Reply to: Adhesion proteins: Suitable therapeutic targets or biomarkers of therapy response for endometriosis?

Sir, We were pleased to read the recent Letter to the Editor by Barra and Ferrero,1 who were interested in our recent publication in AOGS.2 In that report, we demonstrated the decreased expression of Tensin 1 (TNS1) in tissue and serum of women with endometriosis after receiving gonadotropin-releasing-hormone agonist (GnRHa) treatment. In our study, we only recruited patients with ovarian endometriosis, as mentioned in the Material and methods section. We agree that the expression and the changes of TNS1 might be different across endometriosis subtypes such as peritoneal endometriosis and deep infiltrating endometriosis. Further studies will be needed to investigate whether TNS1 is also significantly expressed in the other endometriosis subtypes. These studies will be helpful to understand the possible underlying molecular mechanism of TNS1 in the pathogenesis of endometriosis. We also agree with Barra and Ferrero that different hormone therapies have their own targeting mechanism and particular pharmacokinetics and pharmacodynamics. In our recently published study, the patients who were recruited in the treated group received only one type of GnRHa, leuprorelin acetate (Leuplin Depot, Takeda Pharmaceutical Company Ltd., Osaka, Japan) 1.875 mg/month by subcutaneous injection, and we followed TNS1 expression 1-2 months after the treatment. We excluded patients who received other hormonal treatments or received a different dosage. TNS1 is involved in adhesion formation3 and promotes cell migration.4 Treatment with a high affinity estrogen receptor antagonist downregulated TNS1 expression in murine uterus.5 Our recent report provided new evidence that GnRHa treatment reduced the expression of TNS1 in women with endometriosis. Down-regulated TNS1 might suppress the migration and adhesion of endometriotic tissues. Further investigations are required to clarify TNS1 as a hormonal-responsive molecule in the pathogenesis of endometriosis. We thank Barra and Ferrero for their interest in our findings and for pointing out that adhesion molecules such as TNS1 could be potential therapeutic targets or biomarkers for monitoring the efficacy of GnRHa treatment in women with endometriosis.