Manipulation of the low-metastatic TM40D mammary cancer cell line to over-express COX2 (TM40D-COX2) resulted in an increase in PGE2 production and exacerbated bone degradation due to an increase in osteoclast formation, an effect which was abrogated by treatment of the TM40D-COX2 cells with the COX2 inhibitor NS-398 [25]. This evidence concerns the gene PTGS2 and breast cancer.