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Intrahepatic cholangiocarcinoma (iCCA) is a rare and complex malignancy of the biliary epithelium. Due to its silent presentation, patients are frequently diagnosed late in their disease course, resulting in poor overall survival. Advances in molecular profiling and targeted therapies have improved medical management, but long-term survival is rarely seen with medical therapy alone. Surgical resection offers a survival advantage, but negative oncologic margins are difficult to achieve, recurrence rates are high, and the need for adequate future liver remnant limits the extent of resection. Advances in neoadjuvant and adjuvant treatments have broadened patient treatment options, and these agents are undergoing active investigation, especially in the setting of advanced, initially unresectable disease. For those who are not able to undergo resection, liver transplantation is emerging as a potential curative therapy in certain cases. Patient selection, favorable tumor biology, and a protocolized, multidisciplinary approach are ultimately necessary for best patient outcomes. This review will discuss the current surgical management of locally advanced, liver-limited intrahepatic cholangiocarcinoma as well as the role of liver transplantation for select patients with background liver disease.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8199311 | PMC |
http://dx.doi.org/10.3390/jcm10112428 | DOI Listing |
Arterioscler Thromb Vasc Biol
September 2025
Department of Medicine/Division of Cardiology, University of California Los Angeles. (S.S., C.R.S., L.F., M.P., C.P., Z.Z., J.J.M., R.C.D., D.S., A.J.L.).
Background: In genetic studies with the Hybrid Mouse Diversity Panel, we previously identified a chromosome 9 locus for atherosclerosis. We now identify NNMT (nicotinamide -methyltransferase), an enzyme that degrades nicotinamide, as the causal gene in the locus and show that the underlying mechanism involves salvage of nicotinamide to nicotinamide adenine dinucleotide (NAD).
Methods: Gain/loss of function studies in macrophages were performed to examine the role of NAD levels in macrophage proliferation and apoptosis in atherosclerosis.
Mol Ther
September 2025
Center of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China; Institute of Precision Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China. Electronic address:
The reduction of TCF-1 during CD8 T cell exhaustion leads to attenuated antitumor activity and diminished responsiveness to immune checkpoint inhibitors. However, how TCF-1 is downregulated remains unclear. Here, we showed that during CD8 T cell exhaustion, lnc-SUMF2-8, induced by transcription factor TOX, can bind to cytosolic TCF-1, and direct it to the lysosome for degradation.
View Article and Find Full Text PDFKidney Blood Press Res
August 2025
Primary hyperoxaluria type 1 (PH1) is a rare autosomal recessive disorder caused by a deficiency of the hepatic peroxisomal enzyme alanine-glyoxylate aminotransferase (AGT), which catalyses the conversion of glyoxylate to glycine, resulting in increased oxalate production. The clinical consequences of the progressive build up of oxalates include nephrocalcinosis, nephrolithiasis, chronic kidney disease and ultimately renal failure with extra-renal involvement. The diagnosis of PH1 is challenging due to the non-specific nature of its symptoms and the need for costly genetic testing.
View Article and Find Full Text PDFEndocrinol Diabetes Metab
September 2025
Liver Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Introduction: Liver transplantation is associated with various metabolic disorders. Peri-transplant hyperglycemia is among the most frequent metabolic disorders among liver transplant recipients. Hyperglycemia following liver transplantation can increase the risk of post-transplant complications, potentially impacting both graft and recipient outcomes.
View Article and Find Full Text PDFNature
September 2025
Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Key Laboratory of RNA Innovation Science and Engineering, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Antigen-induced clustering of cell surface receptors, including T cell receptors and Fc receptors, represents a widespread mechanism in cell signalling activation. However, most naturally occurring antigens, such as tumour-associated antigens, stimulate limited receptor clustering and on-target responses owing to insufficient density. Here we repurpose proximity labelling, a method used to biotinylate and identify spatially proximal proteins, to amplify designed probes as synthetic antigen clusters on the cell surface.
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