Dr. Jan Vijg

Jan Vijg, Ph.D. is Professor at the Buck Institute for Age Research, Novato, California. He is the author of more than 200 scientific publications and holds eight patents in research processes and methodologies. In 1989 he helped develop the MutaMouse™, the first transgenic animal engineered to detect gene mutations in a living organism. This allowed scientists to monitor the effects of toxic agents on mouse DNA in any of its tissues or organs. Since that time, he has developed new versions of this mouse model, which make it easy for researchers to monitor ongoing changes in DNA in different tissues or during various developmental stages of the mouse lifespan.
 
Research at the Vijg Lab is focused on genome instability and the mechanisms through which this may cause human disease and aging. Genome instability is generally considered as a cause of cancer since Theodor Boveri proposed, over 100 years ago, that cancer is based on aberrant chromosome combinations. When in the late 1940s it was discovered that low, daily doses of radiation accelerated symptoms of normal aging in rodents (including non-cancer, degenerative symptoms), the possibility was considered — by such eminent scientists as Leo Szilard, Frank Macfarlane Burnet and Howard Curtis — that genome instability could play a general role in the etiology of human aging and disease.
 
This possible connection between damage to the genome and aging found strong support in the discovery that heritable defects in genome maintenance are often associated with premature aging, as for example in Werner Syndrome and Hutchinson Gilford Progeria Syndrome. The DNA repair defects present in these conditions, and other defects as well, have been engineered in mice and shown to also cause premature aging in these animals. Interestingly, while such defects sometimes increase both cancer and non-cancer, degenerative symptoms, they often greatly reduce spontaneous tumor formation. This antagonism between cancer and aging is still incompletely understood. In general, research in this area has now begun to attract increased attention and is the main topic of his NIH program project “DNA repair, mutations and cellular senescence” which began in 1999.
 
Jan authored Aging of the Genome: The Dual Role of DNA in Life and Death and coauthored Two-Dimensional DNA Typing: A Parallel Approach To Genome Analysis, Efficient Rescue of Integrated Shuttle Vectors from Transgenic Mice: A Model for Studying Mutations in vivo, Aging and Genome Maintenance: Lessons from the Mouse?, Rapid accumulation of genome rearrangements in liver but not in brain of old mice, Plasmid-based transgenic mouse model for studying in vivo mutations, Genetic testing: The problems and the promise, and Somatic mitochondrial DNA (mtDNA) mutations in papillary thyroid carcinomas and differential mtDNA sequence variants in cases with thyroid tumors. Read the full list of his publications!
 
Watch his SENS 3 talk Age-related stochastic dysfunction of the genome: a natural limit to life span?.
 
Jan earned his BS, MSc and PhD from the State University of Leiden in the Netherlands.