The Michael E. DeBakey M.D. Award for Excellence in Research recognizes outstanding members of the Baylor College of Medicine faculty for their published scientific contributions to clinical or basic science research over the past three years.

The 2019 recipients of the DeBakey Research Awards are Dr. Carl Allen, assistant professor of pediatrics – hematology/oncology; Dr. Christie Ballantyne, professor, chief of the section of cardiology and vice chair of research in the Department of Medicine; Dr. Robert Britton; professor of molecular virology and microbiology; Dr. Aleksandar Milosavljevic, professor of molecular and human genetics; and Dr. Marco Sardiello, assistant professor of molecular and human genetics.

“These five awardees are representative of the quality and scope of research at the College. Their work has made significant contributions to their fields of study and to improving human health,” said Dr. Adam Kuspa, senior vice president and dean of research at Baylor.

The awards, named in honor of pioneering heart surgeon Dr. Michael DeBakey, the first president of Baylor College of Medicine, were presented at a ceremony and scientific symposium May 15. Sponsored by the DeBakey Medical Foundation, the award includes a commemorative medallion and funds to support further research.

Kuspa presented the awards along with Dr. George Noon, professor of surgery and president of the DeBakey Medical Foundation, who was a colleague of DeBakey.

Dr. Carl Allen is an assistant professor of pediatrics – hematology/oncology and a member of the Dan L Duncan Comprehensive Cancer Center. Allen’s work has focused on defining mechanisms of pathogenesis of Langerhans cell histiocytosis (LCH). Uncertain classification of LCH as a disorder of immune dysregulation versus neoplastic disease has blocked access to research support from National Cancer Institute-supported organizations, limiting opportunities to improve outcomes for patients through clinical trials. The paradigm-changing work by Dr. Allen and colleagues has re-defined LCH as a myeloproliferative disorder. This work has not only uncovered novel therapeutic opportunities, but it also has contributed to the NCI including LCH in its portfolio of diseases that may benefit from translational research and clinical trial support.

Dr. Christie Ballantyne is professor of medicine, chief of the section of cardiology, vice chair of research for the Department of Medicine, director of the Center for Cardiometabolic Disease Prevention and director of the Maria and Alando J. Ballantyne, M.D., Atherosclerosis Clinical Research Laboratory. He also holds the J. S. Abercrombie Chair in Atherosclerosis and Lipoprotein Research. Ballantyne is one of the foremost experts on lipids, atherosclerosis and heart disease prevention. He leads the Reduction of Cardiovascular Events with Icosapent Ethyl–Intervention Trial, or REDUCE- IT, which recently found that patients with high triglycerides, despite statin therapy, had a lower risk of cardiovascular events when taking icosapent ethyl, a type of omega-3 fatty acid, compared to placebo. His recent work also has found that troponin I, a protein that is most commonly used to diagnose heart attack, can be detected in adults without prior cardiovascular disease or heart failure, and by adding this protein to a commonly used risk prediction model, led to more accurate risk prediction for heart attack, stroke and heart failure hospitalization.

Dr. Robert Britton is professor of molecular virology and microbiology and a member of the Dan L Duncan Comprehensive Cancer Center and the Center for Metagenomics and Microbiome Research at Baylor. His research and that of his lab is focused on the study of C. difficile, a bacterium that can cause serious infections in humans. The impact of C. diff, as it is commonly called, is staggering – about 14,000 deaths annually result from C. diff infection in the U.S. alone, and 200,000 worldwide. What’s particularly troubling is that antibiotics used to treat infections are actually a risk factor for C. diff infection by clearing away beneficial bacteria and allowing C. diff to gain a stronghold in the gastrointestinal tract. His recent work has focused on how changes in food additives can drive the emergence of pandemic strains of pathogenic bacteria such as C. diff in the human GI tract and is likely to inform FDA policy on the approval of such additives.

Dr. Aleksandar Milosavljevic is a professor of molecular and human genetics, director of the Program in Quantitative and Computational Biosciences, co-director of Computational and Integrative Biomedical Research Center and a member of the Dan L Duncan Comprehensive Cancer Center. His laboratory develops bioinformatics methods and advanced data platforms while contributing to the fields of genomics, clinical genomics, epigenomics and extracellular RNA communication. Milosavljevic’s lab leads the development of the FDA-recognized ClinGen database to inform clinical interpretation of genetic variation, and the lab currently serves as the Data Coordination Center for the NIH Extracellular RNA Communications project, which produced the ExRNA Atlas and developed the first comprehensive map of extracellular RNA in human biofluids. Developments in his work have been published in recently in Science, Genome Medicine and the American Journal of Human Genetics.

Dr. Marco Sardiello is assistant professor of molecular and human genetics at Baylor and member of the Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital. The Sardiello lab has quickly become a leader in the field of lysosome-autophagy biology that studies the waste disposal system of the cell and how its malfunction leads to the accumulation of cellular waste and lysosomal storage disorders, including Batten disease and other neurodegenerative conditions. Most recently, in 2019, the Sardiello lab set the foundation for a better understanding and treatment of tuberous sclerosis, a disease characterized by the formation of tumors in multiple organs and glycogen accumulation. mTORC1, a protein complex that regulates cell metabolism, has long been considered the major driving force behind tuberous sclerosis but the Sardiello lab has uncovered a second mechanism independent of mTORC1. This work could guide novel approaches to treat the disease.