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 identifies stromal-derived Prostaglandin E2 as a dominant spatial regulator that drives colorectal cancer cell-fate plasticity by converting chemosensitive DACH1+ stem cells into chemorefractory, prometastatic states, a process that can be reversed by inhibiting stromal COX2.
By applying the novel CardamomOT framework to single-cell RNA-seq data from neuroblastoma tumoroids, this study infers a dynamic gene regulatory network that identifies *tcf4* as a critical hub whose inhibition via BET drugs alters cell fate proportions, thereby revealing new therapeutic avenues for this pediatric cancer.
This study reveals that the complex, patient-specific DNA methylation patterns in leukemia are not random but are orchestrated by reproducible, genome-wide epigenetic networks that transcend individual mutations, extend across diverse cancer types, and share underlying regulatory mechanisms with non-malignant cells.
By performing TCRbeta sequencing on paired primary melanomas and sentinel lymph nodes from 24 patients, this study reveals that tumors exhibit reduced diversity and clonal dominance with patient-specific antigen recognition, while distinct spatial TCR architectures and limited shared clonotypes highlight the unique organization of anti-tumor immunity across these compartments.
This study identifies septin-2 overexpression in ovarian cancer and demonstrates that the small molecule UR214-9 disrupts canonical septin hetero-octamer assembly to induce aberrant higher-order structures, thereby inhibiting cancer cell proliferation and migration while showing efficacy and safety in xenograft models across multiple cancer types.
This study demonstrates that the PET radiotracer [18F]FSPG serves as a non-invasive, real-time imaging tool to detect early redox remodeling linked to ferroptosis and monitor immunotherapeutic efficacy in cancer.
This study demonstrates that a genetically engineered murine osteosarcoma model faithfully recapitulates the complex genomic rearrangements, structural variant landscape, and key driver alterations (such as *Myc* amplification and *PTEN* loss) observed in human osteosarcoma, thereby providing a robust preclinical platform for investigating tumor evolution and therapeutic development.
This study utilizes spatial transcriptomics and single-cell profiling to reveal that chemoradiotherapy-resistant residual esophageal squamous cell carcinoma is characterized by a spatially organized microenvironment featuring SPP1+ macrophage accumulation, microvascular rarefaction, and immune exclusion, which collectively drive treatment resistance and predict poor patient survival.
Using engineered murine colorectal cancer organoids, this study demonstrates that while specific combinations of Kras, Apc, and Trp53 mutations drive tumor growth, the temporal order of these mutations critically influences tumorigenic potential, particularly by altering immunological features and reducing tumor formation in immunocompetent hosts when Trp53 loss precedes Apc inactivation.
This study demonstrates that the loss of Kindlin-1 in cutaneous squamous cell carcinoma disrupts the coupling between extracellular matrix organization and vascular architecture, leading to a dysfunctional, dense vascular network and persistent hypoxia that drives tumor progression.