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PhenoSwitch SIGNED

Phenotype switching: plasticity and/or differentiation of stromal cells and their progenitors within the tumour microenvironment regulate tumour fate.

Total Cost €

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EC-Contrib. €

0

Partnership

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 PhenoSwitch project word cloud

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

thoroughly    maintaining    phenotypes    levels    aggressiveness    prognosis    outcome    reside    restrict    strategy    tumour    strategies    plasticity    phenotype    function    predominantly    thereby    sometimes    screen    characterise    commitment    proliferate    hscs    aggressive    molecules    predict    endothelial    tools    molecular    fight    contribution    throughput    lineage    warrants    elucidate    largely    therapy    inducing    metastases    dichotomous    found    hypothesis    functional    fibroblasts    limited    microenvironment    clinical    differentiation    differentiated    haematopoietic    progression    hence    cancer    significantly    metastasise    progenitor    mesenchymal    pharmacological    supporting    blocking    unknown    disease    systematically    fate    restricting    hypothesise    nature    inhibit    cells    adipose    skews    cell    stromal    cellular    switch    reassessment    tumours    niche    trigger    immune    patients    technologies    metastatic    stem    phenotypic    track    mature   

Project "PhenoSwitch" data sheet

The following table provides information about the project.

Coordinator
TECHNION - ISRAEL INSTITUTE OF TECHNOLOGY 

Organization address
address: SENATE BUILDING TECHNION CITY
city: HAIFA
postcode: 32000
website: www.technion.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]
 Project website https://shakedlab.net.technion.ac.il/
 Total cost 1˙906˙250 €
 EC max contribution 1˙906˙250 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2017-COG
 Funding Scheme ERC-COG
 Starting year 2018
 Duration (year-month-day) from 2018-04-01   to  2023-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    TECHNION - ISRAEL INSTITUTE OF TECHNOLOGY IL (HAIFA) coordinator 1˙906˙250.00

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 Project objective

The limited success of cancer therapy especially in advanced metastatic disease warrants a reassessment, especially given our limited understanding of the nature of cancer cells and the factors that allow them to proliferate and metastasise. Stromal cells of the tumour microenvironment, including fibroblasts, endothelial, immune, adipose and mesenchymal cells, significantly affect cancer cell characteristics and tumour fate; however, their sometimes dichotomous function in high- and low-aggressive tumours has not been thoroughly investigated. Here, we propose to elucidate the largely unknown role of haematopoietic stem and/or progenitor cells (HSCs) on tumour growth and metastases. We found that such cells reside in the tumour niche predominantly in non-aggressive tumours. We hypothesise that cancer cells trigger the differentiation of HSCs into haematopoietic tumour-supporting stromal cells, thereby inducing a phenotypic and functional switch that skews them towards a tumour-promoting phenotype, hence promoting tumour cell aggressiveness and metastases. To test our hypothesis, we will use high-throughput technologies to track the lineage, differentiation and commitment of HSCs during tumour progression. Our specific aims are therefore: (a) To systematically analyse tumour-promoting and tumour-restricting stromal phenotypes at the cellular and molecular levels. (b) To characterise stromal cell plasticity and the contribution of tumour cells to the phenotype switch. (c) To determine whether differentiated stromal cells and HSCs in cancer patients can predict clinical outcome. (d) To screen for molecules that inhibit the tumour-promoting stromal switch. Blocking the tumour-promoting phenotypic switch and maintaining a pre-mature tumour-restricting stromal microenvironment represent a novel strategy in the fight against cancer. This study will lead to the development of new tools to predict prognosis and pharmacological strategies to restrict tumour growth.

 Publications

year authors and title journal last update
List of publications.
2019 Yuval Shaked
The pro-tumorigenic host response to cancer therapies
published pages: 667-685, ISSN: 1474-175X, DOI: 10.1038/s41568-019-0209-6
Nature Reviews Cancer 19/12 2020-01-29
2019 Michael Timaner, Kelvin K Tsai, Yuval Shaked
The multifaceted role of mesenchymal stem cells in cancer
published pages: , ISSN: 1044-579X, DOI: 10.1016/j.semcancer.2019.06.003
Seminars in Cancer Biology 2020-01-29
2019 Kelvin K. Tsai, Tze-Sian Chan, Yuval Shaked
Next Viable Routes to Targeting Pancreatic Cancer Stemness: Learning from Clinical Setbacks
published pages: 702, ISSN: 2077-0383, DOI: 10.3390/jcm8050702
Journal of Clinical Medicine 8/5 2020-01-29
2019 Michael Timaner, Yuval Shaked
Elucidating the roles of ASPM isoforms reveals a novel prognostic marker for pancreatic cancer
published pages: , ISSN: 0022-3417, DOI: 10.1002/path.5355
The Journal of Pathology 2020-01-29
2019 Shimrit Avraham, Ben Korin, Sharon Aviram, Dvir Shechter, Yuval Shaked, Ami Aronheim
ATF3 and JDP2 deficiency in cancer associated fibroblasts promotes tumor growth via SDF-1 transcription
published pages: 3812-3823, ISSN: 0950-9232, DOI: 10.1038/s41388-019-0692-y
Oncogene 38/20 2020-01-29
2019 Michael Timaner, Ruslana Kotsofruk, Ziv Raviv, Ksenia Magidey, Dvir Shechter, Tal Kan, Alexander Nevelsky, Shahar Daniel, Elisabeth G. E. de Vries, Tongwu Zhang, Orit Kaidar-Person, Robert S. Kerbel, Yuval Shaked
Microparticles from tumors exposed to radiation promote immune evasion in part by PD-L1
published pages: , ISSN: 0950-9232, DOI: 10.1038/s41388-019-0971-7
Oncogene 2020-01-29

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The information about "PHENOSWITCH" are provided by the European Opendata Portal: CORDIS opendata.

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