411 papers
This confirmatory study demonstrates that miR-15a and miR-16 regulate the oncogene BCL2 by specifically repressing its translation via 3'-UTR binding without degrading the mRNA, thereby providing a precise post-transcriptional mechanism for tumor suppression in malignancies like chronic lymphocytic leukemia.
Zinc-doped Ag2S nanostructures synthesized via cation exchange (specifically ZSS(0.15)) significantly enhance red-light-driven photothermal and photodynamic therapies by improving charge separation and ROS generation, achieving ~97% tumor regression in breast cancer models without systemic toxicity.
This study utilizes a deep neural network model trained on a five-protein stem cell signature (BAX, MLKL, FLIP, GLUT1, and CDX2) derived from single-cell spatial profiling of 493 stage III colorectal cancer patients to accurately predict tumor relapse and identify potential combinatorial therapeutic targets.
This study establishes a comprehensive, genomically diverse mouse mammary tumor dataset with linked treatment outcomes to train and validate machine learning models that successfully predict human breast cancer prognosis and immune checkpoint inhibitor response, highlighting conserved biological mechanisms between species.
This study demonstrates that abolishing mitochondrial Complex I in high-grade serous ovarian cancer cells impairs tumor growth by disrupting hypoxia response and vascular development, thereby sensitizing the tumors to anti-angiogenic therapy with bevacizumab.
This study demonstrates that the mechanical stress experienced by breast cancer cells during intravasation from engineered microtumors triggers distinct mechanotranscriptomic programs, characterized by upregulated YAP/TAZ signaling and increased biomechanical activity, which drive malignant progression beyond the effects of cell-cell contact alone.
This study demonstrates that early suppression of the pro-inflammatory senescence-associated secretory phenotype (SASP) using the JAK inhibitor ruxolitinib effectively mitigates chronic radiation-induced bone loss, improves bone architecture, and reduces associated tissue damage in both prostate cancer patients and mouse models.
This paper introduces SPICE, a novel framework that deconvolves somatic copy-number alteration profiles into discrete evolutionary events to model focal selection, thereby identifying 460 cancer-relevant loci and expanding the understanding of mutational processes and selective forces in cancer genomes.
This study demonstrates that a replication-competent Delta-24-RGD adenovirus platform can serve as an in situ factory for producing and releasing tumor-targeting RNA aptamers against 4-1BB, effectively remodeling the tumor microenvironment and inducing antitumor immunity comparable to protein-based benchmarks.
This study demonstrates that delivering membrane-localized xenoantigens, particularly when combined with checkpoint blockade, effectively redirects pre-existing antiviral immunity against tumors by enhancing CD4+ T cell responses and inflammatory cell recruitment, offering a promising strategy for treating poorly immunogenic cancers.
This study demonstrates that inhibiting the mRNA 3' end processing endonuclease CPSF73 induces widespread 3'UTR lengthening via alternative polyadenylation, which reverses the epithelial-mesenchymal transition (EMT) and suppresses metastasis in multiple cancer cell lines, highlighting APA modulation as a promising therapeutic strategy.
This study reveals that the synthetic lethality observed in acute myeloid leukemia cells upon combined glutaminase and TOFA inhibition stems from TOFA's non-canonical blockade of protein S-acylation, a mechanism essential for maintaining mitochondrial respiration in cancer cells but dispensable in healthy hematopoietic progenitors, thereby exposing a unique metabolic vulnerability for targeted therapy.
This study reveals that nutrient stress within the pancreatic cancer microenvironment induces a drug-tolerant state by suppressing apoptotic priming, a mechanism that can be reversed by targeting the anti-apoptotic regulator BCL-XL.
This study proposes a pathogen-driven model of colorectal carcinoma where Neuro-Immune Crypt-Associated (NICA) cells serve as a cellular origin, EBV-infected B-lineage cells induce HERV-H/F expression via paracrine signaling, and compromised antiviral surveillance allows these viral elements to persist, collectively redefining CRC as a disruption of the neuro-immune niche driven by chronic inflammatory pressure.
This study reveals that Coronin1A, stabilized by SUMOylation via SENP5 and Raftlin, drives colitis-associated colorectal cancer by regulating TGF-β signaling endosome stability to promote M2-like macrophage polarization and a pro-tumorigenic tumor microenvironment.
This study utilizes integrated multi-omics profiling of 16 patient-derived models to reveal that while biallelic SMARCB1 loss is the universal driver of malignant rhabdoid tumors, tumor heterogeneity, progression, and therapeutic vulnerabilities are shaped by diverse inactivation mechanisms, extensive structural variations, and dynamic epigenetic modulation of DNA repair and immune pathways.
This study reveals that the MYC-ATF4-ASS1 axis in melanoma regulates intracellular arginine synthesis and shapes the tumor immune microenvironment, thereby determining tumor sensitivity to arginine-depleting therapies and enhancing CD8+ T cell-mediated antitumor immunity.
This study demonstrates that optimized L1CAM.III-CAR T cells, engineered with a long hinge and CD28 domain, effectively overcome low antigen density to achieve potent, persistent, and safe antitumor activity against relapsed pediatric rhabdomyosarcoma, establishing L1CAM as a promising therapeutic target.
This study integrates experimental findings into a nonlinear dynamical model to demonstrate that p53 restoration suppresses retrotransposon-driven chromosomal instability by triggering a threshold-dependent collapse in L1 burst frequency via a let-7 feedback loop, thereby significantly reducing structural genome rearrangements in early tumorigenesis.
This study identifies PSMD14 as a critical epigenetic regulator that drives melanoma survival and MAPK inhibitor resistance by deubiquitinating histone H2A to maintain pro-survival gene expression, establishing it as a promising therapeutic target to overcome drug tolerance and prevent tumor relapse.