411 papers
Pharmacological inhibition of mucin-type O-glycosylation using Ac5GalNTGc impairs melanoma progression by simultaneously disrupting melanin biosynthesis and blocking Siglec-mediated immune evasion, thereby reducing tumor growth and metastasis.
This study identifies a rare tumor-intrinsic neurovascular progenitor (NVP) cell that serves as a critical lineage intermediate in glioblastoma, capable of generating diverse malignant cell types and acting as a functional nexus that links major organizational axes within the tumor hierarchy.
This study presents GT220, a novel, highly selective, and AI-designed small-molecule inhibitor of PI3Kβ that demonstrates potent, context-dependent antitumor efficacy and safety specifically in PTEN-deficient cancers while sparing normal and wild-type cells.
This study reveals that Keratin 17 (KRT17) promotes ovarian cancer progression and chemoresistance by stabilizing EPN1 through the inhibition of SMURF1-mediated ubiquitination, thereby enhancing Wnt/β-catenin signaling and stem-like traits.
The study demonstrates that the harmine derivative ACB1801 overcomes anti-PD-1 resistance in microsatellite stable colorectal cancer by activating STAT1 signaling to suppress glycolysis, promote ferroptosis, and enhance tumor immunogenicity, thereby significantly improving therapeutic efficacy through increased CD8+ T cell infiltration.
This study identifies that breast cancer cells hijack a conserved developmental program driven by the galectin-1 (GAL1)-glycan axis to enable early dissemination and metastasis, revealing GAL1 as a critical therapeutic target for preventing disease progression.
This study demonstrates that structurally unique benzoxaboroles selectively and stereoselectively bind to the cap-binding pocket of eukaryotic translation initiation factor 4E (eIF4E) through specific hydrogen bonding interactions, offering a promising new avenue for targeting this challenging drug site.
This study establishes that Activation-induced cytidine deaminase (AID) acts as a critical regulator in diffuse large B-cell lymphoma by driving cell cycle progression and reinforcing the activated B-cell-like (ABC) subtype identity through the modulation of MYC, E2F, IRF4, and NF-κB pathways.
This study reveals that deactivating the oncogene Myc in pancreatic ductal adenocarcinoma triggers rapid tumor regression through a latent morphogenic program initiated by the transient release of GM-CSF from tumor cells, which recruits type 1 conventional dendritic cells to orchestrate the dismantling of both neoplastic and stromal components.
This study introduces Polymer-based Leukemic STem-cell Cultures (PLSTCs) to efficiently expand and trace Acute Myeloid Leukemia stem cells, revealing distinct clonal drivers of therapy resistance and identifying chondroitin-sulfate synthesis as a critical target for maintaining primitive stem cell states.
This study identifies iron metabolism as a critical therapeutic vulnerability in stem cell-like castration-resistant prostate cancer (CRPC-SCL), demonstrating that inhibiting the iron-regulatory factor NRF2 induces ferroptosis in CD44-high cells by elevating intracellular free iron, thereby offering a novel treatment strategy for this aggressive disease subtype.
This study demonstrates that the novel EED inhibitor ORIC-944 is a more effective therapeutic strategy for incurable neuroendocrine prostate cancer than the PRC2 inhibitor tazemetostat, as it induces significant dose-dependent growth inhibition and apoptosis by simultaneously reactivating both PRC1 and PRC2 target genes.
This study identifies and characterizes M36 as the first small-molecule inhibitor of Ran GTPase, demonstrating its specificity, synergistic potential with Olaparib, and efficacy in inhibiting tumor growth in epithelial ovarian cancer models.
This study presents the scTumor Atlas, a high-quality pan-cancer single-cell resource of over 135,000 malignant cells across 36 cancer types, which enables precise tumor identity inference, cell line benchmarking, and the systematic mapping of cancer-specific genetic dependencies.
This study introduces Computational Scattered Light Imaging (ComSLI) as a cost-effective, whole-slide microscopy technique capable of mapping collagen fiber architecture in paraffin-treated tumor tissues to visualize growth pathways and support personalized cancer prognoses.
This study reveals a "capacity-contribution paradox" in cancer metabolism where upregulated fatty acid oxidation serves not as a primary fuel source but as a compensatory mechanism to maintain mitochondrial acetyl-CoA levels when glucose-derived synthesis is limited, working in concert with glutamine-driven anaplerosis rather than suppressing glucose oxidation.
This study demonstrates that Sox10 is essential for tumor initiation, cancer stem cell activity, and metastasis in HER2+ mammary cancers, as its genetic ablation prevents tumor formation and reprograms luminal tumor cells into a basal phenotype.
This study introduces MOBA-seq, a high-throughput in vivo platform that quantitatively maps genetic regulators of the metastatic cascade at single-colony resolution in small cell lung cancer, revealing that metastatic seeding is the predominant determinant of progression and identifying CREBBP as a key suppressor whose loss enhances metastasis through both tumor-intrinsic and immune-modulatory mechanisms.
This study reveals that cancer cells adapting to drug stress undergo a non-random, selection-independent process of mega-frequency mutagenesis during pseudo-senescence, generating tens of thousands of precise, recurrent mutations at specific transcription factor binding sites that drive drug resistance.
This study demonstrates that estradiol promotes breast cancer brain metastasis by reprogramming microglia into an immunosuppressive state that hinders anti-tumor immunity, suggesting that estrogen-depletion therapies combined with radiotherapy could effectively treat these metastases.