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Inhibiting tumor cell plasticity by targeting the epigenome in breast cancer

Total Cost €


EC-Contrib. €






 EPICAN project word cloud

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

therapy    interactions    hyperactive    conditional    spatio    transformation    multipotency    cancers    fate    oncogene    mechanisms    anti    progenitors    hurdle    epigenetic    reprograms    cancer    plasticity    tracing    malignancy    underlying    pi3k    epigenome    cell    cells    committed    phosphoinositide    classified    demonstrates    lineage    mice    resistance    histological    microenvironment    regulate    diversity    tumor    mutations    mostly    expression    unknown    disease    multipotent    presenting    outcomes    alterations    overarching    e545k    h1047r    genetic    paramount    participate    ill    70    activating    molecular    hypothesize    epithelial    regulation    kinases    validate    giving    inhibitors    transgenic    oncogenic    downstream    situ    combined    regulators    inhibition    reactivates    mammary    akt    driver    block    pik3ca    synergize    reduce    mediated    outgrowth    pik3cah1047r    breast    activation    clinical    tumors    subgroups    prevent    demonstrated    heterogeneous    heterogeneity    mutant    single    signaling    kinase    temporal   

Project "EPICAN" data sheet

The following table provides information about the project.


Organization address
address: PETERSPLATZ 1
city: BASEL
postcode: 4051

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 Switzerland [CH]
 Total cost 191˙149 €
 EC max contribution 191˙149 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2020
 Duration (year-month-day) from 2020-05-01   to  2022-04-30


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITAT BASEL CH (BASEL) coordinator 191˙149.00


 Project objective

Breast cancer is a heterogeneous disease which is classified into different histological and molecular subgroups presenting different clinical outcomes. Also, the diversity of genetic/epigenetic alterations in cancer cells and their interactions with the microenvironment enhance cell plasticity and result in intra-tumor heterogeneity. While tumor heterogeneity is a major hurdle to anti-cancer therapy, its underlying molecular mechanisms remain ill-defined. The Phosphoinositide 3-kinase (PI3K) pathway, which is hyperactive in more than 70% of breast cancers mostly due to oncogenic activating mutations (PIK3CA-E545K & PIK3CA-H1047R), is a major driver of cell transformation. Using spatio-temporal conditional expression of the mutant PIK3CAH1047R combined with in situ lineage tracing in transgenic mice, recent studies demonstrated that the PIK3CA-H1047R oncogene reprograms lineage-committed mammary epithelial progenitors into a multipotent state, giving rise to heterogeneous mammary tumors. However, the mechanisms by which the PIK3CA-H1047R oncogene reactivates multipotency in breast cancer remain unknown. An increasing number of studies demonstrates that epigenetic regulators participate downstream of PI3K/AKT kinases to regulate the epigenome and contribute to tumor malignancy. Given the importance of epigenetic regulation for cell fate, I hypothesize that the effects of PIK3CA-H1047R signaling on tumor cell plasticity are mediated by epigenetic regulators. Because single inhibition of the PI3K pathway often results in resistance, it is of paramount interest to identify new targets whose inhibition can synergize with PI3K inhibitors to block tumor outgrowth, reduce tumor heterogeneity and prevent resistance. The overarching goal of this proposal is to identify epigenetic regulators downstream of oncogenic activation of the PI3K pathway leading to tumor cell plasticity, and to validate them as new targets in breast cancer.

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

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