395 papers
This study reveals that the RNA demethylase FTO localizes to centrosomes to regulate NuMA and KIFC1 for proper spindle assembly and mitotic fidelity, making FTO inhibition a promising therapeutic strategy for selectively targeting cancers with chromosomal instability.
This study demonstrates that LARP1 overexpression drives endometrial cancer progression and chemoresistance by upregulating E2F1 and suppressing apoptosis, while its inhibition sensitizes tumors to carboplatin and reduces growth, highlighting LARP1 as a promising therapeutic target.
This study reveals that the tumor suppressor p73 transcriptionally upregulates the antiapoptotic protein c-FLIP to inhibit extrinsic apoptosis, but demonstrates that a novel small-molecule "switcher" compound can degrade c-FLIP to sensitize p53-mutant cancer cells to p73-mediated therapeutic killing.
This study identifies fibroblast-derived collagen VI as a critical regulator of clear cell renal cell carcinoma biology that organizes the extracellular matrix to restrict T-cell infiltration, while demonstrating that tyrosine kinase inhibitors like cabozantinib suppress collagen VI expression, thereby revealing a novel mechanism of drug action with potential implications for combination immunotherapy.
This study reveals that spatial polarization of endothelial ICAM-1 at the tumor periphery drives T-cell exclusion from melanoma cores, and that blocking the ICAM-1/LFA-1 axis restores intratumoral T-cell infiltration to enhance antitumor immunity and sensitize tumors to immunotherapy.
This study demonstrates the safety and feasibility of infusing ex vivo expanded allogeneic natural killer cells, derived from healthy canine donors and activated with specific cytokines and feeder cells, for the treatment of metastatic solid tumors in dogs, showing successful cell expansion, in vitro potency against osteosarcoma, and well-tolerated administration in a phase 1 clinical trial.
This study presents a comprehensive cross-species single-cell atlas of pancreatic ductal adenocarcinoma that integrates over 1.6 million cells from human and mouse models to define a hierarchical taxonomy of cell states, reveal therapy-driven microenvironmental remodeling, and validate orthotopic syngeneic allografts as superior models for recapitulating advanced human disease.
This study reveals that the asymmetric inheritance and resulting plasticity of extrachromosomal DNA (ecDNA) copy numbers drive rapid tumor evolution by generating functional heterogeneity, modulating cell division timing, and enabling dynamic adaptation to drug selection pressures and the tumor microenvironment to enhance tumorigenicity.
This paper presents a novel 3D tumor-on-a-chip platform that mimics the dynamic tumor-endothelium interface to enable real-time imaging and quantification of breast cancer cell intravasation, demonstrating its utility in identifying anti-metastatic drugs like Dactolisib.
This study demonstrates that focal adhesion kinase (FAK) promotes metastasis in BRAF-mutant melanoma through a kinase-dependent mechanism downstream of PTEN, supporting the therapeutic potential of FAK inhibition to improve outcomes for patients with metastatic disease.
This study identifies a stable, treatment-resilient lipid metabolic program in temozolomide-resistant glioblastoma cells, characterized by the accumulation of lysophospholipids and cholesteryl esters alongside depleted glycerolipid pools, which maintains membrane integrity and suggests cholesterol storage pathways as a potential therapeutic target to overcome chemoresistance.
This study challenges the traditional view of myelofibrosis by revealing that a single clonal driver mutation triggers a unified osteochondral injury program involving THBS1+ stromal cells, which drives both pathological bone formation and resorption across distinct skeletal lineages, thereby establishing THBS1 inhibition combined with JAK blockade as a promising therapeutic strategy to halt disease progression and restore bone homeostasis.
This study demonstrates that TET2 loss promotes MYC-driven B cell lymphoma development by enhancing the survival and clonal selection of premalignant IgM+ B cells through reduced apoptotic sensitivity.
This study demonstrates that in a zebrafish melanoma model, keratinocytes undergoing an EMT-like transformation driven by Twist overexpression restrain tumor invasion and improve survival by altering cell-cell interactions, specifically through homotypic jam3b and pgrn-sort1a signaling.
This study reveals that metastatic progression in melanoma is driven by a cooperative mechanism where physical constriction and epigenetic reprogramming (specifically CTCF repositioning and heterochromatin loss) jointly remodel chromatin architecture to enhance nuclear deformability and activate mesenchymal-like gene networks.
Researchers developed refined USP25/28 inhibitors that eliminate off-target translation effects to selectively induce cell death in c-Myc-driven squamous lung cancer cells via the TP63/FBW7/c-MYC axis while sparing breast cancer cells.
This study demonstrates that FDA-approved NTRK inhibitors like entrectinib can effectively prevent and reduce brain metastases in lung cancers lacking NTRK fusions by blocking wild-type NTRK2 signaling activated by brain-derived neurotrophic factor (BDNF) within the central nervous system niche.
Researchers developed fibrinogen-drug nanoparticles that exploit the clotting cascade to form sustained intratumoral drug depots, successfully eradicating advanced triple-negative breast and pancreatic cancers in mice through a single, brief treatment.
This study identifies a novel vulnerability in glioblastoma by demonstrating that highly efficient, structured migratory behaviors, quantified via Diffusion Entropy Analysis and strongly associated with poor patient survival, are driven by distinct molecular signatures, particularly PTEN gain-of-function alterations.
This study identifies TGS1 as a critical regulator in acute myeloid leukaemia that promotes oxidative phosphorylation and cell survival by mediating cap trimethylation of mitochondrial protein-encoding mRNAs, thereby establishing it as a promising therapeutic target whose depletion impairs mitochondrial function and sensitizes cancer cells to ferroptosis.