© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 1, 86-88,
January 6, 1999
© 1999 Oxford University Press
BRIEF COMMUNICATION |
Relationship Between p53 Mutations and Inducible Nitric Oxide Synthase Expression in Human Colorectal Cancer
Affiliations of authors: S. Ambs, W. P. Bennett, W. G.Merriam, M. O. Ogunfusika, S. M. Oser, A. M. Harrington, P. G. Shields, S. P. Hussain, C. C. Harris, Laboratory of Human Carcinogenesis, Division of Basic Sciences, National Cancer Institute, Bethesda, MD; E. Felley-Bosco, Institute of Pharmacology and Toxicology, University of Lausanne, Switzerland.
Correspondence to: Curtis C. Harris, M.D., National Institutes of Health, Bldg. 37, Rm. 2C01, 37 Convent Dr. MSC 4255, Bethesda, MD 20892-4255 (e-mail: Curtis_Harris@nih.gov).
Inducible Ca2+-independent nitric oxide synthase (NOS), also referred to as NOS2, which is expressed in a variety of human cancers (1-4), can generate mutagenic concentrations of nitric oxide (NO) in mice (5). NOS2 is the most active isoform among the three known nitric oxide synthases (6), which also include the neuronal (NOS1) and endothelial (NOS3) isoforms. Only NOS2 is capable of producing sustained NO concentrations in the micromolar range (7).
We investigated the hypothesis that NO generated by NOS2 is capable of
inducing mutations in the p53 (also known as TP53) gene and contributes
to human colon carcinogenesis. We analyzed 118 sporadic colon tumors
for NOS2 expression and p53 gene mutations. Colon tumors and
surrounding normal tissues were collected from the Cooperative Human
Tissue Network and the Department of Pathology, University of
Baltimore, with the approval of local boards
NOTES
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