401 papers
This study demonstrates that in *Drosophila*, RasG12V-induced epithelial senescence triggers a systemic senescence-associated secretory phenotype via the cytokine Upd1/IL6, leading to host metabolic syndrome characterized by obesity and insulin resistance, which can be mitigated by suppressing Upd1 or administering Metformin.
This study presents the design, radiosynthesis, and in vitro evaluation of [123I]Italia, a novel talazoparib-derived Auger electron-emitting agent that demonstrates potent PARP1 inhibition, specific nuclear accumulation via PARP trapping, and selective cytotoxicity against PARP-expressing cancer cells, establishing it as a promising candidate for targeted radionuclide therapy.
This study reveals that in small-cell lung cancer, ATM functions as a critical metabolic rheostat by sustaining an ATF4-MYC feedback loop essential for redox homeostasis, such that its inhibition disrupts this axis to induce ferroptotic cell death, thereby identifying a novel therapeutic vulnerability beyond its canonical role in DNA damage repair.
The paper introduces SubNetDL, a robust and interpretable deep learning framework that integrates subclonal mutation profiles with protein-protein interaction networks via network propagation to accurately predict cancer therapy responses and identify novel biomarkers across diverse cancer types and treatment modalities.
This study integrates a spatially resolved agent-based model with an interpretable machine learning surrogate to demonstrate that combination therapy targeting both HER2-positive and HER2-negative cell populations effectively overcomes phenotypic plasticity-driven resistance in heterogeneous breast cancer, offering a scalable framework for predicting and optimizing treatment strategies.
This study demonstrates that the protein phosphatase activity of PTEN, distinct from its lipid phosphatase function, is essential for normal embryonic development and tumor suppression in mice, as evidenced by the embryonic lethality and increased tumorigenesis observed in mice expressing a mutant PTEN lacking protein phosphatase activity.
This study identifies the non-canonical translation initiation factor eIF4G2 as a critical checkpoint that restrains pancreatic cancer progression by selectively suppressing the translation of tumor suppressors and transcriptional regulators, thereby maintaining epithelial identity and preventing metastasis.
This study identifies the POLQ-driven MMEJ Deletion Footprint (MDF) as a key genomic marker in homologous recombination-deficient pancreatic cancer that promotes immunogenicity by increasing neoantigens, remodeling myeloid cells to enhance antigen presentation, and fostering productive T-cell interactions, thereby linking specific DNA repair mechanisms to favorable clinical responses to immunotherapy.
This paper presents a piecewise-linear mathematical model of a three-transcription-factor gene regulatory network to demonstrate how strong intercellular signaling drives travelling waves of gene expression, ultimately determining the dominant cell-state characteristic in melanoma populations.
This study utilizes patient-derived xenograft models to demonstrate that T-cell acute lymphoblastic leukemia relapse is driven by the selection of pre-existing cells with a deregulated OXPHOS and MYC signature, which acquire *TP53* inactivation to enhance leukemia-initiating capacity and treatment resistance.
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.