ArticleMolecular cancer therapeutics2012
Discordant cellular response to presurgical letrozole in bilateral synchronous ER+ breast cancers with a KRAS mutation or FGFR1 gene amplification.
Article in Molecular cancer therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 21 citations in OpenAlex.
- MEK activation modulates glycolysis and supports suppressive myeloid cells in TNBC.JCI insight · 2020Article
- Article
- Article
- The Modulatory Role of MicroRNA-873 in the Progression of KRAS-Driven Cancers.Molecular therapy. Nucleic acids · 2019Article
- Association of FGFR1 with ERα Maintains Ligand-Independent ER Transcription and Mediates Resistance to Estrogen Deprivation in ERClinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Genomic profiling of ERScience translational medicine · 2017Article
- Interaction between the estrogen receptor and fibroblast growth factor receptor pathways in non-small cell lung cancer.Oncotarget · 2017Article
- Inhibition of the fibroblast growth factor receptor (FGFR) pathway: the current landscape and barriers to clinical application.Oncotarget · 2017Review
- FGFR-1 amplification in metastatic lymph-nodal and haematogenous lobular breast carcinoma.Journal of experimental & clinical cancer research : CR · 2012Article
- FGFR1 Is Associated With Tamoxifen Resistance and Poor Prognosis of ER-Positive Breast Cancers by Suppressing ER Protein Expression.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
We describe herein a patient presenting with bilateral estrogen-receptor-positive (ER+) breast tumors who was enrolled in a clinical trial exploring molecular aberrations associated with hormone-refractory tumor cell proliferation. Short-term (two week) hormonal therapy with the aromatase inhibitor letrozole substantially reduced proliferation as measured by Ki67 immunohistochemistry in one tumor, whereas the second was essentially unchanged. Extensive molecular and genetic work-up of the two tumors yielded divergent lesions in the two tumors: an activating KRAS mutation in the responsive tumor and an amplification of the fibroblast growth factor receptor-1 (FGFR1) locus in the treatment-refractory tumor. These findings provide an insight to possible mechanisms of resistance to antiestrogen therapy in ER+ breast cancers. First, they illustrate the necessity of clinically approved assays to identify FGFR1 gene amplification, which occur in approximately 5% of breast tumors and have been linked to antiestrogen resistance. It is quite possible that the addition of FGFR inhibitors to ER-targeted therapy will yield a superior antitumor effect and improved patient outcome. Second, they suggest that the role of activating mutations in RAS, although rare in breast cancer, may need to be explored in the context of ER+ breast tumors.
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Registered trials
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.