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Inducible nitric oxide synthase (iNOS) immunoreactivity and its relationship to cell proliferation, apoptosis, angiogenesis, clinicopathologic characteristics, and patient survival in pancreatic cancer

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Summary

Background. The clinicopathological and biological significance of the expression of iNOS in pancreatic cancer remains unclear. The goal of this study was to determine the possible roles and clinical significance of iNOS expression in pancreatic cancer.

Methods. Seventy-two pancreatic adenocarcinoma tissue specimens were obtained by surgical resection. We investigated the immunohistochemical expression of iNOS in 72 patients with pancreatic cancer with respect to variable clinicopathological characteristics, proliferation activity (assessed by Ki-67 expression), apoptosis (assessed by TUNEL stain), and microvessel density (assessed by CD34 expression; angiogenesis).

Results. Immunohistochemical investigations demonstrated immunolabeling of tumor cells with anti-iNOS antibody. Positivity for iNOS was observed in 48/72 (66.7%). The expression of iNOS protein did not correlate with age, bilirubin, tumor marker, location, size, AJCC stage, differentiation, distant metastasis, or patient survival. No significanct association was found between iNOS expression and proliferation or microvessel density in pancreatic cancer. Apoptotic index (AI) of positive iNOS expressions were significantly higher than negative expression (p<0.001).

Conclusion. Inducible nitric oxide synthase (iNOS) is expressed by human pancreatic cancer, and its presence is positively correlated with apoptosis of cancer cells that could provide the basis for the development of therapeutic strategies in human pancreatic cancer.

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Correspondence to Kyu Taek Lee.

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Kong, G., Kim, E.K., Kim, W.S. et al. Inducible nitric oxide synthase (iNOS) immunoreactivity and its relationship to cell proliferation, apoptosis, angiogenesis, clinicopathologic characteristics, and patient survival in pancreatic cancer. International Journal of Pancreatology 29, 133–140 (2001). https://doi.org/10.1385/IJGC:29:3:133

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  • DOI: https://doi.org/10.1385/IJGC:29:3:133

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