In addition to its role in regulating proliferation and cell death, the PTEN tumor suppressor regulates epithelial morphogenesis through the PDK1 kinase.
Evolution of tumor suppressor genes can involve a trade-off because the acquisition of certain anti-cancer characteristics diminishes the ability to regenerate damaged tissue.
Reduced expression of MYBL2 contributes to malignancies of the blood by permitting uncontrolled expansion of blood cell progenitors, implying a tumor suppressor function for this gene.
Nutrient limitation elicits differential responses in cells lacking the tumor suppressor PTEN and in normal cells, resulting in hyperplastic overgrowth of PTEN mutant tissue independent of additional mutations.
Major secondary tumor suppressors in kidney cancer are required to maintain the activity of a tumor suppressive transcription factor after the loss of the primary tumor suppressor VHL.
The chromatin remodeler and tumor suppressor SMARCB1 acts to restrict superenhancer function to direct neural differentiation of embryonic stem cells while repressing bivalent gene activity in the pluripotent state.
The first global analysis of the effects of the transcription factor p53 on RNA synthesis illuminates several novels aspects of the molecular mechanism of action of this potent tumor suppressor.
