Milen [National Mah Jongg League Scholar] was born and raised in Nashville, Tennessee, to parents who emigrated from Eritrea. As an undergraduate at Harvard College, where she majored in Neuroscience and minored in Global Health and Health Policy, she became interested in the phenomena of neurodevelopment and neuroplasticity. Seeking deeper insight into these processes, she joined the lab of Dr. Michael E. Greenberg at Harvard Medical School (HMS) and conducted research under Dr. Xin Gu (who was a Damon Runyon Fellow at that time). There, she investigated the function of the protein midnolin and explored its structural, spatial, and physiological properties, elucidating its regulation of key neuronal proteins. This research earned her the HMS “Outstanding Undergraduate Research Award in the Lefler Center” and the Harvard “Herchel Smith Undergraduate Science Fellowship.” Working in Dr. Gu’s independent lab at Dana-Farber Cancer Institute, her scientific interests have widened from neuroscience to the broader processes of cellular growth, development, and death. She is drawn to the field of cancer biology not only for its scientific complexity but also for its human urgency and its therapeutic potential to prevent people’s stories from being cut too short. Outside of the lab, Milen immerses herself in the arts through volunteer work with local museums, creates her own art, and serves as paint charge for several student-run theatrical productions.  

Interoceptive neural circuits are responsible for sensing internal changes in the body and initiating appropriate responses. In the context of female reproduction, these neurons sense internal states within the reproductive tract and maintain homeostasis by modulating functions like smooth muscle contractions, fluid flow, and communication with the central nervous system. The female reproductive tract undergoes major changes throughout life, ranging from pregnancy to gynecological cancers like high-grade ovarian carcinoma. Dr. Greenberg is investigating how interoceptive neurons monitor the female reproductive tract and modulate essential physiologies in these changing hormonal and biological states. Her research on the typical functions of reproductive neurons and on the neuronal contribution to tumor progression may suggest novel therapeutic approaches for gynecological cancer treatment.

The cellular response to DNA damage is coordinated by an enzyme known as ATM kinase. Mutations in ATM are found in approximately 1% of the population and contribute to an increased risk of both hereditary and sporadic cancers, including breast cancer. Dr. Kim’s [Lallage Feazel Wall Fellow] research investigates how ATM suppresses the production of double-stranded RNAs (dsRNAs) in response to DNA damage. These dsRNAs play a critical role in tumor progression. Dr. Kim aims to identify the key molecular players involved in ATM-mediated suppression of dsRNAs and elucidate how the loss of ATM function triggers inflammatory responses through dsRNA sensing pathways. By uncovering these mechanisms, Dr. Kim aims to deepen our understanding of how ATM mutations drive cancer development and uncover novel therapeutic strategies for ATM-associated cancers. Dr. Kim received his PhD and BS from the Ulsan National Institute of Science and Technology, Ulsan.

Only up to 20% of patients with advanced ovarian cancer will survive five years after diagnosis. This is largely due to the cancer’s resistance to traditional chemotherapy and the current lack of targeted therapies that work with chemotherapy to improve response. Dr. Mullen’s lab has identified a new target, COP9 Signalosome Subunit 5 (COPS5), to treat ovarian cancer. Her team has found that inhibiting COPS5 with a drug called CSN5i-3 drastically improves ovarian cancer response to chemotherapy. She now aims to test the effectiveness of CSN5i-3 and chemotherapy against patient-derived, therapy-resistant ovarian cancer tumors. She will also investigate the mechanism of COPS5, believed to be involved in the repair of DNA damage caused by chemotherapy. Dr. Mullen hopes this innovative target will transform the care of patients with ovarian cancer.

Chromatin remodelers are complex protein machines responsible for packaging DNA and regulating gene expression. Their dysfunction is strongly implicated in cancer. For example, certain types of sarcoma and ovarian cancer are driven by mutations in a chromatin remodeler called BAF. Combining experiments with theoretical work, Dr. Owen’s research aims to understand how remodelers recognize their target sites in the cell’s nucleus. By expanding our understanding of chromatin remodeling, the findings of this research will provide the groundwork for more effective cancer treatments—suggesting how drugs might target chromatin remodelers—as well as enhance our understanding of how existing drugs that target remodeler-adjacent mechanisms might work.

A central aim of this project is the development of new, quantitative models to explain the behavior of chromatin remodelers seen in experiments. Dr. Owen will achieve this by successive rounds of passing between theory and experiments repeatedly—measuring, modeling, then measuring again. For comparison to experiments, model predictions will be extracted computationally (e.g., numerically solving ODEs, or by exact stochastic simulation using Gillespie’s algorithm) or analytically (e.g., by the King-Altman procedure, and variants), as appropriate.