When PI3K (phosphatidylinositol 3 kinase) is activated by receptor tyrosine kinases, itphosphorylates PIP2 to generate PIP3 and activates the signaling pathway. PTEN (phosphataseand tensin homologue deleted on chromosome 10) dephosphorylates PIP3 to PIP2, and thus, negatively regulates the pathway. AKT (v-akt murine thymoma viral oncogene homolog; Proteinkinase B) is activated downstream of PIP3 and mediates physiological processes. Furthermore, substantial crosstalk exists with other signaling networks at all levels of the PI3K pathway. Because of its diverse array gene mutations and amplifications and also as a consequence of itscentral role in several signal transduction pathways, the PI3K-dependent axis is frequentlyactivated in many tumors and is an attractive therapeutic target. The preclinical testing andanalysis of these novel therapies requires appropriate and well-tailored systems. Mouse models inwhich this pathway has been genetically modified have been essential in understanding therole this pathway plays in the tumorigenesis process. Here, we review cancer mouse models inwhich the PI3K/AKT pathway has been genetically modified.
Carnero, A., & Paramio, J. M. (2014). The PTEN/PI3K/AKT Pathway in vivo, cancer mouse models. Frontiers in Oncology, 4(SEP). https://doi.org/10.3389/fonc.2014.00252