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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.

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

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.
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surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
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 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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