Single Copies of Mutant KRAS and Mutant PIK3CA Cooperate in Immortalized Human Epithelial Cells to Induce Tumor Formation

Abstract excerpt

The selective pressures leading to cancers with mutations in both KRAS and PIK3CA are unclear. Here, we show that somatic cell knockin of both KRAS G12V and oncogenic PIK3CA mutations in human breast epithelial cells results in cooperative activation of the phosphoinositide 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways in vitro, and leads to tumor formation in immunocompromised mice....

Topics

Share this publication in a Topic to start or enrich a Post.

• Share to Cancer-related Molecular Pathways
• Share to PI3K/AKT/mTOR signaling in cancer
• Share to Ubiquitin and proteasome pathways