ArticleNeoplasia (New York, N.Y.)2026
Rational payload selection enables high antitumoral efficacy of an anti-EGFR antibody-drug conjugate against ovarian tumors.
Article in Neoplasia (New York, N.Y.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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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
1 citing paper in PubMed.
- Oncogenic EGFR Signaling as a Central Regulator of Chemoresistance in Ovarian Cancer: A Mechanistic Review.International journal of molecular sciences · 2026Review
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3 authors.
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Abstract
The epidermal growth factor receptor (EGFR) is frequently expressed in ovarian cancer, yet its potential as a therapeutic target remains underexplored. We investigated EGFR expression and its therapeutic exploitation using antibody-drug conjugates (ADCs) based on the clinical anti-EGFR antibody cetuximab. EGFR protein and mRNA levels were evaluated in patient-derived tumors and ovarian cancer cell lines by western blotting and qPCR, and cell surface localization was analyzed by flow cytometry. Several cetuximab-based ADCs were generated using clinically validated cytotoxics: DM1, deruxtecan (DXd), and monomethyl auristatin F (MMAF), with cleavable or non-cleavable linkers. Their structural integrity, antiproliferative activity, internalization dynamics, and mechanisms of action were examined in vitro, and in vivo efficacy and pharmacokinetics were assessed in SKOV3 and OVCAR8 xenograft models. All ADCs showed successful conjugation and preserved antibody integrity. MMAF-conjugated ADCs displayed superior antiproliferative effects, particularly the cleavable cetuximab-vc-MMAF, while A2780 and PEO4, which showed low EGFR expression, were less responsive. Cetuximab alone or free MMAF were markedly less active. Mechanistic studies revealed rapid internalization and lysosomal trafficking of cetuximab-vc-MMAF, leading to G2/M arrest, increased mitotic markers, spindle defects, DNA damage, and apoptosis. In vivo, cetuximab-vc-MMAF significantly inhibited tumor growth and prolonged survival without systemic toxicity. Pharmacokinetic analyses confirmed selective intratumoral accumulation of the ADC and its payload with minimal off-target distribution. Treated tumors exhibited reduced proliferation and increased markers of mitotic arrest, DNA damage, and apoptosis. These results demonstrate that cetuximab-based EGFR-targeting ADCs exert potent and selective antitumor activity in ovarian cancer, supporting their further preclinical and clinical development.
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