Trial reportBreast cancer research : BCR2019
Impact of aromatase inhibitor treatment on global gene expression and its association with antiproliferative response in ER+ breast cancer in postmenopausal patients.
Trial report in Breast cancer research : BCR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Characterization of breast cancer tumors in older patients who show de novo resistance to endocrine therapy.Scientific reports · 2024Article
- Immune infiltration correlates with transcriptomic subtypes in primary estrogen receptor positive invasive lobular breast cancer.NPJ precision oncology · 2024Article
- EMBER creates a unified space for independent breast cancer transcriptomic datasets enabling precision oncology.NPJ breast cancer · 2024Article
- DREAM On, DREAM Off: A Review of the Estrogen Paradox in Luminal A Breast Cancers.Biomedicines · 2024Review
- Breast cancers with high proliferation and low ER-related signalling have poor prognosis and unique molecular features with implications for therapy.British journal of cancer · 2023Article
- The impact of poor metabolic health on aggressive breast cancer: adipose tissue and tumor metabolism.Frontiers in endocrinology · 2023Review
- [miR-16-5p regulates apoptosis and migration of drug-resistant breast cancer cells by targeting YWHAQ].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Impact of Duration of Neoadjuvant Aromatase Inhibitors on Molecular Expression Profiles in Estrogen Receptor-positive Breast Cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- DREAM, a possible answer to the estrogen paradox of the Women's Health Initiative Trial.Heliyon · 2022Article
- TP53 mutations are associated with primary endocrine resistance in luminal early breast cancer.Cancer medicine · 2021Article
- Oestrogen deprivation induces chemokine production and immune cell recruitment in in vitro and in vivo models of oestrogen receptor-positive breast cancer.Breast cancer research : BCR · 2021Article
- Endogenous and Therapeutic Estrogens: Maestro Conductors of the Microenvironment of ER+ Breast Cancers.Cancers · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 7 institutions in 1 country.
Funding
Abstract
backgroundEndocrine therapy reduces breast cancer mortality by 40%, but resistance remains a major clinical problem. In this study, we sought to investigate the impact of aromatase inhibitor (AI) therapy on gene expression and identify gene modules representing key biological pathways that relate to early AI therapy resistance.
methodsGlobal gene expression was measured on pairs of core-cut biopsies taken at baseline and at surgery from 254 patients with ER-positive primary breast cancer randomised to receive 2-week presurgical AI (n = 198) or no presurgical treatment (control n = 56) from the POETIC trial. Data from the AI group was adjusted to eliminate artefactual process-related changes identified in the control group. The response was assessed by changes in the proliferation marker, Ki67.
resultsHigh baseline ESR1 expression associated with better AI response in HER2+ tumours but not HER2- tumours. In HER2- tumours, baseline expression of 48 genes associated with poor antiproliferative response (p < 0.005) including PERP and YWHAQ, the two most significant, and the transcription co-regulators (SAP130, HDAC4, and NCOA7) which were among the top 16 most significant. Baseline gene signature scores measuring cell proliferation, growth factor signalling (ERBB2-GS, RET/GDNF-GS, and IGF-1-GS), and immune activity (STAT1-GS) were significantly higher in poor AI responders. Two weeks of AI caused downregulation of genes involved in cell proliferation and ER signalling, as expected. Signature scores of E2F activation and TP53 dysfunction after 2-week AI were associated with poor AI response in both HER2- and HER2+ patients.
conclusionsThere is a high degree of heterogeneity in adaptive mechanisms after as little as 2-week AI therapy; however, all appear to converge on cell cycle regulation. Our data support the evaluation of whether an E2F signatures after short-term exposure to AI may identify those patients most likely to benefit from the early addition of CDK4/6 inhibitors.
trial registrationISRCTN, ISRCTN63882543, registered on 18 December 2007.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.