dc.contributor.author | Scabia, V | |
dc.contributor.author | Ayyanan, A | |
dc.contributor.author | De Martino, F | |
dc.contributor.author | Agnoletto, A | |
dc.contributor.author | Battista, L | |
dc.contributor.author | Laszlo, C | |
dc.contributor.author | Treboux, A | |
dc.contributor.author | Zaman, K | |
dc.contributor.author | Stravodimou, A | |
dc.contributor.author | Jallut, D | |
dc.contributor.author | Fiche, M | |
dc.contributor.author | Bucher, P | |
dc.contributor.author | Ambrosini, G | |
dc.contributor.author | Sflomos, G | |
dc.contributor.author | Brisken, C | |
dc.coverage.spatial | England | |
dc.date.accessioned | 2022-08-23T10:55:00Z | |
dc.date.available | 2022-08-23T10:55:00Z | |
dc.date.issued | 2022-06-06 | |
dc.identifier | ARTN 3127 | |
dc.identifier | 10.1038/s41467-022-30898-0 | |
dc.identifier.citation | Nature Communications, 2022, 13 (1), pp. 3127 - | en_US |
dc.identifier.issn | 2041-1723 | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/5310 | |
dc.identifier.eissn | 2041-1723 | |
dc.identifier.eissn | 2041-1723 | |
dc.identifier.doi | 10.1038/s41467-022-30898-0 | |
dc.description.abstract | Estrogen and progesterone receptor (ER, PR) signaling control breast development and impinge on breast carcinogenesis. ER is an established driver of ER + disease but the role of the PR, itself an ER target gene, is debated. We assess the issue in clinically relevant settings by a genetic approach and inject ER + breast cancer cell lines and patient-derived tumor cells to the milk ducts of immunocompromised mice. Such ER + xenografts were exposed to physiologically relevant levels of 17-β-estradiol (E2) and progesterone (P4). We find that independently both premenopausal E2 and P4 levels increase tumor growth and combined treatment enhances metastatic spread. The proliferative responses are patient-specific with MYC and androgen receptor (AR) signatures determining P4 response. PR is required for tumor growth in patient samples and sufficient to drive tumor growth and metastasis in ER signaling ablated tumor cells. Our findings suggest that endocrine therapy may need to be personalized, and that abrogating PR expression can be a therapeutic option. | |
dc.format | Electronic | |
dc.format.extent | 3127 - | |
dc.language | eng | |
dc.language.iso | eng | en_US |
dc.publisher | NATURE PORTFOLIO | en_US |
dc.relation.ispartof | Nature Communications | |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | en_US |
dc.subject | Animals | |
dc.subject | Breast Neoplasms | |
dc.subject | Estradiol | |
dc.subject | Female | |
dc.subject | Humans | |
dc.subject | Mice | |
dc.subject | Progesterone | |
dc.subject | Receptors, Estrogen | |
dc.subject | Receptors, Progesterone | |
dc.title | Estrogen receptor positive breast cancers have patient specific hormone sensitivities and rely on progesterone receptor. | en_US |
dc.type | Journal Article | |
dcterms.dateAccepted | 2022-05-24 | |
dc.date.updated | 2022-08-23T10:53:51Z | |
rioxxterms.version | VoR | en_US |
rioxxterms.versionofrecord | 10.1038/s41467-022-30898-0 | en_US |
rioxxterms.licenseref.startdate | 2022-06-06 | |
rioxxterms.type | Journal Article/Review | en_US |
pubs.author-url | https://www.ncbi.nlm.nih.gov/pubmed/35668111 | |
pubs.issue | 1 | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Breast Cancer Research | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Breast Cancer Research/Endocrine control mechanisms | |
pubs.publication-status | Published online | |
pubs.volume | 13 | |
icr.researchteam | Endocrine control mechans | en_US |
dc.contributor.icrauthor | Brisken, Cathrin | |
icr.provenance | Deposited by Mr Arek Surman on 2022-08-23. Deposit type is initial. No. of files: 1. Files: Estrogen receptor positive breast cancers have patient specific hormone sensitivities and rely on progesterone receptor.pdf | |