298 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 introduces BioBombe, an AI/ML framework that analyzes DepMap data to identify complex gene process dependencies beyond single-gene targets, thereby revealing novel cancer vulnerabilities and enabling the prediction and validation of effective drug candidates for precision oncology.
This study demonstrates that in non-small cell lung cancer, the initial proportion of resistant cells critically determines the fitness consequences of resistance evolution and treatment efficacy, suggesting that personalized evolutionary therapy strategies should account for both the abundance and the dynamic fitness effects of resistant subpopulations rather than relying solely on maximum tolerated dosing.
This study identifies a reciprocal positive-feedback loop between the deubiquitinase USP15 and the oncogenic transcription factor ZNF217 that stabilizes ZNF217 to drive ovarian cancer progression and therapeutic resistance, suggesting that targeting USP15 offers a viable indirect strategy to suppress ZNF217-driven malignancies.
This study demonstrates that a human 3D neural tissue model derived from L-Myc immortalized neural stem cells effectively recapitulates chemotherapy- and radiation-induced neurotoxicity, while showing that extracellular vesicles derived from these cells promote neuroprotection and restore transcriptional programs associated with inflammation, stress, and metabolism.
This study demonstrates that cancer-associated fibroblasts in male breast cancer exhibit distinct transcriptional and functional profiles compared to those in females, leading to denser extracellular matrices and altered vascular organization, thereby highlighting the critical need to integrate biological sex into precision oncology strategies.
This study analyzes 5,528 samples across eight cancer types using seven epigenetic clocks to reveal that tumor tissues generally exhibit significant age acceleration and shared methylation remodeling compared to normal tissues, while highlighting notable heterogeneity and specific exceptions such as the uterus cohort.
This study utilizes TruSeq methyl capture sequencing on the UK Prostate ICGC cohort to identify novel methylation-based molecular signatures—including patterns in driver genes, strand-specific methylation, and mitochondrial reads—that effectively distinguish cancerous from benign tissue and serve as independent predictors of prostate cancer relapse.
This study identifies ABCB1-mediated drug efflux as the primary mechanism of resistance to VpreB1-targeted calicheamicin antibody-drug conjugates in B-cell acute lymphoblastic leukemia and demonstrates that this resistance can be overcome by combining the ADCs with ABCB1 inhibitors or by utilizing non-ABCB1 substrate payloads.
This study demonstrates that elevated APOBEC3B mRNA expression in breast cancer correlates with specific mutational signatures and is associated with reduced tamoxifen activation via downregulated CYP enzymes, alongside downregulated pyrimidine metabolism genes that may create therapeutic vulnerabilities to pyrimidine-based chemotherapies.
This study demonstrates that the impact of ARID1A loss on gastric cancer immunity is not intrinsic but strictly determined by tumor context, as it drives immune evasion in vivo through GM-CSF suppression and interferon-gamma resistance in genomically stable subtypes, whereas in vitro deletion or loss in chromosomal instability subtypes fails to produce the same immune-cold phenotype.