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 sanguinarine induces p53-dependent apoptosis in the *C. elegans* germline by elevating reactive oxygen species, which subsequently activate the ATM/ATR-mediated CHK-1 DNA damage signaling pathway.
This study utilizes multimodal functional genomics to map drug-specific on-target resistance mechanisms for clinical WRN inhibitors in microsatellite-unstable cancers and identifies synthetic vulnerabilities, such as NHEJ factors and WIP1, to guide resistance-aware therapeutic strategies.
This study reveals that mammalian neuraminidase-1 (NEU1) acts as a critical regulator of platelet-derived thromboxane A2-mediated T-cell immunosuppression and tumor progression, explaining the comparable clinical efficacy of both aspirin and celecoxib in treating PIK3CA-mutant colorectal cancer by inhibiting NEU1 activity and preserving T-cell function.
By applying spatial profiling to over 300 histological domains in primary cutaneous melanoma, this study reveals that tumor cell dedifferentiation and plasticity are driven by complex, non-stochastic spatial interactions with immune cells and perivascular environments, which collectively map disease progression onto a landscape defined by MITF activity and neural crest-like phenotypes.