Marino Schuhmacher

TL;DR: Serial analysis of gene expression has identified the cyclin-dependent kinase 4 (CDK4) gene as a transcriptional target of c-MYC, and it is shown that CDK4 provides a direct link between the oncogenic effects of c -MYC and cell-cycle regulation.

TL;DR: The identification of potential Myc target genes in a human B cell line that grows and proliferates depending on conditional myc expression support the current view that myc acts as a master gene for growth control and increases transcription of a large variety of genes.

TL;DR: It is shown that division of P493-6 cells was strictly dependent on the expression of the conditional myc allele and the presence of foetal calf serum, and direct evidence is provided that Myc induces cell growth, that is, an increase in cell size, uncoupled from cell division.

TL;DR: It is suggested that myc triggers proliferation of P493‐6 cells by promoting the expression of a set of cell cycle activators but not by inactivating cell cycle inhibitors.

TL;DR: Using a cell line in which EBNA2 and c‐myc can be regulated at will, c‐MYC negatively regulates STAT1, the central player linking the Type‐I and Type‐II interferon response, and implies that immune escape of tumor cells is not only a matter of in vivo selection but may be additionally promoted by activation of a cellular oncogene.