395 papers
This study establishes a low-dose PBMC-engrafted humanized mouse model using CD47-deficient triple-knockout mice that achieves stable human leukocyte reconstitution and a significantly prolonged experimental window by mitigating lethal graft-versus-host disease, offering a versatile platform for immuno-oncology and radiotherapy research.
This study introduces a spike-in probe-enhanced single-cell RNA-seq workflow that enables robust detection and high-resolution transcriptomic profiling of synNotch-CAR-T cells in vivo, revealing their tissue-specific activation, differentiation, and therapeutic dynamics within a glioblastoma model.
This study identifies a robust, lineage-agnostic RNA splicing signature induced by PRMT5 inhibition in MTAP-deleted cancers, establishing it as a specific pharmacodynamic and predictive biomarker for monitoring the efficacy of MTA-cooperative PRMT5 inhibitors.
This study demonstrates that BRAFV600E-driven thyroid tumor development in mice triggers a heterogeneous pro-inflammatory response characterized by early cytokine expression and variable lymphocytic infiltration, which correlates with clonal differences in tumor progression and the inconsistent efficacy of BRAF inhibitor therapy.
By integrating single-nuclei RNA sequencing and spatial transcriptomics, this study reveals that pituitary neuroendocrine tumors arise from developmental plasticity and stromal co-option, forming a transcriptional continuum that challenges traditional discrete classifications and highlights the tumor's dependence on microenvironmental crosstalk.
This study demonstrates that acute RUNX1 ablation in human mammary epithelial cells selectively disrupts enhancer activity and chromatin accessibility, thereby epigenetically driving epithelial destabilization and the acquisition of cancer hallmarks such as stemness, plasticity, and chemoresistance.
This study reveals that mutant p53 (specifically the R273H variant) hijacks PARP via its C-terminal domain to facilitate replication stress adaptation and drive breast cancer metastasis, a mechanism that can be selectively targeted by the synergistic combination of the PARP inhibitor talazoparib and the alkylating agent temozolomide to suppress tumor growth and metastasis in triple-negative breast cancer models.
This study presents a highly potent, multi-armoured IL13Rα2-targeting CAR-T cell therapy that effectively overcomes the immunosuppressive microenvironment of glioblastoma through enhanced persistence, TGF-β resistance, and IL-12 secretion, while maintaining a favorable safety profile and manufacturability.
By integrating multi-omics data from 3,628 samples across 24 cancers using the parseMetab R package, this study reveals that pan-cancer metabolic reprogramming is characterized by the consistent upregulation of glycan biosynthesis and nucleotide metabolism, uncovering universal vulnerabilities that could be targeted for therapeutic intervention.
This study demonstrates that tunneling nanotubes facilitate the horizontal transfer of BMPR1b from transformed to non-transformed mammary cells, triggering a BMP-dependent cascade that propagates a preneoplastic phenotype and anchorage-independent growth during the early stages of luminal breast cancer initiation.
This study establishes a proteogenomic framework for soft tissue leiomyosarcoma by identifying three distinct molecular subtypes with unique signaling pathways, clinical outcomes, and therapeutic vulnerabilities, including a validated immunohistochemical classifier for clinical application.
This study characterizes the childhood cancer-linked BRIP1 R162Q germline variant as a hyperactive helicase that induces genomic instability through the accumulation of G-quadruplexes and R-loops, thereby creating specific vulnerabilities to targeted therapies involving G4-ligands and DNA damage kinase inhibitors.
This study demonstrates that the MEK inhibitor mirdametinib exhibits single-agent activity against atypical teratoid rhabdoid tumor (ATRT) and, when combined with the CDK4/6 inhibitor abemaciclib, significantly suppresses tumor proliferation and extends survival in orthotopic xenograft models.
This study demonstrates that extracellular vesicles released by senescent tumor cells are both necessary and sufficient to induce paracrine senescence in neighboring cells, acting as key autonomous effectors of the senescence-associated secretory phenotype (SASP) distinct from soluble factors.
This study reveals that in breast cancer, A-to-I RNA editing landscapes are shaped by a two-tier model where a dominant ADAR1-driven program targeting intramolecular Alu repeats is augmented by an independent, additive pathway of intermolecular dsRNA formation driven by antisense lncRNA transcription, collectively generating subtype-specific editing patterns that link epitranscriptomic regulation to metabolic phenotypes.
This paper proposes the Homeostatic Theory of Resistance (HTOR), which argues that cancer's robustness against therapy stems not just from genetic mutations but from the preservation of normal tissue-level homeostatic feedback loops that inadvertently help malignant cells survive treatment.
This study demonstrates that combining pharmacologic inhibition of fatty acid synthase (FASN) with dietary polyunsaturated fatty acid (PUFA) supplementation suppresses prostate cancer progression by inducing lethal oxidative stress through increased lipid peroxidation and mitochondrial dysfunction.
This study identifies 3-mercaptopyruvate sulfurtransferase (3-MST) as a critical metabolic vulnerability in colorectal cancer stem cells, demonstrating that its inhibition disrupts bioenergetics and membrane integrity to induce cell death and suppress tumor growth.
This study reveals that breast cancer tumor heterogeneity drives distinct myeloid cell remodeling and a shift from anti- to pro-metastatic monocyte phenotypes during lung metastasis, mediated by specific myeloid-derived suppressor cell signatures and impaired monocyte differentiation, thereby identifying new targets for metastasis-specific therapies.
This study identifies OXA1L-dependent mitochondrial protein translation as a critical driver of chemoresistance in triple-negative breast cancer and demonstrates that repurposing the antibiotic tigecycline to inhibit this process effectively sensitizes resistant tumors to chemotherapy.