ArticleMolecular medicine (Cambridge, Mass.)2023
Targeting CLDN6 in germ cell tumors by an antibody-drug-conjugate and studying therapy resistance of yolk-sac tumors to identify and screen specific therapeutic options.
Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Targeting histone deacetylation, cell cycle regulators and heat shock proteins as novel therapeutic strategies for penile cancers.NPJ precision oncology · 2026Article
- MicroRNAs and immunotherapy in testicular germ cell tumors: opportunities and challenges for modulation of the immune microenvironment.Frontiers in immunology · 2026Review
- Molecular Characterization of Seminoma Utilizing the AACR Project GENIE: A Retrospective Observational Study.Cancers · 2025Article
- [New insights from basic research on testicular germ cell tumors and updated tumorigenesis].Urologie (Heidelberg, Germany) · 2025Review
- Development of a bispecific antibody-drug conjugate targeting EpCAM and CLDN3 for the treatment of multiple solid tumors.Experimental hematology & oncology · 2025Article
- Article
- Antibody-mediated targeting of Claudins in cancer.Frontiers in oncology · 2024Review
- Molecular characterization of the CXCR4 / CXCR7 axis in germ cell tumors and its targetability using nanobody-drug-conjugates.Experimental hematology & oncology · 2023Article
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13 authors.
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Abstract
backgroundBeing the standard-of-care for four decades, cisplatin-based chemotherapy is highly efficient in treating germ cell tumors (GCT). However, often refractory patients present with a remaining (resistant) yolk-sac tumor (YST(-R)) component, resulting in poor prognosis due to lack of novel treatment options besides chemotherapy and surgery. The aim of this study was to identify novel targets for the treatment of YST by deciphering the molecular mechanisms of therapy resistance. Additionally, we screened the cytotoxic efficacy of a novel antibody-drug-conjugate targeting CLDN6 (CLDN6-ADC), as well as pharmacological inhibitors to target specifically YST.
methodsProtein and mRNA levels of putative targets were measured by flow cytometry, immunohistochemical stainings, mass spectrometry of formalin-fixed paraffin-embedded tissues, phospho-kinase arrays, or qRT-PCR. Cell viability, apoptosis and cell cycle assays of GCT and non-cancerous cells were performed using XTT cell viability assays or Annexin V / propidium iodide flow cytometry, respectively. Druggable genomic alterations of YST(-R) tissues were identified by the TrueSight Oncology 500 assay.
resultsWe demonstrated that treatment with a CLDN6-ADC enhanced apoptosis induction specifically in CLDN6
conclusionsIn summary, this study offers a novel CLDN6-ADC to target GCT. Additionally, this study presents novel pharmacological inhibitors blocking FGF, VGF, PDGF, mTOR, CHEK1, AURKA, or PARP signaling for the treatment of (refractory) YST patients. Finally, this study shed light on the mechanisms of therapy resistance in YST.
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