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Defining hormonal cross-talk and the role of mutations in estrogen receptor positive breast cancer

Project description

Investigation of hormonal cross-talk in breast cancer

The majority of breast cancers are driven by oestrogen receptors (OER), and anti-oestrogenic drugs represent the standard treatment for these cancers. Recent studies support the activation of the progesterone receptor (PR) for the treatment of those cases where cancer becomes resistant to anti-oestrogenic drugs. The controversy regarding the role of progestogens in this disease prevents the clinical application of PR-targeted therapies. The ERC-funded ER_disease project focuses on investigating the crosstalk between nuclear receptors in breast cancer. The main goal is to test the hypothesis that other nuclear receptors that are present in these cancer tissues could be activated to interfere with the OER function and prevent the progression of breast cancer.

Objective

Estrogen Receptor (ER) is the driving transcription factor in ~75% of all breast cancers. ER antagonists are routinely used for treatment, but significant variability exists in clinical response. We are interested in explaining this heterogeneity and exploiting the mechanistic insight. We have recently identified important, but previously uncharacterised cross-talk between ER and the progesterone receptor (PR) and androgen receptor (AR) pathways, both of which are commonly expressed in ER+ tumours. Recently, ER has been shown to be mutated in ~18-55% of metastatic breast cancers. In addition, two key ER-chromatin regulatory proteins, FoxA1 and GATA3, are mutated in primary ER+ disease. Finally we have discovered three previously unknown phosphorylation events on FoxA1.

Aim 1: We will comprehensively explore the cross-talk that exists between ER and PR and AR pathways to determine the physiological effects on ER function. Aim 2: We will recapitulate the key mutations observed in ER, FoxA1 and GATA3, to assess the impact on ER-DNA interactions, ER transcriptional activity and cell growth and drug response. This will be explored under different hormonal contexts to identify how the mutational spectrum influences the cross-talk between ER and the parallel PR and AR pathways. Aim 3: We will identify upstream kinase pathways that influence FoxA1 and GATA3 function. Aim 4: We will establish a novel single locus chromatin purification method for isolation of specific chromatin loci, followed by Mass Spectrometry to characterise the potential role of PR and AR variants and to identify unknown regulatory factors.

Given recent biological discoveries and technological advances, we are perfectly positioned to apply cutting-edge tools to glean mechanistic insight into the factors that determine variability within ER+ disease. This proposal aims to advance our understanding of ER+ tumour heterogeneity, revealing ways of exploiting this in a clinically meaningful manner.

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Topic(s)

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Funding Scheme

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ERC-COG - Consolidator Grant

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Call for proposal

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(opens in new window) ERC-2014-CoG

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Host institution

THE CHANCELLOR MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 1 987 273,75
Address
TRINITY LANE THE OLD SCHOOLS
CB2 1TN Cambridge
United Kingdom

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Region
East of England East Anglia Cambridgeshire CC
Activity type
Higher or Secondary Education Establishments
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Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 1 987 273,75

Beneficiaries (1)

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