Three-dimensional (3D) cell culture systems provide superior simulation of the tumour microenvironment compared to traditional two-dimensional (2D) cultures. Chemoprevention agent curcumin analog-1.1 (CCA-1.1), a synthetic curcumin derivative, has demonstrated promising anticancer properties against triple-negative breast cancer (TNBC). This study aimed to develop and use a 3D agarose-based culture system for MDA-MB-231 cells to comprehensively evaluate the efficacy of CCA-1.1 as an anticancer agent.

MDA-MB-231 breast cancer cells were cultured in both a 2D monolayer and a 3D agarose-based spheroid system. Cytotoxicity was assessed using CCK-8 assays, and IC50 values were determined. Spheroid formation capacity was evaluated and compared with that of doxorubicin. Propidium iodide staining was performed to assess cell viability and structural integrity. Gene expression analysis of epithelial-mesenchymal transition (EMT) markers and metastasis-related proteins (E-cadherin, MMP2, and MMP9) was conducted using qRT-PCR.

CCA-1.1 demonstrated IC50 values of 1.48±0.28 µM in 2D cultures versus 6.12±0.27 µM in 3D cultures, while doxorubicin showed IC50 values of 0.79±0.22 µM (2D) and 2.65±0.3 µM (3D). CCA-1.1 reduced spheroid formation by 40% compared to controls, whereas doxorubicin achieved 96% inhibition. Propidium iodide staining showed that CCA-1.1 induced cell death while preserving the spheroid structure, unlike doxorubicin, which disrupted the architecture. Expression level analysis revealed that CCA-1.1 reduced MMP2 (0.15-fold, p=0.0001) and MMP9 (0.25-fold, p<0.0001) levels while increasing E-cadherin levels by 1.54-fold (p=0.379).

Our study using a 3D agarose-based spheroid culture confirms the cytotoxicity of CCA-1.1 against MDA-MB-231 and showed that the compound inhibited spheroid formation and epithelial-mesenchymal transition, and reduced the expression levels of matrix metalloproteinases. These data support the development of CCA-1.1 as a candidate chemotherapeutic agent for TNBC.

Breast cancer is a heterogeneous disease consisting of molecular subtypes with varying aggressiveness, growth rates, and therapeutic responses. MicroRNAs (miRNAs) hold potential as biomarkers owing to their role in gene expression regulation in cancer, as well as their specificity and stability in clinical samples. The mapping of miRNAs associated with disease recurrence and progression in each breast cancer subtype remains limited. This scoping review aimed to map the scientific literature on miRNAs related to recurrence and disease progression in TNBC, luminal, and HER2+ breast cancer subtypes.

Literature searches were conducted in the Scopus and PubMed electronic databases using predefined keywords. Retrieved records were screened, and duplicates were removed. Selection based on title, abstract, and full text was performed according to the established inclusion criteria. Data extracted from eligible studies included cancer subtype, stage, type and timing of sample collection, treatment, miRNA identification technique, miRNA expression patterns, target genes and molecular pathways, clinical outcomes, and biomarker types. This scoping review was developed using the PRISMA-ScR checklist.

A total of 28 studies were included and reviewed. miRNAs associated with the TNBC subtype were the most investigated in both profiling and non-profiling studies. The patterns of miRNA expression varied among the TNBC, luminal, and HER2+ subtypes. Of the 74 miRNAs identified across all breast cancer subtypes, only two miRNAs (miR-30c-5p and miR-195-5p) were found in different subtypes. The miRNAs in each breast cancer subtype were demonstrated to be prognostic, predictive, or both.

This scoping review provides an overview of the unique miRNA expression patterns associated with recurrence and disease progression in TNBC, luminal, and HER2+ breast cancer subtypes. The differences in miRNA expression between breast cancer subtypes emphasize the importance of investigating miRNA biomarkers specific to breast cancer subtypes.

Breast cancer stem cells (BCSCs) are responsible for chemotherapy resistance, metastasis, and tumor recurrence. Paclitaxel-primed mesenchymal stem cells (MSCs) can activate T cells, offering a novel immunotherapeutic approach. However, the molecular mechanisms underlying BCSC-immune interactions remain poorly understood.

To identify overlapping gene networks between BCSCs, paclitaxel-treated cells, activated T cells, and paclitaxel-primed MSCs, and to validate their functional relevance in targeting BCSCs.

Comparative transcriptomic analysis was performed using data from TCGA to identify genes co-expressed across BCSCs, paclitaxel-treated cells, activated T cells, and MSCs. Protein-protein interaction network analysis, Gene Ontology (GO) enrichment, and KEGG pathway mapping were conducted using STRING-DB, DAVID, and cBioPortal. Mutation analysis and survival correlations were assessed across 151 breast cancer samples. Experimental validation was performed using MTT viability assays and qRT-PCR in metastatic breast cancer cells treated with paclitaxel, activated T cell-conditioned medium, and MSC-derived factors.

We identified 158 genes co-expressed across all four conditions, forming a highly interconnected PPI network (136 nodes, 524 edges). Network centrality analysis revealed TP53, AKT1, and STAT3 as top hub genes. GO enrichment analysis demonstrated significant involvement in epithelial cell proliferation, stress responses, and transcriptional regulation. KEGG pathway analysis revealed enrichment in the PI3K-Akt signaling pathway, the PD-L1/PD-1 checkpoint pathway, and Th1/Th2 differentiation. TP53 was the most frequently mutated gene (77.5%), which correlated with a poor prognosis. Experimental validation demonstrated that combined paclitaxel and activated T cell treatment reduced BCSC viability by 75%, upregulated TP53 expression, and suppressed PIK3CA expression by 85%.

This study reveals critical molecular networks connecting BCSCs and immune activation, identifying TP53, AKT1, and STAT3 as central therapeutic targets. Paclitaxel-primed MSC-activated T cells synergize with chemotherapy to suppress BCSC viability by modulating the TP53 and PIK3CA pathways, providing a mechanistic rationale for combinatorial immunotherapy in breast cancer.

Cancer continues to pose a significant worldwide health concern, underscoring the need for the identification of innovative, safer, and more effective therapeutic agents. Phytochemicals obtained from medicinal plants are progressively acknowledged for their anticancer efficacy. This work investigates the antimitotic and antiproliferative properties of the ethanolic extract of Benincasa hispida seeds (EeBHS), known as winter melon, from the Cucurbitaceae family.

Antimitotic activity was assessed using the Allium cepa root tip meristem test and the seed germination assay. The mitotic index and the distribution of cells throughout several mitotic stages were examined after treatment with EeBHS at varying doses. Methotrexate, a recognized antineoplastic agent, served as the standard control. The antiproliferative activity of EeBHS was evaluated using the MTT assay on HepG2 liver cancer cell lines to determine cytotoxicity and growth suppression.

EeBHS exhibited a notable dose-dependent suppression of mitotic activity in Allium cepa root tips and sprouted seeds (p < 0.001). The mitotic index significantly decreased in EeBHS-treated groups (57 ± 0.5 in root tips and 44 ± 1.2 in seeds) relative to controls (67 ± 1.2 and 96 ± 1.2, respectively). Methotrexate also lowered the mitotic index, thereby corroborating the concept. An increased percentage of cells in prophase and metaphase in treated groups signified mitotic arrest. In HepG2 cells, doses of EeBHS ranging from 5 to 7 ng/μL markedly suppressed cell growth, indicating potent cytotoxicity.

EeBHS has significant antimitotic and antiproliferative properties, presumably attributable to its bioactive constituents, including flavonoids, alkaloids, and phenolics, underscoring its potential as a natural anticancer agent that merits further investigation.

Acute myeloid leukemia (AML) is a biologically heterogeneous hematologic malignancy in which cytogenetic and molecular abnormalities critically influence prognosis and treatment decisions. Since the identification of isocitrate dehydrogenase (IDH) mutations in AML in 2009, growing evidence has highlighted their role in leukemogenesis through aberrant cellular metabolism and epigenetic dysregulation. IDH1 mutations, occurring predominantly in cytogenetically normal AML and frequently co-existing with mutations such as NPM1 and DNMT3A, have demonstrated context-dependent prognostic implications rather than uniformly adverse outcomes.

Several studies associate IDH1 mutations with inferior clinical outcomes, including reduced remission rates, poorer overall survival, and global DNA hypermethylation, particularly in specific biological and therapeutic contexts influenced by co-mutational profiles and treatment era.

Recent therapeutic advancements have introduced selective IDH1 inhibitors targeting these mutations. Ivosidenib and Olutasidenib, have demonstrated efficacy in relapsed/refractory (r/r) AML and have received United States Food and Drug Administration (USFDA) approval for these indications. Notably, Ivosidenib has also been approved for newly diagnosed (ND) IDH1-mutated AML patients who are ineligible for intensive chemotherapy. These IDH1 inhibitors, often combined with agents like Azacitidine and Venetoclax, represent a promising shift toward personalized medicine, offering effective, less toxic alternatives for challenging AML cases, including those in elderly patients or individuals with comorbidities.

This review summarizes the prognostic implications of IDH1 mutations in AML and critically examines emerging IDH1 targeted therapies, highlighting their impact on disease biology and evolving treatment algorithms.

Carcinoma ex pleomorphic adenoma (Ca-ex-PA) is a rare salivary gland malignancy with limited therapeutic options. Molecular targets such as androgen receptor (AR) and epidermal growth factor receptor (EGFR) may offer prognostic and therapeutic value.

To systematically review the current literature regarding the role of AR and EGFR in the pathogenesis, progression, and management of Ca-ex-PA.

The review adhered to Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines and was registered in PROSPERO with the registration number CRD420251118578. A systematic literature search was conducted in PubMed, Scopus, Google Scholar, and EBSCOhost databases for studies published upto January, 2026. Inclusion criteria were studies assessing AR and/or EGFR in Ca-ex-PA using immunohistochemistry, molecular techniques, or clinical data. Risk of bias was assessed using the ROBINS tool, and pooled prevalence estimates were calculated using random-effects models.

Eighteen studies were included for qualitative synthesis and meta-analysis. AR expression was found to be highly prevalent in CXPA, particularly in cases with salivary duct carcinoma components, while benign pleomorphic adenoma consistently showed minimal or absent AR expression. EGFR expression demonstrated marked heterogeneity across studies but was generally higher in malignant components compared with benign areas. Overall, included studies exhibited moderate to high risk of bias, mainly related to confounding, post-exposure interventions, and selective reporting.

AR is a consistently expressed and biologically relevant biomarker in CXPA, supporting its diagnostic and potential therapeutic role. EGFR expression reflects molecular heterogeneity and may contribute to malignant progression, although its clinical utility remains uncertain. Standardized biomarker assessment and prospective studies are required to strengthen evidence and guide targeted therapy in CXPA.

Colorectal cancer (CRC) continues to be a significant global health issue. Thymoquinone (TQ), a bioactive component of Nigella sativa, has shown anticancer capabilities by inducing apoptosis. This systematic review and meta-analysis aim to assess the impact of TQ on the levels of pro-apoptotic (BAX, CASP3) and anti-apoptotic (BCL2) markers in colorectal cancer cells.

An extensive literature search was performed in Scopus, BASE, PubMed, and Web of Science for articles published from 2004 to 2025, adhering to PRISMA guidelines. Eligible in vitro and in vivo studies provided numerical data on gene or protein expression levels for BAX, BCL2, and CASP3, along with standard deviations. Effect sizes (g) were computed using a random-effects model, and heterogeneity and publication bias were evaluated.

A total of ten qualifying studies were incorporated. The meta-analysis indicated that TQ significantly (p < 0.001) increased BAX mRNA (g = 3.901) and protein levels (g = 4.232), decreased BCL2 mRNA (g = -3.680) and protein levels (g = -3.328), and markedly upregulated CASP3 mRNA (g = 5.669) and protein levels (g = 6.336). Subgroup analyses revealed consistent effects across CRC cell lines (HT29, SW480, SW620, HCT-15, and HCT116). Heterogeneity varied from low to moderate, and publication bias was low or not significant.

The findings demonstrate that TQ exerts pro-apoptotic effects in colorectal cancer (CRC) models through the upregulation of BAX and CASP3 and the downregulation of BCL2. This suggests its potential therapeutic relevance rather than definitive biomarker utility. Nevertheless, further in vivo studies and early-phase clinical investigations are required to clarify its translational significance and to explore its possible implications for treatment responsiveness.

Oral squamous cell carcinoma (OSCC), the most common oral cancer, presents a clinical challenge due to its complex tumor microenvironment (TME), dysregulated pathways, and poor prognosis. Current methods of diagnosing OSCC use liquid biopsy technologies (ctDNA/microRNAs/exosomes) instead of relying solely on traditional methods such as open surgical biopsy. Liquid biopsy technologies provide non-invasive ways to detect and monitor OSCC in early stages, compared with traditional open surgical biopsy methods. Treatment of OSCC currently relies on chemotherapeutics (cisplatin/5-FU), radiotherapy, and targeted agents (cetuximab). However, resistance is acquired due to TME remodelling (tumor microenvironment) and/or due to epithelial-mesenchymal transition (EMT) through processes such as ABC transporter efflux. This review elucidates key molecular mechanisms, including PD-L1-mediated immune evasion, PI3K/AKT/mTOR hyperactivation, EGFR overexpression, and NF-κB-driven inflammation, which promote proliferation, metastasis, and therapy resistance. One area of study involves the use of nanotechnology to convert phytocompounds (medicinal plants) into therapeutic agents by embedding phytocompounds into nanoparticles created using green synthesis techniques. EPR (Enhanced Permeability and Retention), ligand functionalization for OSCC targeting, improved bioavailability, and reduced toxicity are all advantages that the aforementioned systems provide, offering an opportunity to synergistically develop new therapies with chemotherapeutics for overcoming resistance.

While numerous preclinical studies demonstrate that these newly developed therapies show increased efficacy compared with current therapy options, further work is needed in areas such as standardization, scaling, and clinical translation. As such, the importance of developing pathway-informed diagnostic tests and developing therapies that exploit pathway-specific activity with phytocompounds is emphasized. In addition, large-scale studies should be considered to evaluate the effectiveness of a pathway-informed approach in assessing and differentiating OSCC and personalized therapy strategies, to improve OSCC survival outcomes.

Bloodstream infections are a significant complication in cancer patients and play an important role in morbidity and mortality, especially in immunocompromised populations. It is crucial that clinically derived bacterial strains be molecularly documented to aid infection surveillance and future translational research in oncology practice.

This brief communication describes the identification and National Center for Biotechnology Information (NCBI) GenBank registration of two bacterial strains isolated from bloodstream infections in oncology patients. Partial 16S ribosomal RNA gene sequencing was used for molecular identification.

One isolate was identified as Escherichia coli strain OncoEval 1, and the second as Pseudomonas aeruginosa strain OncoEval 2. Validated and quality-screened sequences of both were deposited in the GenBank database to provide public genomic references derived from cancer-associated bloodstream infections.

The registration of these strains broadens the molecular resource base for pathogens isolated from oncology patients and drives continued studies in infection surveillance and research in the setting of cancer care.

Gastric cancer is a major global health concern characterized by high incidence and mortality rates. One of the key challenges in treating gastric cancer is the development of resistance to chemotherapy drugs like cisplatin (DDP). This study aimed to investigate the efficacy of Zuo Jin Wan (ZJW), a traditional Chinese medicine, in overcoming DDP resistance in gastric cancer cells.

The research employed gastric cancer cells with DDP resistance, namely SGC7901/DDP and AGS/DDP, to explore the molecular mechanisms underlying ZJW's effects.

ZJW significantly reduced DDP resistance by inhibiting the phosphorylation and preventing mitochondrial translocation of Dynamin-related protein 1 (DRP1). ZJW treatment suppressed DRP1-mediated mitochondrial fission and mitophagy, thereby enhancing the sensitivity of resistant cells to DDP. Additionally, ZJW was observed to downregulate the AMPK signaling pathway, which plays a crucial role in DRP1 activation.

By modulating mitochondrial dynamics, ZJW disrupts protective mechanisms in resistant cancer cells, highlighting its potential as an adjunct therapy. This study underscores the therapeutic potential of integrating traditional Chinese medicine with conventional chemotherapy to combat drug resistance in gastric cancer.