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New Insights into Anticancer Strategies
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New Insights into Anticancer Strategies

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: closed (31 May 2026) | Viewed by 8325

Editor

Dr. Yong Teng

E-Mail Website
Guest Editor
Department of Hematology and Medical Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA
Interests: metastasis; molecular pathway; cancer models; metabolism; tumor microenvironment; drug screening and development
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recent advances in anticancer strategies have introduced several promising approaches aimed at increasing treatment efficacy while minimizing side effects. These new strategies against cancer include, but not are limited to, immunotherapy (e.g., immune checkpoint inhibitors, CAR-T cell therapy, and cancer vaccines), targeted therapy (e.g., tyrosine kinase inhibitors and monoclonal antibodies), nanotechnology, combination therapy, gene editing techniques, advanced imaging techniques, cancer metabolic pathway targeting, and tumor microenvironment modulation. Most recently, artificial intelligence (AI) and machine learning have been used to analyze large datasets to identify new drug targets, predict patient responses to treatments, and develop personalized treatment plans. These new approaches can accelerate the discovery of new anticancer drugs and personalized medicine that can be tailored to the individual characteristics of each patient’s cancer. All these strategies represent a shift towards more precise, personalized, and effective cancer treatments. Ongoing research and clinical trials continue to refine and expand these approaches, offering hope for improved cancer outcomes in the future.

This Special Issue aims to advance our understanding of novel anticancer strategies so as to improve early detection and prevention, overcome resistance, and increase patient survival rates. Original research articles and comprehensive reviews are welcome for submission to this Special Issue. Through our efforts, we hope that the impact of developing novel anticancer strategies will extend beyond the basic research paradigm and contribute to the broader goals of improved public health, medical innovation, and healthcare sustainability.

Dr. Yong Teng
Guest Editor

Manuscript Submission Information

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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-anonymized 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.

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Keywords

  • novel targeted therapy
  • personalized medicine
  • nanotechnology
  • AI and machine learning
  • combination therapy

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Published Papers (4 papers)

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Research

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21 pages, 6989 KB  
Article
Investigating the Mechanisms Underlying Cell Death Induction by a Tributyltin Molecule in HTLV-1-Infected Cells Dependent or Not on IL-2 as a Growth Factor
by Valeria Stefanizzi, Evariste Molimbou, Emanuela Balestrieri, Antonella Minutolo, Franca M. Cordero, Sandro Grelli, Antonio Mastino, Claudia Matteucci, Beatrice Macchi and Francesca Marino-Merlo
Int. J. Mol. Sci. 2026, 27(14), 6165; https://doi.org/10.3390/ijms27146165 - 10 Jul 2026
Abstract
Human T-Lymphotropic virus type 1 (HTLV-1) lifelong infects at least 5–10 million people worldwide, a minority of whom develop severe lethal diseases including adult T-cell Leukemia/lymphoma and HTLV-1-associated myelopathy or tropical spastic paraparesis. Currently, no vaccines or curative therapies to fight HTLV-1 infection [...] Read more.
Human T-Lymphotropic virus type 1 (HTLV-1) lifelong infects at least 5–10 million people worldwide, a minority of whom develop severe lethal diseases including adult T-cell Leukemia/lymphoma and HTLV-1-associated myelopathy or tropical spastic paraparesis. Currently, no vaccines or curative therapies to fight HTLV-1 infection or diseases are available. Recently we found that a tributyltin molecule, Bu3SnOCOCF3 (TBT), which is more potent than cisplatin in inducing cytotoxic effects towards a panel of cell lines including high-tumorigenic cells, also exerted potent cytotoxic effects even towards HTLV-1-infected cell lines, mimicking different states of virus-driven transformation. The type of cell death involved was elusive. In the present study, the effects of TBT on virological and cell death parameters were investigated in HTLV-1-infected immortalized lymphocytes generated by in vitro infection and rendered with or without progressive independence from interleukin-2 as a growth factor. Molecular studies demonstrated that TBT affected HTLV-1 viral gene expression, especially HBZ. TBT confirmed its high cytotoxic potential on the HTLV-1-infected cell lines assayed, especially towards the IL-2-independent HTLV-1-infected cells. Investigation of mechanisms involved in cell death induced by TBT in HTLV-1-infected cells confirmed that caspase 3 and 8 activation, as well as apoptotic response, were relevant. In addition, pyroptosis as well as other unspecifed forms of lytic death presumably contribute to cell death induced by TBT in HTLV-1-infected cells, while a concomitant activation of an autophagic response by this compound seems to mitigate it. Overall, these experimental results outline a particular profile of TBT-induced cell death in HTLV-1-infected cells that is useful for future studies aimed at verifying the real potential of tin-based compounds to contrast diseases caused by HTLV-1. Full article
(This article belongs to the Special Issue New Insights into Anticancer Strategies)
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19 pages, 2995 KB  
Article
Characterization of the D8P1C1 Anti-ADAM17 Inhibitory Monoclonal Antibody and Generation of Its Bispecific T-Cell Engager Derivative
by Nayanendu Saha, Sang Gyu Lee, Elisa de Stanchina, Rachelle P. Mendoza, Darren R. Veach and Dimitar B. Nikolov
Int. J. Mol. Sci. 2026, 27(7), 2936; https://doi.org/10.3390/ijms27072936 - 24 Mar 2026
Viewed by 694
Abstract
EGFR signaling, which requires ligand shedding by ADAM proteases, drives the progression of a variety of cancers, including breast, ovarian and lung. We previously reported the generation and characterization of a fully human, affinity-matured anti-ADAM17 monoclonal antibody, D8P1C1, which inhibits both the proliferation [...] Read more.
EGFR signaling, which requires ligand shedding by ADAM proteases, drives the progression of a variety of cancers, including breast, ovarian and lung. We previously reported the generation and characterization of a fully human, affinity-matured anti-ADAM17 monoclonal antibody, D8P1C1, which inhibits both the proliferation of an array of cancer cell lines in vitro as well as breast cancer growth in a mouse xenograft model. Here, we show that the mAb inhibits the shedding of EGFR ligands and EGFR phosphorylation in cancer cell lines, thus explaining its anti-tumor effects. In a xenograft model with a high-grade serous ovarian cancer (HGSOC) cell line, D8P1C1 showed only modest therapeutic effect, without any discernible toxicity. These results suggest that ovarian cancers are less susceptible than breast cancers to therapeutic targeting of ADAM17- or EGFR-dependent signaling. Radioimmuno PET imaging with 89Zr-DFO-D8P1C1 confirmed tumoral accumulation of the mAb in high-grade and non-high-grade serous ovarian tumor xenografts. Furthermore, we report the generation and preliminary characterization of a bispecific T cell engager derivative of D8P1C1 with improved anti-tumor efficacy in vitro. Full article
(This article belongs to the Special Issue New Insights into Anticancer Strategies)
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Review

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30 pages, 1009 KB  
Review
Advances in the Treatment of Ulcerative Colitis—From Conventional Therapies to Targeted Biologics and Small Molecules
by Aleksandra Wilk, Mateusz Pawłowski, Ewa Balcerczak, Agnieszka Jeleń, Marek Mirowski and Dagmara Szmajda-Krygier
Int. J. Mol. Sci. 2026, 27(3), 1534; https://doi.org/10.3390/ijms27031534 - 4 Feb 2026
Cited by 5 | Viewed by 3989
Abstract
The goals of ulcerative colitis (UC) treatment are focused on improving quality of life, achieving steroid-free remission, and minimizing the risk of cancer. In UC traditional management, a step-up strategy involves introducing increasingly more immunosuppressive medications, thus avoiding unnecessary overexposure to more potent [...] Read more.
The goals of ulcerative colitis (UC) treatment are focused on improving quality of life, achieving steroid-free remission, and minimizing the risk of cancer. In UC traditional management, a step-up strategy involves introducing increasingly more immunosuppressive medications, thus avoiding unnecessary overexposure to more potent drugs. However, in cases of severe, acute UC, priority is rapid and effective treatment to minimize the risk of complications such as bleeding, intestinal perforation, toxic megacolon or the need for colectomy. Modern approach to UC management shifts to an “accelerated step-up” or “top-down” approach in high-risk patients to prevent bowel damage. A holistic approach—integrating molecular research, clinical management and patient-centered care—enhances our understanding of disease mechanisms and therapeutic strategies, ultimately supporting improved outcomes and overall quality of life. This review aims to present the treatment options for UC along with an overview of the most modern therapies and experimental agents. Full article
(This article belongs to the Special Issue New Insights into Anticancer Strategies)
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25 pages, 2353 KB  
Review
Membrane Stress and Ferroptosis: Lipid Dynamics in Cancer
by Jaewang Lee, Youngin Seo and Jong-Lyel Roh
Int. J. Mol. Sci. 2026, 27(2), 690; https://doi.org/10.3390/ijms27020690 - 9 Jan 2026
Cited by 2 | Viewed by 1622
Abstract
Membrane rupture, induced by lipid peroxidation, is a severe threat to osmotic balance, as membrane pores contribute to ferroptosis, an iron-dependent cell death. To alleviate osmotic stress, membrane constituents dynamically reconstruct the membrane and interact with intracellular molecules. Tumor-derived acidosis shift glycolysis-dependent metabolism [...] Read more.
Membrane rupture, induced by lipid peroxidation, is a severe threat to osmotic balance, as membrane pores contribute to ferroptosis, an iron-dependent cell death. To alleviate osmotic stress, membrane constituents dynamically reconstruct the membrane and interact with intracellular molecules. Tumor-derived acidosis shift glycolysis-dependent metabolism toward lipid metabolism, increasing polyunsaturated fatty acids (PUFAs). PUFAs enhance membrane fluidity but make cancer susceptible to lipid peroxidation. Also, the ionization of phospholipids under low pH can accelerate membrane rupture. This stress can be mitigated by the redistribution of cholesterol, which maintains tension–compression balance and acts as antioxidants. When excessive reactive aldehydes—byproducts of lipid peroxidation—overwhelm cholesterol’s protective role, lipid peroxides promote membrane cracks. Moreover, a deficiency in glutathione can alter cholesterol’s function, turning it into a pro-oxidant. In contrast, ceramide, derived from membrane lipids, indirectly prevents ferroptosis by facilitating cytochrome c release. This review integrates recent findings on how membrane components and environmental stressors influence ferroptosis. It also suggests potential therapeutic strategies. This could advance our understanding of ferroptosis in cancer. Full article
(This article belongs to the Special Issue New Insights into Anticancer Strategies)
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