390 papers
This paper introduces the CIViC MCP server, a tool that integrates large language models with the CIViC knowledgebase to enable users to query cancer variant data and receive rapid, natural language summaries of expertly curated clinical interpretations.
This study identifies FILIP1L as a critical regulator that coordinates epithelial-to-mesenchymal transition (EMT), cell cycle progression, and invadopodia activity to drive breast cancer invasion and metastasis, with its expression shifting from the G2 to G1 phase as EMT advances and correlating with poor patient outcomes.
This study identifies HVEM as a critical driver of mesenchymal glioblastoma progression and drug resistance via APRIL-induced NF-κB signaling, demonstrating that a novel anti-HVEM nanobody effectively suppresses tumor growth and invasion by blocking this pathway and immune evasion interactions.
This study demonstrates that NG2-targeting chimeric antigen receptor macrophages (CAR-Ms) not only engulf patient-derived glioblastoma cells but also significantly inhibit their 3D invasion in a manner independent of macrophage polarization, offering new insights for optimizing CAR-M therapies.
This study utilizes single-nuclei RNA sequencing and spatial transcriptomics to identify the keratin-positive, HMGA2::NCOR2-fusion cells as the rare neoplastic drivers in KPGCT that activate the Hippo pathway to stimulate CSF1-mediated recruitment and differentiation of macrophages, thereby establishing KPGCT as a distinct entity from TGCT and supporting the therapeutic potential of CSF1R inhibitors.
This study identifies the AIF/CHCHD4 complex as a druggable target in pediatric osteosarcoma and demonstrates that combining mitoxantrone, which inhibits this complex, with the glutaminase inhibitor telaglenastat synergistically overcomes chemoresistance by exploiting metabolic vulnerabilities.
By employing SPEND-hSRS microscopy to achieve high-sensitivity, sub-millimolar imaging of fumarate, this study reveals mitochondrial metabolic heterogeneity and localized lipid-fueled TCA cycle activity in chemotherapy-stressed bladder cancer cells, providing new insights into cancer cell adaptation to stress.
This study reveals that therapeutic stress induces polyploid giant cancer cells (PGCCs) to undergo a distinct endoreplication-based life cycle characterized by senescence-associated secretory phenotype (SASP)-driven reprogramming, which enables the acquisition of drug resistance and the formation of structured tissues through multilineage differentiation.
This study demonstrates that extending 3D culture of pancreatic ductal adenocarcinoma cells to form mature tumoroids reveals clinically relevant drug resistance and context-dependent vulnerabilities driven by time-dependent adaptation and ABC transporter upregulation, thereby addressing the translational gap between conventional short-term assays and patient outcomes.
This study identifies a specific subset of cancer-associated fibroblasts characterized by high NFATC2 expression that suppresses tumor growth and enhances sensitivity to both chemotherapy and ERBB-targeted therapies, offering a promising biomarker and therapeutic target for improving outcomes in pancreatic ductal adenocarcinoma.
This study defines the RNA modification landscape of multiple myeloma and identifies METTL3-dependent m6A methylation of the lncRNA NEAT1 as a critical epitranscriptomic mechanism driving malignant plasma cell survival.
This study characterizes the neoantigen landscape of malignant peripheral nerve sheath tumors (MPNSTs), revealing that while PRC2-loss and PRC2-wildtype subtypes share private neoantigens, PRC2-loss tumors exhibit immune resistance and reduced antigen presentation, thereby necessitating a dual therapeutic strategy of personalized neoantigen vaccines for all patients and cell-surface TAA-directed therapies specifically for PRC2-loss cases.
This study demonstrates that breast cancer cells interacting with osteoclasts in the bone microenvironment undergo dynamic non-canonical cell fusion and cell-in-cell processes to form hybrid-like cells that acquire osteoclast traits, thereby facilitating bone metastasis.
This study utilizes spatial transcriptomics to reveal that non-small cell lung cancer tumors resistant to neoadjuvant chemoimmunotherapy are characterized by a distinct spatial architecture featuring fibroblast-mediated immune exclusion, metabolic rewiring, and TROP2-associated DNA damage repair pathways, which collectively sustain residual cancer cells by physically and functionally decoupling them from immune recognition and therapeutic efficacy.
This study identifies cyclin-G associated kinase (GAK) as a novel, tumor-selective mitotic kinase essential for diffuse large B-cell lymphoma (DLBCL) survival, particularly in RB1-deficient cases, and proposes repurposing existing potent GAK inhibitors like OTS167 as a rapid therapeutic strategy for this disease.
Time-resolved transcriptomics reveals that crocin induces hepatocellular carcinoma cell senescence and suppresses proliferation by disrupting spliceosomal machinery and reprogramming metabolic pathways, offering a novel therapeutic mechanism for treating liver cancer.
This study demonstrates that heterogeneous sensitivity to Src inhibitors in oral squamous cell carcinoma is driven by variable pathway activation, and that combining these inhibitors with cisplatin enhances antitumor efficacy while allowing for a significant reduction in cisplatin dosage to mitigate toxicity.
Under amino acid starvation, oncogenic RAS mutations drive the upregulation of α2 integrin via the RAS/MAPK pathway and mTOR inhibition, thereby enhancing ECM uptake, cell motility, and poor prognosis in pancreatic cancer.
This study introduces an ex vivo "resistant GSC families" platform derived from matched primary glioblastoma samples to dissect the distinct genetic and phenotypic mechanisms of temozolomide and radiation resistance, revealing specific pathways like MMR-dependent stability and adaptive DNA damage responses that drive therapeutic failure.
This study demonstrates that a novel, homogeneous KIM-1-targeted antibody-drug conjugate (LT-025) engineered via microbial transglutaminase exhibits potent, specific cytotoxicity against renal cell carcinoma and shows synergistic antitumor efficacy when combined with sunitinib in mouse models.