Browse our latest Cancer Biology articles

The ISR kinase GCN2 is critical for maintaining tumor amino acid levels to facilitate growth, suggesting a novel therapeutic strategy for the treatment of prostate cancer by inducing starvation for essential amino acids.

In vivo and in vitro experiments confirm the conspicuous antineoplastic efficacy of NIR-III photothermal therapy under the premise of ensuring biosafety.

Novel variants in the BRC repeat region of BRCA2 were identified and comprehensively characterized as either deleterious or benign.

Imaging studies of connexin-coupled networks of colorectal cancer cells reveal that cells carrying a genetic defect in an essential metabolic pathway can be rescued by diffusive exchange with neighboring wild-type cells via gap junctions, particularly Cx26, thereby evading negative selection.

Unbiased proteomics and molecular analysis revealed a new role for S6K1 in regulating DNA repair through the orchestrated phosphorylation of CDK1 and MSH6. The findings may explain why RPS6KB1 gene amplification contributed to breast cancer drug resistance.

An original molecular multi-step approach integrating DNA methylome and chromosome-cluster localization cross-analysis identified a DNA methylation signature of patient outcome supporting that the core DNA methylation for a given trait is independent of the physiological context under which it arises.

Arbidol is a ATR inhibitor to reduce the phosphorylation and activation of MCM2 at Ser108, and innhibits the cell proliferation of ESCC in vitro and in vivo through the DNA replication and cell cycle pathway.

RNA-level regulation of gene expression is negatively associated with protein-level regulation across cellular pathways in normal tissues and cancer.

Tumors escape killing by the immune system through generating transient spatial cell-in-cell structures that are impenetrable to cytotoxic compounds including lytic granules and chemotherapy.

Interplay between AML and stromal cells can initiate a mechanism involving gap junctions where ROS is transferred from cancer cells to stromal cells which then produce acetate which can in return be absorbed/utilised by the cancer cells.