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Novel therapeutic strategies to treat pancreatic and lung cancer

Total Cost €


EC-Contrib. €






 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.

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

Project "THERACAN" data sheet

The following table provides information about the project.


Organization address
city: MADRID
postcode: 28029

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


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 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.


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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