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Innovative Approaches for Targeted Cancer Therapies
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Innovative Approaches for Targeted Cancer Therapies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 January 2025 | Viewed by 5804

Special Issue Editor

Prof. Dr. Maria Gazouli

E-Mail Website
Guest Editor
Department of Biology, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece
Interests: genetics; molecular biology; proteomics; microbiome; cancer; inflammation; nanomedicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is well accepted that tumor heterogeneity, systemic toxicities, and drug resistance are major problems in cancer therapy. Targeted therapy is the basis of precision medicine. As we learn more about the genomic alterations, protein expression, metabolomics and metagenomics that drive cancer, we will be able to design treatments that target these molecules more effectively. With advancements in a number of innovative approaches, e.g., artificial intelligent, CRISP, CAR-T, mRNA approaches, and nanotechnology, we are in position in all major areas of cancer therapy to advance therapeutic efficiency, reduce off-target effects, and deploy drugs effectively at target sites.

This Special Issue aims to gather original research articles and reviews on innovative approaches for targeted cancer therapies.

Prof. Dr. Maria Gazouli
Guest Editor

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Published Papers (3 papers)

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Research

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22 pages, 6663 KiB  
Article
Chemotherapeutic Drug Delivery Nanoplatform Development: From Physicochemical to Preclinical Evaluation
by Orestis Kontogiannis, Dimitrios Selianitis, Konstantinos Palikaras, Natassa Pippa, Stergios Pispas, Efstathios Efstathopoulos and Maria Gazouli
Int. J. Mol. Sci. 2024, 25(21), 11520; https://doi.org/10.3390/ijms252111520 - 26 Oct 2024
Viewed by 1046
Abstract
Through this study, the synergistic behavior of small-molecular-weight, amphiphilic surfactant molecules and the triblock copolymer Pluronic 188 was extensively evaluated based on their ability to formulate nanocarriers with novel properties for the delivery of class II and IV (biopharmaceutical classification system) chemotherapeutic compounds. [...] Read more.
Through this study, the synergistic behavior of small-molecular-weight, amphiphilic surfactant molecules and the triblock copolymer Pluronic 188 was extensively evaluated based on their ability to formulate nanocarriers with novel properties for the delivery of class II and IV (biopharmaceutical classification system) chemotherapeutic compounds. The combination of four different surfactants at multiple weight ratios and twelve initially formulated nanosystems resulted in four hybrid delivery platforms, which were further studied in terms of multiple physicochemical characteristics, as well as their stability in protein-rich media (fetal bovine serum/phosphate-buffer saline). Finally, we obtained a single final nanoformulation that exhibited a high loading capacity (%EE ≥ 75%) and a sustained drug release profile under physiological conditions (model drug methotrexate), without altering the original physicochemical characteristics of the carrier. With a mean hydrodynamic radius (Rh) of less than 70 nm, a polydispersity index of 0.219, and no protein complexation, the system is a suitable candidate for in vivo, intravenous, and/or intramuscular administration. The cytotoxicity and genotoxicity of both loaded and unloaded carriers were evaluated through the examination of the upregulation or downregulation of apoptosis-related pathways. Multiple conventional 2D and 3D spheroidal conformations were used for these assessments, including HEK293, HCT-116, and MCF-7 cell lines, the results of which stressed the safety and biocompatibility of the empty nanocarrier. Additionally, experiments on Caenorhabditis elegans were conducted to evaluate the system’s in vivo toxicity, focusing on developmental stages, egg-laying behavior, and locomotion. Nanosystems studied in terms of chemotherapeutic encapsulation have mostly focused on the physiochemical aspect of the development of such novel delivery platforms, with only few exceptions proceeding step-by-step from cellular 2D to 3D to in vivo experimentation. The present study offers a holistic view of the behavior of such a novel system, advancing our understanding of the capabilities of polymeric/surfactant-based nanodelivery platforms. Full article
(This article belongs to the Special Issue Innovative Approaches for Targeted Cancer Therapies)
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22 pages, 4731 KiB  
Article
VRK1 Regulates Sensitivity to Oxidative Stress by Altering Histone Epigenetic Modifications and the Nuclear Phosphoproteome in Tumor Cells
by Elena Navarro-Carrasco, Eva Monte-Serrano, Aurora Campos-Díaz, Frank Rolfs, Richard de Goeij-de Haas, Thang V. Pham, Sander R. Piersma, Paula González-Alonso, Connie R. Jiménez and Pedro A. Lazo
Int. J. Mol. Sci. 2024, 25(9), 4874; https://doi.org/10.3390/ijms25094874 - 30 Apr 2024
Cited by 1 | Viewed by 1443
Abstract
The chromatin organization and its dynamic remodeling determine its accessibility and sensitivity to DNA damage oxidative stress, the main source of endogenous DNA damage. We studied the role of the VRK1 chromatin kinase in the response to oxidative stress. which alters the nuclear [...] Read more.
The chromatin organization and its dynamic remodeling determine its accessibility and sensitivity to DNA damage oxidative stress, the main source of endogenous DNA damage. We studied the role of the VRK1 chromatin kinase in the response to oxidative stress. which alters the nuclear pattern of histone epigenetic modifications and phosphoproteome pathways. The early effect of oxidative stress on chromatin was studied by determining the levels of 8-oxoG lesions and the alteration of the epigenetic modification of histones. Oxidative stress caused an accumulation of 8-oxoG DNA lesions that were increased by VRK1 depletion, causing a significant accumulation of DNA strand breaks detected by labeling free 3′-DNA ends. In addition, oxidative stress altered the pattern of chromatin epigenetic marks and the nuclear phosphoproteome pathways that were impaired by VRK1 depletion. Oxidative stress induced the acetylation of H4K16ac and H3K9 and the loss of H3K4me3. The depletion of VRK1 altered all these modifications induced by oxidative stress and resulted in losses of H4K16ac and H3K9ac and increases in the H3K9me3 and H3K4me3 levels. All these changes were induced by the oxidative stress in the epigenetic pattern of histones and impaired by VRK1 depletion, indicating that VRK1 plays a major role in the functional reorganization of chromatin in the response to oxidative stress. The analysis of the nuclear phosphoproteome in response to oxidative stress detected an enrichment of the phosphorylated proteins associated with the chromosome organization and chromatin remodeling pathways, which were significantly decreased by VRK1 depletion. VRK1 depletion alters the histone epigenetic pattern and nuclear phosphoproteome pathways in response to oxidative stress. The enzymes performing post-translational epigenetic modifications are potential targets in synthetic lethality strategies for cancer therapies. Full article
(This article belongs to the Special Issue Innovative Approaches for Targeted Cancer Therapies)
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Review

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21 pages, 847 KiB  
Review
Agnostic Administration of Targeted Anticancer Drugs: Looking for a Balance between Hype and Caution
by Svetlana N. Aleksakhina, Alexander O. Ivantsov and Evgeny N. Imyanitov
Int. J. Mol. Sci. 2024, 25(7), 4094; https://doi.org/10.3390/ijms25074094 - 7 Apr 2024
Cited by 2 | Viewed by 1997
Abstract
Many tumors have well-defined vulnerabilities, thus potentially allowing highly specific and effective treatment. There is a spectrum of actionable genetic alterations which are shared across various tumor types and, therefore, can be targeted by a given drug irrespective of tumor histology. Several agnostic [...] Read more.
Many tumors have well-defined vulnerabilities, thus potentially allowing highly specific and effective treatment. There is a spectrum of actionable genetic alterations which are shared across various tumor types and, therefore, can be targeted by a given drug irrespective of tumor histology. Several agnostic drug-target matches have already been approved for clinical use, e.g., immune therapy for tumors with microsatellite instability (MSI) and/or high tumor mutation burden (TMB), NTRK1-3 and RET inhibitors for cancers carrying rearrangements in these kinases, and dabrafenib plus trametinib for BRAF V600E mutated malignancies. Multiple lines of evidence suggest that this histology-independent approach is also reasonable for tumors carrying ALK and ROS1 translocations, biallelic BRCA1/2 inactivation and/or homologous recombination deficiency (HRD), strong HER2 amplification/overexpression coupled with the absence of other MAPK pathway-activating mutations, etc. On the other hand, some well-known targets are not agnostic: for example, PD-L1 expression is predictive for the efficacy of PD-L1/PD1 inhibitors only in some but not all cancer types. Unfortunately, the individual probability of finding a druggable target in a given tumor is relatively low, even with the use of comprehensive next-generation sequencing (NGS) assays. Nevertheless, the rapidly growing utilization of NGS will significantly increase the number of patients with highly unusual or exceptionally rare tumor-target combinations. Clinical trials may provide only a framework for treatment attitudes, while the decisions for individual patients usually require case-by-case consideration of the probability of deriving benefit from agnostic versus standard therapy, drug availability, associated costs, and other circumstances. The existing format of data dissemination may not be optimal for agnostic cancer medicine, as conventional scientific journals are understandably biased towards the publication of positive findings and usually discourage the submission of case reports. Despite all the limitations and concerns, histology-independent drug-target matching is certainly feasible and, therefore, will be increasingly utilized in the future. Full article
(This article belongs to the Special Issue Innovative Approaches for Targeted Cancer Therapies)
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