CANCERDIP

The use of Methylated DNA Immunoprecipitation MeDIP in cancer for better clinical management

 Coordinatore FUNDACIO INSTITUT D'INVESTIGACIO BIOMEDICA DE BELLVITGE 

 Organization address address: AVENIDA GRAN VIA HOSPITALET 199-203
city: L'HOSPITALET DE LLOBREGAT
postcode: 8908

contact info
Titolo: Ms.
Nome: Vistoria
Cognome: Cochrane
Email: send email
Telefono: +34 93260 7226
Fax: +34 93260 7224

 Nazionalità Coordinatore Spain [ES]
 Sito del progetto http://www.cancerdip.eu/
 Totale costo 3˙922˙042 €
 EC contributo 2˙999˙994 €
 Programma FP7-HEALTH
Specific Programme "Cooperation": Health
 Code Call FP7-HEALTH-2007-A
 Funding Scheme CP-FP
 Anno di inizio 2008
 Periodo (anno-mese-giorno) 2008-01-01   -   2011-06-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    FUNDACIO INSTITUT D'INVESTIGACIO BIOMEDICA DE BELLVITGE

 Organization address address: AVENIDA GRAN VIA HOSPITALET 199-203
city: L'HOSPITALET DE LLOBREGAT
postcode: 8908

contact info
Titolo: Ms.
Nome: Vistoria
Cognome: Cochrane
Email: send email
Telefono: +34 93260 7226
Fax: +34 93260 7224

ES (L'HOSPITALET DE LLOBREGAT) coordinator 0.00
2    Nome Ente NON disponibile

 Organization address address: VIALE BENEDUCE 10
city: CASERTA
postcode: 81100

contact info
Titolo: Dr.
Nome: Annunziata
Cognome: Valente
Email: send email
Telefono: -5667603
Fax: -450211

IT (CASERTA) participant 0.00
3    DIAGENODE

 Organization address address: RUE DU BOIS SAINT JEAN 3 LIEGE PARK SCIENCE
city: SERAING
postcode: 4102

contact info
Titolo: Mr.
Nome: Didier
Cognome: Allaer
Email: send email
Telefono: +32 4 364 20 50
Fax: +32 4 364 20 51

BE (SERAING) participant 0.00
4    FUNDACION CENTRO NACIONAL DE INVESTIGACIONES ONCOLOGICAS CARLOS III

 Organization address address: CALLE MELCHOR FERNANDEZ ALMAGRO 3
city: MADRID
postcode: 28029

contact info
Titolo: Mr.
Nome: Juan José
Cognome: Collazo Nieto
Email: send email
Telefono: -7328057
Fax: -2247037

ES (MADRID) participant 0.00
5    MAX PLANCK GESELLSCHAFT ZUR FOERDERUNG DER WISSENSCHAFTEN E.V.

 Organization address address: Hofgartenstrasse 8
city: MUENCHEN
postcode: 80539

contact info
Titolo: Mr.
Nome: Volker
Cognome: Geiss
Email: send email
Telefono: +49 681 9325-799
Fax: +49 681 9325-799

DE (MUENCHEN) participant 0.00
6    STICHTING KATHOLIEKE UNIVERSITEIT

 Organization address address: GEERT GROOTEPLEIN NOORD 9
city: NIJMEGEN
postcode: 6525 EZ

contact info
Titolo: Mr.
Nome: Ivo
Cognome: Hauer
Email: send email
Telefono: +31 24 3653306
Fax: +31 24 3652126

NL (NIJMEGEN) participant 0.00
7    UNIVERSITE LIBRE DE BRUXELLES

 Organization address address: Avenue Franklin Roosevelt 50
city: BRUXELLES
postcode: 1050

contact info
Titolo: Dr.
Nome: François
Cognome: Fuks
Email: send email
Telefono: -5556215
Fax: -5556227

BE (BRUXELLES) participant 0.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

suppressor    scientists    occurs    tools    promoter    hypermethylated    hypermethylation    epigenetics    alterations    cancerdip    gene    tumour    leukaemia    epigenetic    regions    samples    cells    treatment    prognostic    island    immunoprecipitation    medip    methylation    genes    mechanisms    islands    genome    regulation    technique    cancer    methylated    bioinformatics    pattern    clinical    tissue    predictor    dna    molecular    tumours    expression    aberrant    colon    sequencing    biomarkers    cpg    profile    data   

 Obiettivo del progetto (Objective)

'Aberrant DNA methylation is the most common molecular lesion of the cancer cell. Neither gene mutation nor cytogenetic abnormalities are as common in human tumours as DNA methylation alterations. The stability of our genome and correct gene expression is maintained to a great extent thanks to a perfectly preestablished pattern of DNA methylation and histone modifications. In cancer this idealistic scenario breaks down due to an interesting phenomenon whereby the regulatory regions (CpG islands) of certain tumour suppressor genes become hypermethylated, inactivating the gene as a consequence, whilst a wave of hypomethylation occurs in the genome. Indeed, CpG island promoter hypermethylation has a tumour-type-specific pattern, where each gene tends to be methylated in the cancer cells driven from a particular tissue, but not from others. It is also widely accepted that the multiprotein complex associated with the methylated DNA is also crucially involved in the repression of gene expression. Another aspect crucial for the interest of epigenetics in cancer is that promoter hypermethylation of the CpG island of tumours suppressor genes occurs early in tumorigenesis. Furthermore, it has been extensively reported that CpG promoter hypermethylation can be used as predictor of cancer behaviour and a predictor of response to treatment. This characteristic makes promoter hypermethylation combined with the epigenetic associated proteins profile, a potential biomarker for early detection of cancer and for the individualization of cancer treatment. We are going to use a novel technique based in chromatin immunoprecipitation, the Methylated DNA Immunoprecipitation (MeDIP) technique that will easily permit us to obtain an epigenomic profile which will be used to personalize cancer treatment and facilitate tumour diagnosis, prognosis and monitoring.'

Introduzione (Teaser)

The CANCERDIP initiative explored the use of the epigenetic profile of cancers as a predictor of cancer behaviour. Consortium members also developed molecular and bioinformatics tools that are expected to significantly aid the future analysis of DNA methylation.

Descrizione progetto (Article)

Apart from genetic mutations, the instability of cancer cells is also defined by epigenetic alterations involving, among others, aberrant methylation of gene promoters. This occurs at specific sites known as CpG islands and compromises the physiological gene expression pattern, thereby contributing further to malignancy.

To define and delineate the role of the epigenetic profile in colon cancer and leukaemia, the EU-funded project 'The use of methylated DNA immunoprecipitation MeDIP in cancer for better clinical management' (CANCERDIP) brought together leading European researchers in the field. The ultimate objective was to generate insight into the mechanisms of epigenetic regulation, focusing on DNA methylation.

To this end, partners used state-of-the-art techniques to identify differentially methylated regions in cancer samples that could potentially serve as biomarkers or therapeutic targets. For such high-throughput analysis, the consortium developed the MethylCap method of capturing methylated DNA using a methyl-binding domain (MBD) followed by genomic sequencing.

Bioinformatics analysis of the sequencing data verified the potential of this information to discriminate cancer from normal tissue. It also identified genes such as CSPG2/VCAN that are hypermethylated in colon cancer on a regular basis. By comparing the gene expression and DNA methylation profiles of leukaemia samples before treatment and after relapse, scientists were able to pinpoint candidate genes with a prognostic value.

Regarding the mechanisms that regulate DNA methylation, scientists focused on the impact of polycomb genes and their association with DNA methyltransferases. Phosphorylation of these enzymes was discovered as a previously unrecognised mechanism for the regulation of methylation.

Central to CANCERDIP project work was the development of tools for large-scale analysis of the DNA methylation pattern. With the use of magnetic beads for immunoprecipitation, the MeDIP kit accelerated the analysis of DNA methylation while at the same time improving its sensitivity. Furthermore, through the development of specialised software, the CANCERDIP consortium provided invaluable tools for validating DNA methylation biomarkers based on large-scale methylation data.

Taken together, the accomplishments of the participants in the CANCERDIP project offered novel basic knowledge on cancer epigenetics. The identified biomarkers and genes have high prognostic significance and may be exploited for clinical stratification of cancer patients.

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