ArticlePloS one2018
ER-positive breast cancer cells are poised for RET-mediated endocrine resistance.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 42 citations in OpenAlex.
- A long-chain heparan sulfate capture mechanism directs paracrine GDNF-GFRα1 signalling through RET.bioRxiv : the preprint server for biology · 2026Article
- Outcome prediction of oestrogen receptor-positive breast cancer based on a panel of oestrogen receptor-regulated genes.Histopathology · 2025Article
- Enhanced prediction of breast cancer patient response to chemotherapy by integrating deconvolved expression patterns of immune, stromal and tumor cells.bioRxiv : the preprint server for biology · 2025Article
- REThinking the role of the RET oncogene in breast cancer.Frontiers in oncology · 2024Review
- Expert consensus on the diagnosis and treatment of RET gene fusion non-small cell lung cancer in China.Thoracic cancer · 2023Article
- RET signaling in breast cancer therapeutic resistance and metastasis.Breast cancer research : BCR · 2023Review
- GDNF-RET signaling and EGR1 form a positive feedback loop that promotes tamoxifen resistance via cyclin D1.BMC cancer · 2023Article
- A Distinct Chromatin State Drives Therapeutic Resistance in Invasive Lobular Breast Cancer.Cancer research · 2022Article
- The Emerging Portrait of Glial Cell Line-derived Neurotrophic Factor Family Receptor Alpha (GFRα) in Cancers.International journal of medical sciences · 2022Review
- JMJD6 orchestrates a transcriptional program in favor of endocrine resistance in ER+ breast cancer cells.Frontiers in endocrinology · 2022Article
- Prolactin and endocrine therapy resistance in breast cancer: The next potential hope for breast cancer treatment.Journal of cellular and molecular medicine · 2021Review
- CATCH: A Prospective Precision Oncology Trial in Metastatic Breast Cancer.JCO precision oncology · 2021Article
- Chromatin run-on sequencing analysis finds that ECM remodeling plays an important role in canine hemangiosarcoma pathogenesis.BMC veterinary research · 2020Article
- Advances in Targeting RET-Dependent Cancers.Cancer discovery · 2020Review
- Ret Receptor Has Distinct Alterations and Functions in Breast Cancer.Journal of mammary gland biology and neoplasia · 2020Review
- Rationale and Roadmap for Developing Panels of Hotspot Cancer Driver Gene Mutations as Biomarkers of Cancer Risk.Environmental and molecular mutagenesis · 2020Review
- RET in breast cancer: pathogenic implications and mechanisms of drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2019Review
- Design, synthesis and biological evaluation of 3-(2-aminooxazol-5-yl)-2H-chromen-2-one derivatives.Chemistry Central journal · 2018Article
- A bi-stable feedback loop between GDNF, EGR1, and ERα contribute to endocrine resistant breast cancer.PloS one · 2018Article
- GDNF and the RET Receptor in Cancer: New Insights and Therapeutic Potential.Frontiers in physiology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The RET tyrosine kinase signaling pathway is involved in the development of endocrine resistant ER+ breast cancer. However, we know little about how ER+ cells activate RET signaling and initiate an endocrine resistant phenotype. Here we show that both ER+ endocrine resistant and sensitive breast cancers have a functional RET tyrosine kinase signaling pathway, but that endocrine sensitive breast cancer cells lack RET ligands that are necessary to drive endocrine resistance. Transcription of one RET ligand, GDNF, is necessary and sufficient to confer resistance in the ER+ MCF-7 cell line. Endogenous GDNF produced by endocrine resistant cells is translated, secreted into the media, and activates RET signaling in nearby cells. In patients, RET ligand expression predicts responsiveness to endocrine therapies and correlates with survival. Collectively, our findings show that ER+ tumor cells are "poised" for RET mediated endocrine resistance, expressing all components of the RET signaling pathway, but endocrine sensitive cells lack high expression of RET ligands that are necessary to initiate the resistance phenotype.
Indexed as
Identifiers
What OpenQuestion holds
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.