Truncated DAPK Variants Restore Tumor Suppressor Activity and Synergize with Standard Therapies in High-Grade Serous Ovarian Cancer
Reactivation of DAPK1, particularly through truncated variants, represents a promising therapeutic strategy to overcome chemoresistance in HGSOC. The dual mechanisms of tumor suppression provide a strong rationale for developing DAPK1-based therapies to enhance the efficacy of standard chemotherapy, especially in patients with chemoresistant or p53-deficient tumors. Future work should focus on optimizing delivery approaches for DAPK1 variants and assessing their synergistic potential with emerging targeted treatments in clinical settings.
Authors
- Monika Raab (ORCID: https://orcid.org/0000-0002-8081-0905)
- Balázs Győrffy (ORCID: https://orcid.org/0000-0002-5772-3766)
- Sven Becker (ORCID: https://orcid.org/0000-0003-1972-3797)
- Khayal Gasimli (ORCID: https://orcid.org/0000-0003-1874-0341)
- Samuel Peña‐Llopis (ORCID: https://orcid.org/0000-0003-3847-1353)
- Mourad Sanhaji (ORCID: https://orcid.org/0000-0001-8202-0694)
Institutions
- Semmelweis University (HU)
- Goethe University Frankfurt (DE)
- German Cancer Research Center (DE)
- Heidelberg University (DE)
- University Hospital Heidelberg (DE)
- University of Pecs (HU)
Publication Details
- Journal
- Cancers
- Published
- 2025-06-08
- DOI
- https://doi.org/10.3390/cancers17121910
- Primary Topic
- Cancer-related Molecular Pathways
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Deutsche Krebshilfe