Low-grade serous ovarian cancer (LGSOC) accounts for about 5–10% of ovarian cancers. Although patients are typically prescribed cytoreductive surgery followed by platinum-based chemotherapy, approximately 80% of patients tend to have disease recurrence. Currently, there is no established standard of care for recurrent LGSOC. A defining feature of LGSOC is activation of the MAPK pathway with about 50% of LGSOC tumors harbor MAPK-activating mutations such as KRASG12V/D, NRASQ61R/K, or BRAFV600E. To target the known mutations, clinical trials evaluating MEK inhibitor (MEKi) alone or in combination with FAK inhibitor(FAKi), have demonstrated an improvement in progression-free survival, but not in overall survival. This highlights the limited molecular understanding of LGSOC , which hinders the improvement of effective treatments and remains a major barrier to improving patient outcomes. My research investigates alternative transcriptional pathways that may regulate MAPK signaling. Specifically, I am studying how the tumor suppressor CIC controls expression of ETV1, ETV4, and ETV5, which are part of the PEA3 family of transcription factors. Overexpression of these transcription factors has been shown to lead to resistance in other cancers, yet this has never been explored in LGSOC. This work aims to uncover mechanisms driving MEK/FAKi therapies resistance and identify biomarkers to improve treatment outcomes for patients with recurrent LGSOC.

Honors/Awards:

Genetics T-32 Pre-doctoral Training Grant (2025 - 2026)

Travel Award - Health and Human Physiology, University of Iowa (2024)

Travel Grant - Graduate Student Senate, University of Iowa (2024)

Travel Grant - Graduate and Professional Student Government, University of Iowa (2024)