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Selenium deficiency abrogates inflammation-dependent plasma cell tumors in mice
Klaus Felix1, Simone Gerstmeier, Antonios Kyriakopoulos
1Laboratory of Genetics, Center for Cancer Research, National Cancer Institute and Veterinary Resources Program, NIH, Bethesda, Maryland, USA.
Cancer Research
|April 17, 2004
Summary
Selenium deficiency completely prevented inflammation-induced peritoneal plasmacytomas (PCTs) in mice by inhibiting inflammatory tissue formation. This suggests selenoproteins are key in promoting these cancers, offering potential therapeutic targets.
Area of Science:
- Oncology
- Immunology
- Nutritional Science
Background:
- The role of selenium in cancers linked to chronic inflammation and infection is unclear.
- Peritoneal plasmacytomas (PCTs) in BALB/c mice serve as a model for inflammation-dependent plasma cell transformation.
Purpose of the Study:
- To investigate the significance of selenium in neoplastic development using an inflammation-induced PCT mouse model.
- To determine if selenium deficiency affects the induction of PCT.
Main Methods:
- BALB/c mice were fed either a low-selenium or selenium-adequate diet.
- PCTs were induced using pristane, and tumor development was monitored.
- Inflammatory tissue formation and inflammatory cell responsiveness were assessed.
Main Results:
- Selenium-depleted mice were completely refractory to pristane-induced PCT development.
- PCT incidence in control mice was 42.3% and 37.5% on adequate diets.
- Selenium deficiency inhibited pristane granuloma formation and reduced inflammatory cell chemoattractant responsiveness.
Conclusions:
- Selenium, through selenoproteins, promotes inflammation-induced PCT development.
- Selenium deficiency abrogates PCT by inhibiting inflammatory responses.
- Inhibitors of selenoproteins may offer a strategy for preventing chronic inflammation-associated cancers.