Female fertility preservation: a clinical perspective.

For patients with cancer, preserving the ability to start a family at a time of their choosing is especially important and may influence decisions pertaining to cancer treatment. For other women who have delayed childbearing for personal or professional reasons, fertility preservation offers the possibility of having a biological child regardless of age. Though these women may be interested in or benefit from fertility preservation, fertility preservation services remain underutilized. While embryo and oocyte cryopreservation remain the standard strategies for female fertility preservation recommended by the American Society of Reproductive Medicine, the American Society of Clinical Oncology and the European Society of Medical Oncology, other strategies (e.g. pharmacological protection of the ovaries and ovarian tissue cryopreservation) are the subject of increasing research. This review will present new data that have become available over the past few years pertaining to all available methods of fertility preservation.

Steroidogenic factor-1 and endometriosis.

Endometriosis is a common and chronic disease characterized by persistent pelvic pain and infertility. Estradiol is essential for growth and inflammation in endometriotic tissue. The complete cascade of steroidogenic proteins/enzymes including aromatase is present in endometriosis leading to de novo estradiol synthesis. PGE(2) induces the expression of the genes that encode these enzymes. Upon PGE(2) treatment, coordinate recruitment of the nuclear receptor SF-1 to the promoters of these steroidogenic genes is the key event for estradiol synthesis. SF-1 is the key factor determining that an endometriotic cell will respond to PGE(2) by increased estradiol formation. The presence of SF-1 in endometriosis and its absence in endometrium is determined primarily by the methylation of its promoter. The key steroidogenic enzyme in endometriosis is aromatase encoded by a single gene because its inhibition blocks all estradiol biosynthesis. Aromatase inhibitors diminish endometriotic implants and associated pain refractory to existing treatments in affected women.