PTEN is a tumor suppressing protein that carries out important cell functions such as inhibiting cell growth and promoting genomic stability. Somatic variants of PTEN can lead to cancer, and PTEN mutational status has shown to be an indicator of patient survival and prognosis. However, it is not clear whether cancer-associated PTEN variants affect cell growth, genome stability, or both. Here, we demonstrate that simple competition assays can quantitatively assess PTEN variants for their effect on these two important cellular functions. Cells expressing cancer-associated PTEN variants tagged to blue fluorescent protein are mixed with cells expressing wild-type (WT) PTEN tagged with a red fluorescent protein. The proportion of blue and red cells are analyzed over several days using flow cytometry. If the variant does not repress cell growth, variant (blue) cells will outcompete their WT (red) counterparts. To modify the competition assay for genome stability assessment, cells are treated with a PI3K inhibitor and the genotoxic chemotherapeutic temozolomide. These drugs isolate the genomic stability function of PTEN by removing its role in cell growth and causing genome instability, respectively. Here, cells harboring variants that cannot repair temozolomide-induced DNA lesions will be outcompeted by their WT counterparts. The assay generates a score that is based on the rate of change of variant populations relative to the WT population to quantitatively define the phenotype. Results can be interpreted to establish a relationship between a PTEN variant and its quantitative effect on the cell growth or genomic stability functionality of PTEN. Furthermore, the growth-based nature of these assays means that in future work they can be adapted to a pooled library format, allowing the simultaneous, quantitative assessment of thousands of PTEN variants. Data from both low-throughput and high-throughput experiments bring clarity to the relationship between specific PTEN functions and patient prognosis.