Drug repurposing can accelerate the identification of novel therapeutic candidates for rare cancers such as inflammatory breast cancer (IBC), an aggressive type with limited therapeutic options. Here, we report an experimental validation study of compounds previously identified through two computational approaches: Literature Wide Association Studies (LWAS) and Gene Reversal Rate (GRR). Candidate compounds were tested using orthogonal cell viability assays in 2D models across IBC and non-IBC cell lines. In the SUM149 IBC cell line, repurposed compounds predicted from LWAS achieved a 70% success rate, with several showing nanomolar potency, while those predicted from GRR showed a 38% success rate. Through systematic combination screening in both 2D and 3D-spheroid SUM149 models, we identified novel synergistic compound pairs targeting crosstalk between IGF-1R, EGFR and PI3K/Akt/mTOR pathways, with high synergy scores across multiple reference models. Using these combinations, western blott analysis revealed significant suppression in the phosphorylation of key signaling proteins and downstream effectors, while wound healing assays showed reduced cell migration with some combination treatments, suggesting effective pathway inhibition. To further validate these findings at the transcriptional level, RNA-Seq analysis in SUM149 cells confirmed that the GRR drug combinations significantly reversed the IBC gene expression signature (IBC-GES) and identified several clinically relevant genes whose expression was significantly altered. Together, these findings validate our computational predictions and identify candidate combination strategies that may help address therapeutic resistance in IBC. This integrated computational-experimental approach establishes a pipeline for systematic drug repurposing and highlights novel therapeutic combinations for further investigation.

Living with the consequences of rectal cancer treatment, with symptoms that can include bowel dysfunction, can be difficult. Patients need the tools to self‑manage these symptoms and they also need information and support to do so. Using information gained from patients and healthcare specialists it was possible to gain a deeper understanding of what patients want to know about low anterior resection syndrome (LARS). Although each individual will have differing symptoms, goals and treatment preferences, the two LARS toolkits, which are described in this article, can assist the nurse to improve quality of life. The patient toolkit was developed for people living with LARS, and designed to be used in conjunction with clinical discussion. The clinician toolkit aims to assist nurses in understanding assessment processes and interventions such as conservative management of LARS. It is important to live well after cancer treatment and nurses need to support people to do so.

Glioblastoma (GBM) is a highly aggressive brain cancer characterized by rapid growth, extensive infiltration, significant molecular diversity, and notable resistance to standard treatments, resulting in a poor prognosis for patients. This emphasizes the necessity for innovative therapeutic strategies based on novel mechanisms.

GBM tumorigenesis, glioma stem cell maintenance, immunological evasion, and treatment resistance are significantly influenced by the abnormal activation of various oncogenic signaling pathways, such as PI3K/Akt/mTOR, JAK/STAT, NF-κB, MAPK, Wnt/β-catenin, and receptor tyrosine kinases like EGFR and Axl. Phytochemicals such as quercetin, curcumin, resveratrol, and epigallocatechin gallate influence crucial signaling pathways in GBM by inhibiting specific pathways, inducing apoptosis and autophagy, suppressing glioma stemness, and modifying the tumor microenvironment. Furthermore, nano-based delivery systems such as dendrimers, lipid-based nanocarriers, polymeric nanoparticles, and biomimetic exosome-inspired systems enhance stability, bioavailability, and targeted delivery, thereby improving therapeutic efficacy.

This review i) explores the potential of phytochemicals in targeting these pathways, ii) summarizes current evidence on phytochemicalmediated modulation of dysregulated signaling pathways in GBM, and iii) highlights emerging nanobased delivery strategies to improve therapeutic efficacy. Overall, phytochemical modulation of signaling pathways paired with nano-based drug delivery shows potential for enhancing treatment efficacy in GBM.

O^6^-methylguanine-DNA methyltransferase (MGMT) promoter methylation is a key predictive biomarker for temozolomide (TMZ) response in glioma. MGMT status is routinely assessed at diagnosis; however, its utility at recurrence remains incompletely characterized. We aimed to quantify MGMT methylation stability and assess the clinical relevance of reported status changes in recurrent glioma.

We analyzed paired tumor samples from 426 patients with recurrent glioma in a large commercial molecular database containing quantitative methylation percentage and binary methylation status at two sample time points. A separate multi-institutional clinical cohort (n = 27) with detailed treatment annotation was analyzed to explore associations between MGMT status at recurrence and treatment decision-making. Statistical analyses assessed quantitative methylation dynamics and time between samples as a surrogate for disease course.

MGMT status remained unchanged in 84% of tumors across recurrence. 16% demonstrated a status change, commonly among tumors with low baseline methylation near classification thresholds. Longitudinal quantitative methylation changes were modest overall. Tumors that remained, gained, or lost hypermethylation demonstrated longer intervals between samples compared to consistently unmethylated tumors (p < 0.01). In the clinical cohort, TMZ rechallenge was more frequently pursued in patients retaining hypermethylation at recurrence.

MGMT promoter methylation is quantitatively stable in the majority of recurrent gliomas. Status changes predominantly occur in tumors with borderline methylation, highlighting the limitations of binary classification. These findings support routine reassessment of MGMT at recurrence and underscore the value of quantitative reporting to better inform therapeutic decision-making, particularly regarding TMZ rechallenge.

To map the global development, collaboration structure, intellectual foundations, thematic evolution, and translational fronts of robotic technologies relevant to brain tumor surgery and cranial neuro-oncology. The Web of Science Core Collection was searched on August 25, 2026. English-language records were manually screened to include both clinically deployed robotic applications and engineering/preclinical systems with an explicit cranial tumor-related use case. Bibliometric and science-mapping analyses were performed with R/Bibliometrix-Biblioshiny and CiteSpace 6.4.R1. Of 329 records identified, 106 publications were included (98 article-type records and 8 reviews). The corpus spanned 1997-2026, 47 sources, and 620 authors, and accumulated 2,195 citations. The USA led country production (30 records) and citations (748). Universite Paris Cite was the most frequent affiliation (12 records), Sutherland GR the most prolific author (5 publications), and the International Journal of Computer Assisted Radiology and Surgery the leading source (9 publications). Keyword clustering identified ten communities spanning image-guided targeting, robotic biopsy, force feedback, continuum/concentric-tube systems, frameless navigation, sensing, pediatric brainstem biopsy, and robot-guided local therapy. Recent bursts centered on diagnostic yield, efficacy, safety, and brain tumors. The mapped literature represents a translational continuum from clinically integrated stereotactic biopsy and tumor-directed intervention to emerging sensing, continuum robotics, and data-driven control. Bibliometric prominence does not establish clinical effectiveness. Further translation will require reliable sensing, compensation for tissue deformation, workflow integration, standardized reporting, and multicenter validation.

Natural killer (NK) cell-based immunotherapy has shown limited efficacy against solid tumors due to impaired NK cell activation and intrinsic tumor resistance. This study investigated whether lipoteichoic acid isolated from Latilactobacillus sakei K101 (sLTA) could overcome NK resistance in HT-29 colon cancer cells.

Using an NK3.3/HT-29 co-culture system, we found that IL-2-activated NK cells alone were insufficient to induce robust cytotoxicity, whereas sLTA restored NK-mediated tumor cell killing. sLTA upregulated NK activating receptors, including NKG2D and natural cytotoxicity receptors, while enhancing MICB expression and suppressing Bcl-2 and other anti-apoptotic genes in HT-29 cells. siRNA-mediated knockdown and Western blot analysis confirmed the involvement of Caspase-3-dependent apoptosis. Transwell and neutralization assays further demonstrated that sLTA-primed HT-29 cells were sensitized to contact-independent cytotoxicity mediated by NK-derived TNF-α and IFN-γ.

sLTA functions as a dual-action immune sensitizer by enhancing NK effector activation and lowering the apoptotic threshold of resistant tumor cells. These findings suggest that sLTA may serve as an adjunct strategy to improve NK cell-based immunotherapy against solid tumors.

GlycoRNAs are a newly identified class of post‑transcriptionally modified small non‑coding RNAs that carry covalently attached N‑ and O‑linked glycans. This discovery challenges the conventional view that glycosylation is exclusive to proteins and lipids, and places RNA at the interface of glycobiology and immune recognition. Emerging evidence implicates glycoRNAs in tumor biology, where they function as cell‑surface ligands for Siglecs and P‑selectin, thereby modulating three interconnected processes: immune escape and immune regulation, intercellular communication and adhesion, and tumor metastasis and metabolic crosstalk. Recent technological advances-including single‑cell imaging (ARPLA), FRET‑based sEV analysis, and chemoenzymatic profiling-have enabled sensitive detection and revealed aberrant glycoRNA patterns across malignancies. Notably, tumor‑specific glycoRNA signatures correlate with immune checkpoint glycosylation (such as PD‑1/PD‑L1) and metabolic reprogramming. This review synthesizes current understanding of glycoRNA biosynthesis, structure, and function, with an emphasis on its emerging roles in the tumor microenvironment. We also outline the potential of RNA‑centric glycobiology for developing liquid biopsy biomarkers and mechanism‑informed immunotherapeutic strategies.

Hepatocellular carcinoma (HCC), an aggressive cancer predisposed to notable metabolic alterations, including an imbalance in amino acid transporters, remains a global concern. Amino acid transporters such as proton-assisted amino acid transporter (PAT), sodium-coupled neutral amino acid transporter (SNAT), cysteine/glutamate transporter (xCT), L-type amino acid transporter (LAT1), and Alanine-serine-cysteine transporter 2 (ASCT2). The tumour microenvironment (TME), cellular signalling pathways, tumour survival, and proliferation all depend heavily on these transporters. Current investigation of these transporters is fundamental in regulating the imbalance. Emerging therapeutics, including RNA-based therapeutics, small-molecule inhibitors and combinational treatment strategies with dietary intervention in metabolic reprogramming and oncological signalling are also discussed. The emergence of problems like tumour heterogeneity, transporter redundancy, off-target toxicity, and resistance mechanisms is substantial, even with available treatment options. A thorough understanding of amino acid transporters in HCC, including their emerging functions, might reveal metabolic vulnerabilities that could inform creative treatments for better outcomes.

Glioblastoma (GBM) contains spatially organized stress-adaptive and vascular niches. Because transcript abundance does not measure UFM1 conjugation, we asked whether a UFMylation-related transcriptional axis identifies a reproducible tissue program and alters candidate prioritization. In 518 unique primary TCGA-GBM tumors profiled on the Affymetrix HT Human Genome U133A array, weighted gene co-expression network analysis of 8,000 variable genes yielded 12 modules. The 278-gene green module ranked first across nine prespecified traits (mean |r|=0.637). Direct overlap comprised 1/3 measurable UFMylation-core, 5/19 ER-stress/UPR, and 2/15 proteostasis genes; after excluding overlapping genes, correlations with the green eigengene remained significant (r = 0.373, 0.831, 0.639, and 0.699 for UFMylation-core, ER-stress/UPR, proteostasis, and composite scores, respectively). The green score was associated with overall survival per standard-deviation increase (HR 1.17, 95% CI 1.07-1.28), although clinical adjustment attenuated the estimate. In a 10-sample single-cell dataset, sample-level scores were higher in pericytes and endothelial cells than in malignant cells. Donor-aware IvyGAP analysis supported regional organization, whereas one Visium section showed stronger concordance with ER-stress/UPR and mesenchymal scores than with the UFMylation-core score. CellChat indicated pathway-selective rather than global remodeling of inferred vascular communication. Layer ablation moved WWTR1 from rank 48 using WGCNA alone to rank 4 overall and rank 1 among non-common-essential genes after cross-platform integration. These findings define an ER-stress/mesenchymal-weighted, UFMylation-related vascular-stromal transcriptional association and nominate WWTR1 for experimental testing.

Collagen is a defining feature of breast tumors and is increasingly recognized as a regulator of tumor progression and immune exclusion. However, the tumor cell-matrix interaction that link collagen sensing to immune suppression remains poorly understood.

The primary objective of this study was to identify the role of integrin α2 (CD49b/ITGA2) in promoting collagen-dependent tumor growth and immune evasion in breast cancer.

Integrated bulk and single cell transcriptomic analyses reveal that ITGA2 is broadly expressed across breast cancer subtypes and is preferentially localized to malignant epithelial cells. Functional assays demonstrate that CD49b is a dominant receptor mediating breast cancer cell adhesion to collagen I and IV. Genetic ablation or antibody-mediated blockade of CD49b suppresses tumor growth in vivo and profoundly remodels the tumor immune microenvironment, characterized by increased infiltration of CD8⁺ T cells and antigen-presenting dendritic cell subsets, alongside reduced immunosuppressive myeloid populations. Consistent with these findings, ITGA2 expression in human breast cancer cohorts correlates with stromal enrichment and immune exclusion signatures. Importantly, CD49b blockade synergizes with PD-L1 immune checkpoint inhibition, enhancing T cell activation, effector function, and tumor control.

Together, these results identify CD49b mediated tumor collagen interactions as a key driver of immune suppression and resistance to immunotherapy, and provide a mechanistic rationale for targeting integrin α2β1 to enhance antitumor immunity in the 4T1 breast cancer model.