Abstract: Breast cancer remains one of the leading causes of morbidity and mortality among women worldwide, underscoring the critical need for early and accurate diagnostic methodologies. This review describes an advanced breast cancer detection system that integrates Artificial Intelligence (AI) with sophisticated imaging mechanisms to improve diagnostic precision. The system employs highresolution imaging technology to non-invasively visualize and isolate successive layers of breast tissue, thereby providing detailed, multi-planar views of targeted anatomical regions. This approach facilitates deeper examination of tissue architecture. Through subsequent AI-driven computational analysis, potential malignant areas, including microcalcifications and subtle structural distortions, are identified and highlighted in real time. This integrated approach enables faster and more reliable interpretation of complex imaging data while reducing the cognitive burden on radiologists. The core mechanism enhances diagnostic accuracy by detecting aberrant tissue patterns and generating comprehensive layered insights, including quantitative assessments of tissue density and vascularization, to support clinical decision-making and risk stratification. By combining depth-resolved visualization with automated interpretation, this approach has the potential to advance beyond conventional twodimensional screening paradigms. The integration of AI and advanced imaging contributes to a more sensitive and specific diagnostic workflow. Consequently, this review presents SDSND as a hypothetical and emerging framework integrating AI and nanoscale detection. However, its clinical applicability remains unvalidated and requires experimental and clinical investigation.
Abstract: Plant-based natural chemicals remain a viable resource for identifying original active ingredients. Sesquiterpene Lactones (SLs) are available, low-toxicity compounds with a broad spectrum of therapeutic applications. Inula contains a high concentration of flavonoids and SLs, which hold significant therapeutic promise. For centuries, the Asteraceae family, particularly Artemisia britannica L., has been used to treat gastrointestinal and inflammatory disorders. Among them, the pseudo- guaianolide-type SL Britannin (BRT) has shown promise as an anti-cancer and anti-inflammatory compound. By inducing apoptosis, autophagy, and cell death, BRT can cause cell cycle arrest and exhibit cytotoxic effects across various cancer types, including leukemic, hepatic, pancreatic, gastric, colon, and breast cell lines. Mechanistically, BRT prevents tumors from growing, forming new blood vessels, spreading, and evading the immune system by disrupting the following pathways: PD-L1, AMPK-mTOR, c-Myc/HIF-1α, Keap1-Nrf2, and NF-κB signaling. Its therapeutic profile is also enhanced by its immunosuppressive and antioxidant activities. This article concludes that the combined therapy of BRT with chemotherapy and immunotherapy has emerged as a strong candidate for development as a novel anticancer therapy.
It has come to the publisher’s attention that an identical version of this article was previously published in the International Journal of All Research Education & Scientific Methods (IJARESM) under the following link: "https://www.ijaresm.com/ uploaded_files/document_file/Jain_Pk_2tsi0.pdf". As duplicate publication violates ethical publishing standards, the publisher has informed the authors and has decided to retract the article from Current Cancer Therapy Reviews. Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused. The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php.
Introduction: Cancer remains a major global health challenge, accounting for nearly one in six deaths worldwide, with treatment often limited by drug resistance, tumour heterogeneity, and therapy-related side effects. Natural plant-derived compounds have gained attention as potential therapeutic leads owing to their structural diversity and multi-targeted mechanisms. Acteoside (Verbascoside), a phenylethanoid glycoside obtained from medicinal plants, exhibits diverse biological and promising anticancer effects. However, information on acteoside remains scattered across phytochemical, pharmacological, and experimental studies. This review integrates current evidence to provide a comprehensive overview of acteoside in cancer research. Methods: Literature retrieval for this study was conducted using the Scopus database due to its extensive coverage of peer-reviewed journals, robust metadata indexing, and suitability for ethnopharmacological, bibliometric, and pharmacognostic analyses. The study included four analytical components, viz., cataloguing plant sources of acteoside to establish a pharmacognostic repository, bibliometric analysis of acteoside-related cancer research (1990-2024) to identify trends, mapping of cancer types investigated in acteoside studies, and predictive acteoside-disease target mapping using network pharmacology to evaluate oncological relevance. Results: The former two analyses highlight the broad botanical distribution of acteoside and increasing interest in its anticancer potential. Cancer-type mapping showed investigations across multiple malignancies. Predictive acteoside-disease target mapping revealed that cancer exhibited the highest number of connections with acteoside-associated targets. Discussion: These findings reinforce the growing relevance of acteoside in cancer research. Conclusion: Overall, this integrative overview provides a foundation for future experimental and translational research on acteoside as a promising natural anticancer lead.
Introduction: Non-Small Cell Lung Cancer (NSCLC) often occurs with Chronic Obstructive Pulmonary Disease (COPD), a disorder of chronic inflammation of the airways and associated predisposition to bacterial infections. This prospective multicenter cohort study investigates the association between Klebsiella pneumoniae–related neutrophil-driven inflammation and chemotherapy response in patients with stage III NSCLC and COPD. Methods: In this prospective multicenter cohort study, patients with stage III Non-Small-Cell Lung Cancer (NSCLC) and Chronic Obstructive Pulmonary Disease (COPD) were stratified depending on the presence or absence of confirmed infection with K. pneumoniae in the lungs. The chemotherapeutics used in all patients were carboplatin-paclitaxel. Serum interleukin-8 (IL-8) and calprotectin (S100A8/A9) were assessed as indicators of neutrophil recruitment and activation, whereas Carcinoembryonic Antigen (CEA) was assessed as an indicator of chemotherapy response. Biomarkers were assessed over time at baseline and during treatment. K. pneumoniae isolates were tested for biofilm formation ability and MDR phenotype. Results: Infected patients had significantly higher baseline levels of IL-8, calprotectin, and CEA than non-infected patients (p < 0.0001). Although chemotherapy was associated with significant decreases in inflammatory biomarkers in both groups, infected patients had persistent elevations throughout treatment (p < 0.0001). Discussion: CEA levels in infected patients decreased after the first chemotherapy cycles; no significant reduction was seen during subsequent chemotherapy cycles (p = 0.131). Conclusion: K. pneumoniae infection is strongly associated with persistent neutrophil-mediated inflammation and correlates with altered behavior of chemotherapy-related biomarkers in patients with Non-Small Cell Lung Cancer (NSCLC) who also have Chronic Obstructive Pulmonary Disease (COPD).
Abstract: Curcumin is the primary curcuminoid present in the Curcuma longa rhizome, commonly known as turmeric, and because of its potential as a natural anticancer drug, it has drawn a lot of scientific attention. Curcumin has a broad range of pharmacological activities, such as antioxidant, antiinflammatory, antimicrobial, antiangiogenic, anticancer, antiproliferative, and many more. Curcumin has been demonstrated in numerous in vitro and in vivo investigations to be capable of preventing the development and spread of a number of malignancies, including those of the breast, colon, prostate, lung, stomach, brain, and pancreas. Curcumin’s capacity to alter a broad spectrum of molecular targets implicated in tumor initiation, development, and progression is thought to be the cause of its anticancer properties. These include the control of tumor suppressor genes, apoptotic proteins, inflammatory mediators, and angiogenic factors, as well as important signaling pathways like NF-κB, PI3K/ Akt, Wnt/β-catenin, and MAPK. Although curcumin has a potential pharmacological profile, its therapeutic effectiveness is severely limited by its low bioavailability. Numerous formulation techniques, such as the use of adjuvants (such as piperine), liposomes, nanoparticles, and micelles, have shown promising results in improving systemic availability and therapeutic potency. This study demonstrates the complex role curcumin plays in the fight against cancer and stresses how crucial it is to get past pharmacokinetic obstacles in order to fully utilise its therapeutic potential. Curcumin shows promise as an efficient, low-toxicity drug in integrative cancer therapy with additional study and clinical validation. This review provides an integrated cross-cancer analysis of curcumin-mediated signaling networks and translational strategies to overcome pharmacokinetic limitations.
Introduction: To investigate the role of Intermediate Filament Family Orphan Protein 2 (IFFO2) in Liver Hepatocellular Carcinoma (LIHC), we systematically evaluated mRNA expression and analyzed the correlation between IFFO2 expression and clinicopathological information, patient prognosis, and the immune microenvironment. In this study, the influence of IFFO2 on LIHC proliferation, clone formation, migration, and invasion was demonstrated using in vitro experiments. This will provide a theoretical basis for IFFO2 to be developed into a biomarker and therapeutic target for LIHC. Materials and Methods: IFFO2 expression in pan-cancer and LIHC tissues was analyzed in the Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) databases. For assessing diagnostic value, Receiver Operating Characteristic (ROC) curves were used, and Kaplan-Meier (KM) and Cox regression were used for Prognostic analysis. The single-sample Gene Set Enrichment Analysis (ssGSEA) algorithm was used to examine the relationship between IFFO2 expression and immune cell infiltration. In vitro experiments used siRNA to knock down IFFO2 in HUH7 and HepG2 cells, followed by CCK-8 proliferation assays, clone formation, scratch wound-healing assays, transwell invasion assays, and other experiments to examine changes in cellular behavior. Results: IFFO2 expression was obviously upregulated in the LIHC tissues (p < 0.05). The results of the ROC analysis showed a high diagnostic ability, with an Area Under the Curve (AUC) of 0.790. Increased IFFO2 is associated with high pathological stages, high levels of Alpha-Fetoprotein (AFP), prolonged prothrombin time, and shortened overall survival (OS) (p < 0.05). Functional enrichment analysis revealed that IFFO2 is significantly associated with immune regulation, cell cycle, and complement activation pathways. Immune infiltration analysis demonstrated the presence of various immune cell subtypes that exhibited both positive and negative correlations with IFFO2. In vitro experiments have demonstrated that IFFO2 knockdown remarkably diminishes the proliferation, clone formation, migration, and invasion capacities of LIHC cells (p < 0.05). Discussion: The findings suggest that IFFO2 functions as an oncogene in LIHC. Its strong association with adverse prognosis and its potential to modulate the immune microenvironment underscore its dual potential as a diagnostic biomarker and a promising therapeutic target, warranting further mechanistic and clinical investigation. Conclusion: IFFO2 is significantly upregulated in LIHC and promotes tumor progression; its expression is associated with unfavorable prognostic outcomes, suggesting its potential utility as a biomarker for diagnosis and a therapeutic target.
Abstract: Triple-Negative Breast Cancer (TNBC), defined by the lack of Estrogen Receptors (ER), Progesterone Receptors (PR), and human epidermal growth factor receptor 2 (HER2), remains one of the most aggressive and therapeutically challenging subtypes of breast cancer. The absence of these traditional molecular targets limits the effectiveness of conventional hormone and HER2-targeted therapies, necessitating the exploration of alternative therapeutic strategies. Recent attention has shifted toward ER-α36, a structurally distinct isoform of the classical estrogen receptor α (ER-α66), which lacks the AF-1 and AF-2 transactivation domains but retains the ability to mediate nongenomic estrogen signaling. ER-α36 is implicated in activating critical oncogenic pathways, including EGFR/Src/ERK, MAPK/ERK, and PI3K/AKT/mTOR, all of which contribute to enhanced proliferation, survival, and metastasis in TNBC. Therapeutic approaches targeting these downstream signaling cascades have shown promise in preclinical and early clinical studies. Notably, combinations such as pan-PI3K inhibitors with fulvestrant, and agents like BYL719 (alpelisib) and AZD5363 (capivasertib) with chemotherapeutics like docetaxel, have demonstrated significant antitumor efficacy. Additionally, monoclonal antibodies such as trastuzumab and seribantumab have been found to selectively inhibit components of the MAPK/ERK and PI3K/AKT pathways, respectively, offering further avenues for targeted intervention. Moreover, tyrosine kinase inhibitors that disrupt EGFR signaling are emerging as valuable tools to suppress cancer cell viability and proliferation. This review highlights ER-α36 not only as a key player in the molecular pathology of TNBC but also as a promising therapeutic target. By focusing on ER-α36-mediated signaling mechanisms, researchers and clinicians may develop more effective, personalized strategies for treating TNBC. Targeting ER-α36 and its associated pathways represents a forward-looking approach that could address the pressing need for novel therapies in this difficult-to-treat breast cancer subtype.
Ferroptosis, an iron-dependent form of regulated cell death characterized by lipid peroxidation, has emerged as a promising therapeutic target in cancer treatment. This review critically evaluates recent advances in understanding the molecular mechanisms of ferroptosis and its application in oncology. We analyzed preclinical and clinical studies published between 2015 and 2025, sourced from major scientific databases including PubMed, Scopus, and Web of Science. Key findings highlight an expanding range of small molecules, natural compounds, and nanomedicines that induce or inhibit ferroptosis through pathways involving GPX4, SLC7A11, FSP1, and iron metabolism. Ferroptosis has been shown to enhance the efficacy of chemotherapy, radiotherapy, and immunotherapy while overcoming mechanisms of drug resistance. Despite these advances, translational challenges, such as off-target toxicity, tumor heterogeneity, and limited biomarkers for patient selection, remain. This review emphasizes the therapeutic potential of ferroptosis modulation and outlines future directions for integrating ferroptosis-targeted strategies into precision cancer therapy
Introduction: Glioblastoma (GBM) is the most common primary intrinsic brain tumor in adults and represents the most aggressive diffuse astrocytic glioma. This study aimed to identify Differentially Expressed Genes (DEGs) in GBM, elucidate their functional roles, and validate potential hub genes as independent prognostic biomarkers through integrated bioinformatics analysis. Methods: We conducted an integrated bioinformatics analysis using publicly available datasets from the Gene Expression Omnibus (GEO). The GSE4290 and GSE50161 datasets were analyzed to identify DEGs between GBM and normal brain tissue. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to explore the biological functions of DEGs. Protein-Protein Interaction (PPI) networks were constructed using the STRING database and Cytoscape to identify hub genes. Genetic alterations of hub genes were examined through cBioPortal. Prognostic relevance was assessed using Cox regression analysis in the Chinese Glioma Genome Atlas (CGGA), and expression levels were validated in UALCAN. Results: A total of 467 overlapping DEGs were identified, including 94 upregulated and 373 downregulated genes in GBM. GO and KEGG analyses revealed enrichment mainly in synaptic signaling and neurotransmitter release. PPI network analysis identified 10 downregulated hub genes: SNAP25, SYN2, SYN1, RAB3A, SYT1, SLC17A7, CPLX1, RIMS1, STX1A, and STXBP1. Genetic alterations in these genes were observed in 73 (12%) of 585 GBM patients. Higher expression of SYN2 and CPLX1 correlated with improved overall survival, and UALCAN confirmed their reduced expression in GBM compared with normal brain. Discussion: SYN2, encoding a neuronal phosphoprotein critical for synaptic plasticity and vesicle trafficking, and CPLX1, encoding complexin-1, which regulates neurotransmitter release via SNARE complex interaction, emerged as key modulators of neuron-glioma interaction. Their downregulation in GBM and association with improved survival when expressed suggest that dysregulation of the synaptic communication may drive tumor progression. These findings align with mounting evidence that GBM exploits neural signaling circuits, including synaptic and neurotransmitter pathways, to sustain growth and invasion. Conclusion: This study highlights synaptic-related genes as key contributors to GBM pathology and suggests that synaptic dysregulation may present novel prognostic markers. Further experimental validation is required to confirm their clinical utility.
Abstract: Non-Small Cell Lung Cancer (NSCLC), the predominant lung cancer subtype, causes high morbidity and mortality due to its complex pathogenesis, late diagnosis, and multidrug resistance, which limit effective treatment. Physiological barriers, nonspecific drug distribution, and systemic toxicity of the current traditional therapies and current nanocarrier systems have limited their success. The next-generation drug delivery system, engineered liposomes, has emerged to overcome these limitations to enhance the site-specific delivery and improve the therapeutic outcomes. This review examines the engineering and utilization of engineered liposomes to address NSCLC therapy. It begins with an overview of NSCLC and the biological and physiological obstacles associated with its treatment. Limitations of current nano-formulations highlight the rationale for engineered liposomes, which offer improved permeability, targeted delivery, controlled release, and co-delivery of drugs and genetic materials. Special emphasis is placed on their design features, including surface modifications, ligand conjugation, and stimuli-responsive mechanisms that improve tumor targeting and cellular uptake. Mechanistic insights into how engineered liposomes interact with tumor cells, bypass efflux pumps, and facilitate intracellular delivery are presented. Their use in chemotherapy, combination therapy, RNA/gene therapy, and theranostic monitoring is demonstrated in current in vitro, in vivo, and clinical studies. This review also addresses regulatory and safety considerations and concludes with future perspectives, including the potential translation of these systems to other malignancies such as glioblastoma.
Abstract: Hematologic malignancies, such as leukemia and lymphoma, have demonstrated the effectiveness of CAR-T cell therapy, which is a recent innovation in cancer immunotherapy. Ongoing research is focused on the ability to treat solid tumors, autoimmune diseases, and cell platforms that have been genetically altered. There are issues such as tumor heterogeneity, immune evasion, and limited tumor infiltration that limit the effectiveness of therapies against solid tumors. CRISPR/Cas9- based genetic modifications and the targeting of multiple antigens are innovative solutions to these problems. There are also "armored" CAR-Ts that secrete cytokines to aid in therapy. Furthermore, promising, safer, and more scalable substitutes are provided by CAR-NK and CAR-Treg treatments. When taken as a whole, these developments portend a new generation of accurate, readily accessible, and adaptive cellular immunotherapies for a number of diseases.
Abstract: Diabetes and Cancer are global chronic ailments with a significant impact on expectancy and quality of life. Metabolic disorders analysed during the progression and onset of diabetes may have a crucial function in the progression and initiation of carcinogenesis. Although there is growing evidence linking diabetes to some types of cancer, the fundamental processes of this possible relationship remain unclear. Insulin is a potent growth factor that either directly or indirectly stimulates cell division and carcinogenesis through the insulin-like growth factor 1 (IGF-1) pathway. To date, there is no critical data regarding the mechanism responsible for the relationship between diabetes and different types of cancer in humans. Although the latest evidence proposes that both hyperinsulinemia and hyperglycemia in diabetes could bring about pro-carcinogenic stress responses, for instance, lipotoxicity, glucotoxicity, and oxidative stress, which are involved in the process of transformation, increasing the chances of developing cancer. Because hyperinsulinemia inhibits IGF binding protein-1, it increases the bioactivity of IGF-1. Excess hyperglycemia may encourage the growth of cancer cells both directly and indirectly. Additionally, clinical studies have discovered that various anti-diabetic treatments may potentially cause the risk of cancer via undefined mechanisms. Natural compounds (p- and ricinoleic acid, epigallocatechin, coumaric acid, ricinine) targeting both ailments are described, along with their mechanisms of action. Thus, through this review, we targeted the pathophysiological and epidemiological aspects of diabetes, which further direct the process of cancer progression and initiation.
Abstract: The chemotherapeutic agent paclitaxel is being presented as a promising antiendometriotic treatment. Endometriosis is a common gynecological disorder that leads to chronic peritoneal pain and infertility. It is characterized by the presence of endometrial tissue outside the uterus. In this review, the anti-endometriotic features of paclitaxel are analyzed and discussed from both pharmacological and biomolecular perspectives. Paclitaxel acts pharmacologically as a microtubule- stabilizing agent, interfering with the cell cycle and preventing the formation of new cells. It also exhibits anti-angiogenic activity, inhibiting the growth of new blood vessels and thereby reducing the vascularization of endometriotic lesions. Moreover, paclitaxel modulates immune responses, inducing an anti-inflammatory environment during endometriosis. At the biomolecular level, paclitaxel affects important signaling pathways involved in endometriotic pathogenesis. It acts on molecules such as transforming growth factor-beta (TGF-β), vascular endothelial growth factor (VEGF), nuclear factor-kappa B (NF-κB), and matrix metalloproteinases (MMPs), which play roles in inflammation, neovascularization, and tissue remodeling associated with endometriosis. This review provides detailed insights into the research conducted on paclitaxel, including its safety and efficacy as a treatment for endometriosis. It also examines different methods of administration, dosage schedules, and combination strategies aimed at enhancing its therapeutic effects. In conclusion, paclitaxel represents a potential therapeutic strategy for endometriosis by acting not only through its pharmacological properties but also through its biomolecular effects on the disease. Additional investigations are needed to elucidate its mechanisms of action, determine optimal treatment schedules, and explore new combination therapies to improve outcomes in patients with endometriosis.
This review outlines the evolution of molecular techniques used to understand the clinical and molecular heterogeneity of leukemia. These technical advances are reshaping disease classification, prognosis, and therapeutic strategies. The diagnostic journey has progressed from foundational methods like karyotyping and fluorescence in situ hybridization (FISH) to higher-resolution analyses. Techniques such as microarrays, optical genomic mapping (OGM), and next-generation sequencing (NGS) have enabled the identification of copy number variations, complex chromosomal rearrangements, and comprehensive mutational landscapes in key genes like FLT3, NPM1, and TP53. Furthermore, advanced methods have provided deeper insights. RNA-seq has revealed novel transcriptome components, including fusion genes and non-coding RNAs (ncRNA). The role of extrachromosomal DNA (ecDNA) in oncogene amplification and therapeutic resistance has recently been highlighted. Epigenetic dynamics are being explored through techniques like chromatin immunoprecipitation sequencing (ChIP-seq) and the assay for transposase-accessible chromatin (ATAC-seq). Integrating these complementary tools is crucial for identifying therapeutic vulnerabilities cost-effectively. Finally, targeted assays like RT-qPCR and Sanger sequencing remain essential for confirmatory diagnosis and the technical validation of whole-genome or transcriptome-wide assays.
Background: Traditional cancer treatments have increased survival, but their efficacy is frequently constrained by toxicity and drug resistance. Cancer is still a major global health concern. Although resistance, notably to PARP1 inhibitors, has emerged as a significant therapeutic obstacle, PARP inhibitors have demonstrated promise, particularly in BRCA-mutated and HR-deficient malignancies. Objective: Furthermore, highlighting current developments in addressing these treatment obstacles, this review investigates the molecular and cellular mechanisms driving acquired and inherent resistance to PARP inhibitors. Methods: A thorough review of the literature was conducted using specific keywords from Google Scholar, PubMed, and Scopus. To gather relevant information on resistance mechanisms and therapeutic options, 119 peer-reviewed articles were carefully analyzed. Result: Replication fork protection, drug efflux through ABC transporters, homologous recombination restoration, and PARP1 mutations are important resistance mechanisms to PARP inhibitors. Combination treatments, epigenetic modulators, and next-generation PARP inhibitors with enhanced target selectivity are methods for overcoming resistance. Conclusion: For researchers seeking to develop more effective and long-lasting anti-cancer treatments, this review provides a comprehensive framework for understanding PARP inhibitor resistance and exploring new therapeutic approaches.
Introduction: Cancer-Induced Anemia (CIA) in treatment-naïve patients is a common yet under-investigated complication that significantly impacts quality of life (QoL) and survival. This review consolidates evidence on the CIA's baseline prevalence, pathophysiology, clinical implications, and management. Methods: A narrative literature review was conducted using databases like PubMed and Scopus to identify studies on prevalence, pathophysiology, and management of CIA in treatment-naïve patients. Key articles and guidelines were included to synthesize current evidence. Results: The prevalence of CIA varies widely (18-87%), with the highest rates in gastrointestinal, gynecologic, and hematologic cancers. Its pathophysiology is driven by inflammation-mediated hepcidin upregulation, functional iron deficiency, and suppressed erythropoiesis. Clinically, CIA exacerbates fatigue and cognitive dysfunction, acting as an independent prognostic factor for treatment resistance and decreased survival. Current management relies on erythropoiesis-stimulating agents (ESAs), intravenous iron, and transfusions, which offer symptomatic relief but are limited by thromboembolic risks and transient efficacy. Emerging therapies, such as anti-hepcidin agents and HIF stabilizers, show promise by targeting underlying disease mechanisms. Discussion: The findings underscore the multifactorial nature of CIA and highlight the need for early diagnosis and multidisciplinary management. While novel therapies are promising, their long-term efficacy and safety require validation. Regional disparities in prevalence and management call for international guidelines and biomarker-directed approaches Conclusion: Integrating CIA management into initial oncology care, supported by standardized screening and research, is crucial for improving patient outcomes and QoL.
Abstract: Cancer is one of the leading causes of death around the globe. The conventional cancer therapies have several drawbacks, like non-specific biodistribution, poor stability, and significant systemic toxicity. Nanogels are increasingly recognized as a promising type of nanocarrier for cancer therapy because of their structural versatility, biocompatibility, and remarkable drug-loading efficiency. As cross-linked polymeric hydrogel nanoparticles, they offer multiple benefits, including enhancing the solubility of hydrophobic drugs, enabling controlled and stimulus-responsive release, improving tumour-specific delivery through the enhanced permeability and retention (EPR) effect, and reducing systemic toxicity. Recent progress in nanogel engineering has introduced smart modifications such as pH-, temperature-, enzyme-, and redox-responsive designs, which allow exact and localized drug release within the tumor microenvironment. The present review provides a comprehensive overview of nanogels, their types, and effects on various types of cancers.
One of the most aggressive and therapy-resistant brain cancers is glioblastoma (GBM), posing significant challenges in neuro-oncology. The prognosis for individuals with GBM is poor, with median survival rates usually ranging between 12 and 15 months, even with advances in traditional therapies including radiation, chemotherapy, and surgical resection. This review focuses on the emerging role of immunotherapy as a potentially effective therapeutic approach for GBM and describes the immunological mechanism's capacity to identify and eradicate cancerous cells. Recent studies have shown that various immunotherapeutic strategies, including oncolytic viral therapies, dendritic cell vaccines, and immune checkpoint blockers, can elicit robust anti-tumor responses. Nevertheless, these methods' efficacy is frequently constrained by the unique immunosuppressive microenvironment of GBM, characterized by a low mutational burden**,** and a complex immunological response influenced by the presence of T-cell regulators. The review integrates current literature on the immunobiology of GBM and discusses ongoing clinical trials aimed at integrating immunotherapeutic approaches into standard treatment regimens. By providing a thorough analysis of immunotherapy's current status for GBM, this work aims to inform future research directions and clinical practices. The exploration of combination therapies and novel agents holds promise for enhancing the efficacy of immunotherapy in GBM, ultimately striving to improve patient outcomes and survival rates in this challenging malignancy.
Kaposi’s sarcoma-associated herpesvirus (KSHV) is a pathogen associated with Kaposi's sarcoma (KS), multicentric Castleman disease (MCD), primary effusion lymphoma (PEL), and KSassociated inflammatory cytokine syndrome malignancies. Similar to other gamma-herpesviruses, KSHV exhibits both latent and lytic phases. The genes expressed during these phases contribute to maintaining viral infection, promoting the survival of infected cells, and driving tumor development. Redox homeostasis is a central component in the regulation of cell proliferation, apoptosis, and immune response. The delicate balance between oxidative systems (reactive oxygen species and reactive nitrogen species) and antioxidant systems (GSH, thioredoxin, Nrf2, etc.) is crucial for viral replication and the remodeling of the tumor microenvironment. KSHV alters the host redox network through multiple mechanisms. The latent protein promotes Nrf2 nuclear translocation, which enhances antioxidant defenses and protects infected cells from ROS damage. Additionally, the cleavage protein vGPCR activates NADPH oxidase (NOX) to induce a reactive oxygen species burst, promoting angiogenesis and amplifying inflammatory signals. Therefore, an in-depth analysis of the KSHV-host redox interaction network and the development of intervention strategies targeting viral redox regulatory nodes are expected to enable precise antiviral and antitumor therapies. The review highlights the potential of redox targets as therapeutic agents for KSHV-associated diseases. It summarizes potential drug molecules and targets that achieve survival inhibitory effects by disrupting redox homeostasis in the KSHV host.
