ArticleOncotarget2016
Targeting MET and EGFR crosstalk signaling in triple-negative breast cancers.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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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
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Unraveling Biomarker Signatures in Triple-Negative Breast Cancer: A Systematic Review for Targeted Approaches.International journal of molecular sciences · 2024Pooled it
- Targeting EGFR Endocytosis and Signaling for Cancer Drug Delivery and Cancer Treatment.Cancers · 2026Review
- High TRIM28 Expression Defines an Aggressive, Immune-Cold Phenotype with Worse Survival Outcomes in ERα-Positive Breast Cancer.Biomedicines · 2026Article
- A tri-specific EGFR/cMet/VEGF antibody demonstrates potent multi-mechanistic activity in preclinical triple-negative breast cancer models.The Journal of biological chemistry · 2026Article
- Targeting of a novel interplay between MET tyrosine kinase and NRF2 enhances sensitivity to Paclitaxel in triple negative breast cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Review
- Enhancing immunotherapy efficacy in colorectal cancer: targeting the FGR-AKT-SP1-DKK1 axis with DCC-2036 (Rebastinib).Cell death & disease · 2025Article
- Comparison of the effects of crizotinib as monotherapy and as combination therapy with butyric acid on different breast cancer cells.Oncology letters · 2025Article
- Review
- Prognostic Markers in Tyrosine Kinases Specific to Basal-like 2 Subtype of Triple-Negative Breast Cancer.International journal of molecular sciences · 2024Article
- Cabozantinib inhibits tumor growth in mice with ovarian cancer.American journal of cancer research · 2024Article
- Exploring the multifaceted role of obesity in breast cancer progression.Frontiers in cell and developmental biology · 2024Review
- Targeting isoforms of RON kinase (MST1R) drives antitumor efficacy.Cell death and differentiation · 2023Article
- Suppression of TNBC metastasis by doxazosin, a novel dual inhibitor of c-MET/EGFR.Journal of experimental & clinical cancer research : CR · 2023Article
- Combinations of EGFR and MET inhibitors reduce proliferation and invasiveness of mucosal melanoma cells.Journal of cellular and molecular medicine · 2023Article
- An Observatory for theCancers · 2023Review
- HER3 functions as an effective therapeutic target in triple negative breast cancer to potentiate the antitumor activity of gefitinib and paclitaxel.Cancer cell international · 2023Article
- Sorting nexin-dependent therapeutic targeting of oncogenic epidermal growth factor receptor.Cancer gene therapy · 2023Article
- SynDISCO: A Mechanistic Modeling-Based Framework for Predictive Prioritization of Synergistic Drug Combinations Targeting Cell Signalling Networks.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Foretinib Is Effective against Triple-Negative Breast Cancer Cells MDA-MB-231 In Vitro and In Vivo by Down-Regulating p-MET/HGF Signaling.International journal of molecular sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is a vital need for improved therapeutic strategies that are effective in both primary and metastatic triple-negative breast cancer (TNBC). Current treatment options for TNBC patients are restricted to chemotherapy; however tyrosine kinases are promising druggable targets due to their high expression in multiple TNBC subtypes. Since coexpression of receptor tyrosine kinases (RTKs) can promote signaling crosstalk and cell survival in the presence of kinase inhibitors, it is likely that multiple RTKs will need to be inhibited to enhance therapeutic benefit and prevent resistance. The MET and EGFR receptors are actionable targets due to their high expression in TNBC; however crosstalk between MET and EGFR has been implicated in therapeutic resistance to single agent use of MET or EGFR inhibitors in several cancer types. Therefore it is likely that dual inhibition of MET and EGFR is required to prevent crosstalk signaling and acquired resistance. In this study, we evaluated the heterogeneity of MET and EGFR expression and activation in primary and metastatic TNBC tumorgrafts and determined the efficacy of MET (MGCD265 or crizotinib) and/or EGFR (erlotinib) inhibition against TNBC progression. Here we demonstrate that combined MET and EGFR inhibition with either MGCD265 and erlotinib treatment or crizotinib and erlotinib treatment were highly effective at abrogating tumor growth and significantly decreased the variability in treatment response compared to monotherapy. These results advance our understanding of the RTK signaling architecture in TNBC and demonstrate that combined MET and EGFR inhibition may be a promising therapeutic strategy for TNBC patients.
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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.