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Advances in Molecular Target and Anti-Cancer Therapies
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Advances in Molecular Target and Anti-Cancer Therapies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 July 2026 | Viewed by 3674

Special Issue Editor

Dr. Laura Denisa Dragu

E-Mail Website
Guest Editor
Cellular and Molecular Pathology Department, Stefan S. Nicolau Institute of Virology, 285 Mihai Bravu, 030304 Bucharest, Romania
Interests: antimicrobials; oncology; RNA interference; targeted anti-tumor therapy

Special Issue Information

Dear Colleagues,

The identification of new biomarkers and molecular targets, as well as the development of safe and effective anticancer treatments, continues to be a priority in the healthcare field, especially in the context of the global increase in cancer cases. Currently, therapies include small molecules, enzymatic inhibitors, natural products, agents targeting DNA, and metal complexes. These research efforts open up prospects for creating new compounds with enhanced activity, superior bioavailability, and the ability to overcome treatment resistance, thereby contributing to the development of more personalized and effective therapies for oncology patients. This Special Issue, "Advances in Molecular Target and Anti-Cancer Therapies", aims to investigate current research on the identification of new biomarkers and molecular targets, as well as the design and development of safer and more precise anti-tumor drugs capable of overcoming existing limitations and addressing the urgent needs of oncology patients. It also examines emerging technologies such as nanomedicine and genetic editing, which promise more personalized and efficient therapies. Original research articles, review articles, and short communications within (but not restricted to) the described research fields are welcome.

Dr. Laura Denisa Dragu
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • cancer
  • conventional therapy
  • targeted therapy
  • immunotherapy
  • natural compounds
  • combinatorial therapy
  • molecular target
  • molecular mechanism
  • drug design
  • drug resistance

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Published Papers (3 papers)

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Research

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16 pages, 2268 KB  
Article
MicroRNA Mimics Based on the miR-15/107 Consensus Sequence Sensitise NSCLC Cells to Targeted Therapy
by Carien Carpenter, Nina Simmons, William J. H. Davis, Madeleine Thompson, Nico van Zandwijk, Catherine J. Drummond and Glen Reid
Int. J. Mol. Sci. 2026, 27(6), 2701; https://doi.org/10.3390/ijms27062701 - 16 Mar 2026
Viewed by 524
Abstract
Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer deaths, with resistance to targeted therapies posing a major clinical challenge. Drug-tolerant persister (DTP) cells are key contributors to resistance, and targeting them offers new strategies to enhance existing treatments. MicroRNAs [...] Read more.
Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer deaths, with resistance to targeted therapies posing a major clinical challenge. Drug-tolerant persister (DTP) cells are key contributors to resistance, and targeting them offers new strategies to enhance existing treatments. MicroRNAs (miRNAs), particularly the tumour-suppressive miR-15/107 family, offer promise due to their ability to target multiple oncogenic pathways. This study evaluated a synthetic consensus miRNA mimic, conmiR-15/107, in NSCLC cell line models. Dose–response assays showed robust, dose-dependent growth inhibition in both EGFR-mutant (PC9) and KRAS-mutant (H358 and A549) lung adenocarcinoma cells, but not in the human bronchial epithelial cell line BEAS-2B. When combined with EGFR inhibitors (osimertinib and gefitinib) in PC9 cells, the mimics showed a higher rate of growth inhibition compared with the controls and reduced IC50 values. Similarly, conmiR-15/107 enhanced growth inhibition by the KRAS inhibitors sotorasib and adagrasib in H358 cells. RT-qPCR confirmed downregulation of conmiR-15/107 targets, including MEK1, BCL2 and BRCA1, suggesting a multi-target mechanism of action. Long-term assays showed that the mimics reduced the survival and delayed the proliferation of DTPs in osimertinib-treated PC9 cells as well as sotorasib-treated H358 cells. These findings support conmiR-15/107 as a potential adjunct to targeted therapy, capable of enhancing treatment efficacy and delaying resistance in lung adenocarcinoma. Full article
(This article belongs to the Special Issue Advances in Molecular Target and Anti-Cancer Therapies)
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Review

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32 pages, 2875 KB  
Review
Advances in Breast Cancer Research: Immunological, Pathological, and Pharmacological Perspectives for Improving Patient Outcomes
by Susanne Crocamo, Everton Cruz dos Santos and Eliana Abdelhay
Int. J. Mol. Sci. 2026, 27(4), 1902; https://doi.org/10.3390/ijms27041902 - 16 Feb 2026
Viewed by 1076
Abstract
Breast cancer remains the most frequently diagnosed malignancy worldwide. Over the past decade, advances in molecular biology have expanded beyond tumor-intrinsic features to encompass the immune microenvironment and patient-specific pharmacogenomic profiles, profoundly reshaping diagnostic, prognostic, and therapeutic paradigms in breast oncology. Owing to [...] Read more.
Breast cancer remains the most frequently diagnosed malignancy worldwide. Over the past decade, advances in molecular biology have expanded beyond tumor-intrinsic features to encompass the immune microenvironment and patient-specific pharmacogenomic profiles, profoundly reshaping diagnostic, prognostic, and therapeutic paradigms in breast oncology. Owing to rapid technological progress and an expanding therapeutic armamentarium, periodic synthesis of both foundational principles and emerging evidence remains essential for the critical interpretation of ongoing advances. This review provides a comprehensive overview of the contemporary global landscape of breast cancer, integrating developments in diagnosis, risk stratification, and therapeutic innovation. We examine the emerging technologies that are redefining tumor characterization, including digital pathology, artificial intelligence-assisted morphological and molecular analyses, and advanced molecular profiling approaches that increasingly inform prognostic and predictive assessment. We further discuss how these diagnostic frameworks are translating into therapeutic advances, with emphasis on immunotherapy, antibody-drug conjugates, mutation-directed targeted agents, therapeutic vaccines, and bispecific antibodies. Collectively, these developments highlight key translational research priorities, support evidence-based clinical decision-making, and explicitly acknowledge disparities in access and implementation between high-income settings and low- and middle-income countries (LMICs). Full article
(This article belongs to the Special Issue Advances in Molecular Target and Anti-Cancer Therapies)
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26 pages, 2824 KB  
Review
The Mechanisms of Resistance to JAK Inhibitors in Lymphoid Leukemias: A Scoping Review of Evidence from Preclinical Models and Case Reports
by Daniel Martínez Anaya, Marian Valladares Coyotecatl, Maria del Pilar Navarrete Meneses, Sergio Enríquez Flores and Patricia Pérez-Vera
Int. J. Mol. Sci. 2025, 26(18), 9111; https://doi.org/10.3390/ijms26189111 - 18 Sep 2025
Viewed by 1703
Abstract
The use of JAK inhibitors (JAKi) represents a promising therapeutic approach for patients with lymphoid leukemias (Lym-L). Clinical trials are ongoing to evaluate the safety and efficacy of JAK inhibitors. Over the last years, there have been reports of preclinical Lym-L models that [...] Read more.
The use of JAK inhibitors (JAKi) represents a promising therapeutic approach for patients with lymphoid leukemias (Lym-L). Clinical trials are ongoing to evaluate the safety and efficacy of JAK inhibitors. Over the last years, there have been reports of preclinical Lym-L models that developed JAKi resistance, and reports of patients treated with JAKi who experienced treatment failure. Although evidence shows that there are diverse JAKi mechanisms, no review studies have been performed that summarize and discuss this information. This scoping review aimed to provide an updated overview of the mechanisms underlying JAKi molecular resistance in Lym-L. According to a scoping review PRISMA guidelines, a search was conducted in the PubMed and Europe PMC databases for studies published from 2010 to 2024. We included articles that described the molecular resistance to JAKi in Lym-L preclinical models or patients. The search was complemented by a review of laboratory-engineered resistant mutations in genomic datasets to obtain more information about their presence in patients with Lym-L. Twenty-two articles were eligible for this review, and six different mechanisms of molecular resistance were identified: (1) point mutations in the kinase domain, (2) cooperation between double-JAK mutants, (3) inactivation of phosphatases, (4) evasion of JAK inhibition due to trans-phosphorylation of JAK family proteins, (5) upregulation of pro-survival proteins, and (6) activation of kinase cross-signaling pathways. The integrated evidence enabled the identification of specific mechanisms of molecular resistance to JAKi in Lym-L, as well as promising therapeutic approaches to prevent them. These include selecting a sensitive JAKi, choosing an effective dosage regimen, and combining inhibitory molecules. Full article
(This article belongs to the Special Issue Advances in Molecular Target and Anti-Cancer Therapies)
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