he irradiated lungs of normal mice. The lungs of engineered mice also contained less hydroxyproline, a marker of fibrous collagen build-up, than the lungs of normal mice. Moreover, mice lacking ICAM-1 had a lower incidence of respiratory distress and required higher doses of radiation than normal mice to show signs of distress.

In an accompanying editorial, Lisa A. Kachnic, M.D., of the Boston Medical Center, and Simon N. Powell, M.D., Ph.D., of the Massachusetts General Hospital in Boston, point out that loss of ICAM-1 function resulted in only a small increase in radiation tolerance. They say that although modulation of ICAM-1 may well help improve radiation tolerance of the lungs, it is unlikely to completely prevent lung injury.

However, Kachnic and Powell note that ICAM-1 deficiency could be integrated with other factors affecting radiation-induced lung damage and that future studies looking at these relationships may yield more insight into therapy-induced lung injury.

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Contact: Linda Wang
jncimedia@oupjournals.org
301-841-1287
Journal of the National Cancer Institute
14-May-2002

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