Hepatocellular carcinoma (HCC) is a major cause of death among patients with liver cirrhosis. The rise of immuno-oncology has revolutionized treatment for advanced HCC. However, most pivotal randomized controlled trials have excluded patients with moderate liver dysfunction (Child-Pugh-Turcotte B), despite the high incidence of liver disease in patients with HCC at the time of diagnosis. Overall survival in patients with HCC and moderate liver dysfunction treated with sorafenib has been found to be only approximately 3-5 months, underlining the need for improved treatment algorithms for this increasingly important subgroup of patients. In this review, we summarize available data on the treatment of patients with HCC and moderate liver dysfunction. Opportunities, as well as clinical challenges, are discussed in detail, highlighting potential changes to the therapeutic landscape.
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http://dx.doi.org/10.1002/cam4.6033 | DOI Listing |
Curr Nutr Rep
January 2025
Faculty of Pharmaceutical Science, Assam down town University, Sankar Madhab Path, Gandhi Nagar, Panikhaiti, Guwahati, Assam, India, PIN - 781026.
Purpose Of Review: The term metabolic dysfunction-associated steatotic liver disease (MASLD) refers to a group of progressive steatotic liver conditions that include metabolic dysfunction-associated steatohepatitis (MASH), which has varying degrees of liver fibrosis and may advance to cirrhosis, and independent hepatic steatosis. MASLD has a complex underlying mechanism, with patients exhibiting diverse causes and phases of the disease. India has a pool prevalence of MASLD of 38.
View Article and Find Full Text PDFJ Gen Intern Med
January 2025
College of Medicine, Mohammed Bin Rashid University of Medicine and Health Sciences, Dubai, United Arab Emirates.
Background: Type 2 diabetes mellitus (T2DM) and metabolic dysfunction-associated steatotic liver disease (MASLD), which have a reciprocal relationship compounded by obesity, are highly prevalent in the Middle East affecting morbidity, mortality, and healthcare costs.
Objective: This study aimed to assess the severity of MASLD and liver fibrosis among adult Emirati patients with long-standing T2DM.
Design And Participants: This cross-sectional study used noninvasive methods to assess the severity of MASLD and fibrosis progression in an adult cohort of Emirati patients (N = 546) with a mean T2DM duration of 16 years.
Proc Natl Acad Sci U S A
January 2025
Gene Expression Laboratory, Salk Institute, La Jolla, CA 92037-1002.
Nutritional status is a determining factor for growth during development and homeostatic maintenance in adulthood. In the context of muscle, growth hormone (GH) coordinates growth with nutritional status; however, the detailed mechanisms remain to be fully elucidated. Here, we show that the transcriptional repressor B cell lymphoma 6 (BCL6) maintains muscle mass by sustaining GH action.
View Article and Find Full Text PDFParasite
January 2025
National Engineering Research Center of Marine Facilities Aquaculture, Marine Science and Technology College, Zhejiang Ocean University, Zhoushan, Zhejiang 316022, PR China.
The aim of this study was to clarify the taxonomic identification of a hemoflagellate and assess the effect of trypanosome infection on Larimichthys crocea. Giemsa staining showed the presence of three morphotypes of trypomastigotes. The trypanosomes had the following morphological characteristics: a slender body with a long flagellum at the front; body size 12.
View Article and Find Full Text PDFLiver Int
February 2025
Department of Digestive and Hepatobiliary Medicine, CHU Clermont-Ferrand, Clermont-Ferrand, France.
Background And Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common cause of hepatocellular carcinoma (HCC). In this study, we combine metabolomic and gene expression analysis to compare HCC tissues with non-tumoural tissues (NTT).
Methods: A non-targeted metabolomic strategy LC-MS was applied to 52 pairs of human MASLD-HCC and NTT separated into 2 groups according to fibrosis severity F0F1-F2 versus F3F4.
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