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EMT and Inflammation: Crossroads in HCC

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dc.contributor.author Sengez, B.
dc.contributor.author Carr, B.I.
dc.contributor.author Alotaibi, H.
dc.date.accessioned 2022-10-06T12:55:09Z
dc.date.available 2022-10-06T12:55:09Z
dc.date.issued 2022
dc.identifier.issn 19416628 (ISSN)
dc.identifier.uri http://hdl.handle.net/11616/72613
dc.description.abstract Hepatocellular carcinoma is one of the major causes of cancer-related deaths worldwide and is associated with several inflammatory mediators, since 90% of HCCs occur based on chronic hepatitis B or C, alcoholism or increasingly metabolic syndrome-associated inflammation. EMT is a physiological process, with coordinated changes in epithelial gene signatures and is regulated by multiple factors, including cytokines and growth factors such as TGFβ, EGF, and FGF. Recent reports propose a strong association between EMT and inflammation, which is also correlated with tumor aggressiveness and poor outcomes. Cellular heterogeneity results collectively as an outcome of EMT, inflammation, and the tumor microenvironment, and it plays a fundamental role in the progression, complexity of cancer, and chemoresistance. In this review, we highlight recent developments concerning the association of EMT and inflammation in the context of HCC progression. Identifying potential EMT-related biomarkers and understanding EMT regulatory molecules will likely contribute to promising developments in clinical practice and will be a valuable tool for predicting metastasis in general and specifically in HCC. © 2022, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
dc.source Journal of Gastrointestinal Cancer
dc.title EMT and Inflammation: Crossroads in HCC


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