411 papers
Using a patient-derived orthotopic HNSCC model, this study reveals that a subset of clonogenic cancer cells can uncouple terminal differentiation from the loss of self-renewal, thereby escaping differentiation-inducing therapies and driving drug resistance.
This study demonstrates that PRMT5 is frequently upregulated in MTAP-deficient malignant peripheral nerve sheath tumors (MPNSTs) and serves as a promising therapeutic target, as its inhibition selectively suppresses tumor growth by inducing DNA damage and shows synergistic effects when combined with standard chemotherapies.
This study utilizes CRISPR-Cas9 knockouts and whole-genome sequencing of lung adenocarcinoma clones to demonstrate that APOBEC3A and APOBEC3B exhibit heterogeneous, context-dependent mutagenic activities that cannot be predicted by expression levels, while providing the first causal evidence linking these enzymes to the InD9a indel signature.
Chromosomal instability-induced aneuploidy triggers a senescence-associated secretory phenotype in *Drosophila* tumours, which activates a feed-forward loop where secreted proteins kill neighbouring host tissues to non-autonomously drive malignant tumour growth.
This paper presents a refined virtual cohort framework that generates over 10,000 simulated mice to capture treatment response variability and stratify individuals, demonstrated through its application to gemcitabine and OT-1 cell therapy in a murine bladder cancer model.
This study demonstrates that growing glioblastoma-myeloid organoids on the International Space Station for 40 days produces a superior, more reproducible model of advanced disease with enhanced immunosuppressive, architectural, and molecular features that better mimic human tumor progression compared to Earth-based controls.
This study introduces a novel, reliable, and tolerable mouse model combining a lifelong Western diet with sequential low-dose diethylnitrosamine, thioacetamide, and sucrose water that successfully induces advanced-stage hepatocellular carcinoma in nearly 100% of both male and female mice while recapitulating human disease signatures.
This study reveals that in pancreatic ductal adenocarcinoma, tumor-secreted L-lactate is consumed by macrophages to induce site-specific lactylation of the transcriptional co-regulator BCL3 at lysine 21, which drives nuclear translocation and NF-κB p50-mediated transcriptional reprogramming that suppresses inflammation, promotes tumor progression, and correlates with poor patient survival.
The study identifies SSL-0024, a novel niclosamide prodrug with enhanced solubility and bioavailability, as a potent oral therapeutic that effectively suppresses hepatocellular carcinoma in vivo by concurrently inhibiting multiple oncogenic signaling pathways and PD-L1 expression.
This study demonstrates that growth hormone drives triple-negative breast cancer progression by activating DRP1-mediated mitochondrial fission, which is essential for linking metabolic reprogramming toward glycolysis with cell proliferation and the modulation of the inflammatory tumor microenvironment.
This study demonstrates that DuoHexaBody-CD37 induces direct cytotoxicity in diffuse large B-cell lymphoma by promoting CD37 clustering and surface retention, which triggers distinct signaling pathways involving SHP1 upregulation and inhibition of pro-survival signals, thereby offering a promising strategy for combination immunotherapy.
This study demonstrates that increased extracellular matrix stiffness, such as that occurring after surgical remodeling in plexiform neurofibromas, drives tumor growth, invasion, and resistance to MEK inhibitors by inducing specific mechanobiological changes in patient-derived cells.
This study utilizes an integrated multi-omics approach on bioengineered, vascularized pancreatic cancer spheroids to characterize a therapy-resistant, immunosuppressive tumor niche that recapitulates patient heterogeneity and provides a powerful translational platform for developing new PDAC treatments.
By analyzing RNA sequencing data from 721 renal cell carcinoma samples, this study identifies a robust 13-gene transcriptomic signature characterized by loss of epithelial identity and mitochondrial dysregulation that accurately predicts intravascular tumor extension.
This study employs high-stringency computational analysis to predict a high-affinity interaction between the plant-derived *Moringa oleifera* miR156 and the human CDK4 3'UTR, suggesting a potential cross-kingdom mechanism for regulating cell-cycle progression in triple-negative breast cancer.
This study identifies MRPL47 as a novel mitochondrial biomarker that is frequently amplified and overexpressed in ovarian cancer, where it drives metabolic fitness and cisplatin resistance, thereby serving as a valuable indicator for early diagnosis, prognosis, and therapeutic response.
This study demonstrates that integrating video thermometry with concanamycin-sensitive proton pump measurements in canine mammary cancer reveals distinct metabolic signatures of tumour heterogeneity, offering a promising bioenergetic proof-of-concept for improving diagnostic, prognostic, and therapeutic approaches in both veterinary and preclinical human medicine.
By integrating multi-omics profiling across 51 breast cancer cell lines with functional siRNA screening, this study characterizes subtype-specific metabolic heterogeneity and identifies key metabolic genes, including glycosyltransferases, nucleotide metabolism enzymes, and transporters, as promising therapeutic targets for aggressive breast cancer.
This paper proposes a theoretical framework linking normal tissue dynamics and tumor malignancy through distinct sets of N- and T-gene markers, respectively, with NT-genes mediating the transition, and validates this model using prostate, lung, and liver cancer expression data to identify small, perfect gene panels that characterize these biological states.
This study constructs a single-cell atlas of gastric cancer patients treated with chemo-immunotherapy to reveal that intrinsic resistance is driven by CEACAM5/6+ tumor cells forming immune-excluded niches, while acquired resistance stems from IL-1β+ macrophage expansion that activates NF-κB signaling, thereby identifying these pathways as key targets for overcoming treatment failure.