Treatment of bile acid amidation defects with glycocholic acid

James E. Heubi, Kenneth D.R. Setchell, Pinky Jha, Donna Buckley, Wujuan Zhang, Philip Rosenthal, Carol Potter, Simon Horslen, David Suskind – 28 August 2014 – Bile acid amidation defects were predicted to present with fat/fat soluble vitamin malabsorption with minimal cholestasis. We identified and treated five patients (one male, four females) from four families with defective bile acid amidation due to a genetically confirmed deficiency in bile acid CoA:amino acid N‐acyl transferase (BAAT) with the conjugated bile acid, glycocholic acid (GCA).

FAK Is required for c‐Met/β‐catenin‐driven hepatocarcinogenesis

Na Shang, Maribel Arteaga, Ali Zaidi, Jimmy Stauffer, Scott J. Cotler, Nancy J. Zeleznik‐Le, Jiwang Zhang, Wei Qiu – 28 August 2014 – Hepatocellular carcinoma (HCC) is the third most common cause of cancer death worldwide and most patients with HCC have limited treatment options. Focal adhesion kinase (FAK) is overexpressed in many HCC specimens, offering a potential target for HCC treatment. However, the role of FAK in hepatocarcinogenesis remains elusive.

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