161 papers
Cancer biology explores the complex ways cells grow out of control, investigating the genetic mutations and environmental factors that drive tumor formation. This field seeks to understand how healthy cells transform into malignant ones and how these rogue cells spread throughout the body. By decoding these fundamental mechanisms, researchers aim to develop more effective treatments that target the disease at its source while sparing healthy tissue.
At Gist.Science, we process every new preprint published in this category directly from bioRxiv to ensure you stay ahead of the curve. Our team provides both accessible plain-language overviews and detailed technical summaries for each study, bridging the gap between raw research data and practical understanding. Whether you are a specialist or a curious reader, our goal is to make these critical findings clear and actionable.
Below are the latest papers in cancer biology, offering fresh insights into the ongoing fight against this disease.
This study demonstrates that adipocyte-derived signals reprogram triple-negative breast cancer cells by coupling metabolic rewiring with selective chromatin opening to activate stress-adaptive gene programs, thereby enhancing their ability to buffer oxidative stress and survive.
This study demonstrates that intratumoral delivery of lipid nanoparticle-formulated mRNA encoding a membrane-bound IFNγ-FasICD fusion protein effectively drives tumor regression by simultaneously inducing direct Fas-mediated apoptosis in cancer cells and remodeling the tumor microenvironment to enhance systemic anti-tumor immunity.
This paper introduces a hierarchical graph neural network that leverages spatial transcriptomics to accurately distinguish between immunogenic and tolerogenic tertiary lymphoid structures in renal cell carcinoma, revealing that bulk CXCL13 expression often reflects non-TLS exhaustion rather than productive immunity and demonstrating the model's robustness through high clinical validation and cross-cancer generalization.
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 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.
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 integrates transcriptomic analysis and machine learning to demonstrate that the temporal accumulation of extrachromosomal DNA (ecDNA) and associated mutations in TNBC tumors drives chemotherapy resistance by altering gene expression and reducing drug binding affinity, with ecDNA burden identified as a dominant predictive feature for resistance to agents like paclitaxel and doxorubicin.
This study demonstrates that engineered *E. coli* outer membrane vesicles displaying multiple cytokines, particularly a combination of TNF and IL-2, effectively eradicate syngeneic tumors in over 95% of mice by remodeling the tumor microenvironment through enhanced immune cell recruitment and activation.
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.
Sustained interferon exposure in inflamed regions of primary melanoma tumors drives the emergence of a hyper-metastatic subpopulation of cells with elevated CD47 expression that evades macrophage phagocytosis, illustrating how macrophages can paradoxically promote metastasis while attempting to suppress it.