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.
Discover the role of genetic testing in diagnosing imatinib-resistant Philadelphia chromosome-positive leukemia and explore advancements in targeted therapies for improved…
Aberrant transcription from exon 6A of the LHCGR gene leaves Leydig cells less responsive to luteinizing hormone, lowering testosterone in 46,XY individuals.
Variation in T cell immune response pathways, smoking-linked pathway alterations and polygenic risk models are tied here to lung cancer outcomes and LDCT screening.
Not every smoker develops lung cancer. Markers such as GSTM1 deletion and EGFR mutations, plus gene-based risk scores, are explained as tools for risk assessment.
NSCLC accounts for about 85% of cases and SCLC the rest; adenocarcinoma and squamous subtypes, imaging and biopsy, and immune-related genetic findings are described.
Head circumference charts, MRI or CT and genetic testing all feed the work-up; PTEN, Ptch1, SUFU, mTOR and DICER1 mutations converge on mTOR signaling.
Researchers link the Pbr9 locus and a Piezo1 allele that dehydrates red blood cells to lower Plasmodium infection, work that could shape malaria therapies.
Sickle cell trait, G6PD deficiency, thalassemias and a missing Duffy receptor all change how Plasmodium affects the body, and testing can shape treatment.