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StroMaP SIGNED

Stromal stress networks underlying phenotypic plasticity and tumor fitness

Total Cost €

0

EC-Contrib. €

0

Partnership

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 StroMaP project word cloud

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

signatures    patterns    hoemostasis    complement    tradeoffs    cytoprotective    cultures    leads    heterogeneity    tumors    cycles    first    epigenetic    resolution    stress    hypothesize    adapt    hsf1    progression    malignant    stable    diverse    tfs    tumor    heterogeneously    massive    co    malignancies    overarching    nodes    vital    me    aggressive    view    tissue    activation    phenotypic    discover    network    biology    discovered    evolution    actionable    outcome    treatments    multiplexed    time    heat    stroma    transcription    cell    implicated    ways    space    single    hypothesis    reprogramming    genomically    landscape    interrogate    tf    theory    intervention    rewired    mice    tme    player    aggressiveness    diversity    mouse    sequencing    evolve    transcriptional    context    evolutionary    rna    contribution    immunofluorescence    microenvironment    models    rewiring    orchestrated    genetic    disease    map    lack    shock    malignancy    cancer    patients    generally    reprogrammed    valuable    cells    despite    global    plasticity    patient   

Project "StroMaP" data sheet

The following table provides information about the project.

Coordinator
WEIZMANN INSTITUTE OF SCIENCE 

Organization address
address: HERZL STREET 234
city: REHOVOT
postcode: 7610001
website: www.weizmann.ac.il

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 Israel [IL]
 Total cost 1˙499˙990 €
 EC max contribution 1˙499˙990 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2017-STG
 Funding Scheme ERC-STG
 Starting year 2017
 Duration (year-month-day) from 2017-10-01   to  2022-09-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    WEIZMANN INSTITUTE OF SCIENCE IL (REHOVOT) coordinator 1˙499˙990.00

Map

 Project objective

The contribution of genetic and epigenetic changes to rewiring of cancer cells into their malignant state has been much studied. But tumors are more than cancer cells and the tumor microenvironment (TME) is a key player in tumor progression. We lack an overarching view of how, despite being genomically stable, the TME is heterogeneously reprogrammed across time and space to promote evolution of aggressive disease. Recently I discovered that Heat-Shock Factor 1 (HSF1), a cytoprotective transcription factor (TF), is vital to this reprogramming, promoting malignancy in patients and mice upon activation in the stroma. Other stress TFs have also been implicated. This leads me to hypothesize that stress responses help tumors adapt and evolve into aggressive malignancies, by enabling heterogeneity and phenotypic diversity in the TME. This plasticity is achieved through cycles of massive transcriptional rewiring orchestrated by a network of stress TFs. To test this hypothesis in a global way we will proceed in three aims. First we will define patterns of stress response activation in the TME by multiplexed immunofluorescence of patient tumors. Then, we will map the associated transcriptional landscape in patients by RNA-sequencing down to single cell resolution and interrogate it in the context of a novel theory of evolutionary tradeoffs so as to discover signatures that promote tumor aggressiveness. Next, we will identify actionable nodes for intervention and test them in cell co-cultures and mouse models. The expected outcome of the proposed research is a detailed network of stress responses that can explain how the TME is rewired in tumors and how variable this rewiring is. This knowledge will provide new ways to target the TME in order to complement treatments focused on cancer cells. More generally, we address key aspects of stress responses, tissue plasticity, hoemostasis and evolution that are expected to be valuable across diverse fields of biology.

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