ArticleOncotarget2016
Anti-EGFR monoclonal antibodies and EGFR tyrosine kinase inhibitors as combination therapy for triple-negative breast cancer.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
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
65 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.
- Signaling Pathways and Natural Compounds in Triple-Negative Breast Cancer Cell Line.Molecules (Basel, Switzerland) · 2022Pooled it
- Basal-like Phenotype Identifies Immunotherapy-Responsive Subset of HR+/HER2- Breast Cancer with Aggressive Clinical Behavior.Cancers · 2026Article
- Retargeted adenoviruses for local IgA and CD47 blocker production as a novel cancer therapy.EMBO molecular medicine · 2026Article
- [Breast cancer research : BCR · 2026Article
- Decyl caffeate inhibits the proliferation of human triple negative breast cancer cells.BioMedicine · 2026Article
- Synthesis and anti-cancer activity of naphthalimide-organylselanyl conjugates.Beilstein journal of organic chemistry · 2026Article
- Article
- Combine mitochondrial-targeted gene therapy and chemotherapy to treat triple-negative breast cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Real-Time Monitoring of DNA Origami-Cell Interactions via Single Particle Tracking.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- The Therapeutic Potential of Photoimmunotherapy as a Safe, Effective and Non-Toxic Treatment Option for Superficial Triple Negative Breast Cancer.Cancer medicine · 2025Review
- Tailored therapies for triple-negative breast cancer: current landscape and future perceptions.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Triazole-Estradiol Analogs Induce Apoptosis and Inhibit EGFR and Its Downstream Pathways in Triple Negative Breast Cancer.Molecules (Basel, Switzerland) · 2025Article
- Advances in Monoclonal Antibody Therapies for Triple-Negative Breast Cancer: Immunotherapeutic and Targeted Strategies.Current molecular medicine · 2025Review
- Rhodanine-Piperazine Hybrids as Potential VEGFR, EGFR, and HER2 Targeting Anti-Breast Cancer Agents.International journal of molecular sciences · 2024Article
- The molecular basis of the anticancer effect of statins.Scientific reports · 2024Article
- Article
- Caspase-9 suppresses metastatic behavior of MDA-MB-231 cells in an adaptive organoid model.Scientific reports · 2024Article
- Migratory Tumor Cells Cooperate with Cancer Associated Fibroblasts in Hormone Receptor-Positive and HER2-Negative Breast Cancer.International journal of molecular sciences · 2024Article
- Small molecule agents for triple negative breast cancer: Current status and future prospects.Translational oncology · 2024Review
- The Agonistic Activity of the Human Epidermal Growth Factor is Reduced by the D46G Substitution.Protein and peptide letters · 2024Article
5 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
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) is characterized by overexpression of epidermal growth factor receptor (EGFR) and activation of its downstream signaling pathways. Dual targeting of EGFR using one monoclonal antibody (mAb; cetuximab or panitumumab) and one tyrosine kinase inhibitor (EGFR-TKI; gefitinib or erlotinib) is a potential therapeutic approach. We investigated the effect of these therapies in EGFR-expressing TNBC cell lines that do or do not harbor the main activating mutations of EGFR pathways. Cell lines were sensitive to EGFR-TKIs, whereas mAbs were active only in MDA-MB-468 (EGFR amplification) and SUM-1315 (KRAS and PTEN wild-type) cells. MDA-MB-231 (KRAS mutated) and HCC-1937 (PTEN deletion) cells were resistant to mAbs. The combined treatment resulted in a synergistic effect on cell proliferation and superior inhibition of the RAS/MAPK signaling pathway in mAb-sensitive cells. The anti-proliferative effect was associated with G1 cell cycle arrest followed by apoptosis. Sensitivity to therapies was characterized by induction of positive regulators and inactivation of negative regulators of cell cycle. These results suggest that dual EGFR inhibition might result in an enhanced antitumor effect in a subgroup of TNBC. The status of EGFR, KRAS and PTEN could be used as a molecular marker for predicting the response to this therapeutic strategy.
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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.