While intact mir-17-92 acts as a potent oncogene in a mouse model of Burkitt’s lymphoma, one of the six mir-17-92 components antagonizes its oncogenic cooperation with c-Myc by promoting c-Myc-induced apoptosis.
Spontaneous growth arrest of transformed melanocytes (resulting in benign “moles”) does not result from cell-autonomous oncogene-induced senescence, but can be explained by collective mechanisms used in normal tissue size control.
The basic helix-loop-helix transcription factor, HES3, acts downstream of the PAX3-FOXO1 fusion oncogene to impair muscle differentiation and promote tumorigenesis in rhabdomyosarcoma, a childhood muscle cancer.
Skin epithelium can tolerate oncogene-expressing clones through a novel cellular mechanism of inter-clonal competition between renewing progenitors along the clone's edge and differentiating progenitors within the clone's core.
HNF1A, a risk factor gene for pancreatic ductal adenocarcinoma, is critical to maintaining pancreatic cancer stem cell properties through regulating POU5F1 (OCT4) expression, providing a novel role for HNF1A in maintenance of the disease.