Human Reproduction Update Advance Access originally published online on January 9, 2007
Human Reproduction Update 2007 13(3):265-273; doi:10.1093/humupd/dml060
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The Anti-Mullerian hormone and ovarian cancer
MotherInfant Department, Institute of Obstetrics and Gynecology, University of Modena and Reggio Emilia, Modena, Italy
1 To whom correspondence should be addressed at: MotherInfant Department, Institute of Obstetrics and Gynecology, University of Modena and Reggio Emilia, Policlinico di Modena, Largo del Pozzo, 41100 Modena, Italy. Tel: 39 0 594 224 379; Fax: 39 0 594 224 394; E-mail: antlamarca{at}libero.it
The Anti-Mullerian hormone (AMH), which is produced by fetal Sertoli cells, is responsible for regression of Mullerian ducts, the anlagen for uterus and Fallopian tubes, during male sex differentiation. Ovarian granulosa cells also secrete AMH from late in fetal life. The patterns of expression of AMH and its type II receptor in the post-natal ovary indicate that AMH may play an important role in ovarian folliculogenesis. Recent advances in the physiological role of AMH has stimulated interest in the significance of AMH as a diagnostic marker and therapeutic agent for ovarian cancer. Currently, AMH has been shown to be a circulating marker specifically for granulosa cell tumour (GCT). Its diagnostic performance seems to be very good, with a sensitivity ranging between 76 and 93%. In patients treated for GCT, AMH may be used post-operatively as marker for the efficacy of surgery and for disease recurrence. Based on the physiological inhibitory role of AMH in the Mullerian ducts, it has been proposed that AMH may inhibit epithelial ovarian cancer cell both in vitro and in vivo. These observations will be the basis for future research aiming to investigate the possible clinical role of AMH as neo-adjuvant, or most probably adjuvant, therapy for ovarian cancer.
Key words: AMH / cancer therapy / diagnostic markers / epithelial ovarian cancer / granulosa cell tumour
Received on July 10, 2006; revised November 3, 2006; accepted on November 29, 2006