Can Some Anticancer Treatments Preserve the Ovarian Reserve?

Abstract Background Preventing premature ovarian failure (POF) is a major challenge in oncology. With conventional regimens, cytotoxicity-associated POF involves primordial follicles (PF) pool depletion by apoptosis or overactivation mechanisms, notably mediated the ABL/TAp63 and PI3K/Akt/mTOR pathways. New anticancer treatments have been designed to target pathways implicated tumor growth. Although concerns regarding fertility arise with these targeted therapies, we hypothesized that therapies may exert off-tumor effects on PF might delay POF. We provide an overview of evidence concerning PF. Limitations future potential implications findings are discussed. Design PubMed was searched combining Boolean operators following keywords: fertility, ovarian, follicle, anti-tumoral, cancer, targeted, cytotoxic, chemotherapy. Results Cisplatin-related via pathway tyrosine kinase inhibitor, imatinib, mice, but were recently challenged human xenografts mice. In cyclophosphamide-treated inhibition mTOR inhibitors AS101 preserved pool. Proteasome GSK3 evaluated for direct indirect follicle DNA damage prevention. Surprisingly, cytotoxic drug association preservation found. also describe selected non-anticancer molecules minimize gonadotoxicity. Conclusion Not all associated POF, particularly since advent therapies. The feasibility associating protective targeting exhaustion mechanisms should be evaluated, as way decreasing need techniques. Further evaluations required transfer into clinical practice. Implications Practice Anticancer infertility 10%–70% patients, which result depletion. Alone gonadotoxic treatments, some favorable off-targets slowing down their exhaustion. Current relies murine models vitro models. Evaluation strategies humans challenging; however, if results confirmed biological data, it not only could new approach female would change standard strategies.