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TARGEPILIVER

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

Total Cost €

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EC-Contrib. €

0

Partnership

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 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.

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

Project "TARGEPILIVER" data sheet

The following table provides information about the project.

Coordinator
FUNDACION PARA LA INVESTIGACION MEDICA APLICADA FIMA 

Organization address
address: AVENIDA DE PIO XII 55
city: PAMPLONA
postcode: 31008
website: www.cima.es

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 https://cima.unav.edu/en/investigacion/programas-verticales/hepatologia/respuesta-hepatica-al-dano-agudo-y-cronico-desarrollo-de-estrategias-terapeuticas
 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

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    FUNDACION PARA LA INVESTIGACION MEDICA APLICADA FIMA ES (PAMPLONA) coordinator 170˙121.00

Map

 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.

 Publications

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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