MD · MBA
Physician specializing in genetic analysis and personalized preventive medicine, and author of Outsmart Your Genes.
Brandon Colby is a physician-expert in the fields of genetic analysis and Personalized Preventive Medicine. He holds an MD from the Mount Sinai School of Medicine, an MBA from Stanford University's Graduate School of Business, and a degree in Genetics from the University of Michigan.
Dr. Colby is the author of the book Outsmart Your Genes and has developed numerous technologies that improve the analysis, interpretation, and actionability of genome sequencing data. He is an Affiliate Specialist of the American College of Medical Genetics and Genomics (ACMG), an Associate of the American College of Preventive Medicine (ACPM), and a member of the National Society of Genetic Counselors (NSGC).
Articles by Brandon Colby, MD are reviewed for accuracy by Sequencing's medical and scientific team. This page is for informational purposes and does not constitute medical advice.
A single vessel leaving the heart mixes oxygen-rich and oxygen-poor blood, causing cyanosis and breathing trouble. Echocardiography and surgical repair are covered.
Two urate transporters shape blood uric acid: OAT10/SLC22A13 reabsorbs urate in the kidney and ABCG2 moves it out, so impairment of either raises serum levels.
Vertebral, anal, cardiac, tracheoesophageal, renal and limb anomalies define it; array-CGH and exome sequencing have found CHD7 and other gene changes.
Discover the role of genetic testing in diagnosing vascular dementia, identifying at-risk individuals, and creating personalized treatment plans for better management.
Faults in the ZMPSTE24 gene disrupt lamin A maturation, producing restrictive dermopathy, MADA and MADB. Targeted, sequence and deletion analyses tell them apart.
Easy bruising and prolonged bleeding can trace back to FERMT3, GFI1B or VWF gene changes, as seen in LAD-III and in von Willebrand disease.
Platelets that clump too little or too readily lead to bleeding or clots; GFI1B mutations and sticky platelet syndrome are two causes to tell apart.
Reduced alpha-granule content and a poor aggregation response mark GFI1B-related bleeding, which activity assays and genetic analysis can identify.