LIPOCHEX

The Role of Lipolysis in the Pathogenesis of Cancer-associated Cachexia

 Coordinatore UNIVERSITAET GRAZ 

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 Nazionalità Coordinatore Austria [AT]
 Totale costo 2˙499˙446 €
 EC contributo 2˙499˙446 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2013-ADG
 Funding Scheme ERC-AG
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-04-01   -   2019-03-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITAET GRAZ

 Organization address address: UNIVERSITAETSPLATZ 3
city: GRAZ
postcode: 8010

contact info
Titolo: Dr.
Nome: Barbara
Cognome: Haselsteiner
Email: send email
Telefono: +43 316 380 3398
Fax: +43 316 380 9034

AT (GRAZ) hostInstitution 2˙499˙446.00
2    UNIVERSITAET GRAZ

 Organization address address: UNIVERSITAETSPLATZ 3
city: GRAZ
postcode: 8010

contact info
Titolo: Prof.
Nome: Rudolf
Cognome: Zechner
Email: send email
Telefono: +43 316 380 1901
Fax: +43 316 380 9016

AT (GRAZ) hostInstitution 2˙499˙446.00

Mappa


 Word cloud

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

lipases    loss    tissue    lipase    elucidate    mice    muscle    adipose    cachexia    mechanisms    lipolysis    tg    pathogenesis    cac    induced    cancer    coregulators   

 Obiettivo del progetto (Objective)

'Cachexia is a complex syndrome characterized by massive loss of body weight due to uncontrolled loss of adipose tissue and skeletal muscle. The wasting occurs during late stages of many unrelated chronic diseases and frequently leads to the death of affected individuals. Cachexia is most common in cancer, where an estimated 25% of patients die from cancer-associated cachexia (CAC) rather than from the cancer. Despite the tremendous impact of CAC on morbidity and mortality, the underlying molecular mechanisms are poorly understood.

Recently, we demonstrated that lipase-catalyzed triacylglycerol (TG) catabolism is required for the pathogenesis of CAC. Mice lacking adipose triglyceride lipase, the rate-limiting enzyme for TG hydrolysis (lipolysis), were completely protected from loss of both adipose tissue and muscle in two forms of cancer. This implies an essential role of the lipolytic process in the pathogenesis of CAC. Here we propose to elucidate the causal role of lipases and their coregulators in CAC development. We will determine mechanisms involved and pursue novel treatment strategies.

Our objectives are to: - Investigate how different cancers in mice regulate tissue-specific lipolysis; - Elucidate the functional role of lipases and their coregulators in the pathogenesis of CAC; - Assess whether pharmacological inhibition of specific lipases prevents or delays CAC; - Study the effects of cancer-induced lipolysis on energy dissipating pathways and epigenetic control.

The project enters a largely unexplored field: the role of lipid metabolism in the pathogenesis of CAC. The work will heavily rely on the characterization of induced mutant mouse models with CAC and require extensive collaboration with experts in pathology and large-scale systems analytics. The results are expected to yield new mechanisms of disease development and provide novel therapeutic targets to prevent the devastating and prevalent consequences of CAC.'

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