ECE2016 Symposia New mechanisms to induce and protect from ovarian insufficiency (3 abstracts)
Recent years have seen a dramatic rise in interest in preserving fertility in women facing treatment for cancer and other serious diseases, and fertility preservation is rapidly becoming a mainstream part of reproductive medicine. This approach, however, serves to remove oocytes or ovarian tissue before cancer treatment, rather than directly protecting the ovary itself. Some chemotherapies and radiotherapy have well known adverse effects on follicle number, although the details of the effects and their magnitude for chemotherapeutic agents are often poorly characterised. Thus, emerging evidence suggests that different agents can have differential effects on the oocyte itself, the surrounding granulosa cells, and the ovarian stroma including the ovarian vasculature. This may mean that different protective strategies may be needed for different chemotherapeutic agents. There have been studies for many years investigating the potential protective effect of GnRH agonists on the ovary administered during chemotherapy. Initial studies were underpowered and often uncontrolled, but recently larger well powered RCTs have shown a consistent beneficial effect in reducing the risk of premature ovarian insufficiency after chemotherapy for early breast cancer. Smaller studies have also been undertaken in other cancers, particularly lymphoma, but these have not shown a clear benefit. This may reflect the specific treatment regimens involved in those studies, rather than being a feature of the diagnoses. Non-hormonal approaches have also been investigated, although largely confined to animal studies. These have often focused on the potentially beneficial effects of sphingosine-1-phosphate, and the tyrosine kinase inhibitor, Imatinib. Generally, conflicting results have been reported, thus, there is a need for greater understanding of potential mechanisms of action before introduction to clinical trials.