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.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver condition worldwide and a major contributor to cirrhosis and hepatocellular carcinoma (HCC). While metabolic triggers such as obesity and insulin resistance are key drivers of MASLD, growing evidence has identified defects in intracellular quality control-namely impaired autophagy-as central mechanisms governing disease progression. Autophagy, including selective lipophagy and mitophagy, plays a crucial role in hepatic lipid turnover and mitochondrial homeostasis. In MASLD, disruption of these processes contributes to lipid accumulation and oxidative stress, leading to hepatocellular damage (ballooning), fibrogenesis, and HCC. Experimental studies linked impaired autophagic flux to liver injury, and emerging evidence from human genetics suggests that inter-individual inherited variation influences MASLD susceptibility by impairing autophagy. Specifically, main genetic MASLD modifiers such as the p.I148M variant of Patatin-like phospholipase domain-containing protein 3 (PNPLA3) and loss-of-function and hypomorphic variants in autophagy-related gene 7 (ATG7), a core autophagy gene, predispose to ballooning, fibrosis, and HCC. By outlining emerging therapies that restore autophagic flux and reduce steatosis, lipotoxicity, and fibrosis, we propose an integrated precision-medicine model based on genetics and autophagy dynamics biomarkers, offering a new framework for personalized therapeutics.

Skin cancer remains one of the most preventable yet prevalent malignancies worldwide, with non-melanoma and melanoma skin cancers ranking among the top 5 and top 20 most common cancers, respectively. Rising incidence rates in countries such as the United States and Australia have been linked to high ultraviolet (UV) radiation exposure and modifiable behavioral risk factors. Public health efforts increasingly emphasize sun safety education to reduce UV exposure and mitigate long-term cancer risk.

To summarize the current research landscape of intervention strategies for the primary prevention of skin cancer and the study designs used to evaluate these efforts.

We conducted a scoping review following PRISMA-ScR guidelines across PubMed, CINAHL, Embase, Cochrane Library, and PsycInfo. Included studies assessed original sun safety programs implemented in school, community, and healthcare settings, focusing on behavior change, accessibility, and long-term impact.

This review highlights the variability in intervention design and underscores the need for comprehensive, evidence-based strategies that integrate education with accessible resources.

Strengthening these efforts is essential to improving sun safety practices and reducing the global burden of skin cancer.

Chronic and treatment-resistant dermatologic disorders remain difficult to manage with current therapies because of incomplete efficacy, tolerability limitations, and long-term safety concerns. GZ21T is a topical formulation of curcumin, harmine, and isovanillin that has emerged as a potential novel therapy for inflammatory and neoplastic skin disease.

To review the preclinical evidence, proposed mechanism of action, safety data, and future clinical potential of GZ21T in atopic dermatitis, mycosis fungoides, and actinic keratoses.

A focused literature review was performed using published preclinical and early translational studies evaluating GZ17-6.02 and topical GZ21T in dermatologic disease models, including atopic dermatitis, mycosis fungoides, and actinic keratoses. Studies were included if they reported mechanistic, efficacy, or safety outcomes relevant to dermatologic application; non-dermatologic studies were used selectively to contextualize safety and pharmacology.

Across preclinical models, topical GZ21T reduced inflammation, pruritus, lesion burden, and tumor growth while promoting autophagy and suppressing pro-survival signaling pathways including MAPK, PI3K-AKT, mTOR-related pathways, Wnt, and ERBB signaling. In mycosis fungoides models, GZ17-6.02 increased apoptosis and enhanced tumor cell killing, including in combination with standard agents such as bexarotene. Safety data to date suggest favorable local tolerability, minimal systemic absorption in preclinical topical studies, and reversible liver enzyme elevations in oral phase 1 testing of GZ17-6.02.

GZ21T represents a promising topical, multimodal therapeutic approach for inflammatory and premalignant or malignant skin disease. Further clinical studies are needed to confirm efficacy, define long-term safety, and establish its role relative to current standard therapies.