from the first decade. Clin Cancer Res 2008;14:1649–1657.

endometriosis by blocking proteasome and nuclear factor-kB pathways Sir, I have read with great interest the article by Celik et al. (2008) regard-ing experimental treatment of mouse endometriosis by inhibiting pro-teasome and nuclear factor-kB (NF-kB). The findings are in good concordance with recent works suggesting NF-kB to be a major factor in the pathogenesis of endometriosis (Guo, 2007). In fact, pyr-rolidine dithiocarbamate (PDTC) and other dithiocarbamates are NF-kB inhibitors because of creating copper complexes in the body and inhibiting proteasome (Cvek and Dvorak, 2007); hence, PDTC is proteasome inhibitor as well as bortezomib. On the other hand, bor-tezomib as a proteasome inhibitor inhibits NF-kB pathway as well in humans (Orlowski and Kuhn, 2008). Thus, both bortezomib and PDTC represent the same therapeutic approach towards endometrio-sis: NF-kB blockage is a consequence of proteasome inhibition. There-fore, we suggest that it is worth investigating if proteasome inhibitors (bortezomib and disulfiram are available in the clinic even now, cf. Cvek and Dvorak, 2008) would be sufficiently effective (and safe) against endometriosis in human patients.