Our overall goal is to elucidate the molecular pathways involved in DNA damage repair to maintain genomic stability in cancer cells, with the aim of devising and evaluating innovative treatment combinations to improve outcomes for patients with high-grade serous ovarian cancer (HGSOC).
In HGSOC, understanding DNA damage repair mechanisms is important due to their crucial role in maintaining genomic integrity and influencing therapeutic responses. However, despite advancements, there remains a significant gap in our knowledge regarding the intricate interplay of DNA repair pathways. This lack of comprehensive understanding hampers the development of targeted therapies tailored to exploit DNA repair vulnerabilities in ovarian tumors.
We employ a wide variety of methods to approach this problem. We have the privilege to work with clinical samples directly but also take advantage of model systems in cell culture and mice. Our lab's functional assay measures homologous recombination (HR) repair in ovarian tumors, exploiting HR deficiency for personalized therapy. Simultaneously, we target CCNE1 amplification in ovarian cancer, guiding our search for more precise treatments against heightened genomic instability.
We are also investigating the role of the microbiota, with the goal to determine the role of bacteria and viruses in DNA damage. Additionally, we're investigating the dynamics and evolution of LINE-1 retrotransposon activity in high-grade serous ovarian cancer cells, both in vivo and in vitro, to elucidate their role in genome instability.