David L. Tait, MD Associate Director of Gynecologic Oncology
Department of Obstetrics and Gynecology

Prior Positions and Experience


Gynecologic Oncology Fellowship, University of Texas Southwestern Medical Center at Dallas


Obstetrics and Gynecology Resident, University of Tennessee at Memphis


MD: 1987, University of Tennessee at Memphis
BA: 1983, University of Tennessee at Chattanooga

Research Interests

Dr. Tait's primary interest has been in the field of ovarian cancer and the study of the molecular mechanisms associated with oncogenic transformation. Ovarian cancer is the deadliest of the gynecologic malignancies and is the fourth leading cause of cancer death in women in the United States. Each year, more than 22,000 women will be diagnosed with ovarian cancer, resulting in over 16,000 deaths per year. The majority of patients are diagnosed with an advanced stage of disease with five-year survival rates of only 30 to 40 percent. Despite continued development of cytotoxic and molecular therapeutics, as well as identification of better screening tools, the outcome of most patients with ovarian cancer is poor. Dr. Tait’s interest in the gene expression pathways associated with ovarian cancer carcinogenesis has resulted in previous clinical and translational research studies in retroviral based BRCA1 gene therapy for ovarian cancer. These translational research studies include both clinical evaluations of multiple generations of retroviral vectors, as well as the correlative translational research studies for vector safety and efficacy. In addition, Dr. Tait has been involved with multiple clinical trials for ovarian cancer utilizing new cytotoxic and biologic agents sponsored both through the Gynecologic Oncology Group and industry.

Currently, Dr. Tait is investigating dysregulated gene expression in ovarian cancer to identify candidate genes which may serve as potential biomarkers. Ongoing collection of ovarian tissue and serum samples from patients with ovarian cancer are utilized for both the genomic and proteomic studies. One gene family of particular interest has been the homeobox (HOX) gene family. The HOX genes are a group of transcription factors that are involved in early cell differentiation and maintenance of cell identity. These genes have been associated with several oncogenic pathways to include the RAS signaling cascade and angiogenic pathways involving vascular endothelial growth factor and basic fibroblast growth factor. The potential upstream participation by HOX genes in multiple cell regulatory pathways makes this family of genes an appealing candidate for evaluation as a biomarker tool. Preliminary studies have demonstrated dysregulation of multiple HOX genes in ovarian cancer tissue samples to include HOX B2, HOX B3, HOX B5, HOX B7, HOX A10, HOX D1, HOX C6 and HOX D9. The purpose of continuing studies will be to evaluate these genes with additional candidate genes and their role as potential biomarkers for early detection and monitoring of treatment response in patients with epithelial ovarian cancer.

Dr. Tait is a member of the Gynecologic Oncology Group and served on the Developmental Therapeutics Committee. He was the Principle Investigator for the Phase II GOG trial evaluating gemcitabine in the treatment of recurrent endometrial carcinoma. Dr. Tait is currently the site P.I. for an international Phase III trial for treatment of endometrial carcinoma.

Recent Publications

Lange S, Tait DL, Matthews M. Oncofertility: an emerging discipline in obstetrics and gynecology. Obstet Gynecol Survey 2013;68:582-93. [PMID:23921672]

Tait DL, Blessing JA, Hoffman JS, Moore KN, Sprtos N, LaChance JA, Rotmensch J, Miller DS. A phase II trial of gemcitabine in the treatment of recurrent or persistent endometrial carcinoma: a gynecological oncology group study. Gynecol Oncol 2011;26:990-98. [PMID: 21159366]

Bahrani-Mostafavi Z, Tickle TL, Zhang J, Bennet KE, Vachris JC, Spencer MD,Mostafavi MT, Tait DL. Correlation analysis of HOX, ErbB, and IGFBP family gene expression in ovarian cancer. Cancer Investigation 2008;26:990-98. [PMID: 19093257]