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Next-generation in vivo models for improved pancreatic cancer therapies

Total Cost €


EC-Contrib. €






 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.

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

Project "PanCaT" data sheet

The following table provides information about the project.


Organization address
postcode: 81675

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


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 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.


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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