Inflammatory cell-mediated tumour progression and minisatellite mutation correlate with the decrease of antioxidative enzymes in murine fibrosarcoma cells
1999

Inflammation and Tumor Growth in Mice

Sample size: 6 publication Evidence: moderate

Author Information

Author(s): Okada F, Nakai K, Kobayashi T, Shibata T, Tagami S, Kawakami Y, Kitazawa T, Kominami R, Yoshimura S, Suzuki K, Taniguchi N, Inanami O, Kuwabara M, Kishida H, Nakae D, Konishi Y, Moriuchi T, Hosokawa M

Primary Institution: Laboratory of Pathology, Cancer Institute, Sapporo, Japan

Hypothesis

Tumor progression is influenced by inflammation and the levels of antioxidative enzymes in fibrosarcoma cells.

Conclusion

Tumor progression is accelerated by inflammation-induced active oxygen species, especially when antioxidative enzyme levels are low in tumor cells.

Supporting Evidence

  • The QR clones were unable to grow in normal mice but formed aggressive tumors when co-implanted with a gelatin sponge.
  • There was a significant inverse correlation between tumor formation and levels of manganese superoxide dismutase and glutathione peroxidase.
  • The superoxide-scavenging ability was higher in QR clones with high levels of Mn-SOD compared to those with low levels.
  • Minisatellite mutation rates were higher in subclones with low levels of antioxidative enzymes.
  • The content of 8-hydroxydeoxyguanosine was significantly lower in tumors from QR clones with high levels of Mn-SOD and GPχ.

Takeaway

When certain cells that cause inflammation are present, tumors can grow faster, especially if the tumor cells have low levels of protective enzymes.

Methodology

The study involved isolating fibrosarcoma clones and assessing their tumorigenicity when co-implanted with a gelatin sponge, along with enzyme activity assays and DNA fingerprint analysis.

Participant Demographics

Murine (mice) models were used in the study.

Statistical Information

P-Value

p<0.001

Statistical Significance

p<0.001

Digital Object Identifier (DOI)

10.1038/sj.bjc.6690060

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