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 demonstrates that the chromatin-remodeling protein CHD4 is essential for Foxp3+ Treg cell stability and function, and that its pharmacological inhibition selectively disrupts tumor-associated Tregs to enhance anti-tumor immunity without causing systemic autoimmunity.
This study demonstrates that the long non-coding RNA SOX2OT promotes non-small cell lung cancer progression and metastasis by suppressing miR-143, thereby activating oncogenic pathways and inhibiting tumor suppressors like PTEN, which suggests that targeting the SOX2OT/miR-143 axis offers a promising therapeutic strategy.
This study identifies lysyl oxidase (LOX) as a critical driver of clear cell renal cell carcinoma progression that sustains the HIF-2α transcription program by stabilizing the protein and simultaneously remodels the tumor microenvironment, making it a promising therapeutic target even in cases resistant to current HIF-2α inhibitors.
This study demonstrates that deleting ferritin heavy chain in medulloblastoma creates a therapeutic vulnerability by lowering the threshold for iron toxicity, thereby sensitizing tumor cells—particularly mesenchymal-like subtypes—to iron-dependent cell death and growth inhibition without relying on iron deprivation.
This study demonstrates that microbial riboflavin metabolites, specifically 5-OP-RU and 5-OE-RU, act as potent pharmacologic activators of MR1-restricted MAIT cells to drive cytotoxicity, remodel the immunosuppressive tumor microenvironment, and suppress solid tumor growth, particularly in liver cancer models.
Using single-cell RNA sequencing and functional studies in a triple-negative breast cancer mouse model, this paper reveals that metastatic competence arises from early lineage disruption followed by parallel ERK1/2-low and ERK1/2-high regulatory programs that generate distinct hybrid and mesenchymal-like cell states, rather than converging on a single metastatic phenotype.
This study develops and validates a 30-gene transcriptional signature that identifies functional LKB1 loss driven by non-genomic mechanisms across diverse human cancers, revealing a therapeutically addressable patient population nearly four times larger than that defined by genomic alterations alone and characterized by immune evasion.
This study identifies DUSP15 as a highly selective chromophobe renal cell carcinoma epithelial biomarker that distinguishes the tumor type with high diagnostic accuracy and defines a unique immune-metabolic state characterized by enhanced oxidative phosphorylation and depleted immune infiltration.
By integrating large-scale genetic dependency maps with multivariate analysis of chromatin complexes, this study identifies a melanoma-enriched epigenetic vulnerability on the Set1C/COMPASS complex, revealing that its inhibition suppresses MYC- and E2F-driven transcriptional programs essential for tumor proliferation.
This study identifies WNT11 as a context-dependent tumor suppressor in human epithelial cancers that inhibits cancer stemness, invasion, and tumor formation by inactivating RAC1, thereby providing a mechanistic explanation for its previously ambiguous and opposing roles in cancer.