Presentation description

PTEN is the second most commonly mutated tumor suppressor in cancer, and it encodes a phosphatase with dual activity against lipids and proteins. We have observed that PTEN loss cooperates with activated AKT1 to enhance brain metastasis in our melanoma mouse models. This project aims to determine if this cooperation occurs through loss of PTEN lipid, protein, or non-enzymatic functions by utilizing in-vivo mouse models where we introduce mutant forms of PTEN and assess the effect on metastasis.