KRASMIR

The role of miRNAs in KRAS-driven Non-Small Cell Lung Cancer

 Coordinatore FUNDACION PARA LA INVESTIGACION MEDICA APLICADA FIMA 

 Organization address address: AVENIDA DE PIO XII 55
city: PAMPLONA
postcode: 31008

contact info
Titolo: Ms.
Nome: Ana
Cognome: Iglesias Garcia
Email: send email
Telefono: 34948194700
Fax: 34948194718

 Nazionalità Coordinatore Spain [ES]
 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 FP7-PEOPLE-2013-CIG
 Funding Scheme MC-CIG
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-10-01   -   2017-09-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    FUNDACION PARA LA INVESTIGACION MEDICA APLICADA FIMA

 Organization address address: AVENIDA DE PIO XII 55
city: PAMPLONA
postcode: 31008

contact info
Titolo: Ms.
Nome: Ana
Cognome: Iglesias Garcia
Email: send email
Telefono: 34948194700
Fax: 34948194718

ES (PAMPLONA) coordinator 100˙000.00

Mappa


 Word cloud

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

cell    patients    therapeutic    mutations    nsclc    critical    cluster    downstream    lung    ab    cancer    genes    mutant    clinical    regulated    we    vivo    mir    oncogenesis    human    preliminary    kras    micrornas   

 Obiettivo del progetto (Objective)

'Lung cancer is the leading cause of death by cancer in Europe. Non-small cell lung cancer (NSCLC) represents about 80% of total lung cancers. KRAS is the most commonly mutated oncogene in NSCLC, found in over 20% of patients. Since KRAS mutations are directly responsible for NSCLC, KRAS represents a relevant target to prevent NSCLC development. Yet, efforts to develop therapeutic inhibitors have failed for over 20 years, what represents an unmet clinical need in NSCLC. Thus, it is critical to identify targets of oncogenic KRAS that could unveil novel therapeutic candidates.

In preliminary studies, molecular screening of downstream effectors of activated KRAS led to identification of several microRNAs. MiR-181a and b (miR-181a/b) were among the top microRNAs up-regulated upon KRAS activation. Moreover, genetic deletion of the miR-181ab1 cluster significantly impaired lung tumor development in vivo. These preliminary findings suggest a prominent role for miR-181a/b in KRAS oncogenesis. Thus, this proposal aims to dissect the role of miR-181a/b in the context of mutant KRAS to identify downstream target genes required for KRAS oncogenesis.

We propose the following objectives: 1. To investigate the role of miR-181ab-1 cluster in vivo and the potential therapeutic value of miR-181a and b using a genetically-modified mouse model of Kras-driven NSCLC. 2. To uncover the functional role of miR-181a/b in human KRAS-driven oncogenesis using NSCLC cell lines and primary lung epithelial cells. 3. To identify miR-181a/b-regulated genes functionally critical for KRAS-dependent NSCLC. 4. To characterize the clinical implication of miR-181a/b-regulated genes in human NSCLC: translating in vitro and in vivo findings to human patients.

We believe that results from this proposal will expand our current knowledge of the signaling network regulated by mutant KRAS. We hope to apply these findings to develop innovative therapeutic strategies for NSCLC patients harboring KRAS mutations'

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