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.
Loss of the metabolic enzyme CPT1A in breast cancer cells promotes lung metastasis in immune-competent mice by triggering cytosolic mtDNA release and chronic STING pathway activation, which impairs CD8+ T cell function and facilitates tumor outgrowth.
This study demonstrates that KRAS-driven synthetic lethal dependencies are profoundly tissue-specific, revealing that while KRAS activation induces a universal MYC-driven metabolic signature, the specific genetic vulnerabilities required to sustain this state vary drastically across lineages, necessitating context-aware therapeutic strategies.
This study utilizes a chemoproteomic approach to identify a selective covalent GPX4 inhibitor with a pyrimidinylmethyl isourea warhead and leverages this scaffold to develop both CRBN-dependent and CRBN-independent GPX4 degraders, thereby expanding the chemical tools available for investigating GPX4 biology and ferroptosis.
The study demonstrates that the dual GTP/GDP-bound KRASG12C inhibitor BBO-8520 outperforms the GTP-bound-only inhibitor sotorasib by more durably suppressing KRAS and PI3K-AKT signaling, revealing that targeting the RAS-PI3K interaction is a key strategy to overcome resistance and enhance tumor inhibition in KRASG12C-mutant lung cancer.
This study demonstrates that bidirectional crosstalk between bladder cancer cells and normal fibroblasts drives a pro-migratory phenotypic shift and confers chemoresistance to mitomycin C, suggesting that targeting fibroblast interactions could improve intravesical chemotherapy outcomes.
This paper introduces a teleport-stabilized quantum-walk ranking framework that resolves the fragility of near-tie neoantigen selection by modeling peptides as nodes in an evidence graph, applying symmetry-aware reduction, and utilizing coherent quantum transport with teleportation consensus to generate robust, interpretable shortlists for personalized cancer vaccination.
This study identifies that primary trastuzumab resistance in HER2-positive breast cancer is driven by widespread epigenetic remodeling and 3D chromatin architectural changes, such as altered histone modifications and promoter-enhancer interactions, which reprogram gene expression to support tumor survival and metastasis.
This study identifies XRRA1 as a stress-adaptive protein that acts as a molecular brake on radiation-induced DNA damage signaling and immunogenic cell death, suggesting its potential as a biomarker for radioresistance and a therapeutic target to enhance radiotherapy efficacy.
This study introduces ROSIE, an autonomous multimodal agent framework that leverages large language models to reconstruct transparent, spatiotemporal immune dynamics in pancreatic cancer progression from routine H&E histology, revealing a distinct three-stage trajectory of immune activation, exhaustion, and stromal takeover.
This study demonstrates that circadian disruption drives pulmonary metastatic colonization by eliminating the temporal segregation of pro-metastatic signals, thereby enabling the constitutive convergence of TNF-, TGF-β-, and YAP/TEAD-mediated pathways to induce epithelial-to-mesenchymal transition and extracellular matrix remodeling, a mechanism validated in mouse models and conserved in human metastatic melanoma.