Researching the mechanism of cancer treatment induced ovarian toxicity.
Advancements in cancer treatments have improved patient survival rates; however, the genotoxicity of these lifesaving treatments can leave young female cancer patients and survivors facing premature ovary failure. Genotoxic cancer treatments -such as radiation - induce DNA double strand breaks (DSBs) to target cells. These damaging DSBs preferentially kill cancer cells but can also kill healthy cells. Primordial follicles (PFs), a limited population of ovarian follicles containing immature oocytes, are highly susceptible to DNA damage. Cancer treatment induced DNA damage can deplete the ovary of PFs resulting in premature ovarian failure (POF) and infertility. Existing fertility preservation methods require delaying cancer treatment, invasive surgeries that may reintroduce cancerous cells, and are insufficient for prepubescent females. The goal of my research is to understand the DNA damage response in immature oocytes to establish targets for a non-invasive pharmacological inhibition strategy to preserve ovarian function and fertility in both pre-pubertal female cancer patients without delaying cancer treatment.