298 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 TACC3 as a pivotal regulator that dictates cancer cell susceptibility or tolerance to mitotic stress by coordinating a switch between m7G cap-dependent translation of pro-apoptotic factors and m6A-mediated cap-independent translation of chromosome segregation genes in response to CDK1 signaling.
This study demonstrates that proton FLASH radiotherapy enhances the control of triple-negative breast cancer in mice compared to standard dose-rate irradiation by activating the STING-IRF3 pathway to boost CD8+ T-cell-mediated antitumor immunity, thereby widening the therapeutic window through both normal tissue sparing and improved tumor response.
This paper employs a continuous-time Markov decision framework to demonstrate that the specific structure of objective functions—such as the type of cost penalties and reward constraints—fundamentally dictates whether a tumor population exhibits regulated, dormant-like dynamics or sustained, uncontrolled growth.
This study identifies that rare, peripherally expanding, neoantigen-reactive CD8+ T cell clonotypes are the primary determinant of exceptional survival in pancreatic cancer patients receiving maintenance pembrolizumab and olaparib, while resistance is driven by T cell exclusion, specific stromal and tumor-intrinsic programs, and regulatory T cell expansion.
This study utilizes spatial transcriptomics to identify six distinct tumor microenvironment niches in glioblastoma, demonstrating that specific niche compositions—particularly those enriched with mesenchymal-like cells and monocyte-derived macrophages—are significantly associated with patient survival and immunotherapy response, thereby suggesting their potential as biomarkers for risk stratification and treatment decisions.
This study demonstrates that pharmacological blockade of Na+/K+-ATPase with digoxin induces reversible, concentration-dependent attenuation of proliferation and metabolic function in K562 leukemia cells primarily through ion dyshomeostasis rather than scaffold-mediated signaling, as confirmed by potassium surmountability and the cells' resistance to canonical stress checkpoints.
This study demonstrates that the H3K27M oncohistone is a critical driver of Diffuse Midline Glioma progression by reshaping the tumor microenvironment to enhance excitatory neuron-tumor coupling and immunosuppression, thereby validating its inhibition as a promising therapeutic strategy.
This study demonstrates that inhibiting MNK1/2 kinases synergizes with G1/S cyclin-dependent kinase (CDK4/6) blockade to suppress triple-negative breast cancer growth by altering the translation of genes involved in mitotic checkpoint control and DNA repair, thereby revealing a new therapeutic vulnerability for this challenging disease subtype.
This study demonstrates that dynamic changes in circulating tumor cell subsets defined by PSMA and EpCAM expression during 177Lu-PSMA-617 treatment hold prognostic value for overall survival in metastatic castration-resistant prostate cancer patients, warranting further investigation.
This study demonstrates that the spliced HPV16 E6*I isoform drives aggressive invasion in oropharyngeal cancer by promoting E-cadherin internalization, establishing E6 splicing patterns and E-cadherin localization as valuable biomarkers for predicting poor clinical outcomes and potential therapeutic targets.