Interaction of oncoprotein transcription factor MYC with chromatin-associated protein host cell factor–1 controls expression of genes important for ribosome biogenesis and mitochondrial vigor, loss of which promotes tumor regression.

Differences in promoter affinity and MYC levels explain distinct expression profiles induced by physiological and oncogenic MYC.

MYC and Twist1 drive metastasis by a novel non-cell-autonomous transcriptional mechanism of eliciting a cytokinome that mediates the crosstalk between cancer cells and macrophages, and its therapeutic blockade inhibits metastasis.

Myc-dependent induction of amino acid transporter expression in response to T cell receptor activation is essential to enable T cell proteome remodelling upon immune activation.

A new potent and selective CDK9 inhibitor induces the expression of the proto-oncogene MYC via a mechanism that depends on the bromodomain protein BRD4.

Epstein-Barr virus controls B-cell growth and survival through large-scale reorganization of the enhancers of the MYC and BCL2L11 genes, and may promote MYC translocations as a result.

Single molecule mRNA imaging uncovers post-transcriptional regulation of myc mRNA, via a cell-intrinsic mechanism allowing individualised control of neural stem cell proliferation during Drosophila brain development.

Protein kinase A-driven increases in c-MYC protein expression and tumor cell proliferation can be blocked by eIF4A inhibitors, suggesting a potential new treatment option for patients with oncogenic PKA activation.

Deletion and small-molecule inhibition of ubiquitin-specific protease 28 destabilizes the oncogenes c-MYC, c-JUN, and Δp63, and elicits regression of squamous cell lung carcinoma, a major cancer type with currently limited treatment options.

MYCN and TFIIIC exert a censoring function during early transcription, limiting the accumulation of inactive RNAPII at the promoter and facilitating promoter-proximal degradation of nascent RNA.