ArticleJournal of the National Cancer Institute2016
Targeting a Cancer-Specific Epitope of the Epidermal Growth Factor Receptor in Triple-Negative Breast Cancer.
Article in Journal of the National Cancer Institute, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 35 citations in OpenAlex.
- Targeted biologics for TNBC: Advances in nanobodies, antibodies, peptides, and aptamers.Molecular therapy. Oncology · 2026Review
- EGFR-targeted affibody-polyIC polyplex kills EGFR-overexpressing cancer cells without activating the EGFR.PloS one · 2026Article
- Interplay between malic enzyme 2, de novo serine synthesis, and the malate-aspartate shuttle drives metabolic adaptation in triple-negative breast cancer.Cancer & metabolism · 2025Article
- EGFR as a potent CAR T target in triple negative breast cancer brain metastases.Breast cancer research and treatment · 2023Article
- Expanding the Therapeutic Window of EGFR-Targeted PE24 Immunotoxin for EGFR-Overexpressing Cancers by Tailoring the EGFR Binding Affinity.International journal of molecular sciences · 2022Article
- Review
- Eugenol-Induced Autophagy and Apoptosis in Breast Cancer Cells via PI3K/AKT/FOXO3a Pathway Inhibition.International journal of molecular sciences · 2021Article
- Targeting Receptors on Cancer Cells with Protein Toxins.Biomolecules · 2020Review
- 'Characterization of monoclonal antibodies generated to the 287-302 amino acid loop of the human epidermal growth factor receptor'.Antibody therapeutics · 2019Article
- Targeting dePARylation selectively suppresses DNA repair-defective and PARP inhibitor-resistant malignancies.Science advances · 2019Article
- Anti-metastatic and anti-proliferative activity of eugenol against triple negative and HER2 positive breast cancer cells.BMC complementary and alternative medicine · 2018Article
- Characterization of Apoptosis in a Breast Cancer Cell Line after IL-10 SilencingAsian Pacific journal of cancer prevention : APJCP · 2018Article
- Triple negative breast cancer: shedding light onto the role of pi3k/akt/mtor pathway.Oncotarget · 2016Review
- Immunotoxin Therapies for the Treatment of Epidermal Growth Factor Receptor-Dependent Cancers.Toxins · 2016Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTriple-negative breast cancers (TNBCs) are typically more aggressive and result in poorer outcomes than other breast cancers because treatment options are limited due to lack of hormone receptors or amplified human epidermal growth factor receptor 2 (HER2). Many TNBCs overexpress the epidermal growth factor receptor (EGFR) or manifest amplification of theEGFRgene, supporting EGFR as a therapeutic target. While EGFR-directed small molecule inhibitors have shown limited effectiveness in clinical settings, use of EGFR as a mechanism of delivering enzymatic cytotoxins to TNBC has not been demonstrated.
methodsUsing the single-chain variable fragment (scFv) of the 806 antibody that binds only cells with overexpressed, misfolded, or mutant variants of the EGFR, a recombinant immunotoxin was engineered through gene fusion withPseudomonas aeruginosaExotoxin A (806-PE38). The potency of 806-PE38 on reducing TNBC cell growth in vitro and in xenograft models (n ≥ 6) was examined for six TNBC cell lines. All statistical tests were two-sided.
results806-PE38 statistically significantly reduced the viability of all tested TNBC lines, with IC50values below 10 ng/mL for three of six cell lines, while not affecting cells with wild-type EGFR (IC50>300 ng/mL). Systemic treatments with 806-PE38 vs vehicle resulted in statistically significantly reduced tumor burdens (806-PE38 mean = 128 mm(3)[SD = 46 mm(3)] vs vehicle mean = 749 mm(3)[SD = 395 mm(3)], P = .001) and increased median survival (806-PE38 median = 82 days vs vehicle median = 50 days,P= .01) in a MDA-MB-468 TNBC mouse xenograft. Deletion of the catalytic residue eliminated both cytotoxic activity in vitro and the reduction in tumor burden and survival (P= .52).
conclusionsThese data support the further development of the 806-PE38 immunotoxin as a therapeutic agent for the treatment of patients with EGFR-positive TNBC. Follow-up experiments with combination therapies will be attempted to achieve full remissions.
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