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Panminerva Med. 2018 Jun 28. doi: 10.23736/S0031-0808.18.03494-8. [Epub ahead of print]

Novel insights into the pathophysiology of chemotherapy-induced damage to the ovary.

Author information

1
Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA.
2
Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, São Paulo, Brazil.
3
Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA - info@fertilitypreservation.org.

Abstract

Cancer is a worldwide public health problem and is the second leading cause of death in the United States. Early detection of cancer and advancement of treatment modalities contributed to declining mortality rates. Consequently, survival rates increased, leading to a greater interest in maintaining the quality of life after cancer treatment. Adjuvant chemotherapy results in an improvement in both disease-free and overall survival. However, chemotherapy treatment is associated with acute and long- term complications for cancer survivors. A special concern of women diagnosed with reproductive-age breast cancer is their reproductive potential after chemotherapy. The chemotherapeutic agents act by different mechanisms in the ovary. DNA damage of primordial follicle cells, leading to chemotherapy-induced oocyte apoptosis, was identified as the main mechanism responsible for the decrease of the ovarian reserve. The oocyte initially attempts to repair DNA damage through the DNA damage repair pathway mediated by ataxia-telangiectasia mutated. For cells in which DNA damage cannot be repaired, elimination occurs via apoptosis. In this review, the clinical impact and the major mechanisms of chemotherapy-induced ovarian reserve damage will be briefly described.

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