D. Woodrow Benson, MD, PhD
Title
Director, Cardiovascular Genetics
Appointment
Professor, University of Cincinnati College of Medicine
Email
woody.benson@cchmc.org
Phone
513-636-0389
Fax
513-636-5958
Credentials
MS: Emory University, 1967.
PhD: University of North Carolina, 1970.
MD: Duke University, 1972.
Residency: Pediatrics, Duke University.
Fellowship: Cardiology, Duke University.
Certification: Pediatrics, 1976; Cardiology, 1977.
Recertification: Pediatrics and Cardiology, 1993; Pediatrics, Pediatric Cardiology.
Awards and Honors
1994-2008 The Best Doctors in America
1993-98 Subboard Pediatric Cardiology, Chairman (1996-98)
1996 The Country's Best Heart Doctors (Good Housekeeping)
1995-97 NIH Senior Fellow
2000 Founder, Society of Pediatric Cardiology Training Program Directors
2003 Helen B. Taussig Memorial Lecture, American Heart Association
2006 Keynote Speaker Weinstein Cardiovascular Development Conference
2008 Keynote address Paediatric Research Day, University of Western Ontario
Research
Who says only old people get heart disease?
Cardiovascular disease in the young, which includes congenital heart defects, cardiomyopathy and disorders of heart rhythm (arrhythmias), is an important cause of morbidity and mortality.
My laboratory uses a "bedside-to-bench and back" approach to determine the molecular genetic basis of cardiovascular disease in the young. Our goal is to identify genes and their mutations that cause heart disease in the young.
In order to learn more about how the gene mutation leads to heart malformation or dysfunction, we seek to study mutant gene malfunction in a model system (in vitro assay, cell culture, etc).
Ongoing studies utilize genetic linkage analysis in kindreds (human and canine), positional cloning, characterization of genotype-phenotype relations of heart disease causing mutations.
Identification of gene mutations causing cardiovascular disease in the young, characterization of genotype-phenotype relations and illustration of the functional effects of the mutations will provide important insight into disease pathophysiology; such insight promises to lead to improved diagnosis and therapy.
Research Grants and Contracts
NIH P50 HL74728: SCCOR in Pediatric Heart Disease and Development. 02/15/04 – 01/31/09 (no cost extension to 2010) PI D. W. Benson
NIH K24 HL69712: Genetic mechanisms of cardiac disease in the young. 04/01/01 – 3/31/11. PI D. W. Benson
NIH U01HL085057: Pediatric Heart Network. 09/01/06 – 08/31/11. PI D. W. Benson
Publications, Most Recent
Zhang L, Benson DW, Tristani-Firouzi M, Ptacek LJ, Tawil R, Schwartz PJ, George AL, Horie M, Andelfinger G, Ackerman MJ, Sanguinetti M, Vincent GM. ECG features in Andersen syndrome patients with KCNJ2 mutations - characteristic T-U Waves patterns predict genotype.Circulation 2005:111:2720-26.
Ballester LY, Benson DW, Wong B, Law IH, Mathews KD, Vanoye CG, and George AL, Jr. Trafficking-competent and trafficking-defective KCNJ2 mutations in Andersen syndrome. Hum Mutat 2006;27:388-390.
Hinton, Jr., RB, Lincoln J, Deutsch GH, Osinska H, Manning PB, Benson DW, Yutzey KE. Extracellular matrix remodeling and organization in developing and diseased aortic valves. Circ Res 2006;98:1431-38.
Cripe LH, Barber BJ, Spicer RL, Wong BL, Weidner N, Benson DW, Markham LW. Outpatient continuous inotrope infusion as an adjunct to heart failure therapy in Duchenne muscular dystrophy.Neuromuscul Disord 2006;16:745-748.
Martin LJ, Ramachandran V, Cripe LH, Hinton RB, Andelfinger G, Tabangin M, Shooner K, Keddache M, Benson DW. Evidence in favor of linkage to human chromosomal regions 18q, 5q and 13q for bicuspid aortic valve and associated cardiovascular malformations. Hum Genet 2007;121:275-284.
Zhao B, Etter L, Hinton Jr. RB, Benson DW. BMP and FGF regulatory pathways in semilunar valve precursor cells.Dev Dyn 2007;236:971-980.
Viswanathan S, Burch JBE, Fishmann GI, Moskowitz IP, Benson DW. Immunohistochemical characterization of sinoatrial node in four atrioventricular conduction system marker mice.J Mol Cell Cardiol 2007;42:946-953.
Hinton RB Jr, Martin LJ, Tabangin ME, Mazwi M, Cripe LH, Benson DW. Hypoplastic left heart syndrome is heritable. J Am Coll Cardiol 2007; 50:1590-1595.
Markham LW, Kinnett K, Wong BL, Benson DW, Cripe LH. Corticosteroid treatment retards development of ventricular dysfunction in Duchenne muscular dystrophy.Neuromuscul Disord 2008;18:365-370.
Hinton RB, Jr, Andelfinger G, Sekar P, Hinton AC, Gendron RL, Michelfelder EC, Robitaille Y, Benson DW. Prenatal head growth and white matter injury in hypoplastic left heart syndrome.Ped Res 2008;64:364-369.
Hinton RB, Martin LJ, Rame-Gowda SR, Tabangin ME, Cripe LH, Benson DW. Hypoplastic left heart syndrome links to chromosomes 10q and 6q and is genetically related to bicuspid aortic valve.J Am Coll Cardiol 2008; in press.
Presentations, Most Recent
For more presentations, please see Dr. Benson's Molecular Cardiovascular Biology Page.
Genetic and developmental origins of pediatric heart valve disease. Keynote Speaker. Weinstein Conference on Cardiovascular Development. St Petersburg, FL May 11, 2006.
Cardiac arrhythmias in pediatric syndromes: Transcription factor mutations. Heart Rhythm Society Meeting. Boston, MA May 19, 2006.
Sodium channel mutations and conduction system disorders. NHLBI/ORD Workshop on Rare Inherited Arrhythmias. Bethesda, MD September 14, 2006.
SCN5A and the genetic origins of cardiac arrhythmias in the young. ODICH Meeting, Cincinnati, OH May 18, 2007.
Genetic and developmental origins of pediatric heart disease. Keynote address 2008 Paediatric Research Day, University of Western Ontario. London, Ontario, May 21, 2008.
Andersen-Tawil syndrome: Clinical course and treatment. CardioStim 2008. Nice, France June 19, 2008.
NKX2.5 and the genetic origins of pediatric heart disease. Pediatric Department Grand Rounds, University of Wisconsin, Madison, WI, November 6, 2008.
Professional Organization Memberships
Special Interests
Genetic basis of pediatric heart disease
Cardiovascular disease in the young, which includes congenital heart defects, cardiomyopathy and disorders of heart rhythm (arrhythmias), is an important cause of morbidity and mortality.
My laboratory uses a "bedside-to-bench and back" approach to determine the molecular genetic basis of cardiovascular disease in the young. Our goal is to identify genes and their mutations that cause heart disease in the young.
In order to learn more about how the gene mutation leads to heart malformation or dysfunction, we seek to study mutant gene malfunction in a model system (in vitro assay, cell culture, etc).
Current interests are the genetic basis of bicuspid aortic valve (BAV, the most common cardiovascular malformation) and hypoplastic left heart syndrome. Ongoing studies utilize family-based genetic linkage analysis to identify the genotype-phenotype relations of heart disease causing mutations.
Identification of gene mutations causing cardiovascular disease in the young, characterization of genotype-phenotype relations and illustration of the functional effects of the mutations will provide important insight into disease pathophysiology; such insight promises to lead to improved diagnosis and therapy.
Related Areas
This person works in these other areas at Cincinnati Children's Hospital Medical
Center:
