411 papers
This study demonstrates that the loss of the circadian clock gene *Per1* exacerbates colorectal tumorigenesis in *ApcMin/+* mice by increasing polyp burden and elevating β-catenin protein levels through non-transcriptional mechanisms, thereby establishing a tumor-suppressive role for *Per1*.
This study characterizes triciribine as a potent, pleiotropic antimetabolite in acute lymphoblastic leukemia that induces cytotoxicity through ADK-dependent metabolism and broad disruption of nucleotide synthesis, DNA replication, and protein translation, suggesting ADK levels as a predictive biomarker for patient stratification.
This study reveals that ADAR1 protects triple-negative breast cancer cells from ferroptosis by suppressing MDM2-mediated lipid remodeling to limit polyunsaturated fatty acid accumulation, thereby identifying ADAR1 inhibition combined with cobimetinib as a promising therapeutic strategy.
The study demonstrates that the CK2 inhibitor CX-4945 effectively treats metastatic Ewing sarcoma by inducing the proteasomal degradation of the EWS-FLI1 oncoprotein, thereby suppressing tumor growth and metastasis while showing synergistic efficacy with chemotherapy, which supports its clinical evaluation in relapsed or refractory cases.
By using an epigenetic mitotic clock to estimate tumor ages, this study reveals that aggressive neuroblastomas typically begin growing after infancy, explaining why population screening during that period fails to reduce mortality and suggesting that future early-detection strategies must target older children.
By integrating whole-genome and transcriptome sequencing of 169 laser-capture microdissected biliary tract cancer tumors, this study identifies two consensus cancer subtypes with distinct molecular landscapes and evolutionary processes that better explain tumor biology and improve patient stratification than traditional anatomical classification.
This study establishes a mutation-resolved therapeutic atlas for NRAS-mutant melanoma using a saturation mutagenesis screen, revealing that tri-complex RAS(ON) inhibitors exhibit genotype-selective efficacy across most variants while identifying adaptive STAT3 signaling as a critical resistance mechanism that can be targeted to enhance therapeutic outcomes.
This paper presents a framework that infers the presence and strength of cancer drug cross-resistance using only single-drug exposure lineage tracing data, thereby eliminating the need for complex combinatorial experiments to optimize treatment strategies and identify resistance-minimizing targets.
This study demonstrates that the aberrant expression of the cancer-testis antigen TSSK6 in colorectal cancer promotes tumorigenic growth and invasion by activating a FAK-STAT3 signaling axis that drives STAT3-dependent transcriptional programs for extracellular matrix remodeling and anoikis resistance.
This study demonstrates that sequential [18F]-fluorothymidine PET imaging, rather than baseline uptake, serves as a predictive non-invasive biomarker for monitoring treatment response to combined ATR and Wee1 inhibitors in triple-negative breast cancer models.
This study reveals that tumors induce nephrogenic ascites in Drosophila by triggering the systemic dissemination of the commensal bacterium *Acetobacter aceti*, which activates renal IMD/NF-κB signaling to cause uric acid accumulation and fluid imbalance.
This preclinical study demonstrates that combining the menin inhibitor ziftomenib with the XPO1 inhibitor selinexor synergistically suppresses oncogenic transcription and induces apoptosis in KMT2A-rearranged and NPM1-mutated AML by disrupting menin-chromatin interactions, thereby offering a promising strategy to overcome resistance and improve survival outcomes compared to monotherapy.
This paper extends an individual-based cancer invasion model by incorporating stochastic, force-dependent N-cadherin bond lifetimes fitted to Gamma distributions, thereby linking adhesion dynamics to cell motility and proposing a framework for pattern formation.
This study identifies METTL16 as a critical driver of taxane resistance in triple-negative breast cancer that promotes ABCB1 translation via m6A modification, establishing METTL16 as a cancer-selective therapeutic target to restore drug sensitivity.
This study reveals that the miR-199a-5p/XIAP axis undergoes context-dependent rewiring and spatial reorganization in high-grade serous ovarian cancer, where its loss of regulatory coupling in resistant states and distinct tumor-associated spatial phenotypes drive platinum resistance and offer new targets for biomarker development and therapeutic resensitization.
This study demonstrates that disrupting the Bop1-WDR12 interaction in HCT116 colon cancer cells using peptide mimetics induces nucleolar stress and apoptosis without causing DNA damage, offering a promising non-genotoxic therapeutic strategy for cancer treatment.
This study demonstrates that the pan-Ras tricomplex inhibitor daraxonrasib acts as a pharmacologic GAP mimetic to restore GTPase activity, thereby synergizing with Switch-II pocket inhibitors like adagrasib to enhance K-Ras engagement, accelerate pathway suppression, and improve therapeutic efficacy in mutant cell lines.
This study demonstrates that lipid-rich ascites in ovarian cancer drives T cell dysfunction by altering lipid metabolism, and that removing these lipids restores T cell activation and enhances the efficacy of bispecific T cell engager (BiTE) therapy.
This study demonstrates that engineering a novel anti-FAP single-domain antibody (VHH) into monomeric, dimeric, and Fc-fusion formats allows for the tuning of pharmacokinetic properties to optimize tumor uptake, retention, and radiation dosimetry for improved cancer theranostics targeting fibroblast activation protein.
By integrating spatial transcriptomics and proteomics, this study reveals that IDH-mutant gliomas transition from a brain anatomy-driven spatial organization in low-grade tumors to a hypoxia-associated structural pattern in high-grade tumors, establishing a framework linking tumor grade to specific spatial interactions between malignant and microenvironmental cells.