Transcription beyond annotated gene boundaries expands the diversity of the cancer transcriptome with overexpressed oncogenes and RNA chimeras.

The temporal patterns of MAPK activity differentially regulate cell autonomous and non-cell autonomous effects of oncogene expression.

Co-mutation of two powerful oncogenes in certain cell types may have a lethal effect that explains the mutual exclusivity of the mutations.

G alpha q/11 signaling can either promote or inhibit melanocyte growth through a reversible switch that is controlled by the microenvironment and that shapes the mutational diversity of melanoma subtypes.

Src, an oncogene, promotes both cell proliferation and cell death simultaneously, which can be regulated by dietary methionine.

FOXP2, encoding a forkhead-box transcription factor regarded as vital to proper development of human speech, was revealed to have an oncogenic potential and activate MET signaling in prostate cancer.

Altering the level of different oncogenic mutants of Kras induces unique tumor patterns in mice, suggesting that tissue-specific responses mold the sensitivity of normal tissues to different oncogenic RAS mutations.

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.

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.

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.