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Characterization of Key Epigenetic Targets in Hepatic Fibrosis and Hepatocellular Carcinoma Development. Generation of New Antifibrotic and Antitumoral Drugs.

Total Cost €


EC-Contrib. €






 TARGEPILIVER project word cloud

Explore the words cloud of the TARGEPILIVER project. It provides you a very rough idea of what is the project "TARGEPILIVER" about.

histones    alone    pathological    usa    clds    efficacious    global    background    progression    neoplasm    exposure    safety    burden    amenable    cirrhosis    inflammation    literature    hematological    post    environmental    hepatocellular    marks    diseases    inhibitors    cld    deposition    methyltransferase    intervention    triggers    cellular    stage    observations    carcinoma    quell    preliminary    profile    constitute    viral    dna    critical    events    pharmacological    first    translational    enzymes    despite    modification    treating    therapeutic    steatohepatitis    develops    infection    models    therapies    healthcare    fibrosis    causes    attractive    obesity    prevent    enzymatic    halt    histone    hcc    pathogenic    alcohol    patients    molecular    fastest    function    ways    cancer    altered    epigenetic    incidence    adaptative    methylation    progress    good    hepatocarcinogenesis    gene    chronic    hepatitis    rising    drugs    significance    huge    dynamic    liver    mechanisms    linked    methyltransferases    multistep    ultimately    malignancies    compromised    expression    abuse    context    combination    treat    methyl    alterations   

Project "TARGEPILIVER" data sheet

The following table provides information about the project.


Organization address
address: AVENIDA DE PIO XII 55
postcode: 31008

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Spain [ES]
 Project website
 Total cost 170˙121 €
 EC max contribution 170˙121 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2014
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2015
 Duration (year-month-day) from 2015-12-01   to  2018-03-22


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 Project objective

Liver fibrosis represents a common pathogenic pathway in most chronic liver diseases (CLDs) and cirrhosis, its end stage, is a huge healthcare burden. The main causes of CLD are chronic viral hepatitis B or C infection, alcohol abuse and obesity-linked steatohepatitis, conditions with increasing global incidence. Hepatocellular carcinoma (HCC) develops on this background of CLD as a multistep process in the context of chronic inflammation and cirrhosis. Among all non-hematological malignancies, HCC has the fastest rising incidence of any neoplasm in USA and Europe. Despite all the progress in understanding the cellular and molecular mechanisms of liver fibrosis and hepatocarcinogenesis, there are no effective therapies to halt fibrosis or quell liver cancer. Exposure to environmental factors triggers adaptative epigenetic mechanisms, including alterations in DNA methylation or post-translational modification of histones, which control gene expression and ultimately cellular behaviour in ways critical for the development of CLD and HCC. From the literature and our preliminary observations it is known that many of the enzymes carrying out these epigenetic events, such as DNA and histone methyltransferases, present altered expression and activity in CLD and HCC. The deposition of methyl marks in histones and DNA are very dynamic enzymatic processes, amenable to pharmacological intervention and therefore constitute attractive therapeutic targets. Our proposal has two main objectives: first the analysis of the expression, activity and pathological significance of DNA and histone-methyltransferases in models of CLD and hepatocarcinogenesis; and second the development of new efficacious DNA and histone-methyltransferase specific inhibitors with a good safety profile, which is critical when treating patients with compromised liver function. These new epigenetic therapies could be used to prevent CLD progression, and to treat HCC alone or in combination with existing drugs.


year authors and title journal last update
List of publications.
2018 Gloria Alvarez-Sola, Iker Uriarte, Maria U. Latasa, Maddalen Jimenez, Marina Barcena-Varela, Eva Santamaría, Raquel Urtasun, Carlos Rodriguez-Ortigosa, Jesús Prieto, Pedro Berraondo, Maite G. Fernandez-Barrena, Carmen Berasain, Matías A. Avila
Bile acids, FGF15/19 and liver regeneration: From mechanisms to clinical applications
published pages: 1326-1334, ISSN: 0925-4439, DOI: 10.1016/j.bbadis.2017.06.025
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1864/4 2019-06-13
2017 M.G. Fernandez-Barrena, M. Barcena-Varela, J.M. Banales
New evidence supporting the biliary bicarbonate umbrella theory
published pages: 126-128, ISSN: 2210-7401, DOI: 10.1016/j.clinre.2016.09.004
Clinics and Research in Hepatology and Gastroenterology 41/2 2019-06-13
2017 Gloria Alvarez-Sola, Iker Uriarte, Maria U Latasa, Maddalen Jimenez, Marina Barcena-Varela, Eva Santamaría, Raquel Urtasun, Carlos Rodriguez-Ortigosa, Jesús Prieto, Fernando J Corrales, Anna Baulies, Carmen García-Ruiz, Jose C Fernandez-Checa, Pedro Berraondo, Maite G Fernandez-Barrena, Carmen Berasain, Matías A Avila
Engineered fibroblast growth factor 19 protects from acetaminophen-induced liver injury and stimulates aged liver regeneration in mice
published pages: e3083, ISSN: 2041-4889, DOI: 10.1038/cddis.2017.480
Cell Death and Disease 8/10 2019-06-13
2017 Gloria Alvarez-Sola, Iker Uriarte, M Ujue Latasa, Maite G Fernandez-Barrena, Raquel Urtasun, Maria Elizalde, Marina Barcena-Varela, Maddalen Jiménez, Haisul C Chang, Roberto Barbero, Victoria Catalán, Amaia Rodríguez, Gema Frühbeck, José M Gallego-Escuredo, Aleix Gavaldà-Navarro, Francesc Villarroya, Carlos M Rodriguez-Ortigosa, Fernando J Corrales, Jesus Prieto, Pedro Berraondo, Carmen Berasain, Matias A Avila
Fibroblast growth factor 15/19 (FGF15/19) protects from diet-induced hepatic steatosis: development of an FGF19-based chimeric molecule to promote fatty liver regeneration
published pages: 1818-1828, ISSN: 0017-5749, DOI: 10.1136/gutjnl-2016-312975
Gut 66/10 2019-06-13

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