Selenium deficiency abrogates inflammation-dependent plasma cell tumors in mice

Klaus Felix; Simone Gerstmeier; Antonios Kyriakopoulos; O M Zack Howard; Hui-Fang Dong; Michael Eckhaus; Dietrich Behne; Georg W Bornkamm; Siegfried Janz

doi:10.1158/0008-5472.CAN-03-2672

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Selenium deficiency abrogates inflammation-dependent plasma cell tumors in mice

Journal article

Open access

Peer reviewed

Selenium deficiency abrogates inflammation-dependent plasma cell tumors in mice

Klaus Felix, Simone Gerstmeier, Antonios Kyriakopoulos, O M Zack Howard, Hui-Fang Dong, Michael Eckhaus, Dietrich Behne, Georg W Bornkamm and Siegfried Janz

Cancer research (Chicago, Ill.), Vol.64(8), pp.2910-2917

04/15/2004

DOI: 10.1158/0008-5472.CAN-03-2672

PMID: 15087411

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Abstract

The role of the micronutrient, selenium, in human cancers associated with chronic inflammations and persistent infections is poorly understood. Peritoneal plasmacytomas (PCTs) in strain BALB/c (C), the premier experimental model of inflammation-dependent plasma cell transformation in mice, may afford an opportunity to gain additional insights into the significance of selenium in neoplastic development. Here, we report that selenium-depleted C mice (n = 32) maintained on a torula-based low-selenium diet (5-8 micro g of selenium/kg) were totally refractory to pristane induction of PCT. In contrast, 11 of 26 (42.3%) control mice maintained on a selenium adequate torula diet (300 micro g of selenium/kg) and 15 of 40 (37.5%) control mice fed standard Purina chow (440 micro g of selenium/kg) developed PCT by 275 days postpristane. Abrogation of PCT was caused in part by the striking inhibition of the formation of the inflammatory tissue in which PCT develop (pristane granuloma). This was associated with the reduced responsiveness of selenium-deficient inflammatory cells (monocytes and neutrophils) to chemoattractants, such as thioredoxin and chemokines. Selenium-deficient C mice exhibited little evidence of disturbed redox homeostasis and increased mutant frequency of a transgenic lacZ reporter gene in vivo. These findings implicate selenium, via the selenoproteins, in the promotion of inflammation-induced PCT and suggest that small drug inhibitors of selenoproteins might be useful for preventing human cancers linked with chronic inflammations and persistent infections.

Peritoneal Neoplasms - pathology

Oxidation-Reduction

Mice, Inbred C57BL

Plasmacytoma - genetics

Selenium - deficiency

Male

Mice, Transgenic

Plasmacytoma - pathology

Chemotaxis - drug effects

Plasmacytoma - metabolism

Terpenes - pharmacology

Tissue Distribution

Inflammation - metabolism

Animals

Chemotaxis - physiology

Selenium - metabolism

Diet

Peritoneal Neoplasms - genetics

Peritoneal Neoplasms - metabolism

Mice

Mice, Inbred BALB C

Mutation

Selenium - pharmacokinetics

Selenium - administration & dosage

Details

Title: Subtitle: Selenium deficiency abrogates inflammation-dependent plasma cell tumors in mice
Creators: Klaus Felix - Laboratory of Genetics, Center for Cancer Research, National Cancer Institute and Veterinary Resources Program, NIH, Bethesda, Maryland, USA
Simone Gerstmeier
Antonios Kyriakopoulos
O M Zack Howard
Hui-Fang Dong
Michael Eckhaus
Dietrich Behne
Georg W Bornkamm
Siegfried Janz
Resource Type: Journal article
Publication Details: Cancer research (Chicago, Ill.), Vol.64(8), pp.2910-2917
DOI: 10.1158/0008-5472.CAN-03-2672
PMID: 15087411
NLM abbreviation: Cancer Res
ISSN: 0008-5472
eISSN: 1538-7445
Language: English
Date published: 04/15/2004
Academic Unit: Pathology
Record Identifier: 9984083213802771

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