LAUSR

We read with great interest the study by Seo et al1 entitled “Trichostatin A induces NAG-1 expression and apoptosis in human endometriotic stromal cells” published in your journal. The authors investigated the use of trichostatin A (TPA), a histone deacetylase inhibitor (HDACI), for inducing growth arrest and apoptosis of human endometriotic stromal cells (HESCs) obtained from 15 women with ovarian endometriomas who underwent previous cystectomy. In particular, TPA was effective in enhancing the expression of nonsteroidal anti-inflammatory drug-activated gene 1 (NAG-1), a critical proa-poptotic gene, which has been demonstrated in patients with endometriosis.2 The rational of this study is based on the evidence that epigenetic aberrations may underlie the pathogenesis of endo-metriosis and that the use of HDACIs can modulate the histone acetylation/deacetylation and, thus, protein transcription.3 These drugs have demonstrated to inhibit proliferation and to stimulate apoptosis of various cell types, including HESCs.4–7 Furthermore, their administration has been supported by previous studies on animal model with endometriosis, resulting efficacious in decreasing size and number of implants and in reducing disease-related hyperalgesia.8,9