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Regular Article| Volume 88, ISSUE 2, P130-134, February 2000

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MnSOD Expression Is Increased in Metastatic Gastric Cancer

DOI:https://doi.org/10.1006/jsre.1999.5773
MnSOD Expression Is Increased in Metastatic Gastric Cancer
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      Abstract

      Background. Manganese superoxide dismutase (MnSOD) catalyzes the scavenging of superoxide radicals in order to protect cells from the damage caused by reactive oxygen species. Previous studies implicate MnSOD in cancer progression, but its role in gastric cancer metastasis is poorly understood.
      Materials and methods. To determine whether MnSOD expression correlates with gastric cancer metastasis, we compared immunostaining for MnSOD in the primary tumors of gastric cancer patients with (n = 15) and without (n = 9) nodal metastases. These patients were matched for risk factors associated with gastric cancer metastasis, such as tumor site, depth, and grade. MnSOD expression was scored positive (increased) if MnSOD staining of tumor cells was more intense than MnSOD staining in corresponding normal gastric epithelial cells. Statistical analyses were via χ2 test and Fisher's exact test.
      Results. MnSOD expression was increased in 14 of the 15 (93%) metastatic tumors, compared to only 4 of the 9 (44%) nonmetastatic tumors (P = 0.015). There was no significant difference in staining when the two groups were compared based on tumor grade (P = 0.70) or depth of tumor cell invasion (T stage) (P = 0.22).
      Conclusions. MnSOD expression is upregulated in the primary tumors of gastric cancer patients with lymph node metastases. This finding supports an involvement of MnSOD and possibly the reactive oxygen status of the gastric tumor microenvironment in gastric cancer metastasis.

      Keywords

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      Article info

      Footnotes

      ☆This work was supported by grants from the William E. McElroy Charitable Foundation and a Minority Supplement to NIH Grant RO1 DC02396.

      Identification

      DOI: https://doi.org/10.1006/jsre.1999.5773

      Copyright

      © 2000 Academic Press. Published by Elsevier Inc. All rights reserved.

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