299 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.
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.
This study demonstrates that combining untargeted long-read transcriptome sequencing with in vivo functional validation in Drosophila reveals novel, oncogenic gene fusions in gliomas that are missed by standard targeted short-read fusion panels.
The paper introduces SubNetDL, a robust and interpretable deep learning framework that integrates subclonal mutation profiles with protein-protein interaction networks via network propagation to accurately predict cancer therapy responses and identify novel biomarkers across diverse cancer types and treatment modalities.
This study integrates a spatially resolved agent-based model with an interpretable machine learning surrogate to demonstrate that combination therapy targeting both HER2-positive and HER2-negative cell populations effectively overcomes phenotypic plasticity-driven resistance in heterogeneous breast cancer, offering a scalable framework for predicting and optimizing treatment strategies.
This study demonstrates that the protein phosphatase activity of PTEN, distinct from its lipid phosphatase function, is essential for normal embryonic development and tumor suppression in mice, as evidenced by the embryonic lethality and increased tumorigenesis observed in mice expressing a mutant PTEN lacking protein phosphatase activity.