-
dc.contributor.authorXu, Hongxi-
dc.contributor.authorZheng, Xiaojiao-
dc.date.accessioned2024-04-17T07:05:00Z-
dc.date.available2024-04-17T07:05:00Z-
dc.date.issued2021-
dc.identifier.citationProtein and Cell, 2021, v. 12, n. 5, p. 374-393-
dc.identifier.issn1674-800X-
dc.identifier.urihttp://hdl.handle.net/10722/342607-
dc.description.abstractColorectal cancer (CRC) and hepatocellular carcinoma (HCC) are the second and third most common causes of death by cancer, respectively. The etiologies of the two cancers are either infectious insult or due to chronic use of alcohol, smoking, diet, obesity and diabetes. Pathological changes in the composition of the gut microbiota that lead to intestinal inflammation are a common factor for both HCC and CRC. However, the gut microbiota of the cancer patient evolves with disease pathogenesis in unique ways that are affected by etiologies and environmental factors. In this review, we examine the changes that occur in the composition of the gut microbiota across the stages of the HCC and CRC. Based on the idea that the gut microbiota are an additional “lifeline” and contribute to the tumor microenvironment, we can observe from previously published literature how the microbiota can cause a shift in the balance from normal → inflammation → diminished inflammation from early to later disease stages. This pattern leads to the hypothesis that tumor survival depends on a less pro-inflammatory tumor microenvironment. The differences observed in the gut microbiota composition between different disease etiologies as well as between HCC and CRC suggest that the tumor microenvironment is unique for each case.-
dc.languageeng-
dc.relation.ispartofProtein and Cell-
dc.subjectcolorectal cancer-
dc.subjectgut microbiota-
dc.subjecthepatocellular carcinoma-
dc.titleGut microbiota alterations are distinct for primary colorectal cancer and hepatocellular carcinoma-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s13238-020-00748-0-
dc.identifier.pmid32797354-
dc.identifier.scopuseid_2-s2.0-85089378188-
dc.identifier.volume12-
dc.identifier.issue5-
dc.identifier.spage374-
dc.identifier.epage393-
dc.identifier.eissn1674-8018-
dc.identifier.isiWOS:000559701100001-

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