Winston E. Thompson, Ph.D., M.S. 

Education

POSTGRADUATE: 
Marine Biological Laboratory
Certificate: Embryology

Harvard Medical School
Fellowship: Reproduction


GRADUATE: 
Rutgers University and the University of Medicine & Dentistry
Degree: Doctor of Philosophy in Cell and Developmental Biology

Rutgers University 
Degree: Master of Science in Endocrinology


UNDERGRADUATE: 
Lafayette College
Degree: Bachelor of Art in Biology

Research Interests

Endometriosis

1. Thompson and Dr. Villacorta Laboratories at Morehouse School of Medicine are dedicated to advancing innovative, non-hormonal therapeutic strategies for endometriosis, a debilitating and often under-treated disease that affects at least 10% of reproductive-age women and is a major cause of chronic pelvic pain and infertility. Current medical treatments are largely hormone-based, and while they may reduce symptoms, they often produce unwanted side effects and can interfere with conception, creating a significant challenge for patients seeking both pain relief and fertility preservation. Our research focuses on the STING signaling pathway as a promising non-steroidal target, building on evidence that STING is upregulated in endometriotic lesions and that both type I and type II interferons are associated with more advanced stages of disease. We hypothesize that novel, orally bioavailable STING inhibitors may protect against endometriosis progression and alleviate associated pain by suppressing inflammation and fibrosis. By pursuing this non-hormonal mechanism, the Thompson and Villacorta Laboratories aim to develop more effective and clinically meaningful therapies for individuals living with endometriosis.

Uterine Fibroid

2. The Thompson Laboratory is also dedicated to advancing a deeper understanding of the biological mechanisms that drive uterine fibroid development and the striking health disparities associated with this common gynecologic disease. Uterine fibroids are highly prevalent, benign uterine tumors and a leading source of gynecologic morbidity, yet they disproportionately affect women of African and Afro-Caribbean descent, who often experience earlier onset, more aggressive growth, and more severe symptoms. Our research focuses on ancestry-enriched gene programs as drivers of fibroid growth and fibrotic remodeling, with particular interest in how genetic ancestry interacts with environmental stressors to influence disease susceptibility and progression. Although genome-wide association studies have identified numerous loci linked to fibroid risk, most of these signals lie in noncoding regions and have been derived primarily from populations of European ancestry, limiting their functional interpretation and relevance to the populations most burdened by the disease. To address this critical gap, the Thompson Laboratory uses integrative genomic approaches, including admixture mapping in African ancestry populations, to identify ancestry-informed loci and molecular pathways that may explain differences in fibroid growth rates, disease severity, and treatment response across diverse cohorts. Through this work, we aim to move beyond describing disparities to uncovering the underlying biology that can inform more precise, equitable, and effective approaches to uterine fibroid diagnosis and treatment.

Publications

• Harp D, Driss A, Mehrabi S, Chowdhury I, Xu W, Liu D, Garcia-Barrio M, Taylor RN, Gold B, Jefferson S, Sidell N, Thompson W. Exosomes derived from endometriotic stromal cells have enhanced angiogenic effects in vitro. Cell Tissue Res. 2016 Jul;365(1):187-96. doi: 10.1007/s00441-016-2358-1. Epub 2016 Feb 3. PMID: 26841879; PMCID: PMC4917586.
• Chowdhury I, Banerjee S, Driss A, Xu W, Mehrabi S, Nezhat C, Sidell N, Taylor RN, Thompson WE. Curcumin attenuates proangiogenic and proinflammatory factors in human eutopic endometrial stromal cells through the NF-κB signaling pathway. J Cell Physiol. 2019 May;234(5):6298-6312. doi: 10.1002/jcp.27360. Epub 2018 Sep 27. PMID: 30259980; PMCID: PMC6344303.
• Elkafas H, Ali M, Elmorsy E, Kamel R, Thompson WE, Badary O, Al-Hendy A, Yang Q. Vitamin D3 Ameliorates DNA Damage Caused by Developmental Exposure to Endocrine Disruptors in the Uterine Myometrial Stem Cells of Eker Rats. Cells. 2020 Jun 12;9(6):1459. doi: 10.3390/cells9061459. PMID: 32545544; PMCID: PMC7349254.
• Banerjee S, Xu W, Chowdhury I, Driss A, Ali M, Yang Q, Al-Hendy A, Thompson WE. Human Myometrial and Uterine Fibroid Stem Cell-Derived Organoids for Intervening the Pathophysiology of Uterine Fibroid. Reprod Sci. 2022 Sep;29(9):2607-2619. doi: 10.1007/s43032-022-00960-9. Epub 2022 May 18. PMID: 35585291; PMCID: PMC9444830.
• Banerjee S, Xu W, Doctor A, Driss A, Nezhat C, Sidell N, Taylor RN, Thompson WE, Chowdhury I. TNFα-induced altered miRNA expression links to NF-κB signaling pathway in endometriosis. Inflammation. 2023 Jun 30;: PMID:  37205467.
• Omran MM, Vafaei S, Alkhrait S, Ali FL, Bariani MV, Bai T, Thompson WE, Yang Q, Ali M, Al-Hendy A. Utilising Human Myometrial and Uterine Fibroid Stem Cell-Derived Three Dimentional Organoids as a Robust Model System for Understanding the Pathophysiology of Uterine Fibroids. Cell Prolif. 2025 Sep;58(9):e70025. doi: 10.1111/cpr.70025. Epub 2025 Mar 20. PMID: 40108998; PMCID: PMC12414642.

Honors and Awards

• 2012: Certificate of Teaching Excellence, Frontiers in Stem Cells in Cancer, Advanced Lab Course at Howard University
• 2012: Elected to the Board of Directors, Society for the Study of Reproduction
• 2011: NIH R15 Grant Reviewer, NIH