Fertility reservation in female patients

Ankara University School of Medicine, Ankara, Turkey and The Center for Reproductive Medicine and Infertility, Department of Obstetrics and Gynecology, Joan and Sanford I. Weill Medical College of Cornell University, New York, NY 10021, USA.
Human Reproduction Update (Impact Factor: 10.17). 05/2004; 10(3):251-66. DOI: 10.1093/humupd/dmh021
Source: PubMed


In the USA alone, >650 000 women will be afflicted by cancer in 2003, and 8% of these cases will be aged <40 years. Due to improvements in cancer therapy, cure rates of both adult and childhood cancers increased significantly over the past three decades. However, long-term consequences of cancer therapy and impact on quality of life are now being recognized. One of the major sequelae of cytotoxic chemotherapy is gonadal failure. Cytotoxic chemotherapy and/or radiotherapy are not only used to treat malignant diseases, but also non-malignant systemic conditions. Upon reviewing the extent and mechanism of gonadal damage due to chemo-/radiotherapy, this article discusses indications and the wide range of methods of fertility preservation in a comprehensive manner. All current, emerging, experimental as well as controversial approaches are reviewed. A comprehensive algorithm to manage fertility preservation through an individualized approach is presented.

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    • "Most of the available data for ovarian failure after chemotherapy, is based on leukaemias, lymphomas, Hodgkin's disease, and on some solid tumors such as breast cancer. However, there is an increasing number of patients with no malignancy who are being treated successfully with chemotherapy due to autoimmune diseases, such as systemic erythematosus lupus, rheumatoid arthritis as well as some hematological diseases [1] [3] [4] [5]. "
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    ABSTRACT: Cancer prevalence is high, and of importance to cancer sufferers is the long term survival and normal activities resumption. Moreover, pregnancy is drawing interest for preserving ovarian reserves in post-chemotherapy affected women, especially of younger ages. The gonadotoxic effect of cancer treatment, involves mechanisms that are not fully understood, mainly due to the variety of molecular pathways triggered once therapeutic agents applied. Reported rates of premature ovarian failure after the treatment effect and the application of various treatment protocols, differ extensively due to the protocol itself but also due to the age of treated patients. Several options for preserving ovarian reserves are currently employed in the clinique, such as ovarian transposition, embryos cryopreservation and the use of gonadotropin-releasing hormone (GnRH) and its agonists/antagonists, but most of them are still under investigation. This paper reviews these methods and the molecular mechanisms that are possibly involved in the action of agents such as GnRH.
    Full-text · Article · Aug 2015 · Clinical and experimental obstetrics & gynecology
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    • "Chemotherapy may cause a loss of fertility due to premature ovarian failure [1] [2], and it has been well documented that this failure can be immediate [3] [4]. Alkylating agents such as cyclophosphamide (CTX) are a mainstay of chemotherapy regimens used to treat cancer and autoimmune diseases; however, CTX treatment can lead to impaired fertility or ovarian failure as a result of follicular destruction [5] [6]. Previous studies have shown that follicular decline in the CTX-treated ovaries occurred in a dosedependent manner, and apoptotic changes in granulosa and theca cells have been identified as the mechanism leading to the follicle loss [7] [8]. "
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    ABSTRACT: The adverse effects of the anti-cancer agent cyclophosphamide (CTX) on follicular growth and ovarian angiogenesis were investigated in mice. CTX treatment irreversibly induced a loss of follicles through apoptosis and decreased microvascularization of the corpora lutea and follicles in a dose-dependent manner. Our findings demonstrated that CTX adversely affected the ovaries indicating the need to support an awareness of fertility preservation before chemotherapy is initiated. © 2014 Society for Biology of Reproduction & the Institute of Animal Reproduction and Food Research of Polish Academy of Sciences in Olsztyn.
    Full-text · Article · Sep 2014 · Reproductive biology
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    • "In addition, consistent with the localization of active caspase-3, the decrease in AMH levels indicated that the gonadotoxic effect of busulfan occurs mainly in granulosa cells, affecting ovarian function as well as ovarian tissues. Follicular destruction is the main cause of the ovarian failure and infertility, induced by chemotherapy (Sonmezer and Oktay, 2004). Busulfan may damage the ovaries in a follicle-type-dependent manner. "
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    ABSTRACT: Chemotherapy damages the reproductive system by enhancing apoptosis, and evidence suggests that targeted anti-apoptotic therapy may preserve fertility in patients receiving chemotherapy. To investigate the protective effect of sphingosine-1-phosphate (S1P) on chemotherapeutic agent-induced ovarian gonadotoxicity, busulfan-treated female mice were pre-treated with low (0.5 mM) and high (2.0 mM) doses of S1P or vehicle 1 h before busulfan injection. In the S1P groups, each mouse was injected with low-dose S1P in one ovary and high-dose S1P in the contralateral ovary. Four weeks later, the ovaries were removed for histological and biochemical examinations. Caspase 3 immunoreactivity was greater in mice treated with busulfan compared with mice pre-treated with S1P, in which more primordial follicles were observed (P < 0.05). The mRNA level of anti-Müllerian hormone was higher in mice pre-treated with S1P than those that received busulfan only, indicating a better ovarian function in mice pre-treated with S1P. No difference was observed in the levels of growth differentiation factor-9 among all groups. In conclusion, S1P protects primordial follicles from chemotherapy-induced gonadotoxicity, and may partially preserve ovarian function.
    Full-text · Article · Aug 2014 · Reproductive biomedicine online
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