400 papers
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.
This study demonstrates that pre-treating TRAIL-resistant breast cancer cells with a non-lethal dose of paclitaxel sensitizes them to TRAIL-induced apoptosis by upregulating the pro-apoptotic receptor DR5 and downregulating the decoy receptor DCR2, thereby offering a promising combinatorial therapeutic strategy.
This study reveals that chemotherapy-induced tumor cell death releases ATP to activate P2X7 signaling in pancreatic stellate cells, driving their reprogramming into IL-6-secreting cancer-associated fibroblasts that foster tumor resistance and immune evasion in pancreatic ductal adenocarcinoma.
This study establishes that targeting the mitochondrial one-carbon metabolism enzyme MTHFD2 disrupts redox homeostasis and nucleotide synthesis in acute myeloid leukemia, thereby suppressing disease progression and restoring sensitivity to venetoclax in both treatment-naive and resistant models.
This study demonstrates that Integrin beta 4 (ITGB4) promotes colorectal cancer progression by directly upregulating Ezrin (EZR), which in turn activates the Wnt/β-catenin signaling pathway to drive tumor growth, migration, and invasion.
This study elucidates the cryo-EM structure of the kidney cancer target SLC1A1 bound to a selective inhibitor, revealing an allosteric mechanism that blocks transport, and leverages these insights to design optimized derivatives with enhanced cytotoxicity against renal cell carcinoma.
This study demonstrates that STING overexpression specifically suppresses the migration, but not the proliferation, of murine triple-negative breast cancer cells by significantly upregulating Itgb1 and Itga6 expression.
This study reveals that triple-negative breast cancer-derived extracellular vesicles compromise blood-brain barrier integrity and facilitate brain metastasis by inducing miR-146a-5p and TGF-β1-mediated downregulation of the membrane progesterone receptor PAQR5, which subsequently represses claudin-5 expression and disrupts interendothelial tight junctions.
In HPV-positive head and neck cancer, the ULK1 complex drives the selective autophagic degradation of MARCHF8-ubiquitinated MHC-I via the cargo receptor NDP52, a mechanism that facilitates immune evasion and tumor growth which can be reversed by inhibiting autophagy initiation to restore CD8+ T cell-mediated antitumor responses.
This study establishes a single-cell RNA editing framework that reveals distinct, clinically actionable cellular states in chronic myelomonocytic leukemia (CMML), identifying a high-risk, ADAR1-dysregulated subpopulation associated with adverse outcomes and TET2 mutations, thereby offering novel biomarkers for risk stratification and therapeutic targeting.
This study demonstrates that dual inhibition of PDPK1 and BRAF V600E induces synthetic lethality in anaplastic thyroid cancer by simultaneously suppressing convergent oncogenic signaling pathways, thereby triggering robust oxidative stress, DNA damage, and apoptosis to achieve potent tumor regression.
This study demonstrates that primary breast tumors upregulate endothelial ACKR1 in the lung premetastatic niche to recruit neutrophils, thereby facilitating tumor cell engraftment and metastasis.
This study demonstrates that in early-stage breast cancer, a robust negative association exists between estimated tumor circadian clock function and 10-year survival, indicating that better-preserved clock function paradoxically correlates with poorer patient outcomes.
By applying single-cell multi-omics to 57 patients, this study reveals that subclonal copy number variations generally exert additive transcriptional effects modulated by cancer type and promoter elements, while identifying a distinct class of tumors with transient clonality driven by whole genome duplication.
This study demonstrates that the SSTR2 antagonist [225Ac]Ac-SSO110 achieves superior tumor absorbed dose and retention compared to the internalizing agonist [225Ac]Ac-DOTA-TATE without increased redistribution of daughter radionuclides, challenging the hypothesis that cellular internalization is required for effective daughter retention in targeted alpha therapy.
This study reveals that PI3K-AKT pathway hyperactivation is a critical determinant of oncogenic RAS-induced hypertranscription and replication stress, explaining variability between RAS isoforms and highlighting PI3K inhibition as a potential therapeutic strategy to mitigate transcription-replication conflicts in cancer.
Using a novel computational framework called NicheSphere, this study identifies Spp1⁺ macrophages as central communication hubs that coordinate fibrotic remodeling in myeloproliferative neoplasms by integrating inflammatory and fibrotic signaling with stromal cells, revealing them as promising therapeutic targets for bone marrow fibrosis.