411 papers
By integrating high-complexity DNA barcoding with single-cell transcriptomics in patient-derived glioblastoma, this study reveals that tumor propagation is driven by multiple distinct, non-redundant progenitor lineages rather than a single dominant population, providing a functional framework for designing effective, cell type-specific combination therapies.
This study integrates single-cell RNA-seq data to reveal that breast tumor endothelial cells exhibit an anergic phenotype with a venule predominance and distinct gene expression profiles, identifying novel markers like ADM5 that correlate with poor patient survival and resistance to immunotherapy.
The study demonstrates that a novel HER3-targeting protein-corrole nanocomplex (HPK2.0) effectively treats metastatic triple-negative breast cancer by delivering cytotoxic payloads directly to tumor cells, resulting in significant tumor regression, metastasis suppression, and improved survival with minimal toxicity in mouse models.
This study identifies BRD2 upregulation, driven by the transcription factor NFYA, as a conserved pan-cancer adaptive resistance mechanism to BET inhibitors that compensates for BRD4 loss, suggesting that co-targeting BRD2 could enhance the efficacy of BET-based therapies.
The authors developed the RaDRI agent-based computational model to investigate radiosensitisation by the DNA-PK inhibitor SN39536, revealing that while radiation-induced cell killing is primarily driven by DSB misjoining, the inhibitor enhances cell death mainly by preventing DSB resolution before mitosis and predicting a ~9-hour exposure duration is required for maximal effect.
This study reveals that NFE2L2/KEAP1 mutations drive chemoradiotherapy resistance in esophageal squamous cell carcinoma by activating the NRF2 pathway, which synergizes with SPP1⁺TREM2⁺ macrophages to promote tumor relapse, thereby identifying these mechanisms as key targets for overcoming treatment failure.
This study demonstrates that mannose-weighted CEST MRI can non-invasively detect elevated mannose levels associated with aggressive mesenchymal glioblastoma, establishing it as a promising imaging biomarker for predicting tumor aggressiveness and recurrence.
This study establishes a quantitative transcriptomic framework demonstrating that increasing cancer stemness, driven by therapy-reprogrammed androgen receptor activity, RB1 loss, and MYC activation, serves as a key determinant of prostate cancer progression, lineage plasticity, therapy resistance, and poor patient survival.
This study identifies YES and SRC tyrosine kinases as redundant, essential drivers of malignant peripheral nerve sheath tumors (MPNST), demonstrating that their dual inhibition suppresses tumor growth by rewiring oncogenic signaling and reactivating immune pathways, thereby establishing them as promising therapeutic targets.
This study characterizes the diverse landscape of KIT mutations in Asian melanoma and demonstrates that specific variants exhibit distinct drug sensitivities, thereby establishing a critical evidence base to replace the current "one-size-fits-all" treatment approach with genotype-guided precision medicine strategies.
This study reveals that physiologic hypoxia in lung cancer induces translational arrest and sequestration of MHC class I antigen processing pathway mRNAs into stress granules, thereby blocking immunopeptide presentation and establishing a state of "immunogenic dormancy" that facilitates immune escape.
This study reveals that while *VHL* inactivation drives proliferation in clear cell renal cell carcinoma, co-inactivation of *PBRM1* promotes tumorigenesis not by enhancing transcriptional changes, but by independently disrupting epithelial architecture to remove structural restraints on cell growth.
This study demonstrates that intratumoral plasma cells are essential for activating CD8+ T cells and enabling the success of immune checkpoint blockade therapy in malignant peripheral nerve sheath tumors (MPNSTs), a finding that explains how CDK4/6-MEK inhibition sensitizes these tumors to immunotherapy and suggests plasma cell presence as a key biomarker for treatment response.
This study utilizes spatial multi-omics to identify a distinct population of immunosuppressive, lipid-laden macrophages derived from infiltrating monocytes in primary CNS lymphoma, which are absent in systemic DLBCL and correlate with treatment response, suggesting a novel therapeutic target for immune modulation.
The study presents a personalized microfluidic tumor-on-a-chip platform that co-cultures patient-derived tumor cells with immune cells to generate highly cytotoxic organoid-interacting lymphocytes (OILs), effectively overcoming limitations of current immunotherapies for peritoneal malignancies by enhancing CD8+ T and NK cell activity even when tumor-infiltrating lymphocytes are insufficient.
This study utilizes multi-omic and spatial analyses to reveal that glioblastoma-derived paracrine signals drive immunosuppressive macrophage polarization through the activation of the cAMP-CREB signaling axis.
Using a mosaic Drosophila model, this study reveals that early Ras-driven tumour growth is shaped by interclonal interactions where neighbouring cells either suppress tumours via cell competition regulators or promote them through SWI/SNF chromatin remodelling disruptions that trigger inflammatory and anabolic programs, demonstrating that oncogenic cooperation extends beyond cell-intrinsic mutations to include non-cell-autonomous effects.
This study demonstrates that combining metabolic drugs, such as imipridones and metformin, with conditions forcing reliance on mitochondrial oxidative phosphorylation significantly reduces osteosarcoma cell viability while sparing normal osteoblasts, thereby supporting the development of personalized, mitochondria-targeted combination therapies for this aggressive pediatric bone cancer.
This study integrates network biology and machine learning to identify Aminoadipate Semialdehyde Synthase (AASS) as a novel prognostic metabolic tumor suppressor biomarker in triple-negative breast cancer.
This study demonstrates that Daraxonrasib (RMC-6236), a potent RAS(ON) inhibitor, effectively suppresses tumor growth and induces cell death in RAS-mutant neuroblastoma models by inhibiting MAPK signaling and upregulating BIM, with its efficacy further enhanced when combined with the BCL-2 inhibitor venetoclax, thereby supporting its clinical development for this high-risk patient subset.