Oral Presentation ESA-SRB 2023 in conjunction with ENSA

Development of innovative strategies to preserve oocyte number and quality during cancer treatment (#98)

Karla Hutt 1
  1. Monash Biomedicine Discovery Institute, Department of Anatomy and Developmental Biology, Monash University, Clayton, Australia

Irreversible damage to the ovary and depletion of the ovarian reserve are devastating side effects of many traditional cytotoxic cancer treatments, often leaving young female cancer survivors infertile and at risk of premature menopause. Compounding this issue, our recent studies suggest that new precision drugs, like parp inhibitors and immune checkpoint inhibitors, which promise to deliver better patient outcomes with fewer side effects, may also damage the ovary and compromise fertility. Globally, ~1.4 million women under the age of 45 years are diagnosed with cancer per year and over 80% will survive. Therefore, improving quality of life by mitigating off-target treatment effects has become a critical patient-driven priority. Existing fertility preservation methods are not suitable for all patients, and no broadly effective pharmacological options exist to protect the ovaries of young girls and women receiving cancer treatment. This is due to poor understanding of how different treatments damage the reproductive tract, therefore, a lack of viable pharmacological targets. To begin to address these fundamental knowledge gaps, we are utilising preclinical naive and tumour bearing mice to examine the impact of existing and new cancer treatments on female reproductive health. We are using these models to decipher the precise cellular and molecular mechanisms that contribute to loss of oocyte number and quality during cancer treatment, and then using this knowledge to investigate innovative adjuvant therapies to protect the ovary from damage. Our long-term goal is to expand and improve fertility preservation options available to women, and thereby optimise the health and well-being of female cancer survivors world-wide.