411 papers
This study reveals that asparagine-rich microenvironments in the bone and lung drive prostate cancer organotropism by suppressing asparagine synthetase to activate an mTORC1-dependent translational program that enhances N-glycosylation of adhesion proteins like CD44, thereby facilitating metastatic colonization.
This study introduces Single cell Correlation Analysis (SCA), a statistically rigorous computational framework that successfully identifies a conserved, prognostic self-renewal gene signature in human acute myeloid leukemia stem cells across age groups and genetic subtypes, offering a robust solution for overcoming the limitations of existing single-cell annotation tools.
This study reveals that aberrant oxidative metabolism drives the selective expansion of TET2-deficient hematopoietic stem and progenitor cells in clonal hematopoiesis, a process critically dependent on the pentose phosphate pathway to maintain redox balance and cellular fitness.
This study demonstrates that a novel gorilla-derived oncolytic adenovirus (GRAd32), engineered with a chimeric fiber knob to enhance tumor tropism and armed with an anti-HER3 antibody (EV20), effectively achieves selective replication in cancer cells while inhibiting oncogenic signaling, offering a promising alternative to traditional human adenovirus vectors.
This study demonstrates that inhibiting mSWI/SNF chromatin remodeling complexes, specifically with the SMARCA4/2 inhibitor FHD-286, reverses epithelial-mesenchymal transition-mediated resistance and synergistically enhances the efficacy of KRAS inhibitors in KRAS-mutant non-small cell lung cancer.
This study demonstrates that early pancreatic cancer-induced organ dysfunction triggers systemic nutrient depletion and muscle autophagy, a process that drives peripheral tissue wasting while simultaneously supplying amino acids to fuel both tumor growth and host metabolism.
This study reveals that hypoxia-associated acidosis in glioblastoma drives divergent myeloid responses by enabling infiltrating monocyte-derived macrophages to adapt metabolically and adopt immunosuppressive states while depleting microglia and disrupting their homeostatic identity, thereby reshaping the tumor immune architecture.
By integrating multi-omics and spatial transcriptomics from the MOSAIC cohort, this study reveals a high-risk, progenitor-driven molecular program in glioblastoma that links malignant cells with immunosuppressive microenvironments in hypoxic niches to drive tumor progression and predict poor patient survival.
The nuclear oncoprotein SET is essential for MLL/KMT2A-fusion induced leukemia by acting as a transcriptional activator that stabilizes MLL/KMT2A chromatin binding and transcriptional elongation through the inhibition of PP2A-mediated dephosphorylation of Msk1, thereby maintaining a pro-proliferative gene expression program.
This study identifies EZH1-dependent H3K27me1 as a key adaptive barrier limiting DNMT inhibitor efficacy in colorectal cancer and demonstrates that combining DNMT inhibitors with dual EZH1/2 inhibitors overcomes this resistance by eliminating H3K27 methylation, resolving induced bivalent chromatin states, and suppressing oncogenic transcription to enhance therapeutic response.
This study demonstrates that the anti-diabetic drug repaglinide exerts potent anticancer effects on human breast (MCF-7) and lung (A549) cancer cells by inducing dose-dependent cytotoxicity, triggering apoptosis and G1 cell cycle arrest, and inhibiting cell migration through the downregulation of MMP-2 and MMP-9, thereby supporting its potential as a repurposed therapeutic agent for cancer treatment.
This study introduces TumorSim, an agent-based model analogous to GranSim, to compare the spatiotemporal immune dynamics of small cell lung cancer and tuberculosis granulomas, revealing shared two-phase formation processes and the dual, context-dependent role of CCL5 in tumor progression.
This paper introduces omlta, an NP-hard algorithm for computing the optimal multi-label tree alignment to compare tumor clonal trees by minimizing removed mutation labels, and validates its application on non-small cell lung cancer and melanoma datasets.
This study identifies the mitochondrial enzyme ACSS1 as a critical therapeutic vulnerability in mantle cell lymphoma and related B-cell malignancies, demonstrating that it sustains tumor progression by converting acetate into acetyl-CoA to fuel the TCA cycle and de novo pyrimidine biosynthesis, a process whose disruption significantly suppresses tumor growth both in vitro and in vivo.
This study reveals that the expression of GRIA genes encoding AMPA receptor subunits exhibits distinct, subgroup-specific patterns in medulloblastoma that serve as significant prognostic indicators for patient survival, with high expression of certain subunits correlating with either favorable or unfavorable outcomes depending on the molecular subgroup.
This paper presents an integrated pipeline combining optimized DISCO-based tissue clearing, light-sheet microscopy, and a deep learning model (ColNet) to achieve high-resolution 3D visualization and automated feature extraction of collagen architecture in diverse fibrotic tissues.
By employing a novel dTAG-based system for the acute degradation of the pioneer factor FOXA1, this study reveals that FOXA1 exclusively initiates chromatin opening at its binding sites, a unidirectional mechanism that subsequently drives both transcriptional activation and repression depending on the local chromatin environment to regulate cancer growth.
This study reveals that sympathetic norepinephrine in tumor-draining lymph nodes enhances CD8⁺ T cell cytotoxicity by covalently norepinephrinylating granzyme B at Gln43 to prevent its degradation, thereby establishing a neural mechanism for "arming" T cells that can be leveraged through exercise or ex vivo conditioning to improve anti-tumor immunity.
This study reveals that the vitamin K oxidoreductase paralogue VKORC1L1 protects hepatocytes from oxidative stress and DNA damage via vitamin K reduction, thereby preventing the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) to hepatocellular carcinoma (HCC) independently of its role in coagulation.
This study reveals that CKII-phosphorylated HPV-16 E7 oncoprotein drives cervical cancer invasion by recruiting and disrupting the homeostasis of the planar cell polarity protein Vangl1, thereby remodeling tissue polarity and enhancing tumor aggressiveness.