Since the invasive potential in DCIS.COM positively correlates with, and depends upon, expression and activity of COX-2 [22, 44], we tested the hypothesis that the loss of invasive phenotype observed with blocking of COX-2 expression was due, in part, to re-expression of SIM2s. Thus, we measured SIM2 protein levels by IHC analysis of tumors generated from control and shPTGS2 DCIS.COM cells, which are less invasive [22]. Here, PTGS2 is linked to ductal breast carcinoma in situ.