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Llamoza-Torres et al. Metab Target Organ Damage 2024;4:40             Metabolism and
               DOI: 10.20517/mtod.2024.64
                                                                             Target Organ Damage




               Review                                                                        Open Access


               Metabolic dysfunction-associated steatotic liver
               disease: a key factor in hepatocellular carcinoma

               therapy response


                                                              3
               Camilo Julio Llamoza-Torres 1,2  , María Fuentes-Pardo , Bruno Ramos-Molina 2
               1
                Division of Liver Diseases, Department of Gastroenterology and Hepatology, Virgen de la Arrixaca University Hospital, Murcia
               30120, Spain.
               2
                Obesity, Diabetes and Metabolism Laboratory, Biomedical Research Institute of Murcia (IMIB), Murcia 30120, Spain.
               3
                Family and Community Medicine, Las Torres de Cotillas Health Center, Murcia 30565, Spain.
               Correspondence to: Dr. Camilo Julio Llamoza-Torres, Division of Liver Diseases, Department of Gastroenterology and
               Hepatology, Virgen de la Arrixaca University Hospital, Ctra. Madrid-Cartagena, s/n, El Palmar, Murcia 30120, Spain. Email:
               camiloj.llamoza@carm.es; Dr. Bruno Ramos-Molina, Obesity, Diabetes and Metabolism Laboratory, Biomedical Research
               Institute of Murcia (IMIB), Edificio LAIB, Carretera Buenavista s/n, Murcia 30120, Spain. Email: bruno.ramos@imib.es

               How to cite this article: Llamoza-Torres CJ, Fuentes-Pardo M, Ramos-Molina B. Metabolic dysfunction-associated steatotic liver
               disease: a key factor in hepatocellular carcinoma therapy response. Metab Target Organ Damage 2024;4:40. https://dx.doi.org/
               10.20517/mtod.2024.64

               Received: 31 Jul 2024  First Decision: 29 Aug 2024  Revised: 30 Oct 2024  Accepted: 1 Nov 2024  Published: 13 Nov 2024

               Academic Editors: Gyorgy Baffy, Juan Pablo Arab  Copy Editor: Ting-Ting Hu  Production Editor: Ting-Ting Hu

               Abstract
               The conceptual evolution of non-alcoholic fatty liver disease (NAFLD) to what, since 2023, is called metabolic
               dysfunction-associated steatotic liver disease (MASLD) not only represents a change in the classification and
               definition of the disease but also reflects a broader understanding of this heterogeneous condition, which still with
               many aspects to refine. Although the definition of NAFLD can be interchanged to a high percentage with the new
               MASLD concept in different aspects, MASLD has been proposed as a relevant factor that influences the response
               to new immunotherapeutic treatments in the management of MASLD-related hepatocellular carcinoma (HCC),
               compared to HCC of other etiologies. This indicates that the etiology of HCC plays a relevant role in the prognosis,
               highlighting the urgency of evaluating treatment regimens for this subgroup of patients in upcoming clinical trials.
               A better understanding of the pathophysiology of MASLD generates strategies that not only aid in its management
               but also provide strategies to directly intervene in the carcinogenesis of HCC.

               Keywords: Hepatocellular carcinoma, NAFLD, MASLD, HCC therapy, immunotherapy







                           © The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution 4.0
                           International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing,
                           adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as
               long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and
               indicate if changes were made.

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