Browse our latest Cancer Biology articles

A large-scale single-cell RNA sequencing experiment explores single-cell dynamics in epithelial and immune populations within murine prostates upon cancer initiation and progression and validates key findings across orthogonal models and patient specimens.

Overexpression of VPS9D1-AS1 is a lncRNA to activate TGF-β and IFN signaling pathways, regulates crosstalk between cancer cells and T lymphocytes in the tumor microenvironment.

Comprehensive transcriptomic analyses describe the underlying tumorigenic gene expression state in the invasive Drosophila follicle cells following the loss of epithelial cell polarity and identify a non-canonical role of Keap1-Nrf2 signaling in regulating collective cell invasion.

Non-coding RNAs appear to be good candidates as biomarkers for predicting treatment response and therapeutics for sarcoma, their differential expression across tissues complicates their application.

A proportion of glioblastoma with global hypo-methylation are enriched for an astrocytic signature and display increased invasion and altered immune landscape.

Among multiple myeloma stratified by Revised International Staging System, single-cell transcriptome atlas reveals novel heterogeneities with NKG7+ cytotoxic plasma cells (PCs) enriched in stage II, RRM2+ high proliferative PCs enriched in stage III, and MKI67 up-regulated in EBV-positive patients.

The identification of alternative splicing targets and upstream RNA-binding proteins that underlie EMT and metastasis in colon cancer stratifies patients according to their overall survival and provide new insights on the function of specific isoforms along the migrating cancer stem cell sequence.

Mutual suppression of ETV1 by Capicua (CIC) and ETS2 repressor factor (ERF) limits prostate cancer progression.

Analyzing how gene interaction networks are perturbed in individuals can help identify different types of colorectal cancers, paving the way towards personalized care.

Cellular and molecular analyses of human AML cells reveal a novel pathway activated by the bone marrow microenvironment that confers resistance to FLT3 inhibition and can be exploited to improve the efficacy of FLT3 inhibitor therapy for AML.