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JNCI Journal of the National Cancer Institute 1999 91(1):86-88; doi:10.1093/jnci/91.1.86
© 1999 by Oxford University Press
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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

Stefan Ambs, William P. Bennett, William G. Merriam, Mofolusara O. Ogunfusika, Sean M. Oser, Anita M. Harrington, Peter G. Shields, Emanuela Felley-Bosco, S. Perwez Hussain, Curtis C. Harris

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 . . . [Full Text of this Article]

NOTES

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