Recent Advances in Anticancer Strategies, 2nd Edition

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Dear Colleagues,

The topic "Recent Advances in Anticancer Strategies, 2nd Edition" aims to provide an overview of the latest developments in the field of cancer treatment. Cancer remains one of the leading causes of death worldwide, and researchers have been working to develop more effective and targeted treatments to improve outcomes for patients. The existing cancer therapies suffer from severe side-effects and drug resistance, leading to an increase in cancer incidence and mortality worldwide. Hence, there is a pressing need to develop and discover novel therapeutic strategies that can offer more effective and less-toxic treatment options for cancer patients. Novel anticancer approaches are being developed which can selectively identify and eliminate cancerous cells while minimizing harm to healthy tissues, unlike traditional therapies.

For this Topic, we welcome original articles and comprehensive reviews that showcase the latest advances in novel anticancer strategies with reduced toxicity and improved therapeutic indices. These articles can suggest potential prospects for optimizing cancer therapies with significant clinical value in the near future. We encourage submissions that focus on the development and validation of various anticancer approaches, including ligand-/receptor-based targeting, controlled drug delivery, gene therapy, gene delivery, immunotherapy, targeted anticancer prodrugs and conjugates (such as photoactivatable caged prodrugs, ADEPT, ADAPT, and ADCs), magnetic- and ultrasound-mediated drug targeting, and cancer stem cell therapy, as well as strategies that explore the targeting of signaling cascades and the tumor microenvironment.

Overall, this Topic aims at providing recent advances in anticancer strategies, highlighting the potential impact of these new approaches on cancer treatment and patient outcomes. We eagerly anticipate your valuable contribution to this exciting topic.

Dr. Hassan Bousbaa
Dr. Zhiwei Hu
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Cancers cancers	4.8	9.0	2009	17.5 Days	CHF 2900
Current Oncology curroncol	3.6	6.1	1994	22.6 Days	CHF 2200
International Journal of Molecular Sciences ijms	5.6	10.0	2000	17.5 Days	CHF 2900
Molecules molecules	5.1	10.3	1996	15.6 Days	CHF 2700
Pharmaceuticals pharmaceuticals	5.7	9.0	2004	14.3 Days	CHF 2900
Pharmaceutics pharmaceutics	6.9	12.5	2009	16.3 Days	CHF 2900
Scientia Pharmaceutica scipharm	3.6	5.3	1930	24.8 Days	CHF 1000

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Published Papers (17 papers)

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All Cancers IJMS Pharmaceuticals Pharmaceutics Sci. Pharm. Current Oncology Molecules

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28 pages, 3899 KB  

Open AccessReview

70 Years of DON and Beyond: Glutaminase Inhibition as a Synergistic Strategy in Cancer Combination Therapy

by José A. Campos-Sandoval, Juan De los Santos-Jiménez, Javier Márquez and José M. Matés

Pharmaceutics 2026, 18(7), 850; https://doi.org/10.3390/pharmaceutics18070850 - 13 Jul 2026

Viewed by 795

Abstract

Personalized oncology seeks to selectively block specific dysregulated pathways to arrest cancer development. Increased glutamine metabolism is a hallmark of cancer, and 6-diazo-5-oxo-L-norleucine (DON), a structural analog of L-glutamine, was the first compound used to target the exacerbated nitrogen metabolism observed in cancer [...] Read more.

Personalized oncology seeks to selectively block specific dysregulated pathways to arrest cancer development. Increased glutamine metabolism is a hallmark of cancer, and 6-diazo-5-oxo-L-norleucine (DON), a structural analog of L-glutamine, was the first compound used to target the exacerbated nitrogen metabolism observed in cancer cells. However, its clinical application was limited by unacceptable toxicity. With the same goal of blocking glutamine metabolism, several specific glutaminase inhibitors have been characterized in recent decades, showing promising antitumor activity. Nevertheless, this strategy frequently induces adaptive metabolic resistance that must be counteracted. In this context, glutaminase has become a key target in combination therapies for several tumor types aimed at restricting anabolic adaptation when single metabolic therapy fails, emerging as a possible synergistic therapeutic intervention. Consequently, combination therapies that include glutaminase inhibition alongside additional agents to counteract the metabolic plasticity of cancer have emerged as a promising approach in personalized antitumor pharmacology. This review provides a historical-to-translational overview of glutamine-targeted therapies, with particular emphasis on glutaminase inhibitors, including compound 968, BPTES, CB-839, and next-generation inhibitors, as well as DON-derived prodrugs. We discuss their mechanisms of action and their integration with chemotherapy, targeted therapies, radiotherapy, and immunotherapy, highlighting how glutamine metabolism targeting influences tumor metabolic adaptation, redox homeostasis, therapy resistance, and tumor–immune interactions. Finally, we examine current clinical developments, emerging therapeutic combinations, and the challenges that must be addressed for the incorporation of glutamine metabolism targeting into precision oncology. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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21 pages, 1330 KB  

Open AccessReview

Immunometabolic Stress and Immune Suppression in Clear-Cell Renal Cell Carcinoma: Perspectives in Therapeutic Strategy

by Tuong-Vi Nguyen and Tien Hsu

Int. J. Mol. Sci. 2026, 27(13), 6021; https://doi.org/10.3390/ijms27136021 - 4 Jul 2026

Viewed by 699

Abstract

Solid tumors frequently experience hypoxia during tumor progression, resulting in profound metabolic alterations. This phenomenon is particularly pronounced in clear-cell renal cell carcinoma (ccRCC) because of loss of the von Hippel–Lindau (VHL) tumor suppressor gene and constitutive activation of hypoxia-inducible factor [...] Read more.

Solid tumors frequently experience hypoxia during tumor progression, resulting in profound metabolic alterations. This phenomenon is particularly pronounced in clear-cell renal cell carcinoma (ccRCC) because of loss of the von Hippel–Lindau (VHL) tumor suppressor gene and constitutive activation of hypoxia-inducible factor (HIF) signaling. ccRCC is the most common subtype of kidney cancer, and durable therapeutic responses remain limited despite advances in immune checkpoint inhibition. Owing to its strong pseudohypoxic phenotype and extensive metabolic rewiring, ccRCC is widely regarded as a metabolic disease. These alterations generate a unique immune landscape characterized by abundant immune-cell infiltration together with profound T-cell dysfunction and exhaustion. This paradoxical “immune-hot yet immunosuppressed” phenotype is largely driven by hypoxia-associated immunometabolic reprogramming within tumor cells and the tumor microenvironment (TME). Several metabolic pathways are critically involved in this process, including lactate acidosis, arginine (Arg) depletion, tryptophan (Trp) depletion, kynurenine (Kyn)-mediated T-cell exhaustion, and adenosine-driven immune suppression. This review summarizes the current understanding of hypoxia-driven immunometabolic interactions in ccRCC and discusses how targeting these pathways may improve future therapeutic strategies against this aggressive malignancy. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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20 pages, 7149 KB  

Open AccessArticle

CD40LG/CD28-Mediated Rho GTPase Signaling Drives Survival and Chemoresistance in Non-ETP T-ALL

by Yan Yang, Wei Lu, Zhexi Zhu, Chenyang Li, Zihao Guo and Han Zhang

Int. J. Mol. Sci. 2026, 27(12), 5306; https://doi.org/10.3390/ijms27125306 - 11 Jun 2026

Viewed by 437

Abstract

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subtype of ALL characterized by unfavorable clinical outcomes. Despite significant progress in deciphering the genetic and epigenetic landscapes of T-ALL, the underlying molecular mechanisms, particularly in non-early T-cell precursor (non-ETP) T-ALL, remain incompletely understood. In [...] Read more.

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subtype of ALL characterized by unfavorable clinical outcomes. Despite significant progress in deciphering the genetic and epigenetic landscapes of T-ALL, the underlying molecular mechanisms, particularly in non-early T-cell precursor (non-ETP) T-ALL, remain incompletely understood. In this study, functional assays were performed using three well-characterized non-ETP T-ALL cell lines. In vivo therapeutic efficacy was evaluated using non-ETP T-ALL xenograft models. Transcriptomic profiling was performed by RNA sequencing (RNA-seq) followed by bioinformatic analysis. Publicly available clinical datasets from T-ALL patients were mined to analyze survival outcomes. We found that activation of CD40 ligand (CD40LG) or CD28 accelerates cell-cycle progression and enhances the migratory capacity of non-ETP T-ALL cells, with CD40LG uniquely upregulating CXCR4 to mediate bone marrow tropism. Further RNA-seq and functional validation identified Rho GTPase signaling, specifically RhoA/Rac1/Rac2, as a pivotal downstream effector of CD40LG/CD28, leading to therapeutic resistance to PI3K inhibition. Pharmacological blocking RhoA or Rac1 using small-molecule compounds not only induces remarkable cytotoxicity but also sensitizes resistant cells to PI3K inhibitors, both in vitro and in vivo. Clinically, elevated expression of CD40LG, CD28, RHOA, or RAC2 correlates with poor prognosis in non-ETP T-ALL patients. These findings uncover a novel CD40LG/CD28-Rho GTPase axis as a key driver of pathogenesis and a potential therapeutic vulnerability in non-ETP T-ALL, providing a new target for precision intervention and a promising strategy to overcome therapeutic resistance. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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31 pages, 7553 KB  

Open AccessSystematic Review

Evaluation of Efficacy and Safety of Chimeric Antigen Receptor-Natural Killer (CAR-NK) Cells in Breast Cancer: A Systematic Review and Meta-Analysis

by Nabeel Ahmed, Jawaria Jabeen, Safa Noor, Malja Rehman, Sana Tahseen, Asmaa Qamar, Muhammad Anas, Muhammad Muneeb Khalid, Tao Li, Lechun Lyu and Zhiwei Hu

Cancers 2026, 18(10), 1634; https://doi.org/10.3390/cancers18101634 - 19 May 2026

Cited by 1 | Viewed by 1210

Abstract

Background: For almost two decades now, chimeric antigen receptor-natural killer cells (CAR-NK) have been investigated in pre-clinical breast cancer models, yet clinical evidence on efficacy remains scarce. This meta-analysis provides pooled evidence of pre-clinical CAR-NK effectiveness and safety in breast cancer and [...] Read more.

Background: For almost two decades now, chimeric antigen receptor-natural killer cells (CAR-NK) have been investigated in pre-clinical breast cancer models, yet clinical evidence on efficacy remains scarce. This meta-analysis provides pooled evidence of pre-clinical CAR-NK effectiveness and safety in breast cancer and an overview of current clinical trials to support clinical translation. Methods: Following PRISMA guidelines and a registered protocol (PROSPERO, CRD420251131530), PubMed, Web of Science, and Scopus were searched up to 30 June 2025 for pre-clinical CAR-NK studies in breast cancer. Clinical studies were retrieved from clinicaltrials.gov and the International Clinical Trial Registry Platform (ICTRP) up to 1 March 2026. Pre-clinical studies without in vivo data or non-human CAR-NK cells were excluded. Primary outcomes were tumor burden (ratio of means, ROMs) and survival (median survival ratio, MSR). Data were analyzed in JASP™ and risk of bias (RoB) was assessed using SYRCLE’s tool. Results: Fourteen pre-clinical studies (38 CAR-NK treatment groups targeting EGFR, HER2, tissue factor, CD70, mesothelin, or folate receptor, with peripheral blood as the primary NK source, and a 5–10 million cell dose) and 11 early-phase clinical studies (targeting HER2, TROP2, PD-L1, MUC1, or NKG2D ligands under ongoing investigation) were included. In pooled pre-clinical analysis, CAR-NK significantly reduced tumor burden against untreated and unmodified/mock controls (ROM 0.311 [0.22–0.44] and 0.42 [0.33–0.53], p < 0.001, respectively). Survival was also prolonged significantly (MSR 1.47 [1.15–1.87], p = 0.010 vs. untreated; 1.30 [1.09–1.60], p = 0.007 vs. unmodified/mock NK cells). Subgroup analyses indicated improved efficacy with peripheral blood source and 5–10 M dosing. No treatment-related toxicities were reported. CAR-NK persistence was generally higher than unmodified/mock NK cells. Discussion and Conclusions: Significant heterogeneity was observed in ROM analysis which the multi-level meta-analysis configured as intra-study interventional variability. There was moderate RoB in pre-clinical studies. Published results from clinical trials remain limited, highlighting early stages of investigation. Overall, CAR-NK therapy demonstrated consistent pre-clinical efficacy and safety, supporting further translational and clinical evaluation in breast cancer. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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37 pages, 1703 KB  

Open AccessReview

Linking Iron Metabolism, Ferroptosis, and Cancer: New Targets and Prospects for Effective Anticancer Therapeutic Interventions

by Malamati Kourti and George J. Kontoghiorghes

Cancers 2026, 18(9), 1436; https://doi.org/10.3390/cancers18091436 - 30 Apr 2026

Cited by 2 | Viewed by 1361

Abstract

New anticancer therapeutic strategies, including targeting of iron dysregulation in affected cancer types and stages, are urgently needed to decrease the associated annual cancer death rate of about 10 million worldwide. Many tumours evade treatment and support metastatic potential by effluxing iron and [...] Read more.

New anticancer therapeutic strategies, including targeting of iron dysregulation in affected cancer types and stages, are urgently needed to decrease the associated annual cancer death rate of about 10 million worldwide. Many tumours evade treatment and support metastatic potential by effluxing iron and upregulating antioxidant systems, leading to suppression of lipid peroxidation and ferroptotic cell death. Similarly, many tumours manipulate the tumour microenvironment (TME) by ensuring the continuous supply of iron. This involves phenotypic modulation of immune cells, including macrophages, neutrophils, regulatory T lymphocytes, and natural killer cells, as well as fibroblasts, contributing to immune evasion and tumour growth. In particular, tumour-associated macrophages (TAMs), which may account for about half of the tumour’s bulk, become progressively heavily loaded with iron and can be detected by magnetic resonance imaging (MRI) technologies. Clinically effective iron chelation therapy protocols in iron-overloaded conditions using the chelating drugs deferoxamine, deferasirox, and especially deferiprone can also potentially remove excess iron from TAMs and may decrease tumour malignancy. Deferiprone can also remove excess iron from iron-loaded renal cancer cells and potentially prevent metastasis in renal carcinoma. The anticancer potential of deferiprone has also been shown in other cancers, including iron removal in prostate cancer and through cancer stem cell inhibition in breast cancer. Many ongoing clinical trials using different drugs and experimental agents for inducing or modulating ferroptosis also support the translational potential of ferroptosis-based therapeutic strategies in selected categories of cancer patients. These advances highlight ferroptosis as a potential key metabolic vulnerability with relevance for treatment-resistant and metastatic tumours. Overall, iron chelation therapeutic approaches and ferroptosis-targeting may be considered for significant use as monotherapies or in combination with other anticancer drugs and could potentially improve therapeutic outcomes and limit disease progression and mortality in many cancers. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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13 pages, 1434 KB  

Open AccessReview

Oral Environment of Esophageal Cancer Patients, the Incidence of Complications, and Long-Term Prognoses

by Yusuke Sato, Hiroki Nikawa, Akiyuki Wakita, Yushi Nagaki, Hiroshi Takano and Kazuhiro Imai

Curr. Oncol. 2026, 33(2), 86; https://doi.org/10.3390/curroncol33020086 - 1 Feb 2026

Viewed by 1128

Abstract

Recent studies have increasingly indicated that postoperative complications after esophagectomy are correlated with poor long-term prognoses, making it crucial to prevent such complications. Based on our studies, we believe that central to this issue is the finding that among esophageal cancer patients who [...] Read more.

Recent studies have increasingly indicated that postoperative complications after esophagectomy are correlated with poor long-term prognoses, making it crucial to prevent such complications. Based on our studies, we believe that central to this issue is the finding that among esophageal cancer patients who experience postoperative complications and have poor long-term prognoses there is a high incidence of poor oral environments. Here we review the results of our basic and clinical research studies, as well as evidence from other institutions, on the oral environment of esophageal cancer patients and its association with the incidence of complications and long-term prognoses. We hope these findings, which suggest “improving the oral environment of esophageal cancer patients can reduce the incidence of postoperative complications and improve long-term prognoses”, will gain consensus and lead to safer esophageal cancer surgery. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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25 pages, 11658 KB  

Open AccessArticle

Effect of Treatment with a Combination of Dichloroacetate and Valproic Acid on Adult Glioblastoma Patient-Derived Primary Cells Xenografts on the Chick Embryo Chorioallantoic Membrane

by Rūta Skredėnienė, Donatas Stakišaitis, Aidanas Preikšaitis, Angelija Valančiūtė, Vaiva Lesauskaitė and Ingrida Balnytė

Pharmaceutics 2026, 18(1), 52; https://doi.org/10.3390/pharmaceutics18010052 - 30 Dec 2025

Cited by 1 | Viewed by 1043

Abstract

Background/Objectives: The ineffectiveness of current treatments for glioblastoma underscores the urgent need for effective alternatives. This study aimed to investigate the effectiveness of sodium dichloroacetate (NaDCA) and a sodium valproate NaDCA combination (NaVPA–NaDCA) on formed patients’ primary cell tumors on the chick embryo [...] Read more.

Background/Objectives: The ineffectiveness of current treatments for glioblastoma underscores the urgent need for effective alternatives. This study aimed to investigate the effectiveness of sodium dichloroacetate (NaDCA) and a sodium valproate NaDCA combination (NaVPA–NaDCA) on formed patients’ primary cell tumors on the chick embryo chorioallantoic membrane (CAM). Methods: Glioblastoma tissue samples were obtained from three patients during tumor surgery. WHO grade IV, IDH wild-type, and a strong positive cytoplasmic GFAP reaction in tumor cells characterized the investigated glioblastoma cases. The tumor cells GBM2-2F, GBM2-3F, and GBM-4M from the patients were examined. Histological examination of tumor invasion into CAM, angiogenesis, and immunohistochemical expression of GFAP-, PCNA-, p53-, EZH2- and vimentin-positive cells were examined. Results: No difference in GFAP expression was observed between the patient’s GBM tumor tissue and the tumor formed on CAM from the same patient’s tumor cells. There were no significant differences in invasion or in the frequency of GFAP- and p53-positive cells among the study control groups. The expression of PCNA-, EZH2-, and vimentin-positive cells in control tumors varied significantly. Treatment significantly reduced the incidence of tumor invasion in GBM2-2F and GBM2-4M and did not affect GBM2-3F tumors; treatment also significantly reduced GFAP expression in GBM2-3F and GBM2-4M and did not affect GBM2-2F tumors. The treatment with NaVPA–NaDCA significantly reduced the expression of PCNA, p53, EZH2 and vimentin in the tested tumors. Conclusions: Data demonstrated an antitumor effect of NaVPA–NaDCA in an in vivo model of a patient’s primary glioblastoma cells. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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49 pages, 11865 KB  

Open AccessReview

The Involvement of the Peptidergic Systems in Breast Cancer Development

by Manuel L. Sánchez, Prema Robinson, Zal Italia, Tan Hoang, Miguel Muñoz and Rafael Coveñas

Cancers 2025, 17(22), 3662; https://doi.org/10.3390/cancers17223662 - 14 Nov 2025

Cited by 1 | Viewed by 2393

Abstract

The current known data on the involvement of the peptidergic systems in breast cancer progression is overwhelmingly vast. Peptidergic systems are useful tools for imaging, diagnosis, prognosis and treatment of breast cancer. These systems play a crucial role in both basic and clinical [...] Read more.

The current known data on the involvement of the peptidergic systems in breast cancer progression is overwhelmingly vast. Peptidergic systems are useful tools for imaging, diagnosis, prognosis and treatment of breast cancer. These systems play a crucial role in both basic and clinical breast cancer research by enabling the exploration of novel molecular mechanisms, signaling pathways, and the development of effective drug design strategies. Breast cancer cells overexpress peptide receptors; at the same time they are known to interact with peptides that (a) exert an oncogenic action (adrenomedullin 2, endothelin, gastrin-releasing peptide, neurokinin A, neuromedin, neuropeptide Y, neurotensin, substance P, vasoactive intestinal peptide), (b) exert an anticancer action (angiotensin (1–7), ghrelin, peptide YY) or (c) exert dual oncogenic and anticancer effects (adrenomedullin, angiotensin II, bradykinin, corticotropin-releasing factor, β-endorphin, glucagon-like peptide 1, gonadotropin-releasing hormone, kisspeptin, methionine-enkephalin, oxytocin). This indicates that peptides, as well as peptide receptor agonists and antagonists, may serve as antitumor agents due to their diverse actions against breast cancer development, including the inhibition of cell proliferation, migration and invasion, induction of apoptosis, and anti-angiogenesis. Multiple strategies have been developed to combat breast cancer, including peptide receptor silencing; antibodies conjugated to specific signaling proteins; antibodies targeting specific peptide receptors or oncogenic peptides; and the use of peptides or peptide receptor agonists/antagonists loaded with antitumor cargo. Future lines of research are suggested in breast cancer using promising anti-breast-cancer peptide receptor antagonists (HOE-140, exendin (9–39), bosentan, macitentan, PD168,368, CGP71,683A, SR48,692, aprepitant) or agonists (FR190,997, semaglutide, exendin 4, goserelin) mentioned in this review. Peptidergic systems have tremendous anti-breast-cancer clinical potential which must be exploited and developed. Taken together, the available data highlight the enormous promise of translational research into breast cancer and peptidergic systems for the development of effective treatments. A full understanding of the roles played by the peptidergic systems in breast cancer will serve to improve diagnosis and treatment. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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38 pages, 2078 KB  

Open AccessReview

Kinesin Spindle Protein (KIF11) in Mitosis and Cancer

by João P. N. Silva, Patrícia M. A. Silva and Hassan Bousbaa

Int. J. Mol. Sci. 2025, 26(18), 8975; https://doi.org/10.3390/ijms26188975 - 15 Sep 2025

Cited by 7 | Viewed by 4438

Abstract

Kinesin spindle protein (KSP), also known as KIF11, is a member of the kinesin superfamily of motor proteins that plays a pivotal role in mitosis by regulating spindle assembly, chromosome alignment, and segregation. Its motor activity, which is essential for the proper organization [...] Read more.

Kinesin spindle protein (KSP), also known as KIF11, is a member of the kinesin superfamily of motor proteins that plays a pivotal role in mitosis by regulating spindle assembly, chromosome alignment, and segregation. Its motor activity, which is essential for the proper organization of microtubules during mitosis, is crucial for maintaining genomic stability. KSP overexpression has been observed in several cancer types, where it promotes uncontrolled cell proliferation, making it a promising target for cancer therapy. This review provides a comprehensive analysis of the molecular mechanisms underlying KSP function, including its structural features, ATPase activity, and interactions with other mitotic proteins. Additionally, we review the regulation of KSP through post-translational modifications, such as phosphorylation, as well as the therapeutic strategies currently being explored to inhibit its activity in cancer treatment. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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107 pages, 4728 KB  

Open AccessReview

Molecular and Immunomodulatory Mechanisms of Statins in Inflammation and Cancer Therapeutics with Emphasis on the NF-κB, NLRP3 Inflammasome, and Cytokine Regulatory Axes

by Sara Khan, Bintul Huda, Farida Bhurka, Rajashree Patnaik and Yajnavalka Banerjee

Int. J. Mol. Sci. 2025, 26(17), 8429; https://doi.org/10.3390/ijms26178429 - 29 Aug 2025

Cited by 34 | Viewed by 11859

Abstract

Statins, primarily prescribed for their lipid-lowering effects, have garnered significant attention for their potent anti-inflammatory effects. This review explores the underlying molecular pathways and clinical relevance of statins’ anti-inflammatory actions, extending beyond cardiovascular disease management to chronic inflammatory conditions and oncological applications. The [...] Read more.

Statins, primarily prescribed for their lipid-lowering effects, have garnered significant attention for their potent anti-inflammatory effects. This review explores the underlying molecular pathways and clinical relevance of statins’ anti-inflammatory actions, extending beyond cardiovascular disease management to chronic inflammatory conditions and oncological applications. The lipid-lowering effect of statins stems from their ability to suppress HMG-CoA reductase, a crucial enzyme in cholesterol synthesis; however, their pleiotropic effects include modulation of critical inflammatory pathways such as the inhibition of NF-κB signalling, a reduction in pro-inflammatory cytokine production, and enhancement of endothelial function. We delve into the molecular pathways influenced by statins, including their effects on inflammatory mediators like C-reactive protein (CRP), interleukins (IL-6, IL-1β), and tumour necrosis factor-alpha (TNF-α). Clinical evidence supporting the efficacy of statins in managing chronic inflammatory diseases, such as rheumatoid arthritis, chronic obstructive pulmonary disease, diabetes, and osteoarthritis, is critically reviewed. Additionally, we investigate the emerging role of statins in oncology, examining their impact on inflammation-driven carcinogenesis, tumour microenvironment modulation, and cancer progression. Despite their broad therapeutic potential, the safety profile of statins, particularly concerning adverse effects such as myopathy, hepatotoxicity, and potential diabetes risk, is discussed. Controversies surrounding the extent of their anti-inflammatory benefits and the variability in patient responses are also addressed. This review consolidates the current literature, elucidating the biochemical mechanisms underlying the anti-inflammatory properties of statins and evaluating their clinical applications and associated controversies. Future research directions are identified, including the development of novel statin analogues with enhanced anti-inflammatory effects and the investigation of new therapeutic indications in inflammatory diseases and cancer. By providing an in-depth analysis, this review underscores the expanding therapeutic scope of statins and advocates for their integration into broader clinical strategies for the management of inflammation and cancer. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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13 pages, 2991 KB  

Open AccessArticle

Age-Stratified Clinicopathological Features and Efficacy of Adjuvant Chemotherapy in Resectable Gastric Cancer: An East-West Population-Based Study

by Zijian Deng, Jianping Guo, Zhizhong Xiong, Bin Zhong, Dayin Huang, Haoyang Xu, Shi Chen and Lei Lian

Curr. Oncol. 2025, 32(9), 480; https://doi.org/10.3390/curroncol32090480 - 26 Aug 2025

Viewed by 1477

Abstract

Background: The incidence of early-onset gastric cancer (EOGC) has been steadily increasing in recent years. However, the efficacy of adjuvant chemotherapy (AC) in this population remains unclear. This study aimed to investigate the clinicopathological characteristics, survival outcomes, and efficacy of AC between EOGC [...] Read more.

Background: The incidence of early-onset gastric cancer (EOGC) has been steadily increasing in recent years. However, the efficacy of adjuvant chemotherapy (AC) in this population remains unclear. This study aimed to investigate the clinicopathological characteristics, survival outcomes, and efficacy of AC between EOGC and average-onset gastric cancer (AOGC) patients. Methods: Patients with stage II–III gastric adenocarcinomas who underwent curative D2 gastrectomy at the Sixth Affiliated Hospital of Sun Yat-sen University from January 2014 to December 2021 were enrolled and classified into two groups: EOGC (≤45 years) and AOGC (>45 years) groups. Clinicopathological characteristics, overall survival (OS), and efficacy of AC were compared between the two groups. Western and East Asian cohorts were included as external validation sets to compare the efficacy of AC between different age groups. Results: Compared to AOGC, EOGC patients exhibited a higher proportion of females, poor differentiation, diffuse Lauren type, middle-third GC, perineural invasion (PNI), and receipt of AC. Univariate and multivariate analyses identified that T stage, N stage, PNI, and AC were independent prognostic factors for OS. After balancing the baseline characteristics between patients who received AC and those who did not, the Kaplan–Meier survival curves indicated that AC significantly improved OS across all patients. Further subgroup analysis revealed a survival benefit of AC in AOGC patients, whereas no significant survival difference was observed in the EOGC subgroup. Consistently, external validation in both Western and East Asian cohorts confirmed that AC did not confer a survival advantage in EOGC patients. Conclusions: EOGC exhibits aggressive pathological characteristics, and chemotherapy does not consistently improve survival in EOGC patients. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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14 pages, 1306 KB  

Open AccessReview

Gold Nanoparticles as Targeted Drug Delivery Systems for Liver Cancer: A Systematic Review of Tumor Targeting Efficiency and Toxicity Profiles

by Meda Cosma, Teodora Mocan, Cristian Delcea, Teodora Pop, Ofelia Mosteanu and Lucian Mocan

Int. J. Mol. Sci. 2025, 26(16), 7917; https://doi.org/10.3390/ijms26167917 - 16 Aug 2025

Cited by 23 | Viewed by 5193

Abstract

Hepatocellular carcinoma (HC) ranks as the fifth most prevalent form of cancer among humans and is a significant contributor to cancer-related deaths. During the latest year, an interesting scientific fascination arose around gold nanoparticles (AUNPs) following the recovery of their remarkable properties. Some [...] Read more.

Hepatocellular carcinoma (HC) ranks as the fifth most prevalent form of cancer among humans and is a significant contributor to cancer-related deaths. During the latest year, an interesting scientific fascination arose around gold nanoparticles (AUNPs) following the recovery of their remarkable properties. Some studies suggest that AUNPs can enhance drug targeting in cancer treatment and reduce its toxicity. The major purpose of this paper is to systematically review the effectiveness, safety, and prospective mechanism of gold nanoparticles in delivering drugs for liver cancer treatment. Comprehensive research was conducted using major scientific databases (i.e., PubMed, Web of Science, and Scopus) to identify studies focusing on AUNPs in drug delivery systems. We mainly focused on studies that specifically analyzed liver cancer. The current results of the systematic review show that the application of gold nanoparticles (AUNPs) in liver cancer drug delivery enhances drug targeting to liver tumors. This efficient factor improves the bioavailability and elevates the therapeutic index of chemotherapeutic agents in treatment. This systematic review highlights the significant potential of AUNPs to increase the delivery of drugs for liver cancer treatment effectively. The major findings indicate that AUNPs improve the targeting and bioavailability of chemotherapeutic agents, enhancing therapeutic outcomes such as tumor suppression and improved survival rates. While the results of this review are encouraging; however, further research is necessary to ensure the safety and efficacy of AUNPs in clinical settings. Human trials must address concerns regarding long-term toxicity and regulatory approval. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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28 pages, 732 KB  

Open AccessSystematic Review

Preclinical Trials of Cancer Stem Cells Targeted by Metal-Based Coordination Complexes: A Systematic Review

by Ana Caroline Mafra Bezerra, Lucas Elohim Cardoso Viana Baptista, Maria Núbia Alencar Couto and Milton Masahiko Kanashiro

Pharmaceutics 2025, 17(7), 931; https://doi.org/10.3390/pharmaceutics17070931 - 18 Jul 2025

Cited by 6 | Viewed by 2733

Abstract

Background/Objective: Cancer stem cells (CSCs) are a self-renewing subpopulation within tumors that contribute to heterogeneity and resistance to conventional cancer therapies, including chemotherapy and radiotherapy. Despite growing interest in CSCs as therapeutic targets, effective compounds against these cells remain limited. This systematic [...] Read more.

Background/Objective: Cancer stem cells (CSCs) are a self-renewing subpopulation within tumors that contribute to heterogeneity and resistance to conventional cancer therapies, including chemotherapy and radiotherapy. Despite growing interest in CSCs as therapeutic targets, effective compounds against these cells remain limited. This systematic review aims to assess the potential of metal-based coordination complexes as anti-CSC agents in preclinical models. Methods: A systematic literature search was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Twenty-seven original in vitro studies were included, all evaluating the cytotoxic effects of metal-based compounds on cancer cell lines enriched with CSC subpopulations. To ensure methodological rigor, all articles underwent a critical appraisal by independent reviewers who resolved discrepancies through consensus, and only studies meeting predefined quality criteria were included. Results: Several metal complexes, particularly copper-based compounds, demonstrated significant cytotoxicity toward CSCs, mainly through the induction of apoptosis. Breast cancer was the most frequently studied tumor type. Many studies reported modulation of CSC-related markers, including EPCAM, CD44, CD133, CD24, SOX2, KLF4, Oct4, NOTCH1, ALDH1, CXCR4, and HES1, suggesting effects on CSC maintenance pathways. Most studies were conducted in the United Kingdom and relied on in vitro models. Conclusions: Metal coordination complexes, especially those containing copper, show promise as therapeutic agents targeting CSCs. However, further in vivo studies and mechanistic investigations are essential to advance their translational potential. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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20 pages, 663 KB  

Open AccessSystematic Review

Electrochemotherapy in the Management of Keratinocyte Carcinomas: A Systematic Review

by Yue Ting Nichole Tan and Choon Chiat Oh

Cancers 2025, 17(11), 1766; https://doi.org/10.3390/cancers17111766 - 24 May 2025

Cited by 2 | Viewed by 2426

Abstract

Background: Keratinocyte carcinomas, including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC), presents a growing concern. Electrochemotherapy (ECT), an emerging treatment modality, combines chemotherapy and electroporation to enhance drug delivery into cells. However, reviews evaluating ECT in keratinocyte carcinomas are lacking. Objectives: [...] Read more.

Background: Keratinocyte carcinomas, including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC), presents a growing concern. Electrochemotherapy (ECT), an emerging treatment modality, combines chemotherapy and electroporation to enhance drug delivery into cells. However, reviews evaluating ECT in keratinocyte carcinomas are lacking. Objectives: This study reviews the efficacy and toxicity of ECT in the treatment and palliation of keratinocyte carcinomas. Methods: A systematic search was conducted across PubMed, Cochrane, Embase, and Scopus databases. Patient, tumor, and treatment characteristics, tumor response, long-term disease outcomes, and toxicity data were extracted. Quality of studies was assessed using validated tools. Primary endpoints included tumor response; secondary endpoints included long-term disease outcomes and toxicity. Results: Twenty-one studies were included. Complete response (CR) rates ranged from 50 to 100% and from 10 to 100% for BCC and SCC, respectively. OS rates ranged from 95 (14 months) to 100 (1 year) % and from 64 (1 year) to 85.1 (8.6 months) % for BCC and SCC, respectively. One-year local disease-free survival (LDFS) rates were 89% and 87% for BCC and SCC, respectively. For BCC, local progression-free survival (LPFS) rates were 96% (1 year), 90% (2 year), and 70% (5 year). For SCC, 1-year LPFS rates were 80% on a per-patient basis and 49% on a per-lesion basis. Conclusions: ECT is effective and tolerable in the treatment and palliation of keratinocyte carcinomas. Future studies should focus on improving reporting quality, optimizing treatment protocols, and investigating long-term outcomes. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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32 pages, 6286 KB  

Open AccessArticle

Synthesis and In Vitro Evaluation of the Anticancer Effect of Novel Phosphonium Vindoline Derivatives

by Mónika Halmai, Viktória Donkó-Tóth, Péter Keglevich, Károly Kánai, Márton Weber, Miklós Dékány, Ejlal A. Abdallah, Noémi Bózsity, István Zupkó, Andrea Nehr-Majoros, Éva Szőke, Zsuzsanna Helyes and László Hazai

Int. J. Mol. Sci. 2025, 26(8), 3775; https://doi.org/10.3390/ijms26083775 - 16 Apr 2025

Cited by 4 | Viewed by 2183

Abstract

The Vinca alkaloid vindoline was coupled at position 17 with several trisubstituted phosphine derivatives and their in vitro anticancer activities on 60 human tumor cell lines (NCI60) were investigated. This phosphonium-type ionic side chain is beneficial because it allows therapeutic molecules to pass [...] Read more.

The Vinca alkaloid vindoline was coupled at position 17 with several trisubstituted phosphine derivatives and their in vitro anticancer activities on 60 human tumor cell lines (NCI60) were investigated. This phosphonium-type ionic side chain is beneficial because it allows therapeutic molecules to pass through the cell membrane. Thus, the candidates coupled to it can exert their activities in the mitochondria. The coupling of vindoline with the trisubstituted phosphines was achieved through flexible or rigid linkers. Instead of the ionic phosphonium structural part, a neutral moiety, namely the triphenylmethyl group, was also added to the side chain, being sterically similar but without a charge and phosphorus atom. In addition, the triphenylphosphine element was also built at position 10 of vindoline. Most of the derivatives showed low micromolar growth inhibition (GI₅₀) values against most cell lines. Among them, conjugate 9e was outstanding: it exhibited nanomolar anticancer activity on the RPMI-8226 leukemia cell line (GI₅₀ = 20.0 nM). Compound 9g elicited cell cycle disturbance and apoptosis on A2780 ovary cancer cells and inhibited their migration at subantiproliferative concentrations. The selectivity of the conjugates was determined by their effects on non-tumor Chinese hamster ovary (CHO) cells in the CellTiter-Glo Luminescent Cell Viability Assay. Compound 9e showed an estimated half-maximal inhibitory concentration (IC₅₀) value of 1.36 µM, suggesting good selectivity on cancer cells. These results open new perspectives of novel phosphonium-based vindoline derivatives as anticancer compounds. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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22 pages, 1121 KB  

Open AccessReview

Advancing Cancer Treatment and Diagnosis: A Review on Photodynamic Therapy Using OLED Technology

by Rajesh Kumar Tiwari, Rajesh Mishra, Sanjay Kumar Sharma, Nakshathra Prabhu, Mangey Ram Nagar and Saulius Grigalevicius

Molecules 2025, 30(6), 1305; https://doi.org/10.3390/molecules30061305 - 14 Mar 2025

Cited by 13 | Viewed by 5415

Abstract

Photodynamic therapy (PDT) is an innovative and non-invasive approach to treating apparent tumours with minimal toxicity. PDT has a long-standing application in antitumor treatment utilizing various photosensitizers (PSs) for different tumours. Historically, light has served as a therapeutic tool in many diseases. PDT [...] Read more.

Photodynamic therapy (PDT) is an innovative and non-invasive approach to treating apparent tumours with minimal toxicity. PDT has a long-standing application in antitumor treatment utilizing various photosensitizers (PSs) for different tumours. Historically, light has served as a therapeutic tool in many diseases. PDT involves a dual treatment process in which light energy and PSs are combined to ablate tumour cells following light activation. In general, PDT exhibits reduced side effects and toxicity compared to chemotherapy and radiotherapy, as it spares the extracellular matrix, facilitating excellent tissue healing and minimizing scarring. In addition, PSs can serve in diagnostic roles in tumour identification, termed photodynamic diagnosis (PDD). Advancements in flexible light sources that produce uniform illumination could significantly enhance the consistency of light delivery. This review outlines the clinical applications of OLEDs in PDT for cancer, addressing both diagnostic and therapeutic methods. Furthermore, we will explore various tumour cases using PDT with OLEDs. In particular, antimicrobial PDT targets antibiotic-resistant strains in diabetic foot ulcers, while metronomic PDT promotes cancer cell apoptosis through prolonged, low-intensity light exposure. Our emphasis is on PDT employing organic light-emitting diodes (OLEDs). Furthermore, the combination of PDT with NIR-OLEDs is examined for its potential to enhance tumour-targeting effectiveness, possibly exceeding the results of standalone treatments. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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28 pages, 2851 KB  

Open AccessReview

Targeting c-MYC G-Quadruplexes for Cancer Treatment with Small Molecules

by Prasanth Thumpati, Sachchida Nand Rai, Chandrabhan Prajapati, Kakarla Ramakrishna and Santosh Kumar Singh

Sci. Pharm. 2025, 93(1), 6; https://doi.org/10.3390/scipharm93010006 - 22 Jan 2025

Cited by 66 | Viewed by 6199

Abstract

Novel therapies are required due to the rising cancer burden. Conventional chemotherapeutics tend to be particularly toxic, but there is a promising alternative for oncogenes, such as c-MYC. Often overexpressed in many cancer types, the potential c-MYC oncogene seems essential to the development [...] Read more.

Novel therapies are required due to the rising cancer burden. Conventional chemotherapeutics tend to be particularly toxic, but there is a promising alternative for oncogenes, such as c-MYC. Often overexpressed in many cancer types, the potential c-MYC oncogene seems essential to the development of cancer. Targeting c-MYC protein directly was limited, but these DNA structures composed of guanine-rich sequences suppress c-MYC transcription. This review discusses recent advances in developing small compounds that selectively bind to and stabilize c-MYC G-quadruplexes (G4). These molecules have also shown promise for the inhibition of c-MYC signaling and inhibition of tumor growth, suggesting that G-quadruplex targeting could be a promising therapeutic for cancer. Full article

(This article belongs to the Topic Recent Advances in Anticancer Strategies, 2nd Edition)

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