ArticleThe Journal of experimental medicine2012
MYC pathway activation in triple-negative breast cancer is synthetic lethal with CDK inhibition.
Article in The Journal of experimental medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 220 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
220 citing papers in PubMed, 1 synthesis or guideline pooled it, 390 citations in OpenAlex.
- Comparative oncogenomics identifies combinations of driver genes and drug targets in BRCA1-mutated breast cancer.Nature communications · 2019Pooled it
- CCT2 enhances c-Myc stabilization to drive tumor progression and chemoresistance in head and neck squamous cell carcinoma.Genes & diseases · 2026Article
- Mitochondrial dynamics: A promising tool for personalized TNBC management.Genes & diseases · 2026Review
- Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
- EphB4 inhibition defines a druggable synthetic-lethal vulnerability in MYC-driven triple-negative breast cancer.Cell death & disease · 2026Article
- B.R.E.A.S.T. Breast canceR Enhanced AI-Supported Therapy: A New Interpretable Proteomics-Driven Machine Learning Framework for Therapy Response Prediction in Breast Cancer.International journal of molecular sciences · 2026Article
- Ribosome biogenesis bottlenecks reveal vulnerabilities in cancer.bioRxiv : the preprint server for biology · 2026Article
- Research Progress of PROTACs in Breast Cancer: Subtype-Oriented Target Landscape, Clinical Stratification Evidence, and Engineering Strategies for Translation.Biomedicines · 2026Review
- Integrative CRISPR Screening and RNA Analyses Discover an Essential Role for PUF60 Interactions with 3' Splice Sites in Cancer Progression.Cancer research · 2026Article
- Article
- Methionine metabolism and the NOP2 methyltransferase are essential for MYC-Driven liver tumorigenesis.bioRxiv : the preprint server for biology · 2026Article
- Disrupting CDK9 activity suppresses triple-negative breast cancer and is enhanced by EGFR Inhibition.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Multi-omics comprehensive analysis identified KIF22 and KRAS as highly synthetic lethal pairs for triple-negative breast cancer.Frontiers in oncology · 2026Article
- OGT-Mediated O-GlcNAcylation Stabilizes c-Myc Activity and Promotes Chemoresistance in Triple-Negative Breast Cancer.The breast journal · 2026Article
- The role of pluripotency regulators in triple-negative breast cancer immune response.Frontiers in genetics · 2026Review
- Pan-cancer Myc modulator that targets Myc-α-tubulin interaction to drive selective mitotic catastrophe.Scientific reports · 2025Article
- Targeting c-Myc enhances immunotherapy efficacy in combination with Ras inhibitor in triple-negative breast cancer.Clinical and translational medicine · 2025Article
- Tumor cell-adipocyte gap junctions activate lipolysis and contribute to breast tumorigenesis.Nature communications · 2025Article
- Article
- Targeting miR-32-5p suppresses c-MYC-driven proliferation and induces apoptosis in MCF-7 breast cancer cells.Medical oncology (Northwood, London, England) · 2025Article
160 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
Estrogen, progesterone, and HER2 receptor-negative triple-negative breast cancers encompass the most clinically challenging subtype for which targeted therapeutics are lacking. We find that triple-negative tumors exhibit elevated MYC expression, as well as altered expression of MYC regulatory genes, resulting in increased activity of the MYC pathway. In primary breast tumors, MYC signaling did not predict response to neoadjuvant chemotherapy but was associated with poor prognosis. We exploit the increased MYC expression found in triple-negative breast cancers by using a synthetic-lethal approach dependent on cyclin-dependent kinase (CDK) inhibition. CDK inhibition effectively induced tumor regression in triple-negative tumor xenografts. The proapoptotic BCL-2 family member BIM is up-regulated after CDK inhibition and contributes to this synthetic-lethal mechanism. These results indicate that aggressive breast tumors with elevated MYC are uniquely sensitive to CDK inhibitors.
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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.