Cancer is the second leading cause of death in the USA and is considered a public health issue worldwide. Early diagnosis 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. Overall survival and disease-free survival rates are improved with the use of adjuvant chemotherapy. However, chemotherapy treatment might cause short and long-term side effects for cancer survivors. A special concern of young women diagnosed with cancer is their reproductive potential after chemotherapy. Chemotherapy drugs act by distinct mechanisms in the ovaries. DNA damage of primordial follicle oocytes, leading to chemotherapy-induced apoptosis, was recognized as the principal mechanism responsible for the irreversible decline of the ovarian reserve. The oocyte first attempts to repair DNA damage via the DNA damage repair pathway mediated by ataxia-telangiectasia mutated. Elimination through apoptosis occurs in cells in which DNA damage could not be repaired. In this review, the clinical impact and the major mechanisms of ovarian damage from chemotherapy treatment will be briefly described.
