Nutrient restriction (NR) causes a shift from hypertrophy to hyperplasia in PTEN mutant cells
Tumor cells evade the breaks imposed by cellular stress conditions (e.g., NR, hypoxia, high osmolarity). We induce clonal populations of cells lacking a particular tumor suppressor to study their behavior under cellular stress conditions.
The lipid phosphatase PTEN is a key component of insulin/IGF-1 signaling and is often mutated in human cancer. Clones of PTEN mutant cells grow to slightly larger sizes in Drosophila imaginal discs, mainly due to an increase in cell size. Surprisingly, PTEN mutant cells hyperproliferate upon NR, giving rise to organs that are larger than under normal conditions. We are currently studying the differential response of PTEN mutant cells to starvation.
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