HCC EPIGENETICS

Epigenetic Deregulation of Apoptotic Gene Expression in Hepatocellular Carcinoma (HCC)

Coordinatore	more  Organization address address: "LEOFOROS STAVROS S NIARCHOS, PANEPISTIMIOUPOLI IOANNINON" city: IOANNINA postcode: 45110 contact info Titolo: Prof. Nome: Vasiliki Cognome: Malamou-Mitsi Email: send email Telefono: 302651000000 Fax: 302651000000
Nazionalità Coordinatore	Non specificata
Totale costo	100˙000 €
EC contributo	100˙000 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	F
Anno di inizio	2011
Periodo (anno-mese-giorno)	2011-02-01   -   2015-01-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITY OF IOANNINA  Organization address address: "LEOFOROS STAVROS S NIARCHOS, PANEPISTIMIOUPOLI IOANNINON" city: IOANNINA postcode: 45110 contact info Titolo: Prof. Nome: Vasiliki Cognome: Malamou-Mitsi Email: send email Telefono: 302651000000 Fax: 302651000000	EL (IOANNINA)	coordinator	100˙000.00

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 Obiettivo del progetto (Objective)

'Hepatocellular carcinoma (HCC) is the fifth most common cancer worldwide and thus constitutes a major health problem involving more than half a million new cases every year. During its promotion stage, HCC has been associated with defective apoptosis and increased cell proliferation. Only recently, gene expression has been shown to be regulated by epigenetics (reversible heritable changes in gene regulation that occur without a change in DNA sequence) involving changes in DNA methylation patterns as well as specific histone modifications. Throughout our proposal, we speculate that alterations in DNA methylation patterns trigger specific histone modifications resulting in apoptotic gene silencing during HCC. Thus, we propose to test the hypothesis that epigenetically-induced deregulation of the apoptotic pathway promotes transformation to malignancy. To conclude, although the deregulation of the apoptotic machinery in carcinogenesis is well established, there is a gap in our understanding as to how apoptotic genes are involved and how is their expression regulated in malignancy. Our proposal fills in the gaps in linking the epigenetically-induced alterations in apoptotic gene expression to the defective apoptotic phenotype characteristic of HCC. Furthermore, our proposal elucidates the molecular mechanisms by which specific histone modifications converse with the DNA methylation machinery in order to silence specific apoptotic genes. Finally, determining the molecular identity of these epigenetic modifications is of paramount importance because such information can be utilized in designing more efficient cancer therapeutic strategies based on the concept of selective apoptotic activation in malignant cells thus making such strategies more efficient and less cytotoxic.'