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PanCaT SIGNED

Next-generation in vivo models for improved pancreatic cancer therapies

Total Cost €

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EC-Contrib. €

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Partnership

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 Outcomes and results

 PanCaT project word cloud

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

biological    human    temporal    versatile    had    cutting    maintenance    native    organismal    validation    tumor    patients    applicable    multistep    spatial    gene    formed    autonomous    performed    stroma    autochthonous    drug    fact    players    provides    prognosis    genetic    tool    cre    metastatic    edge    validated    cancers    cells    models    mast    functional    thought    clinical    discover    dual    therapeutic    permits    rigorous    biology    tumors    recombinase    loxp    flp    questions    functions    endogenous    uncovered    pancreatic    deploy    engineering    depends    treatment    inducible    mouse    candidate    insights    pdac    generation    niche    unbiased    carcinogenesis    manipulation    hosting    once    model    combining    showed    cancer    lethal    tools    hallmarks    frt    expression    dispensable    horizons    secondary    host    resistance    microenvironment    therapy    technologies    unparalleled    screening    supports    cell    adenocarcioma    mechanisms    evolution    oncogenic    ductal    pancat    intrinsic   

Project "PanCaT" data sheet

The following table provides information about the project.

Coordinator		 KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN 

Organization address
address: ISMANINGER STRASSE 22
city: MUENCHEN
postcode: 81675
website: http://www.med.tu.muenchen.de

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 Germany [DE]
 Total cost 2˙440˙275 €
 EC max contribution 2˙440˙275 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2014-CoG
 Funding Scheme ERC-COG
 Starting year 2016
 Duration (year-month-day) from 2016-02-01   to  2021-01-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN DE (MUENCHEN) coordinator 2˙440˙275.00

Map

 Project objective

Maintenance and drug resistance of pancreatic ductal adenocarcioma (PDAC) depends on cancer cell intrinsic mechanisms and a stroma that supports tumor growth. Mouse models of human PDAC have provided important insights into the evolution of this highly lethal tumor, but there are no models that allow secondary genetic manipulation of autochthonous tumors, the tumor microenvironment or the metastatic host niche once the tumor has formed.

We generated an inducible dual-recombinase system by combining Flp/frt and Cre/loxP. This novel PDAC model permits spatial and temporal control of gene expression enabling unbiased genetic approaches to study the role of tumor cell-autonomous and non-autonomous functions in endogenous cancers. This tool provides unparalleled access to the native biology of cancer cells and their hosting stroma, and rigorous genetic validation of candidate therapeutic targets. We performed tumor cell-autonomous and non-autonomous targeting, uncovered hallmarks of human multistep carcinogenesis, validated genetic tumor therapy, and showed that mast cells in the tumor microenvironment, which had been thought to be key oncogenic players, are in fact dispensable for tumor formation.

In the proposed research program, we will 1) develop and further improve next-generation PDAC models, 2) deploy these systems to identify and target key features of PDAC maintenance in tumor cells and their microenvironment, and 3) discover mechanisms of treatment resistance. The application of cutting edge genetic engineering and screening technologies will allow us to address biological questions that could not be addressed before. The PanCaT project will open new horizons for the functional understanding of pancreatic cancer biology with a strong impact on clinical management and prognosis of PDAC patients. It will also produce a unique set of highly versatile and widely applicable genetic tools that will facilitate the study of PDAC at an organismal level.

 Publications

year authors and title journal last update
List of publications.
2016 Roman Maresch, Sebastian Mueller, Christian Veltkamp, Rupert Öllinger, Mathias Friedrich, Irina Heid, Katja Steiger, Julia Weber, Thomas Engleitner, Maxim Barenboim, Sabine Klein, Sandra Louzada, Ruby Banerjee, Alexander Strong, Teresa Stauber, Nina Gross, Ulf Geumann, Sebastian Lange, Marc Ringelhan, Ignacio Varela, Kristian Unger, Fengtang Yang, Roland M. Schmid, George S. Vassiliou, Rickmer Braren, Günter Schneider, Mathias Heikenwalder, Allan Bradley, Dieter Saur, Roland Rad
Multiplexed pancreatic genome engineering and cancer induction by transfection-based CRISPR/Cas9 delivery in mice
published pages: 10770, ISSN: 2041-1723, DOI: 10.1038/ncomms10770 		Nature Communications 7 2019-06-06
2017 Günter Schneider, Marc Schmidt-Supprian, Roland Rad, Dieter Saur
Tissue-specific tumorigenesis: context matters
published pages: 239-253, ISSN: 1474-175X, DOI: 10.1038/nrc.2017.5 		Nature Reviews Cancer 17/4 2019-06-06
2018 Sebastian Mueller, Thomas Engleitner, Roman Maresch, Magdalena Zukowska, Sebastian Lange, Thorsten Kaltenbacher, Björn Konukiewitz, Rupert Öllinger, Maximilian Zwiebel, Alex Strong, Hsi-Yu Yen, Ruby Banerjee, Sandra Louzada, Beiyuan Fu, Barbara Seidler, Juliana Götzfried, Kathleen Schuck, Zonera Hassan, Andreas Arbeiter, Nina Schönhuber, Sabine Klein, Christian Veltkamp, Mathias Friedrich, Lena Rad, Maxim Barenboim, Christoph Ziegenhain, Julia Hess, Oliver M. Dovey, Stefan Eser, Swati Parekh, Fernando Constantino-Casas, Jorge de la Rosa, Marta I. Sierra, Mario Fraga, Julia Mayerle, Günter Klöppel, Juan Cadiñanos, Pentao Liu, George Vassiliou, Wilko Weichert, Katja Steiger, Wolfgang Enard, Roland M. Schmid, Fengtang Yang, Kristian Unger, Günter Schneider, Ignacio Varela, Allan Bradley, Dieter Saur, Roland Rad
Evolutionary routes and KRAS dosage define pancreatic cancer phenotypes
published pages: 62-68, ISSN: 0028-0836, DOI: 10.1038/nature25459 		Nature 554/7690 2019-06-06

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