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 reveals that cancer cells develop resistance to doxorubicin by accumulating recurrent mutations at topoisomerase II cleavage sites to prevent drug-induced DNA damage, a mechanism that simultaneously sensitizes the adapted cells to topoisomerase I inhibitors.
Using ultra-deep duplex sequencing, this study reveals that the germline TP53 p.R181H variant in Li-Fraumeni syndrome reshapes baseline somatic mutation patterns and selection dynamics in normal tissues, characterized by increased mutagenesis, reduced positive selection for somatic TP53 mutations, and a distinct preference for mutations occurring on the wild-type chromosomal copy.
The paper introduces cfClone, a Bayesian framework that integrates single-cell whole-genome sequencing with circulating tumor DNA data to enable high-resolution, tissue-informed, and uncertainty-aware tracking of clonal evolution and therapeutic resistance without relying on bulk tissue references.
This study establishes an experiment-anchored abundance coverage frontier that defines conditional RHSVV exposure requirements for TP53-missense tumors by analyzing 809 tumor and 523 normal specimens to identify a pragmatic R≥3 abundance threshold, while explicitly noting that actual therapeutic efficacy and safety remain unmeasured.
This study utilizes single-nucleus RNA sequencing on archival human melanoma metastases from the brain, liver, and lung to construct a multi-organ atlas revealing distinct malignant differentiation states and organ-specific immune and stromal adaptations that define the heterogeneity of the tumor microenvironment across distant sites.
This study reveals that urothelial cancer cells evade terminal differentiation despite expressing master transcription factors because genomic alterations disrupt the balance between chromatin-opening coactivators and chromatin-closing corepressors within the transcriptional hub, a blockage that can be reversed by restoring coactivators or inhibiting corepressors to reactivate differentiation programs.
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.