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 re-engineering prostate cancer cells to express rat CMAH induces Neu5Gc presentation on cell-surface glycans and reveals a bystander effect where Neu5Gc is transferred to neighboring cells, potentially propagating immune suppression within the tumor microenvironment.
This study demonstrates that supplementation with the naturally occurring lipid FuFA-F2 effectively prevents tumor-induced skeletal muscle atrophy and preserves muscle function in a cancer cachexia mouse model by attenuating inflammatory, catabolic, and fibrotic pathways without affecting tumor growth.
This study reveals that interferon gamma drives acute myeloid leukemia growth by triggering a paradoxical intraclonal fate bifurcation where leukemic stem cells deepen their quiescent stemness while progenitor cells undergo rapid but transient differentiation, ultimately enabling long-term disease regeneration despite inflammatory challenges.
This study identifies a specific panel of myeloid lectins associated with immunosuppressive tumor-associated macrophages in breast cancer and demonstrates that pharmacologically targeting their shared SYK signaling node effectively remodels these macrophages to reduce immunosuppression.
This study identifies and characterizes specific long non-coding RNAs, including the pan-cancer regulator CAMOR, that are driven by major oncogenic mutations (MYC, KRAS, TP53) and functionally promote carcinogenesis across colorectal, lung, and pancreatic cancers, thereby offering new potential diagnostic and therapeutic targets.
This study utilizes cross-species analysis of a mouse model and human tissues to demonstrate that cell-cell communication rewiring, specifically driven by NOTCH2 overexpression, is a conserved early event in serous endometrial carcinogenesis that promotes tumor progression and correlates with poor patient survival.
This study demonstrates that patient-derived brain tumor models faithfully recapitulate the molecular and histological heterogeneity of primary tumors, enabling the identification of Stearoyl-CoA Desaturase1 (SCD1) as a promising biomarker and therapeutic target for precision immunotherapy in glioma.
This study identifies that multiple STAG2 mutations in myeloid neoplasms, particularly myelodysplastic syndromes (MDS), arise through convergent evolutionary targeting rather than stepwise allelic inactivation, defining a distinct high-risk subset characterized by increased multilineage dysplasia and inferior overall survival.
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.