400 papers
Using a novel computational framework called NicheSphere, this study identifies Spp1⁺ macrophages as central communication hubs that coordinate fibrotic remodeling in myeloproliferative neoplasms by integrating inflammatory and fibrotic signaling with stromal cells, revealing them as promising therapeutic targets for bone marrow fibrosis.
This study demonstrates that systemic cysteine elevation, achievable through probiotics or oral supplementation, sustains T-cell activation and function to overcome resistance and potentiate anti-PD-1 immunotherapy in pancreatic cancer.
This study identifies a reduction in microbiome-derived acetic acid in pancreatic ductal adenocarcinoma (PDAC) and demonstrates that co-targeting the resulting AMPK-MAPK axis reprograms cancer-associated fibroblasts and suppresses tumor growth in preclinical models, revealing a novel metabolic vulnerability for therapeutic intervention.
This study demonstrates that hypo-fractionated FLASH radiotherapy effectively eradicates medulloblastoma in an orthotopic mouse model by activating tumor-associated microglia for debris clearance, while simultaneously preserving hippocampal cognitive function through enhanced neuron-astrocyte crosstalk and reduced neuroinflammation.
This study identifies the pyruvate branch point as a critical metabolic checkpoint that regulates lymphoid cancer cell dissemination by modulating mitochondrial ROS and HIF-1α signaling through a reprogrammed metabolic profile characterized by reduced pyruvate oxidation and citrate synthase downregulation.
Analysis of Cancer Cell Line Encyclopedia data suggests that ligands for ERBB family receptors, particularly through the G11/Gq pathway, drive the proliferation of BRAF-WT melanomas, identifying new therapeutic targets for these difficult-to-treat tumors and potentially uveal melanomas.
This study identifies that ROCK1 activation drives cell-in-cell invasion during entosis by recruiting the actin-bundling protein Plastin-3 to the plasma membrane, thereby facilitating the cortical tension and cytoskeletal remodeling necessary for one cell to engulf another.
This study develops and validates a robust 26-gene tumor-suppressor signature that effectively stratifies prognosis and predicts recurrence in adenocarcinoma non-small cell lung cancer patients, demonstrating superior performance compared to existing prognostic models across multiple independent cohorts.
This study establishes a robust genomic subtyping of skull base chordoma into four biologically coherent clusters based on distinct copy-number events, linking specific chromosomal architectures to unique transcriptional programs and shared sarcoma aberrations to provide a unifying classification for future therapeutic targeting.
This study reveals that RAS pathway mutations in B-cell acute lymphoblastic leukemia drive an immunosuppressive bone marrow microenvironment enriched with regulatory T cells, which impairs T-cell function but can be overcome by combining blinatumomab with CTLA4 blockade.
This study demonstrates that reporter-labeled estrogen receptor-positive invasive lobular breast carcinoma xenografts faithfully recapitulate the unique single-file histology, specific metastatic patterns (including brain and bone), and robust endocrine therapy response of human disease, establishing them as valuable pre-clinical platforms for therapeutic development.
This study demonstrates that the E3 ubiquitin ligase TRIM9 regulates melanoma cell proliferation and morphology by interacting with VASP to modulate actin organization and adhesion, thereby suppressing mesenchymal motility and influencing tumor growth and metastasis.
This study reveals that castration-resistant prostate cancer (CRPC) cells become dependent on high cyclin-dependent kinase 2 (CDK2) activity and demonstrates that combining CDK2 inhibitors with androgen receptor-targeted therapies selectively enhances anti-tumor efficacy while sparing normal cells.
This study reveals that upregulation of the arginine synthesis enzyme ASS1 drives ICI resistance in cutaneous melanoma by reprogramming mRNA translation via the mTORC1/4EBP1 axis, and demonstrates that pharmacologically targeting ASS1 can resensitize tumors to anti-PD-1 therapy.
This study reveals that cancer-associated fibroblasts support pancreatic ductal adenocarcinoma adaptation to oxidative phosphorylation inhibition by supplying asparagine via SLC38A4-mediated metabolic coupling, a dependency that, when disrupted, converts the tumor's stress response into a therapeutic vulnerability.
This study reveals that while mesenchymal glioblastoma cells exhibit more aggressive migration than proneural cells, their superior survival outcomes are driven by a protective T cell-mediated immune response that counteracts their invasive potential, highlighting a trade-off between migration mechanics and immunogenicity that informs subtype-specific therapeutic strategies.
This study identifies SRRM1 as a key splicing regulator that, often in concert with SRSF11, drives the expression of oncogenic protein isoforms—including those of NUMB and other signaling or cytoskeletal genes—to promote tumor growth, proliferation, and stemness in multiple cancer types, thereby highlighting its potential as a therapeutic target.
This study demonstrates that prolonged PARP inhibitor treatment drives metabolic plasticity in ovarian cancer cells, specifically a shift from glutamine dependence to glycolytic reliance, which confers resistance but also creates a glucose-dependent vulnerability that can be exploited through optimized treatment scheduling.
This study demonstrates that combining untargeted long-read transcriptome sequencing with in vivo functional validation in Drosophila reveals novel, oncogenic gene fusions in gliomas that are missed by standard targeted short-read fusion panels.
This study demonstrates that in *Drosophila*, RasG12V-induced epithelial senescence triggers a systemic senescence-associated secretory phenotype via the cytokine Upd1/IL6, leading to host metabolic syndrome characterized by obesity and insulin resistance, which can be mitigated by suppressing Upd1 or administering Metformin.