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Targeted Therapies and Molecular Methods in Cancer, 3rd Edition

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (20 May 2026) | Viewed by 11744

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Special Issue Information

Dear Colleagues,

This Special Issue of IJMS continues on from “Targeted Therapies and Molecular Methods in Cancer” and “Targeted Therapies and Molecular Methods in Cancer, 2nd Edition”, examining targeted strategies for dealing with cancer. We welcome articles on new targeted anticancer methods, novel drug delivering routes, and innovative approaches including, but not limited to, the following: immunotherapy; new aspects of radiotherapy; methods to facilitate drug delivery, such as pulsed electric fields (PEFs), sonoporation, magnetic fields (MFs), nanotechnology, and nanocarriers; and gene electrotransfer using PEFs. Targeted anticancer methods can focus on membrane proteins and ion channel alterations. Additionally, targets can be specific surface receptors (ERs, estrogen receptors; FARs, folic acid receptors; and HARs, hyaluronic acid receptors) or cancer biomarkers. Research targeting drug resistance (MDR), aimed at bypassing or modifying the activity of drug transporters, i.e., MDR1/P-gp, MRP1, BCRP, and LRP, will be of interest. We also welcome new and more effective protocols which could be developed and find potential applications in pharmacy and medical sciences. This Special Issue will cover the latest research concerning targeted therapies and molecular methods against cancer.

Dr. Julita Kulbacka
Guest Editor

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Keywords

  • immunotherapy
  • radiotherapy
  • methods using facilitated drug delivery such as electroporation, sonoporation, and magnetic fields
  • nanotechnology and nanocarriers
  • gene electrotherapy
  • intelligent predicting methods with AI

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Published Papers (5 papers)

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Research

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25 pages, 5503 KB  
Article
In Silico Approach to Design of New Multi-Targeted Inhibitors Based on Quinoline Ring with Potential Anticancer Properties
by Żaneta Czyżnikowska, Martyna Mysłek, Aleksandra Marciniak, Remigiusz Płaczek, Aleksandra Kotynia and Edward Krzyżak
Int. J. Mol. Sci. 2025, 26(10), 4620; https://doi.org/10.3390/ijms26104620 - 12 May 2025
Cited by 5 | Viewed by 2251
Abstract
Searching for new anticancer drugs is a significant challenge for the medical community due to the current limitations of existing treatments. The primary objective of this study was to design and optimize multi-targeted drug candidates based on a quinoline scaffold. In this paper, [...] Read more.
Searching for new anticancer drugs is a significant challenge for the medical community due to the current limitations of existing treatments. The primary objective of this study was to design and optimize multi-targeted drug candidates based on a quinoline scaffold. In this paper, we adopt various in silico techniques, including molecular docking, molecular dynamics simulations, and ADMET property modeling, to predict the binding affinity and interactions of 7-ethyl-10-hydroxycamptothecin derivatives with multiple biological targets. The interactions of these compounds with three potential molecular targets, topoisomerase I, bromodomain-containing protein 4, and ATP-binding cassette sub-family G member 2 proteins, were analyzed. It has been previously proved that the inhibition of these molecular targets may have beneficial effects on cancer treatment. The designed chemical compounds can effectively interact with selected proteins, thereby establishing their potential as drug candidates. Molecular docking revealed promising binding affinities, with topoisomerase I docking scores ranging from −9.0 to −10.3 kcal/mol, BRD4 scores from −6.6 to −8.0 kcal/mol, and ABCG2 scores from −8.0 to −10.0 kcal/mol. Furthermore, the ADMET property analysis indicates promising pharmacological profiles, protein binding affinity, selectivity, and bioavailability while minimizing toxicity. For example, satisfactory logP values have been demonstrated in the favorable range for bioavailability after oral administration. Additionally, several compounds exhibited predicted aqueous solubility values greater than −3, suggesting moderate-to-good solubility, which is crucial for oral drug delivery. Full article
(This article belongs to the Special Issue Targeted Therapies and Molecular Methods in Cancer, 3rd Edition)
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17 pages, 4554 KB  
Article
Cytotoxic Activity of Curcumin- and Resveratrol-Loaded Core–Shell Systems in Resistant and Sensitive Human Ovarian Cancer Cells
by Joanna Weżgowiec, Zofia Łapińska, Łukasz Lamch, Anna Szewczyk, Jolanta Saczko, Julita Kulbacka, Mieszko Więckiewicz and Kazimiera A. Wilk
Int. J. Mol. Sci. 2025, 26(1), 41; https://doi.org/10.3390/ijms26010041 - 24 Dec 2024
Cited by 5 | Viewed by 3144
Abstract
Due to the high mortality rate of ovarian cancer, there is a need to find novel strategies to improve current treatment modalities. Natural compounds offer great potential in this field but also require the careful design of systems for their delivery to cancer [...] Read more.
Due to the high mortality rate of ovarian cancer, there is a need to find novel strategies to improve current treatment modalities. Natural compounds offer great potential in this field but also require the careful design of systems for their delivery to cancer cells. Our study explored the anticancer effects of novel resveratrol (RSV)- and curcumin (CUR)-loaded core–shell nanoparticles in human ovarian cancer cells. We evaluated the in vitro cytotoxicity of various nanocarriers (CUR 1-3, RSV I-III) delivered to MDAH-2774 and SKOV-3 cells in comparison to free RVS and CUR after 24 h and 72 h treatment. A two-way ANOVA was applied to compare the results of the MTT assay. Confocal laser scanning microscopy was employed to visualize cellular uptake and mitochondrial localization. Our findings revealed that the cytotoxicity of the core–shell nanoparticles with RSV was not significant, but the systems loaded with CUR effectively decreased the viability of cells. The MDAH-2774 cell line was more sensitive to the treatment than SKOV-3. The enhanced cellular uptake of CUR delivered by core–shell systems and its colocalization with mitochondria were demonstrated. Further research focused on the detailed biological effects of the most effective systems (CUR 2 and CUR 3) should be conducted to provide detailed insights. These findings highlight the promising role of CUR-loaded nanoparticles in ovarian cancer treatment. Full article
(This article belongs to the Special Issue Targeted Therapies and Molecular Methods in Cancer, 3rd Edition)
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Review

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22 pages, 3795 KB  
Review
BRCA1 Gene as a Potential Marker for Lung Cancer Therapy
by Matvey M. Tsyganov, Irina A. Tsydenova, Daria S. Dolgasheva and Marina K. Ibragimova
Int. J. Mol. Sci. 2026, 27(14), 6364; https://doi.org/10.3390/ijms27146364 - 17 Jul 2026
Viewed by 450
Abstract
DNA double-strand breaks (DSBs), caused by various endogenous and exogenous factors, pose a significant threat to genomic stability. Several conserved repair pathways address DSBs, with homologous recombination (HR) being the only mechanism capable of accurately restoring the original DNA sequence. The BRCA1 gene [...] Read more.
DNA double-strand breaks (DSBs), caused by various endogenous and exogenous factors, pose a significant threat to genomic stability. Several conserved repair pathways address DSBs, with homologous recombination (HR) being the only mechanism capable of accurately restoring the original DNA sequence. The BRCA1 gene plays a critical role in HR and is involved in maintaining genomic stability, cell cycle regulation, transcription, and tumor angiogenesis. Germline mutations in BRCA1 are strongly associated with increased risks of breast, ovarian, and other cancers. Dysfunction of BRCA1 leads to homologous recombination deficiency (HRD), forcing cells to rely on error-prone repair pathways, which promotes genomic instability and tumorigenesis. Besides hereditary mutations, HRD can also arise in sporadic cancers through epigenetic mechanisms such as promoter hypermethylation and reduced BRCA1 expression. Although BRCA1 deficiency is uncommon in lung cancer, BRCA1 status is considered a potential biomarker for sensitivity to platinum-based chemotherapy and other cytotoxic agents used in lung cancer treatment. However, the impact of BRCA1 on treatment response and prognosis in lung cancer remains controversial and not fully understood. This review summarizes current evidence on the role of BRCA1 in modulating chemotherapy response and disease outcomes in lung cancer patients, highlighting its potential as a biomarker for personalized therapy selection. Thus, in this context, the key unresolved issues critical for the development of personalized treatment strategies for lung cancer associated with BRCA1 alterations include the identification of molecular biomarkers most reliably associated with tumor sensitivity to chemotherapy. In addition, the development of methods for identifying patients with homologous recombination deficiency specifically in lung tumors appears to be of considerable importance, as does a better understanding of how the biological and therapeutic implications of BRCA1-related parameters in lung cancer differ from those observed in other tumor types. Addressing these challenges could substantially improve the efficacy of chemotherapy and patient outcomes, while also expanding the opportunities for a personalized approach to treatment selection in patients with lung cancer. Full article
(This article belongs to the Special Issue Targeted Therapies and Molecular Methods in Cancer, 3rd Edition)
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21 pages, 7721 KB  
Review
CD22 as a Target for Hematological Malignancies and Autoimmune Diseases
by Xin Chen, Jiayi Zhang, Sizhuo Chen, Chaojun Yan, Cefan Zhou, Jingfeng Tang, Rachael Mira McLean and Zhenhuan Zhao
Int. J. Mol. Sci. 2026, 27(12), 5406; https://doi.org/10.3390/ijms27125406 - 16 Jun 2026
Viewed by 1097
Abstract
CD22 is a critical inhibitory coreceptor predominantly expressed on the surface of B cells, playing a pivotal role in modulating B cell receptor (BCR) signaling and maintaining immune homeostasis. Its high B cell lineage specificity, rapid internalization capacity, and signal attenuation mediated by [...] Read more.
CD22 is a critical inhibitory coreceptor predominantly expressed on the surface of B cells, playing a pivotal role in modulating B cell receptor (BCR) signaling and maintaining immune homeostasis. Its high B cell lineage specificity, rapid internalization capacity, and signal attenuation mediated by immunoreceptor tyrosine-based inhibitory motifs (ITIMs) render it an ideal therapeutic target for B cell-related pathologies. In recent years, CD22-targeted therapeutic strategies have demonstrated significant clinical breakthroughs in the treatment of hematological malignancies and autoimmune diseases. These strategies encompass immunotoxins, radioimmunoconjugates, antibody–drug conjugates (ADCs), bispecific antibodies, and chimeric antigen receptor (CAR) T cell therapy. Notably, while monotherapies have achieved high response rates, dual-targeting approaches (e.g., CD19/CD22 CAR-T) have further mitigated the risk of antigen escape and profoundly enhanced long-term durable efficacy. This review systematically summarizes the molecular mechanisms of CD22 and the latest clinical advancements in its targeted therapies. Furthermore, we highlight the promising translational potential of CD22-targeted strategies—particularly CAR-T cell therapy—from oncology to the management of autoimmune disorders, outlining future research priorities within this rapidly evolving field. Full article
(This article belongs to the Special Issue Targeted Therapies and Molecular Methods in Cancer, 3rd Edition)
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20 pages, 1388 KB  
Review
Mismatch Repair Deficiency and the Role of Non-Canonical Functions in Cancer: Diagnosis and Therapeutic Implications
by Alicja Dąbrowska, Jakub Mastalerz, Zofia Łapińska, Iwona Deszcz, Agnieszka Chwiłkowska and Nina Rembiałkowska
Int. J. Mol. Sci. 2025, 26(19), 9312; https://doi.org/10.3390/ijms26199312 - 24 Sep 2025
Cited by 7 | Viewed by 3715
Abstract
The mismatch repair system is critical for correcting base–base mismatches and insertion-deletion loops during DNA replication. Deficiencies in MMR (due to mutations in MLH1, MSH2, MSH6, or PMS2) lead to microsatellite instability and contribute to the development of various cancers, such as Lynch [...] Read more.
The mismatch repair system is critical for correcting base–base mismatches and insertion-deletion loops during DNA replication. Deficiencies in MMR (due to mutations in MLH1, MSH2, MSH6, or PMS2) lead to microsatellite instability and contribute to the development of various cancers, such as Lynch syndrome-related colorectal cancer and sporadic tumors. This review will delve into the molecular basis of MMR deficiency. Additionally, the review will cover diagnostic approaches for detecting MSI and MMR deficiency, including next-generation sequencing and PCR-based methods. The implications for treatment will be discussed, emphasizing immune checkpoint inhibitors (e.g., pembrolizumab) that target tumors with high mutational burdens due to MMR deficiency, as well as novel therapeutic approaches like synthetic lethality exploiting DNA repair vulnerabilities. Full article
(This article belongs to the Special Issue Targeted Therapies and Molecular Methods in Cancer, 3rd Edition)
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