161 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 ultra-rapid FLASH radiotherapy significantly reduces radiation-induced oral mucositis and DNA damage in both wild-type and Fanconi anemia-deficient mice compared to conventional radiotherapy, suggesting a promising normal tissue-sparing approach for treating head and neck cancers in patients with Fanconi anemia.
Using Oxford Nanopore long-read sequencing on 71 human samples, this study characterizes the alternative splicing landscape of acute myeloid leukemia and myelodysplastic syndrome, identifying over 174,000 novel translated isoforms and spliceosome-mutant-enriched transcripts while providing a valuable community resource for exploring these splicing patterns.
This study reveals that de novo lipogenesis drives metastatic immune evasion in triple-negative breast cancer by promoting FASN-mediated EGFR palmitoylation, which sustains a lipid-dependent PI3K-AKT-mTOR signaling axis to suppress MHC-I antigen presentation and enable CD8+ T cell escape, a process that can be reversed by inhibiting FASN to restore anti-tumor immunity and block lung metastasis.
This study demonstrates that the choice of isolation method (ultracentrifugation, size exclusion chromatography, or EXODUS nanofiltration) significantly alters the protein composition and purity of cancer-associated fibroblast extracellular vesicles, proving that MISEV2023 compliance alone does not guarantee biological equivalence and that isolation protocols must be treated as critical biological variables.
This study identifies argininosuccinate synthase (ASS1) deficiency as a defining metabolic vulnerability in Philadelphia chromosome-positive acute lymphoblastic leukemia that renders the disease dependent on extracellular arginine, thereby establishing arginine deprivation with pegargiminase as an effective monotherapy and a potent strategy to overcome tyrosine kinase inhibitor resistance.
This study utilizes mirror-image mRNA display to discover stable, all-D macrocyclic peptides that selectively target a cryptic back pocket on KRAS, offering a novel, isoform-specific therapeutic mechanism distinct from existing switch-II pocket inhibitors.
This study demonstrates that reactivation of the mitochondrial fission protein DRP1, driven by a c-Myc-CDK6 signaling axis, mediates resistance to MEK inhibitors in pancreatic cancer, suggesting that targeting mitochondrial fission could overcome therapeutic resistance.
This study introduces a Composite Driver Score (CDS) framework to systematically prioritize exosomal proteins in triple-negative breast cancer, revealing a coordinated extracellular matrix invasion module and identifying Agrin as a high-priority therapeutic and diagnostic target.
This study reveals that aging-associated macrophage deregulation, characterized by attenuated STAT6-mediated oxidative phosphorylation programs, drives the formation of tumor-like multinucleated syncytia in metastatic cancers, a process that can be modulated by targeting the STAT6-EP2 axis.
This study demonstrates that combining the xanthine oxidase inhibitor febuxostat with 2-fluoroadenine and 5-methylthioadenosine overcomes the limited in vivo efficacy of the original drug pair by preventing 2-fluoroadenine degradation, thereby significantly enhancing tumor regression in MTAP-deleted cancers.