PPARG and neoplasm: Studiesusing dominant-negative PPARγ over-expression orGW9662 revealed thatthe inductionof 15-PGDH by both pioglitazone and rosiglitazone is PPARγ-independent.These findings indicate that it ispossible to use a clinically available pharmacological interventionto suppress tumor-derived PGE2 by enhancing catabolismrather than blocking synthesis.