390 papers
Sustained interferon exposure in inflamed regions of primary melanoma tumors drives the emergence of a hyper-metastatic subpopulation of cells with elevated CD47 expression that evades macrophage phagocytosis, illustrating how macrophages can paradoxically promote metastasis while attempting to suppress it.
By reanalyzing genomic data from 481 DLBCL tumors, this study reveals that EBV-positive cases exhibit distinct genetic patterns that often confound current molecular classification algorithms and demonstrates that existing in vitro models only partially capture the biological heterogeneity of EBV-associated DLBCL.
This study utilizes 3D traction force microscopy to characterize the mechanical dynamics of patient-derived glioblastoma neurosphere invasion in Matrigel, revealing that while actomyosin contractility and microtubules drive robust force generation and directional persistence, a distinct, traction-poor, and MMP-independent invasion mechanism persists even when myosin II activity is inhibited.
This study establishes a comprehensive multi-ancestry compendium of 3,001 prostate methylomes to identify four epigenomic subtypes that risk-stratify patients and reveal complex interactions between genetic and epigenetic alterations, including DNA copy number and methylation, which drive distinct evolutionary trajectories, gene expression programs, and clinical outcomes.
This study demonstrates that the FLASH effect in murine skin is modulated by baseline tissue oxygen levels, showing significant toxicity sparing at moderate to low pO2 values but disappearing under both anoxic and hyperoxic conditions.
This study demonstrates that targeted therapy indirectly selects for cells with heightened phenotypic plasticity in ALK+ lung cancer, a process that not only drives acquired resistance but also enhances the population's capacity to adapt to orthogonal stressors and metastasize, suggesting that constraining plasticity could delay resistance and improve treatment durability.
This study employs a multi-omics approach to demonstrate that the A-to-I edited miR-411-5p (miR-411ed) restores sensitivity to Osimertinib in TKI-resistant NSCLC by downregulating STAT3 and modulating interferon and ERK/MAPK signaling pathways, independent of MET suppression, thereby significantly reducing tumor growth in vivo when combined with the drug.
This study concludes that there is no direct causal relationship between clinical doses of Augmentin and other commonly used drugs with biliary toxicity and the development of cholangiocarcinoma, based on experimental findings showing no increase in malignancy markers and cohort data revealing no statistically significant difference in cancer incidence.
This study identifies that the systemic and tumor-intrinsic expansion of FCRL5-expressing atypical B cells, which form immunosuppressive niches and drive IgG-skewed humoral responses, is a key mechanism underlying poor response to BCG immunotherapy in patients with high-risk non-muscle invasive bladder cancer.
This study demonstrates that basic region missense variants of the MAX protein exhibit reduced homodimeric DNA binding and enhanced heterodimerization with MYC, suggesting that the loss of MAX homodimer-mediated tumor suppression and the consequent preferential formation of oncogenic MYC/MAX heterodimers contribute to tumorigenesis.
This study demonstrates that gallium nitrate induces cytotoxicity in osteosarcoma cells by acting as an iron decoy to inhibit ribonucleotide reductase and disrupt DNA synthesis, rather than through ferroptosis, thereby synergizing with cisplatin to overcome platinum resistance.
KRAS inhibitor-resistant cancer cells overcome treatment by utilizing the ADGRB1 receptor to drive macropinocytosis-mediated fatty acid scavenging and beta-oxidation, a metabolic adaptation that sustains bioenergetics independently of canonical KRAS signaling and can be reversed by disrupting the ADGRB1-PI3Kγ pathway.
This study reveals that in non-small cell lung cancer, the metabolic enzyme QPRT promotes tumor progression through a moonlighting function where it interacts with and inhibits caspase-3 to suppress apoptosis, independent of its canonical role in NAD+ biosynthesis.
This study establishes ARID2 as a critical tumor suppressor in colorectal cancer by demonstrating that its loss destabilizes the PBAF chromatin remodeler complex, leading to the degradation of key subunits and the dysregulation of oncogenic pathways such as Wnt/beta-catenin signaling.
This study reveals that inflammatory signaling establishes a "memory" by silencing the FBXW2-mediated degradation of the collagen receptor DDR1, thereby allowing pancreatic cancer cells to sustain growth-promoting signaling even in metabolically restrictive stromal environments.
This study demonstrates that exposure to physiological mixtures of environmental chemicals, specifically bisphenols, disrupts human mammary development by inducing persistent epigenetic and transcriptional changes associated with epithelial plasticity and increased susceptibility to specific breast cancer subtypes, particularly invasive lobular carcinoma.
This study establishes PARP16 as a druggable regulator of ribosome MARylation and protein homeostasis in ovarian cancer, demonstrating that the selective inhibitor DB008 effectively suppresses tumor growth by disrupting this pathway both in vitro and in vivo.
This study demonstrates that targeting the lncRNA MALAT1 with antisense oligonucleotides in patient-derived organoid xenograft models effectively inhibits triple-negative breast cancer progression by altering alternative splicing and reducing metastatic burden through tumor-stroma crosstalk, thereby validating MALAT1 as a promising therapeutic target.
This study introduces a trajectory-centric framework that integrates agent-based modeling with state space analysis to map static tumor-immune tissue architectures onto dynamic simulated landscapes, revealing that treatment-phase trajectory histories rather than pre-treatment states robustly predict immunotherapy response in triple-negative breast cancer.
This study demonstrates that Aurora kinase A (AURKA) drives collective breast cancer invasion and metastasis by establishing a leader cell phenotype through centrosome polarization and by stabilizing cell-cell cohesion via its interaction with the actin regulator EPLIN.