220 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 glioblastoma invasion in human brain organoids causes profound and persistent dysfunction in GABAergic neurons, specifically through the loss of SLC12A5/KCC2 expression and chloride homeostasis, which remains uncorrected even after temozolomide chemotherapy.
This study utilizes integrated multi-omic analysis of pediatric metastatic osteosarcoma to reveal significant cellular plasticity, demonstrating that endothelial cells adopt osteoblast-like features and that tumor cells exhibit vascular mimicry, thereby challenging current models of the disease's biology and microenvironment.
This study utilizes a clinically calibrated, temporally resolved in vitro model of osteosarcoma to map the evolution of chemoresistance and identify distinct patterns of collateral drug sensitivity, while simultaneously extracting predictive transcriptomic signatures to guide personalized second-line treatment strategies for relapsed or refractory patients.
This study identifies Siglec-15 as a critical glyco-immune checkpoint in prostate cancer that drives immune evasion and bone metastasis by promoting immunosuppressive macrophage and osteoclast differentiation, while demonstrating that therapeutic blockade of Siglec-15 restores CD8+ T-cell responses and inhibits tumor growth in preclinical models.
This study introduces the 3DisoGalaxy atlas to demonstrate that alternative splicing in breast cancer significantly expands the translated proteome by coupling conserved protein structural cores with extensive remodeling of regulatory domains and motifs, particularly within cancer-driver genes.
This study identifies CPA4 as a direct YAP-TEAD transcriptional target that drives NF2-deficient meningioma growth and serves as a potential biomarker for tumors responsive to TEAD inhibition.
By establishing a human B-cell differentiation platform to model inherited risk variants, this study reveals that diverse familial predisposition genes converge on delaying early B-cell development during high RAG activity, thereby increasing the risk of illegitimate recombination and subsequent leukemia transformation.
This study employs a single-cell multiomic framework to map genetic predisposition to childhood B-cell acute lymphoblastic leukemia, identifying 34 high-confidence susceptibility genes and functionally validating ELK3 as a novel regulator of B-cell development and leukemogenesis.
This study reveals that cancer cells acquire resistance to KIF18A inhibitors through two distinct mechanisms—either partially overriding the spindle assembly checkpoint or adapting microtubule dynamics—while identifying specific genetic contexts, such as reduced PP2A or APC/C activity, that create exploitable vulnerabilities to enhance therapeutic efficacy.
This study identifies the long non-coding RNA PURPL as a recurrent copy number alteration and expression biomarker associated with adverse clinical outcomes in Luminal A breast cancer, particularly in TP53 wild-type tumors, suggesting its potential as a prognostic marker for this generally favorable subtype.