Browse our latest Cancer Biology articles

More than 30 published articles have suggested that a protein kinase called MELK is an attractive therapeutic target in human cancer, but three recent reports describe compelling evidence that it is not.

Proteomics and functional genomics coupled to an antibody discovery pipeline revealed the influence of oncogenic RAS signaling on the cell-surface proteome and resulted in the discovery of potential therapeutic targets for RAS-driven cancers.

Antitumor (natural killer) NK cell responses are negatively regulated by interactions between NK cells and endogenous NKG2D ligands constitutively expressed on lymph node endothelial cells and super-induced on tumor-associated endothelium.

A novel RNA-based trans-regulatory system that control gene expression in mammalian cells has been developed and they can be coupled to endogenous signals.

Loss of BAP1 function is associated with increased sensitivity to TRAIL and other death receptor agonists in malignant mesothelioma, where this is a frequent event, with immediate and actionable therapeutic implications.

Driving melanoma differentiation through G protein-coupled estrogen receptor signaling decreases proliferative capacity, decreases expression of the oncodriver and stem cell marker c-Myc, and increases the effectiveness of immunotherapy.

Harnessing female sex hormones may improve how all patients with melanoma respond to treatment.

The transcription factor c-Myc amplifies the transcription of many growth-related genes in cancer cells, but its role as an oncogene is not fully understood.

Editors' Summary: This Replication Study has reproduced some parts of the original paper but other parts could not be interpreted.

A c-Myc-transcribed long noncoding RNA namely LAST (LncRNA-assisted stabilization of transcripts) collaborates with a cellular factor CNBP to promote the stability of CCND1/cyclin D1 mRNA post-transcriptionally, ensuring the proper G1/Sphase transition of the cell cycle.