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 reveals that myeloid cells undergo metabolic reprogramming during head and neck cancer progression by significantly upregulating MCT4-associated lactate export, a feature that is most prominent in SPP1+ macrophages and consistently increases across all patients compared to normal tissue.
This study demonstrates that carcinogen-induced DNA adducts amplify endogenous APOBEC mutagenesis through nucleotide excision repair, creating a synergistic mechanism that generates distinct "didyma" mutation pairs and accelerates cancer development, particularly in smokers.
This paper introduces a self-supervised learning framework that analyzes multiplex immunofluorescence images to autonomously discover novel, prognostic spatial patterns and biological mechanisms in cancer without relying on pre-defined hypotheses, thereby outperforming conventional segmentation methods and transforming high-plex imaging into a powerful hypothesis-generating engine.
This study reveals that glioblastoma cells parasitically hijack ribosomes from surrounding astrocytes via tunneling nanotubes to reprogram their translatome and drive malignancy, a process mediated by INTS12 that represents a novel therapeutic vulnerability.
This study presents the largest multimodal resource of 1,000 treatment-unexposed colorectal cancer cases, integrating deep proteomics, genomics, and histopathology to define six clinically relevant molecular subgroups that improve patient stratification and establish benchmarks for computational pathology.
This study reveals that HoxA9 coordinates hematopoietic differentiation and cell cycle progression through a feedback loop where it sustains Cdk6/CyclinD1 activity to inhibit pRb-mediated repression, while Myc autonomously suppresses differentiation regulators Cebpa and Cdkn2d, collectively maintaining a block in differentiation.
This study reveals that breast cancer, particularly triple-negative and high-grade tumors, exhibits significant cytoplasmic RNA hydroxymethylation (5hmC) driven by TET3 upregulation, which correlates with altered RNA processing and spliceosomal gene expression.
This study introduces ResponseVerdict, a method that reorients and selects immunotherapy response signatures based on measured clinical outcomes to overcome the poor predictive performance and biases of existing computational tools, thereby significantly outperforming all published predictors and identifying substantially more patients who would benefit from treatment.
By integrating spatial transcriptomics with thermodynamic quality control and physiologically informed constraints, this study establishes a robust framework for generating reliable metabolic flux predictions in prostate cancer, revealing spatial metabolic heterogeneity independent of histological grade and identifying localized, condition-specific metabolic vulnerabilities.
This study reveals that radiation-induced accumulation of Collagen I and III drives immunosuppression in recurrent glioblastoma via a DDR1-PI3K/AKT/TGF-β signaling axis, identifying this pathway as a therapeutic target where inhibiting PI3K sensitizes tumors to PD-1 blockade and improves survival.