For more information about this archival news release, please contact Robin Mackar(http://www.niehs.nih.gov/news/media/index.cfm), News Director, Office of Communications & Public Liaison(http://www.niehs.nih.gov/about/od/ocpl/index.cfm) at (919) 541-0073 or by email at email@example.com.
May 3, 2001
3 May 2001: Environmental Health Institute Selects Centers in Ohio, Texas, New York and Washington to Breed Mice with Gene Variants for Disease Studies
The National Institute of Environmental Health Sciences today announced the establishment and funding of five research centers to develop and breed mice with key genetic variations similar to those of humans.
The centers will provide the special, mutant mice for scientists throughout the National Institutes of Health, of which NIEHS is a part, and to other research programs as well, to help scientists study how human bodies repair environment-damaged DNA and control their cell's life cycles.
The centers named by NIEHS today are:
- The Albert Einstein College of Medicine of Yeshiva University, the Bronx, N.Y.; Principal investigator: Raju Kucherlapati, Ph.D.
- University of Washington, Seattle; Principal investigator: Warren Lapiges, DVM.
- University of Cincinnati, Ohio; Principal investigator: Peter Stambrook, Ph.D.
- The University of Texas Health Science Center at San Antonio; Principal investigator: Jan Vijg, Ph.D.
- The University of Texas, MD Anderson Cancer Center, Smithville, Texas; Principal investigator: David Johnson, Ph.D.
NIEHS said that it will spend up to $5 million a year in grants in each of the next five years to establish the five new centers - or about $1 million per center per year - under cooperative agreements with the established laboratories named. The NIEHS centers will sequence mouse genes and compare them to human genes and their sequences, produce mice with mutations or missing genes ("knock-out"mice) and maintain breeding colonies to supply test rodents or breeding stock to other scientists.
NIEHS Director Kenneth Olden, Ph.D., said, "Mice and humans have many similar genes, and by adding a gene, we can make mice even more similar in their susceptibility to human diseases. We can use these mouse models to understand human variabilities to environmental factors that may have a role in human diseases like diabetes, Alzheimer's and Parkinson's diseases, arthritis and heart disease."
Jose Velazquez, Ph.D., NIEHS program director for the mouse centers, said that the animals and the data on them will be made available widely -- to scientists in other parts of the National Institutes of Health and beyond.
The NIEHS mouse centers will support and supplement a $21 million National Institutes of Health-wide effort, announced Oct. 5, 1999, to map the genes of the mouse via a Mouse Genome Sequencing Network. The effort by NIEHS, which is one of the institutes within NIH, will emphasize finding a better understanding of the variations in the genes that make some individuals more sensitive than others to environmental exposures.
Many cases of human disease can be triggered when a natural or man-made substance in the environment causes a genetic mutation or a disturbance in cell growth. Variations in a person's genes make the person more -- or less -- sensitive to these substances, or more - or less - able to resist or repair the damage.
Genetic variations may also explain why one smoker gets cancer or heart disease from that exposure while another smoker doesn't. Or why some members of a family react to environmental substances and develop asthma, while others do not. By modifying the mice to add or subtract a human-like gene with its variations, scientists hope to unlock the secrets of these and other human diseases in a genetically varied humankind.
Earlier NIEHS' studies of lead, asbestos, DES, air pollutants and some pesticide products have led to protective measures that have prevented many human diseases. Today, while continuing such studies, NIEHS scientists have also pushed forward with molecular and genetic studies of the mechanisms by which environmental factors cause disease and the genetic variability of humans' responses to the environment, both natural and man-made.
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