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.
This study demonstrates that depleting the oncogenic factor HSF1 in malignant cells triggers a catastrophic proteomic imbalance and amyloidogenesis that can be exploited for tumor suppression, whereas HSF1 is dispensable for non-transformed cells, highlighting a novel therapeutic strategy to combat malignancy by provoking proteomic catastrophe.
This study demonstrates that canonical NF-κB signaling constrains RAS-driven B-cell acute lymphoblastic leukemia by inducing a mature B-cell receptor state incompatible with oncogenic RAS activity, thereby triggering apoptosis in RAS-mutated cells and explaining the mutual exclusivity of these pathway alterations in leukemia.
This study evaluates the clinical feasibility of evolutionary therapy for metastatic non-small cell lung cancer by demonstrating that while higher containment levels and dynamic protocols can improve outcomes, their success critically depends on minimizing measurement errors and appointment delays, with single-bound protocols proving more robust to these real-world clinical constraints.
This study presents fucoidan-based nanoparticles (SMNPs) that selectively target P-selectin-expressing pathogenic senescent cells to ameliorate fibrosis, reverse immune exclusion, and sensitize tumors to immunotherapy by modulating immune-suppressive macrophages.
This study presents a single-cell framework that leverages temporal delays between mRNA and protein accumulation to identify cancer cell-state transitions, revealing a molecular program linking cell-cycle progression and mitochondrial remodeling to plasticity that serves as a robust prognostic and predictive biomarker across multiple tumor types.
This paper introduces SPICE, a novel framework that deconvolves somatic copy-number alteration profiles into discrete evolutionary events to model focal selection, thereby identifying 460 cancer-relevant loci and expanding the understanding of mutational processes and selective forces in cancer genomes.
This study proposes a pathogen-driven model of colorectal carcinoma where Neuro-Immune Crypt-Associated (NICA) cells serve as a cellular origin, EBV-infected B-lineage cells induce HERV-H/F expression via paracrine signaling, and compromised antiviral surveillance allows these viral elements to persist, collectively redefining CRC as a disruption of the neuro-immune niche driven by chronic inflammatory pressure.
This study reveals that the MYC-ATF4-ASS1 axis in melanoma regulates intracellular arginine synthesis and shapes the tumor immune microenvironment, thereby determining tumor sensitivity to arginine-depleting therapies and enhancing CD8+ T cell-mediated antitumor immunity.
This study integrates experimental findings into a nonlinear dynamical model to demonstrate that p53 restoration suppresses retrotransposon-driven chromosomal instability by triggering a threshold-dependent collapse in L1 burst frequency via a let-7 feedback loop, thereby significantly reducing structural genome rearrangements in early tumorigenesis.
This study demonstrates that inhibiting mSWI/SNF chromatin remodeling complexes, specifically with the SMARCA4/2 inhibitor FHD-286, reverses epithelial-mesenchymal transition-mediated resistance and synergistically enhances the efficacy of KRAS inhibitors in KRAS-mutant non-small cell lung cancer.