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 identifies a large, previously unexplored class of non-canonical cancer-germline microproteins (ncCGAs) encoded by non-coding RNAs and untranslated regions, demonstrating their tumor-specific expression, evolutionary youth, and potential as immunotherapeutic targets through the generation of immunogenic HLA class I peptides.
This study expands the "structural surfaceomics" framework across multiple cancer models and healthy controls to compile a comprehensive crosslinking database, enabling the identification of tumor-specific protein conformations and aberrant epitopes as promising targets for next-generation immunotherapies.
This study reveals that the transcription factor ZEB1 drives astrocyte-mediated immunosuppression in glioblastoma, while its loss or the therapeutic delivery of the cytokine CXCL14 reprograms the tumor microenvironment to recruit T cells, thereby inhibiting tumor growth and extending survival.
This study maps the interactome of the scaffold protein FRS2 in medulloblastoma cells, revealing its role in promoting tumor migration and invasion through the reorganization of signaling complexes and the regulation of cell junction proteins, thereby identifying novel therapeutic targets for FGFR-driven cancers.
This study reveals that early recurrence of bladder cancer following Bacillus Calmette-Guerin (BCG) therapy is driven by a pre-existing state of innate immunosenescence in monocytes, characterized by Activator Protein 1 (AP-1) dysregulation, which prevents the necessary inflammatory response to treatment.
This study proposes a multidimensional benchmarking framework for circulating tumor cell (CTC) isolation technologies that integrates recovery, purity, and post-isolation preservation metrics to demonstrate that the TellDx system outperforms other platforms under spike-in conditions, thereby advocating for evaluation beyond simple capture efficiency.
This study identifies a therapeutic vulnerability in lethal prostate cancer by demonstrating that the synergistic co-inhibition of nuclear export (XPO1) and translation initiation (EIF4A1) effectively overcomes AR-driven resistance and induces tumor regression in preclinical models at significantly lower doses than current single-agent regimens.
This study demonstrates that the CXCL13-CXCR5 signaling axis drives the recruitment, differentiation, and spatial organization of stem-like CD8+ T cells within lymphoid aggregates in clear cell renal cell carcinoma, thereby enhancing anti-tumor immunity and correlating with improved patient survival.
This study demonstrates that phosphoglycerate mutase 5 (PGAM5) regulates lipid metabolism and mitochondrial homeostasis in hepatocellular carcinoma by suppressing glycerophospholipid pathways and fatty acid biosynthesis, thereby influencing tumor progression and patient survival.
Loss of the metabolic enzyme CPT1A in breast cancer cells promotes lung metastasis in immune-competent mice by triggering cytosolic mtDNA release and chronic STING pathway activation, which impairs CD8+ T cell function and facilitates tumor outgrowth.