Q&A with Sumegha Mitra, PhD

Sumegha Mitra, Ph.D., received a four-year, $792,000 research scholar grant from the American Cancer Society (ACS) to study high-grade serous ovarian cancer. Dr. Mitra is a visiting assistant professor of microbiology and immunology at IU School of Medicine and an associate member of the Tumor Microenvironment and Metastasis research program at the IU Simon Comprehensive Cancer Center. 

Dr. Mitra answers a few questions about her ACS-funded project, “Protein Homeostasis Network Regulates Oncogenic Signaling in High-Grade Serous Ovarian Cancer,” and her broad ovarian cancer research efforts.

A. We recently published a study that identified an adaptive mechanism and novel links that maintain protein homeostasis and promote high-grade serous ovarian cancer growth. However, not much is known about the role of the protein homeostasis network in high-grade serous ovarian cancer. This cancer originates from fallopian tube secretory epithelial cells and harbors copy number variations and other stressors that affect the protein quality control pathways. My American Cancer Society grant will help us study the regulation of the protein homeostasis network in high-grade serous ovarian cancer and its role in cancer relapse and chemoresistant growth. Our goal is to target protein homeostasis, an important druggable vulnerability of cancer cells.

A. Ovarian cancer is the most lethal gynecologic malignancy because it is detected at later stages and most ovarian cancer patients experience recurrent and chemoresistant tumors resulting in a poor 5-year survival rate. Other therapies, like immunomodulators, have limited success in treating advanced ovarian cancer patients. My American Cancer Society grant will help us test several novel inhibitors in chemoresistant patient-derived xenograft models and murine models of ovarian cancer relapse. These translational studies will help us understand the mechanisms that promote ovarian cancer relapse and chemoresistant growth.

A. For several decades, ovarian cancer patients have been treated with platinum-taxane-based therapy until they become refractory and die due to chemoresistant tumors. While most cancer therapies target dividing cells, my research will identify molecular targets that mediate cellular homeostasis in cancer cells and promote their survival and growth under various stressors. Targeting these stress-response pathways will enhance cancer cell killing.

A. I am involved with a non-profit organization called Ovar’coming Together, and annually I participate in their Turn the Canal Teal program and interact with ovarian cancer survivors and patient advocates. These people, their zest, and bravery in this fight against ovarian cancer motivate me to understand this deadly disease better to develop novel therapies.