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Biomedicines
Special Issues
Advances in Cancer Treatment
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Advances in Cancer Treatment

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: 31 October 2026 | Viewed by 1728

Special Issue Editors

Dr. Vlasios Karageorgos

E-Mail
Guest Editor
Department of Pharmacology & Anesthesiology, School of Medicine, University of Crete, Crete, Greece
Interests: GPCR’s; CRF; GnRH; AT1R; drug-conjugates
Prof. Dr. George Liapakis

E-Mail Website
Guest Editor
Department of Pharmacology, School of Medicine, University of Crete, Crete, Greece
Interests: GPCRs; CRF; GnRH; AT1R; novel anticancer therapies

Special Issue Information

Dear Colleagues,

We invite you to contribute to a special issue focused on cutting-edge developments in advanced cancer therapies, emphasizing the role of biomolecules in precision oncology. This issue will explore the design, development, and clinical translation of targeted therapies, including bio-conjugates, nucleic acid-based treatments, and other biologic agents engineered for tumor specificity and therapeutic potency. We welcome original research and reviews that address novel biomolecular platforms, mechanisms of action and resistance, optimization of therapeutic conjugates, translational progress, and biomarker-driven strategies for personalized treatment. This special issue aims to showcase the biomolecular innovations transforming cancer therapy and accelerating the path from laboratory discoveries to clinical application.

Dr. Vlasios Karageorgos
Prof. Dr. George Liapakis
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • targeted therapy
  • bio-conjugates
  • biologic agents
  • precision oncology
  • personalized cancer treatment
  • biomarker-guided therapy
  • cancer drug development
  • biopharmaceuticals

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

18 pages, 5108 KB  
Article
DYRK1B Inhibition by AZ191 Sensitizes High-Grade Serous Ovarian Cancer to Niraparib Through Promoting Apoptosis and Ferroptosis
by Yu Gao, Yuanyuan Cao, Junyao Liu, Fang Tong, Xianlin Liu, Jiahui Wang, Peixuan Liu, Yanting Xu, Lu Feng, Pengxin Zhang, Jingchun Gao and Jiwei Liu
Biomedicines 2026, 14(4), 939; https://doi.org/10.3390/biomedicines14040939 - 20 Apr 2026
Viewed by 567
Abstract
Background/Objectives: The clinical challenges of PARP inhibitors in ovarian cancer include the lack of effective maintenance regimens for homologous recombination proficiency (HRP) patients and the emergence of acquired resistance in initially responsive homologous recombination deficiency (HRD) patients. This study aims to explore the [...] Read more.
Background/Objectives: The clinical challenges of PARP inhibitors in ovarian cancer include the lack of effective maintenance regimens for homologous recombination proficiency (HRP) patients and the emergence of acquired resistance in initially responsive homologous recombination deficiency (HRD) patients. This study aims to explore the synergistic effect and molecular mechanism of the bispecific tyrosine phosphorylation-regulated kinase 1B (DYRK1B) inhibitor AZ191 combined with the PARP inhibitor Niraparib on high-grade serous ovarian cancer (HGSOC). Methods: This study first explored the expression and prognostic significance of DYRK1B in ovarian cancer through bioinformatics analysis. Subsequently, the therapeutic effect of the DYRK1B inhibitor AZ191 combined with Niraparib on HGSOC cells and organoids was evaluated by MTT examination. Flow cytometry and Western blot were used to investigate the synergistic mechanism between the two agents. Results: Bioinformatics analysis shows that the high expression of DYRK1B in serous ovarian cancer is associated with poor prognosis of the patients. The experiments in vitro have shown that the DYRK1B inhibitor AZ191 can enhance the therapeutic effect of Niraparib on HGSOC cells and organoids, whether HRD-positive or not. Mechanistic studies have shown that the combination of AZ191 and Niraparib can synergistically increase the accumulation of DNA damage, thereby intensifying the apoptosis of HGSOC cells. In addition, the combination therapy induces ferroptosis by inhibiting the Nrf2/SLC7A11/GPX4 axis, thereby exerting cytotoxic effects. Conclusions: Our results uncover a novel mechanism by which inhibiting DYRK1B enhances the anti-HGSOC efficacy of Niraparib and may offer a promising treatment strategy to improve the maintenance therapy in both HRD and HRP ovarian cancer patients. Full article
(This article belongs to the Special Issue Advances in Cancer Treatment)
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13 pages, 2009 KB  
Article
Resveratrol Mimics Exercise-Induced Metabolic Stress to Suppress CIP2A and Epithelial–Mesenchymal Transition in 3D Renal Carcinoma Spheroids
by Bang Sub Lee, Jong-Shik Kim and Wi-Young So
Biomedicines 2026, 14(3), 599; https://doi.org/10.3390/biomedicines14030599 - 8 Mar 2026
Viewed by 564
Abstract
Background/Objectives: We evaluated a 6-day repeated resveratrol exposure regimen in a three-dimensional (3D) culture model of human renal cell carcinoma (Caki-1) spheroids to examine phenotypic responses and changes in CIP2A abundance and epithelial–mesenchymal transition (EMT)-associated marker expression. Methods: Over 6 days, we assessed [...] Read more.
Background/Objectives: We evaluated a 6-day repeated resveratrol exposure regimen in a three-dimensional (3D) culture model of human renal cell carcinoma (Caki-1) spheroids to examine phenotypic responses and changes in CIP2A abundance and epithelial–mesenchymal transition (EMT)-associated marker expression. Methods: Over 6 days, we assessed morphology and 2D cell viability and quantified CIP2A, fibronectin, and α-SMA by immunoblotting and immunofluorescence. Results: Resveratrol reduced 2D viability and increased cytoplasmic vacuoles, consistent with a stress-associated morphological response. In 3D spheroids, resveratrol treatment was associated with reduced CIP2A protein levels and decreased fibronectin and α-SMA, consistent with attenuation of a mesenchymal marker profile. Conclusions: These proof-of-concept data link 6-day resveratrol exposure to CIP2A reduction and decreased mesenchymal marker expression in a human 3D RCC spheroid system; however, PP2A activity and downstream signaling, AMPK/SIRT1 activation, and EMT-relevant functional assays were not assessed, and validation across additional RCC models will be required. Full article
(This article belongs to the Special Issue Advances in Cancer Treatment)
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