411 papers
This study identifies Glycoprotein non-metastatic B (GPNMB) overexpression as a key driver of resistance to CDK4/6 inhibitors in estrogen receptor-positive breast cancer, establishing it as a promising biomarker for patient stratification and a potential therapeutic target.
By performing spatial single-cell profiling of paired newly diagnosed and recurrent glioblastoma samples, this study identifies five distinct tumor ecosystem trajectories that correlate with clinical outcomes, revealing how specific evolutionary shifts toward either immunomodulatory or immunosuppressive niches under standard therapy can guide prognostic stratification and therapeutic decisions.
This study identifies a co-evolved therapeutic vulnerability in recurrent pancreatic cancer where oncogenic KRAS signaling and LILRB4-expressing macrophages mutually reinforce tumor progression, suggesting that dual targeting of this axis offers a promising strategy to prevent recurrence.
This study demonstrates that depleting the oncogenic factor HSF1 in malignant cells triggers a catastrophic proteomic imbalance and amyloidogenesis that can be exploited for tumor suppression, whereas HSF1 is dispensable for non-transformed cells, highlighting a novel therapeutic strategy to combat malignancy by provoking proteomic catastrophe.
An engineered subtilisin protease (RASp) specifically targets and degrades active KRAS G12C by cleaving its switch II region, thereby disrupting downstream MEK-ERK signaling and inducing selective cell death in KRAS-dependent cancer cells while sparing normal cells.
This study demonstrates that the elevated concentrations and shortened fragment lengths of circulating cell-free DNA (cfDNA) observed in cancer patients are primarily driven by the saturation of hepatic clearance mechanisms rather than tumor-specific processes, revealing a systemic fragmentation signature that serves as an independent prognostic marker.
This study demonstrates the feasibility of generating patient-derived organoids from malignant pleural effusions of lung adenocarcinoma and mesothelioma patients to recapitulate tumor heterogeneity and serve as a translational platform for individualized chemotherapy profiling.
By leveraging single-cell RNA sequencing to map intrinsic and adaptive resistance signatures in platinum-resistant high-grade serous ovarian cancer, this study establishes a translational framework that identifies and validates tumor-specific carboplatin combination therapies, including the promising adjuvant pevonedistat, to overcome treatment heterogeneity and improve therapeutic efficacy.
This study demonstrates that canonical NF-κB signaling constrains RAS-driven B-cell acute lymphoblastic leukemia by inducing a mature B-cell receptor state incompatible with oncogenic RAS activity, thereby triggering apoptosis in RAS-mutated cells and explaining the mutual exclusivity of these pathway alterations in leukemia.
This study reveals that oncogene inactivation-induced senescence (OIIS) acts as a double-edged sword in targeted cancer therapy, initially suppressing tumor growth but ultimately driving relapse by inducing genomic instability, remodeling the tumor microenvironment toward immunosuppression, and facilitating the emergence of resistant clones.
The authors present a high-throughput 384-well microfluidic platform (MPO) that miniaturizes patient-derived organoid cultures to enable multi-parameter phenotypic and omics profiling, thereby facilitating clinical treatment optimization and revealing mechanisms of drug resistance in metastatic colon cancer.
This study demonstrates that combining the CDK4/6 inhibitor palbociclib with the MET/ALK/ROS1 inhibitor crizotinib synergistically induces senescence and enhances immune recognition in melanoma cells regardless of BRAF/NRAS status, effectively suppressing tumor growth through CD8+ T cell-dependent immune surveillance.
This study evaluates the clinical feasibility of evolutionary therapy for metastatic non-small cell lung cancer by demonstrating that while higher containment levels and dynamic protocols can improve outcomes, their success critically depends on minimizing measurement errors and appointment delays, with single-bound protocols proving more robust to these real-world clinical constraints.
This study utilizes quantitative proteomics of primary patient samples to define the protein landscape of B-cell malignancies, revealing a unique 10-protein signature in mantle cell lymphoma (MCL)—seven of which are missed by RNA analysis—that offers novel targets for dual CAR T-cell therapy and personalized treatment strategies.
This study utilizes longitudinal spatial transcriptomics to demonstrate that PARP inhibitor resistance in high-grade serous ovarian cancer is driven by reproducible tumor microenvironment remodeling characterized by hypoxia, increased stromal compartmentalization, and the exclusion of effector immune cells.
This study demonstrates that deoxysphingolipids activate the cGAS-STING1 pathway via mitochondrial stress-induced DNA release, thereby enhancing immune cell infiltration and suppressing tumor growth in colon cancer.
This study demonstrates that targeting the chromatin remodeling enzyme ALC1 safely expands the therapeutic utility of PARP inhibitors across diverse high-grade serous ovarian cancers, including those with homologous recombination deficiency or CCNE1 amplification, by overcoming resistance mechanisms while sparing normal cells through a biomarker-driven safety profile.
This study identifies a novel bivalent binding site formed by the bHLH and eMBII domains of the MYC protein, which is enhanced by lysine acetylation at K148, thereby enabling the selective targeting of oncogenic MYC with small-molecule inhibitors.
This study demonstrates that combining subtotal focused ultrasound thermal ablation with CD40 agonism reprograms breast tumor immunity to drive durable, T cell-dependent tumor regression and systemic immunological memory across diverse murine breast cancer models, offering a promising in situ vaccination strategy for subtypes refractory to checkpoint blockade.
This study presents a single-cell framework that leverages temporal delays between mRNA and protein accumulation to identify cancer cell-state transitions, revealing a molecular program linking cell-cycle progression and mitochondrial remodeling to plasticity that serves as a robust prognostic and predictive biomarker across multiple tumor types.