395 papers
This study demonstrates that in KRAS-driven liver cancer, the cell-of-origin (cholangiocyte versus hepatocyte) rather than the oncogenic driver itself dictates the formation of a desmoplastic, immune-excluded tumor microenvironment, a process mediated by cholangiocyte-specific secreted factors LAMC2 and uPA that activate cancer-associated fibroblasts.
This study establishes a robust biobank of patient-derived organoids from pharyngeal and laryngeal squamous cell carcinomas that faithfully recapitulate the original tumors' histological and molecular heterogeneity, while demonstrating that prior therapy negatively impacts outgrowth and that these models can effectively predict differential therapeutic responses to cisplatin and radiation.
This study introduces a quantitative imaging workflow that elucidates the early heterogeneity and macrophage recruitment in schwannomas while accelerating preclinical testing, revealing distinct therapeutic effects of rapamycin and brigatinib in an NF2-related mouse model.
This study identifies a TROP2-Claudin 7-mediated barrier mechanism that excludes T cells and impedes immunotherapy in triple-negative breast cancer, demonstrating that targeting TROP2 disrupts tight junctions to restore immune infiltration and enhance checkpoint blockade efficacy.
This paper presents the updated MutationAssessor (r4) within cBioPortal, which leverages refined evolutionary conservation analysis and expanded protein sequence data to provide functional impact scores for approximately 4 million somatic mutations across over 320,000 human tumor samples, while validating its predictions against clinical databases and germline variant frequencies.
This study identifies REEP2 as a critical mediator of lung cancer progression, demonstrating that the EMT activator ZEB1 upregulates REEP2 via miR-183 and miR-193a to enhance ER-to-Golgi trafficking, thereby promoting tumor growth, metastasis, and immunosuppression through the secretion of pro-tumorigenic factors.
This study reveals that STING functions as an interferon-independent, cell-autonomous guardian of epithelial genome stability by regulating homologous recombination and ATM signaling to prevent chromosomal instability and tumor evolution, while its loss creates a selective vulnerability to CDK inhibition.
By analyzing ATAC-seq data from 1,563 acute myeloid leukemia cases, this study establishes a novel epigenetic classification system comprising 16 distinct subgroups with unique chromatin landscapes, regulatory networks, and clinical implications that complement and extend beyond traditional genomic profiling.
This study demonstrates that low-intensity alternating magnetic field therapy (Asha) improves survival and reduces metastasis in triple-negative breast cancer by inducing tumor cell ER stress, which triggers interferon-mediated immune reprogramming of the tumor microenvironment and sensitizes tumors to anti-PD1 checkpoint blockade.
This study reveals that the loss of SMAD4 drives chromosomal instability and tumourigenesis by reprogramming translation to downregulate the mitotic protein CDK11B, a mechanism validated in both experimental models and patient tumours.
By integrating multimodal spatial and single-cell transcriptomics, this study identifies plasma cell-dense bone marrow niches enriched with non-canonical Wnt signaling that drive drug resistance, extramedullary progression, and immune suppression, ultimately yielding a 15-gene signature predictive of patient survival in multiple myeloma.
This study demonstrates that the systemically-administered, second-generation STING agonist BI-1703880 is well-tolerated and synergizes with radiotherapy to enhance antitumor immunity and immune memory in preclinical models, particularly when combined with immune checkpoint inhibitors.
This study employs single-nucleus multiome sequencing and spatial transcriptomics to construct a comprehensive atlas of liposarcoma, revealing distinct cellular lineages, immune microenvironments, and gene regulatory circuits that differentiate the aggressive dedifferentiated subtype from the less aggressive well-differentiated subtypes.
This study identifies BAP18 as a novel substrate degraded by the oncogenic E3-ligase adaptors MAGE-A3/6, revealing a molecular mechanism that drives enhanced cancer cell migration and suggesting new therapeutic targets based on aberrant germline protein re-expression.
This paper introduces a mechanistic nonlocal tumour-growth model featuring singular acceleration to explain explosive dynamics, establishes its finite-time blow-up and stability properties under Neumann boundary conditions, and integrates it into a Bayesian inference framework to quantify explosive onset and interaction parameters from empirical data.
This study establishes an aging, male-biased mouse model of tobacco-related oral premalignancy to generate a transcriptomic atlas that reveals enhanced immune responses and stem cell dysregulation as key drivers of oral squamous cell carcinoma progression.
This study establishes YAP1/TAZ-TEAD signaling as a shared oncogenic dependency in meningioma and demonstrates that while TEAD inhibition alone shows variable efficacy, combining it with MEK or mTOR inhibitors effectively overcomes resistance in NF2 wild-type and higher-grade tumors by targeting compensatory signaling pathways.
This study utilizes single-cell RNA sequencing of 72 AML patient samples across disease stages to reveal distinct cellular dynamics, including immature progenitor enrichment, metabolic shifts, and an exhausted immune microenvironment with impaired antigen presentation in relapsed/refractory cases, thereby identifying potential therapeutic targets.
This multi-omics study utilizing bioinformatics analysis of public datasets identifies MACC1 as a potential prognostic biomarker and therapeutic target for colonic adenocarcinoma, characterized by its elevated expression in Wnt and chromatin modifier pathways, association with DNA damage repair, and negative correlation with immune cell infiltration.
This study establishes a stable, long-term biobank of 20 Patient-Derived Tumor Organoids (PDTO) from diverse head and neck squamous cell carcinoma (HNSCC) sites that faithfully recapitulate tumor characteristics and demonstrate a strong predictive correlation between in vitro drug/radiation sensitivity and 24-month patient clinical outcomes, supporting their integration into precision oncology workflows.