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In this issue

DEVELOPMENT IN MICE Release of nitric oxide (NO) by macrophages and epithelial cells leads to DNA damage and to protein nitrosylation and has been implicated in carcinogenesis, particularly in the gastrointestinal tract. The role of inducible nitric oxide synthase (iNOS), an enzyme responsible for increased NO production in response to inflammatory cytokines and bacterial endotoxin, is controversial in breast cancer, with reports of both inhibitory and stimulatory effects. In this issue of the Journal, Ellies and colleagues (pages 1–7), have used the polyoma virus middle T antigen targeted to the mouse mammary gland and bred into an iNOS-deficient mouse strain to examine the role of NO in tumor development in the whole animal. They report that the development of hyperplasia was delayed by 2– 4 weeks in iNOS -/animals. Tumors that developed in those animals were characteristically well differentiated in contrast to tumors that developed in the control animals, which were solid nodular adenocarcinomas with a high mitotic index and pleomorphic nuclei. No effect of iNOS was noted on vascular density, metastatic potential or macrophage infiltration. These interesting observations indicate a role for iNOS in the regulation of early events in tumorigenesis.