Abstract
Endometriosis is a chronic disease where endometrial-like tissue is grows outside of the uterine cavity that impacts around 10% of women of reproductive age (Lebovic et al., 2001). Current available treatments use surgical or hormonal methods to alleviate symptoms, such as pelvic pain and dysmenorrhea, but are not successful in treating the disease (Ellis et al., 2022). Symptom relief is often temporary, and the treatments fail to aid with problems of infertility in endometriosis patients (Lebovic et al., 2001). The mechanisms and cause of endometriosis are not fully understood, so patients can face up to 7-9 years of misdiagnosis and are often treated for other conditions (Kirk et al., 2024). Due to failures in both treatments and diagnosis, around 70% of endometriosis patients live with unresolved pain (Ellis et al., 2022).
For my technical project, my group and I sought to optimize a patient-specific hydrogel model for endometriosis. To validate that hydrogel models are effective in retaining cells and maintaining native cell populations, we analyzed whether cellularity was greater in an endometriosis lesion embedded in a polyethylene glycol (PEG) hydrogel, and the results found that to be true. After confirming the basis for our model, we used a viscometer to test the physical properties and molecular components of PEG hydrogels to see what would affect gelation time. We tested three different weight percentages of PEG (2%, 3%, and 5%), a degradable vs nondegradable crosslinker, and the presence vs absence of Arginylglycylaspartic acid (RGD) peptides. The original model used a degradable crosslinker, but we conducted an experiment to examine if a non-degradable crosslinker would impact tissue viability using mouse uterine tissue samples. Our lab has the unique opportunity to access freshly isolated tissue samples from endometriosis patients, but that is not the case for all institutions. We wanted to test if tissue could be flash frozen, thawed, and used again in experiments on our hydrogel model, so we conducted cellularity and viability analysis on fresh and cryopreserved endometriosis lesions. We plan to publish our results, so that other researchers can use our model to study the prognosis of endometriosis and test how potential treatments affect endometriosis lesions over time to examine their effectiveness.
In my Science, Technology, and Society (STS) research, I examined how endometriosis and other female-specific diseases have failed to have proper funding despite their high disease burdens. I used the global burden of disability adjusted life years (DALYs) to measure the burdens of female-specific diseases such as endometriosis, ovarian cancer, cervical cancer, and polycystic ovarian syndrome (PCOS). Then, I found other male-specific or non-gender specific diseases with similar burdens and compared their National Institute of Health (NIH) funding and grants. Upon finding that female-specific diseases were underfunded, I used Actor-Network Theory (ANT) to investigate the reasons for gender disparity in medical research with the goal of bringing light to these issues in hope to inspire change in the funding distribution system.
Together, these projects tackle both the scientific and societal challenges surrounding endometriosis. While my Capstone group works to advance a patient-specific hydrogel model to better investigate endometriosis behavior and treatment responses, my STS research underscores the broader structural inequities that have limited progress in the field. The lack of effective therapies and delayed diagnosis are not only biological problems but are also shaped by gender disparities in research funding. This work aims to improve the laboratory tools that are available to researchers and the priorities that guide research investment.
