256 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 systematically demonstrates that while ferroptosis induction via the GPX4 axis fails to impact established tumors in vivo, inhibiting cytosolic thioredoxin reductase or GCLC triggers potent tumor regression through a distinct, non-ferroptotic cell death mechanism, revealing that standard cell culture models significantly overestimate the therapeutic potential of ferroptosis.
This study establishes a mutation-resolved therapeutic atlas for NRAS-mutant melanoma using a saturation mutagenesis screen, revealing that tri-complex RAS(ON) inhibitors exhibit genotype-selective efficacy across most variants while identifying adaptive STAT3 signaling as a critical resistance mechanism that can be targeted to enhance therapeutic outcomes.
This preclinical study demonstrates that combining the menin inhibitor ziftomenib with the XPO1 inhibitor selinexor synergistically suppresses oncogenic transcription and induces apoptosis in KMT2A-rearranged and NPM1-mutated AML by disrupting menin-chromatin interactions, thereby offering a promising strategy to overcome resistance and improve survival outcomes compared to monotherapy.
This paper extends an individual-based cancer invasion model by incorporating stochastic, force-dependent N-cadherin bond lifetimes fitted to Gamma distributions, thereby linking adhesion dynamics to cell motility and proposing a framework for pattern formation.
This study demonstrates that the pan-Ras tricomplex inhibitor daraxonrasib acts as a pharmacologic GAP mimetic to restore GTPase activity, thereby synergizing with Switch-II pocket inhibitors like adagrasib to enhance K-Ras engagement, accelerate pathway suppression, and improve therapeutic efficacy in mutant cell lines.
This study demonstrates that lipid-rich ascites in ovarian cancer drives T cell dysfunction by altering lipid metabolism, and that removing these lipids restores T cell activation and enhances the efficacy of bispecific T cell engager (BiTE) therapy.
This study demonstrates that engineering a novel anti-FAP single-domain antibody (VHH) into monomeric, dimeric, and Fc-fusion formats allows for the tuning of pharmacokinetic properties to optimize tumor uptake, retention, and radiation dosimetry for improved cancer theranostics targeting fibroblast activation protein.
This study demonstrates that a non-destructive, single-cell Raman spectroscopy approach combined with machine learning can accurately differentiate melanoma cell phenotypes and predict therapeutic resistance to targeted and immunotherapies in both cell lines and patient-derived samples, offering a rapid and scalable tool for precision medicine.
This study identifies the absence of the tumor suppressor AT2R as a key marker for chemotherapy-resistant leukemic stem cells in acute myeloid leukemia, demonstrating that epigenetic silencing of AT2R drives disease progression through fatty acid metabolism and that its pharmacological activation with the agonist buloxibutid (C21) effectively inhibits leukemogenesis and enhances chemotherapy efficacy.
This study reports the development and preclinical validation of a shark-derived VNAR-based theranostic agent, vMET1-Fc, which enables high-contrast PET imaging and effective targeted radiotherapy for MET-altered non-small cell lung cancer with a favorable safety profile.