by Meredith Jackson
Renal cell carcinoma (RCC) is an aggressive form of kidney cancer that tends to recur even after treatment with targeted cancer therapies or immunotherapies.
One commonly mutated pathway in RCC and in all cancers is the PI3K-AKT signaling axis. P13K and AKT enzymes play key roles in multiple cellular processes including cell proliferation and migration.
A recent study found that RCC cells with mutations in another enzyme-encoding gene, SETD2, were sensitive to a drug that inhibits the enzyme PI3K-beta.
Reporting last month in the journal Oncotarget, Kimryn Rathmell, MD, PhD, and colleagues found that cancer cells in which SETD2 had been inactivated exhibited decreased growth, survival and migration when treated with PI3K-beta inhibitors compared to cancer cells with functional SETD2. Similar treatments were able to significantly reduce tumor growth in mice with SETD2-deficient tumors.
The findings reveal the “tantalizing” therapeutic potential of applying precision medicine to target cells that are mutated for SETD2 using PI3K pathway inhibitors for improved RCC therapies.
The research was supported by the National Institutes of Health (grants CA203012, CA198482, CA231993, CA119925, CA009156, GM007347, CA090625), the Conquer Cancer Foundation of ASCO Young Investigator Award and a Komen Post-Doctoral Award.
