https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.26641

Once-Daily Simeprevir (TMC435) With Pegylated Interferon and Ribavirin in Treatment-Naïve Genotype 1 Hepatitis C: The Randomized PILLAR Study

Cholangiocarcinomas are a heterogeneous group of malignancies arising from a number of cells of origin along the biliary tree. Although most cases in Western countries are sporadic, large population-based studies have identified a number of risk factors. This review summarises the evidence behind reported risk factors and current understanding of the molecular pathogenesis of cholangiocarcinoma, with a focus on inflammation and cholestasis as the driving forces in cholangiocarcinoma development. Cholestatic liver diseases (e.g. primary sclerosing cholangitis and fibropolycystic liver diseases), liver cirrhosis, and biliary stone disease all increase the risk of cholangiocarcinoma. Certain bacterial, viral or parasitic infections such as hepatitis B and C and liver flukes also increase cholangiocarcinoma risk. Other risk factors include inflammatory disorders (such as inflammatory bowel disease and chronic pancreatitis), toxins (e.g. alcohol and tobacco), metabolic conditions (diabetes, obesity and non-alcoholic fatty liver disease) and a number of genetic disorders. Regardless of aetiology, most risk factors cause chronic inflammation or cholestasis. Chronic inflammation leads to increased exposure of cholangiocytes to the inflammatory mediators interleukin-6, Tumour Necrosis Factor-ɑ, Cyclo-oxygenase-2 and Wnt, resulting in progressive mutations in tumour suppressor genes, proto-oncogenes and DNA mismatch-repair genes. Accumulating bile acids from cholestasis lead to reduced pH, increased apoptosis and activation of ERK1/2, Akt and NF-κB pathways that encourage cell proliferation, migration and survival. Other mediators upregulated in cholangiocarcinoma include Transforming Growth Factor-β, Vascular Endothelial Growth Factor, Hepatocyte Growth Factor and several microRNAs. Increased expression of the cell surface receptor c-Met, the glucose transporter GLUT-1 and the sodium iodide symporter lead to tumour growth, angiogenesis and cell migration. Stromal changes are also observed, resulting in alterations to the extracellular matrix composition and recruitment of fibroblasts and macrophages that create a microenvironment promoting cell survival, invasion and metastasis. Regardless of aetiology, most risk factors for cholangiocarcinoma cause chronic inflammation and/or cholestasis, leading to the activation of common intracellular pathways that result in reactive cell proliferation, genetic/epigenetic mutations and cholangiocarcinogenesis. An understanding of the molecular pathogenesis of cholangiocarcinoma is vital when developing new diagnostic biomarkers and targeted therapies for this disease.

/pdf/molecular-pathogenesis-of-cholangiocarcinoma-2loktcbpgk.pdf

Molecular Pathogenesis of Cholangiocarcinoma.

Hepatic encephalopathy in patients with acute decompensation of cirrhosis and acute on chronic liver failure

https://aasldpubs.onlinelibrary.wiley.com/doi/epdf/10.1002/hep.31092

Identification of Four Immune Subtypes Characterized by Distinct Composition and Functions of Tumor Microenvironment in Intrahepatic Cholangiocarcinoma

https://www.natap.org/2014/HCV/PIIS0016508513015643.pdf

Efficacy of an Interferon- and Ribavirin-Free Regimen of Daclatasvir, Asunaprevir, and BMS-791325 in Treatment-Naive Patients With HCV Genotype 1 Infection

47 efficacy and safety of protease inhibitors for severe hepatitis c recurrence after liver transplantation: a first multicentric experience

https://www.hal.inserm.fr/inserm-00515623/document

of cellular targets in human intrahepatic cholangiocarcinoma using laser microdissection and accurate mass and time tag proteomics.

P1319 once-daily simeprevir (tmc435) with peginterferon/ribavirin in treatment-naive or treatment-experienced chronic hcv genotype 4-infected patients: final results of a phase iii trial

https://www.journal-of-hepatology.eu/article/S0168-8278(10)60031-1/pdf

29 early transplantation improves survival of non-responders to corticosteroids in severe alcoholic hepatitis: a challenge to the 6 month rule of abstinence

220 predictive factors of transplant free survival in patients with fulminant and subfulminant hepatic failure: results from a randomized controlled multicenter trial

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