204 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 TET2 loss promotes MYC-driven B cell lymphoma development by enhancing the survival and clonal selection of premalignant IgM+ B cells through reduced apoptotic sensitivity.
Researchers developed fibrinogen-drug nanoparticles that exploit the clotting cascade to form sustained intratumoral drug depots, successfully eradicating advanced triple-negative breast and pancreatic cancers in mice through a single, brief treatment.
This study identifies a novel vulnerability in glioblastoma by demonstrating that highly efficient, structured migratory behaviors, quantified via Diffusion Entropy Analysis and strongly associated with poor patient survival, are driven by distinct molecular signatures, particularly PTEN gain-of-function alterations.
This study demonstrates that STING overexpression specifically suppresses the migration, but not the proliferation, of murine triple-negative breast cancer cells by significantly upregulating Itgb1 and Itga6 expression.
In HPV-positive head and neck cancer, the ULK1 complex drives the selective autophagic degradation of MARCHF8-ubiquitinated MHC-I via the cargo receptor NDP52, a mechanism that facilitates immune evasion and tumor growth which can be reversed by inhibiting autophagy initiation to restore CD8+ T cell-mediated antitumor responses.
This study identifies a reduction in microbiome-derived acetic acid in pancreatic ductal adenocarcinoma (PDAC) and demonstrates that co-targeting the resulting AMPK-MAPK axis reprograms cancer-associated fibroblasts and suppresses tumor growth in preclinical models, revealing a novel metabolic vulnerability for therapeutic intervention.
This study demonstrates that hypo-fractionated FLASH radiotherapy effectively eradicates medulloblastoma in an orthotopic mouse model by activating tumor-associated microglia for debris clearance, while simultaneously preserving hippocampal cognitive function through enhanced neuron-astrocyte crosstalk and reduced neuroinflammation.
This study identifies the pyruvate branch point as a critical metabolic checkpoint that regulates lymphoid cancer cell dissemination by modulating mitochondrial ROS and HIF-1α signaling through a reprogrammed metabolic profile characterized by reduced pyruvate oxidation and citrate synthase downregulation.
This study develops and validates a robust 26-gene tumor-suppressor signature that effectively stratifies prognosis and predicts recurrence in adenocarcinoma non-small cell lung cancer patients, demonstrating superior performance compared to existing prognostic models across multiple independent cohorts.
This study identifies SRRM1 as a key splicing regulator that, often in concert with SRSF11, drives the expression of oncogenic protein isoforms—including those of NUMB and other signaling or cytoskeletal genes—to promote tumor growth, proliferation, and stemness in multiple cancer types, thereby highlighting its potential as a therapeutic target.