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THERACAN SIGNED

Novel therapeutic strategies to treat pancreatic and lung cancer

Total Cost €

0

EC-Contrib. €

0

Partnership

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 THERACAN project word cloud

Explore the words cloud of the THERACAN project. It provides you a very rough idea of what is the project "THERACAN" about.

combination    progression    trials    treatment    events    therapeutic    medical    types    suspected    tumor    functionally    validating    pancreatic    evolution    generate    clinical    mutations    section    activated    hamper    outcome    last    eradicate    survival    molecular    diseases    desmoplasic    ablation    strategies    likewise    implicated    naturally    platforms    reasoned    pro    tumoral    onset    first    separation    deadly    hence    stages    pharmacological    validation    cancer    adenocarcinoma    temporal    accelerate    rates    senescence    guide    occurring    human    class    serves    validate    initial    synergies    manifestations    devise    unmet    preclinical    intend    trial    barrier    ras    stroma    cells    therapies    mutant    responsible    tumors    gem    unacceptable    inactivation    heterogeneity    generation    pathological    maintained    positive    cancers    models    interrogate    inhibitors    lung    ductal    genes    pdx    initiating    treat    reprogramming   

Project "THERACAN" data sheet

The following table provides information about the project.

Coordinator
FUNDACION CENTRO NACIONAL DE INVESTIGACIONES ONCOLOGICAS CARLOS III 

Organization address
address: CALLE MELCHOR FERNANDEZ ALMAGRO 3
city: MADRID
postcode: 28029
website: www.cnio.es

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Spain [ES]
 Total cost 2˙499˙500 €
 EC max contribution 2˙499˙500 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2015-AdG
 Funding Scheme ERC-ADG
 Starting year 2017
 Duration (year-month-day) from 2017-01-01   to  2021-12-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    FUNDACION CENTRO NACIONAL DE INVESTIGACIONES ONCOLOGICAS CARLOS III ES (MADRID) coordinator 2˙499˙500.00

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 Project objective

This proposal is aimed at identifying and functionally validating targets with potential therapeutic value to devise novel strategies to treat two human cancers with unacceptable low survival rates and unmet medical needs: pancreatic ductal adenocarcinoma and K-RAS mutant lung adenocarcinoma. Although these tumor types have distinct pathological and clinical manifestations, they are both driven by K-RAS mutations. Hence, we expect that the proposed studies will generate synergies to accelerate the outcome of the expected results. In the first part of the proposal, we will identify those genes activated in the cancer initiating cells responsible for the onset of pancreatic and lung tumors. We reasoned that genes implicated in the initial stages of tumor development will be maintained during tumor evolution and not be affected by the intra-tumoral heterogeneity generated during tumor progression. We also propose to identify and validate genes capable of reprogramming the desmoplasic stroma characteristic of pancreatic tumors to hamper its pro-tumoral effects. Likewise, we intend to define the molecular events that control senescence, a naturally occurring process that serves as a barrier to tumor development. In the second part of the project, we will interrogate the role of known targets with suspected therapeutic value in tumor progression using a new generation of GEM tumor models that allow the temporal separation of tumor development from target ablation or inactivation. These studies will make it possible to design combination therapies capable of effectively eradicate advanced tumors. The last section of this proposal focuses on the pharmacological validation of these combination therapies using best-in-class inhibitors in state-of-the-art preclinical trial platforms based on GEM and PDX tumor models. The results derived from these studies will guide the design of new clinical trials that should have a positive impact in the treatment of these deadly diseases.

 Publications

year authors and title journal last update
List of publications.
2018 Magdolna Djurec, Osvaldo Graña, Albert Lee, Kevin Troulé, Elisa Espinet, Lavinia Cabras, Carolina Navas, María Teresa Blasco, Laura Martín-Díaz, Miranda Burdiel, Jing Li, Zhaoqi Liu, Mireia Vallespinós, Francisco Sanchez-Bueno, Martin R. Sprick, Andreas Trumpp, Bruno Sainz, Fátima Al-Shahrour, Raul Rabadan, Carmen Guerra, Mariano Barbacid
Saa3 is a key mediator of the protumorigenic properties of cancer-associated fibroblasts in pancreatic tumors
published pages: E1147-E1156, ISSN: 0027-8424, DOI: 10.1073/pnas.1717802115
Proceedings of the National Academy of Sciences 115/6 2019-08-29
2018 Lucía Simón-Carrasco, Gerardo Jiménez, Mariano Barbacid, Matthias Drosten
The Capicua tumor suppressor: a gatekeeper of Ras signaling in development and cancer
published pages: 702-711, ISSN: 1538-4101, DOI: 10.1080/15384101.2018.1450029
Cell Cycle 17/6 2019-08-29
2019 María Teresa Blasco, Carolina Navas, Guillermo Martín-Serrano, Osvaldo Graña-Castro, Carmen G. Lechuga, Laura Martín-Díaz, Magdolna Djurec, Jing Li, Lucia Morales-Cacho, Laura Esteban-Burgos, Javier Perales-Patón, Emilie Bousquet-Mur, Eva Castellano, Harrys K.C. Jacob, Lavinia Cabras, Monica Musteanu, Matthias Drosten, Sagrario Ortega, Francisca Mulero, Bruno Sainz, Nelson Dusetti, Juan Iova
Complete Regression of Advanced Pancreatic Ductal Adenocarcinomas upon Combined Inhibition of EGFR and C-RAF
published pages: 573-587.e6, ISSN: 1535-6108, DOI: 10.1016/j.ccell.2019.03.002
Cancer Cell 35/4 2019-08-29
2018 Matthias Drosten, Carmen Guerra, Mariano Barbacid
Genetically Engineered Mouse Models of K-Ras-Driven Lung and Pancreatic Tumors: Validation of Therapeutic Targets
published pages: a031542, ISSN: 2157-1422, DOI: 10.1101/cshperspect.a031542
Cold Spring Harbor Perspectives in Medicine 8/5 2019-08-29
2018 Manuel Sanclemente, Sarah Francoz, Laura Esteban-Burgos, Emilie Bousquet-Mur, Magdolna Djurec, Pedro P. Lopez-Casas, Manuel Hidalgo, Carmen Guerra, Matthias Drosten, Monica Musteanu, Mariano Barbacid
c-RAF Ablation Induces Regression of Advanced Kras/Trp 53 Mutant Lung Adenocarcinomas by a Mechanism Independent of MAPK Signaling
published pages: 217-228.e4, ISSN: 1535-6108, DOI: 10.1016/j.ccell.2017.12.014
Cancer Cell 33/2 2019-06-13

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