Bradley C. Carthon, MD, PhD


Titles and Roles

Associate Professor, Department of Hematology and Medical Oncology
Emory University School of Medicine
Section Chief of Hematology and Oncology
Winship Cancer Institute at Emory Midtown
Medical Oncologist
Bladder Cancer
Kidney Cancer
Penile Cancer
Prostate Cancer
Testicular Cancer
Uterine Cancer
Research Program
Discovery and Developmental Therapeutics


Bradley C. Carthon, MD, PhD, is interim director of the Division of Medical Oncology and associate professor in Emory University School of Medicine's Department of Hematology and Medical Oncology. Dr. Carthon also serves as section chief of Hematology and Oncology at Winship Cancer Institute at Emory Midtown. He works with the genitourinary oncology team at Winship Cancer Institute in order to discover novel therapeutic targets and carry out clinical trials that utilize novel treatment combinations for our patients with prostate, bladder, and renal and other genitourinary malignancies.

Dr. Carthon previously served as medical director of Inpatient Medical Oncology at Winship Cancer Institute, Clifton campus, during a period of notable growth in staffing and patient volume. He also previously served as Chair of Winship Cancer Institute's Health Disparities, Health Literacy and Minority Accrual Committee. He is a former participant in the Emory University School of Medicine Professional Leadership Enrichment and Development Program.

Dr. Carthon is a member of the Discovery and Developmental Therapeutics research program at Winship. He is also a member of the Annual Meeting Education Committee for American Society of Clinical Oncology.


Dr. Carthon earned his medical degree from Harvard Medical School in Boston, Massachusetts. He completed an internship and residency at Massachusetts General Hospital in Boston, Massachusetts. Dr. Carthon then went on to complete a fellowship at the University of Texas MD Anderson Cancer Center in Houston, Texas. 


Dr. Carthon conducted his PhD thesis work in the Sicinski Laboratory of the Dana Farber Cancer Institute and Harvard Medical School. His research focused on the individual roles of D-type cyclins in the context of mammary gland development and breast cancer, as cyclin had been shown to be overexpressed in various malignancies, including breast cancer. Utilizing knock-in murine mouse models, Dr. Carthon was able to express various D-type cyclins under the control of  the cyclin D1 promoter in order to delineate whether the specific roles of D-type cyclins were due to inherent differences in the family of proteins, or if the differences in the D-type cyclins were due predominantly to tissue specific patterns of expression. Animals expressing cyclin D2 under the control of the cyclin D1 promoter were able to develop normally, and lacked many of the phenotypic abnormalities seen in cyclin D1 null animals. This suggested that the specificity of the D type cyclins were largely controlled by tissue specific expression, and differences in cofactors that bound to each of the D-type cyclin signaling complexes.

Research from Dr. Carthon's clinical fellowship was done in the Thompson Lab at the University of Texas M.D. Anderson Cancer Center. The lab was interested in the role of Caveolin-1 (Cav-1), a Src kinase substrate, as it is overexpressed in primary prostate cancer (PCa) and in PCa bone metastases. In addition, PCa-derived and -secreted Cav-1 contributes to malignant progression. Using samples from patients enrolled on a phase II clinical trial of docetaxel and dasatinib (a Src family kinase [SFK]/abl inhibitor), Dr. Carthon was able to characterize Cav-1 as a biomarker and potential target in castration-resistant prostate cancer. The team stratified responder and non-responder patient data according to patients with locally advanced vs. bone metastatic disease. In brief, their findings suggested that serum Cav-1 can serve as a novel discriminating biomarker for SFK/Abl inhibition in both node-positive and bone-metastatic castration-resistant prostate cancer. Moreover, responding patients with bone predominant prostate cancer demonstrated higher levels of serum Cav-1. In vitro data suggested that this was likely due to a direct effect of Src family kinase inhibition on osteoblasts of the bone microenvironment. Src inhibition in osteoblast cells seemed to promote osteoblast differentiation and provided rationale for the use of dasatinib as a way to target not only prostate cancer cells, but also other cells of the bone microenvironment in prostate cancer bone metastases.

  • Below is a listing of current federal grants for the above principal investigator.



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