A genetic basis for adult leukemia.
That protein, one o! two interferon regulatory factors, keeps cell division in check, report Hisashi Harada, Motoo Kitagawa, and their colleagues at Osaka University in Japan. They monitored the amount of each factor produced by normal mouse cells during growth and division. The level of the second factor remained fairly constant. But the amount of the first factor -- which started out lower than the second factor -- increased, peaking in cells that stopped dividing, say the scientists.
They also discovered that mutant mouse cells that produce way too much of the second factor multiply much like malignant tumor cells. By adding the gene for the first factor to these mutants, however, the scientists were able to restore normal growth. Thus it appears that the two factors work to balance each other and that a deficit in the first factor could lead to a tumor, the researchers conclude in the Feb. 12 SCIENCE.
Even if just one of the two genes coding for that first factor is missing or mutated, cells fail to produce the protein in the right amounts, adds Cheryl L. Willman, a cell biologist at the University of New Mexico School of Medicine in Albuquerque. After conducting genetic analyses of 13 patients with leukemia or preleukemia syndromes, she and her colleagues concluded that the gene for this regulatory protein lies on the stretch of chromosome 5 found faulty in many people with leukemia. They also describe their results in the Feb. 12 SCIENCE.
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|Title Annotation:||protein that regulates interferon is faulty in many adults with leukemia|
|Article Type:||Brief Article|
|Date:||Feb 27, 1993|
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