In a study from the Johns Hopkins Kimmel Cancer Center, researchers described a novel mechanism of tumor formation in kidney cancers driven by overexpression of the mechanistic target of rapamycin complex 1 signaling pathway with loss of the tuberous sclerosis complex tumor suppressor gene.
A genetic mutation that fuses two genes drives several cancer types by forming networks of protein interactions that alter gene expression in cells, a study by UT Southwestern Medical Center researchers suggests.
