A gene previously identified as important in promoting obesity also appears to be responsible for causing a common human tumor, researchers at The Schepens Eye Research Institute have found.
The gene, known as HMG I-C, causes tumors called lipomas, a common tumor in fat tissue in humans. Lipomas start as benign growths, but can become malignant liposarcomas as they grow. Lipomas are the most common form of mesenchymal tumors found in humans.
"There is now strong evidence that targeting this molecule may be useful both for the treatment of obesity in humans and the treatment of lipomas. It is likely that therapeutic agents which block the expression of the HMG I-C would be effective in the treatment of these two major clinical problems ," said Santa J. Ono, Ph.D., Associate Scientist at The Schepens Eye Research Institute and Associate Professor at Harvard Medical School.
Ono and his colleagues report their findings in The Journal of Biological Chemistry, scheduled for publication on May 12, 2000. The paper has been online at the journal's web site (www.jbc.org) since March 15. Coauthors are Paola Arlotta, Ph.D., and Albert K.-F. Tai, both of The Schepens Eye Research Institute; Guidalberto Manfioletti, Ph.D., University of Trieste, Italy; Charles Clifford, Ph.D., Charles Rivers Laboratories, Wilmington, Mass.; and Gilbert Jay, Ph.D., OriGene Technologies, Rockville, Md.
Previous epidemiologic data had shown that the HMG I-C gene is defective in many mesenchymal tumors. The Ono team has proven a direct role for the HMG I-C gene in lipoma formation by creating transgenic mouse lines that overexpress the defective HMG I-C gene in all cells of the body. The transgenic mice are obese early in life and develop tumors of the adipose (fat) tissue in adult life. About 25 percent of the transgenic mice develop tumors, while control mice, or normal mice, showed no evidence of tumor formation.
The researchers also found that no tumors formed in o
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Contact: Larry Bernard
bernard@vision.eri.harvard.edu
617-912-2548
Schepens Eye Research Institute
25-Apr-2000