MITOCANCERSTEM

Role of Mitochondrial Physiology in Tumor Stem Cell Resistance to Chemotherapeutics

 Coordinatore CENTRO DE NEUROCIENCIAS E BIOLOGIACELULAR ASSOCIACAO 

 Organization address address: UNIVERSIDADE DE COIMBRA .
city: COIMBRA
postcode: 3004 517

contact info
Titolo: Prof.
Nome: Euclides
Cognome: Pires
Email: send email
Telefono: -855648
Fax: -855677

 Nazionalità Coordinatore Portugal [PT]
 Totale costo 147˙283 €
 EC contributo 147˙283 €
 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 FP7-PEOPLE-2009-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2010
 Periodo (anno-mese-giorno) 2010-08-01   -   2012-07-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    CENTRO DE NEUROCIENCIAS E BIOLOGIACELULAR ASSOCIACAO

 Organization address address: UNIVERSIDADE DE COIMBRA .
city: COIMBRA
postcode: 3004 517

contact info
Titolo: Prof.
Nome: Euclides
Cognome: Pires
Email: send email
Telefono: -855648
Fax: -855677

PT (COIMBRA) coordinator 147˙283.60

Mappa


 Word cloud

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

driving    hypothesis    varying    tumor    ability    stem    cancer    suggesting    chemotherapeutics    chemotherapeutic    basis    differentiation    past    tumors    organs    cell    decade    re    cells    mitochondrial    force    differentiated   

 Obiettivo del progetto (Objective)

'Although many advances in cancer research have heightened cases of long term survival, tumor re-growth is still a major concern. One hypothesis of the driving force behind tumor re-growth is the subpopulation of cancer stem cells found in varying types of tumors. Cancer stem cells have emerged as an important chemotherapeutic target over the past decade, as their ability to evade treatments provides a likely source for tumor re-growth. Like organs, tumors are composed of a mixture of cells at varying states of differentiation and arise from cells with the ability to proliferate indefinitely and differentiate into multiple lineages. In healthy organs, the cells responsible for organ development are stem cells, suggesting that tumors also have a subset of cells with stem-like characteristics known as cancer stem cells. Over the past decade, support for the existence of cancer stem cells has grown, suggesting that cancer stem cells are a driving force in tumorigenesis.This project is devised to investigate mitochondrial characteristics of cancer stem cells that allow them to survive the effects of chemotherapeutic drugs, especially those targeting apoptotic pathways. Our working hypothesis will be that the differential physiology of mitochondria in tumor stem cells and differentiated cells result into a different susceptibility to chemotherapeutics.To pursue the objective of the present work we will use mouse P19 embryonal carcinoma cells (TSC), which are a unique system on the basis that cancer stem cells can be compared with more differentiated cancer tumor cells in the same cell line under two different conditions. Preliminary data from the host group clearly demonstrates that mitochondrial differentiation accompanies cell differentiation. The consequences for cell metabolism and resistance to pro-oxidants, chemotherapeutics and mitochondrial inhibitors of the different mitochondrial subtypes are not known and constitute the basis of this proposal.'

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