Reduction of murine mammary tumor metastasis by conjugated linoleic acid

Neil Hubbard, Debora Lim, Lauri Summers, Kent L Erickson

Research output: Contribution to journalArticle

70 Citations (Scopus)

Abstract

Recent studies have shown that conjugated linoleic acid (CLA) can inhibit the initiation and thus, incidence of mammary tumors in rodents. The concentration of CLA required for these effects was as low as 0.1% of the diet, with no increased effects above 1%. To date, there is little evidence that CLA has any effect on growth or metastasis of mammary tumors. In this report, we demonstrate that CLA, at the concentrations used in previous studies, had a significant effect on the latency, metastasis, and pulmonary tumor burden of transplantable murine mammary tumors grown in mice fed 20% fat diets. The latency of tumors from mice fed CLA was significantly increased when compared with the 0% CLA control diet. The volume of pulmonary tumor burden, as a result of spontaneous metastasis, decreased proportionately with increasing concentrations of dietary CLA. With 0.5 and 1% CLA, pulmonary tumor burden was significantly decreased compared to mice treated with the eicosanoid inhibitor, indomethacin and fed diets containing no CLA. Tumors of mice fed as little as 0.1% CLA and as much as 1% had significantly decreased numbers of pulmonary nodules when compared with diets containing no CLA. The decrease in the number of pulmonary nodules by CLA was nearly as effective as indomethacin, a known suppressor of tumor growth and metastasis in this malignant model. These data suggest that effects of CLA on mammary tumorigenesis may go beyond the reported alterations in tumor incidence and effect later stages, especially metastasis. (C) 2000 Elsevier Science Ireland Ltd.

Original languageEnglish (US)
Pages (from-to)93-100
Number of pages8
JournalCancer Letters
Volume150
Issue number1
DOIs
StatePublished - Mar 13 2000

Fingerprint

Conjugated Linoleic Acids
Breast Neoplasms
Neoplasm Metastasis
Diet
Lung
Tumor Burden
Indomethacin
Neoplasms
Eicosanoids
Incidence
Growth

Keywords

  • Conjugated linoleic acid
  • Mammary tumor
  • Metastasis
  • Murine

ASJC Scopus subject areas

  • Cancer Research
  • Molecular Biology
  • Oncology

Cite this

Reduction of murine mammary tumor metastasis by conjugated linoleic acid. / Hubbard, Neil; Lim, Debora; Summers, Lauri; Erickson, Kent L.

In: Cancer Letters, Vol. 150, No. 1, 13.03.2000, p. 93-100.

Research output: Contribution to journalArticle

@article{c29a53bac60f45fdb7cef53fa70ed64e,
title = "Reduction of murine mammary tumor metastasis by conjugated linoleic acid",
abstract = "Recent studies have shown that conjugated linoleic acid (CLA) can inhibit the initiation and thus, incidence of mammary tumors in rodents. The concentration of CLA required for these effects was as low as 0.1{\%} of the diet, with no increased effects above 1{\%}. To date, there is little evidence that CLA has any effect on growth or metastasis of mammary tumors. In this report, we demonstrate that CLA, at the concentrations used in previous studies, had a significant effect on the latency, metastasis, and pulmonary tumor burden of transplantable murine mammary tumors grown in mice fed 20{\%} fat diets. The latency of tumors from mice fed CLA was significantly increased when compared with the 0{\%} CLA control diet. The volume of pulmonary tumor burden, as a result of spontaneous metastasis, decreased proportionately with increasing concentrations of dietary CLA. With 0.5 and 1{\%} CLA, pulmonary tumor burden was significantly decreased compared to mice treated with the eicosanoid inhibitor, indomethacin and fed diets containing no CLA. Tumors of mice fed as little as 0.1{\%} CLA and as much as 1{\%} had significantly decreased numbers of pulmonary nodules when compared with diets containing no CLA. The decrease in the number of pulmonary nodules by CLA was nearly as effective as indomethacin, a known suppressor of tumor growth and metastasis in this malignant model. These data suggest that effects of CLA on mammary tumorigenesis may go beyond the reported alterations in tumor incidence and effect later stages, especially metastasis. (C) 2000 Elsevier Science Ireland Ltd.",
keywords = "Conjugated linoleic acid, Mammary tumor, Metastasis, Murine",
author = "Neil Hubbard and Debora Lim and Lauri Summers and Erickson, {Kent L}",
year = "2000",
month = "3",
day = "13",
doi = "10.1016/S0304-3835(99)00379-1",
language = "English (US)",
volume = "150",
pages = "93--100",
journal = "Cancer Letters",
issn = "0304-3835",
publisher = "Elsevier Ireland Ltd",
number = "1",

}

TY - JOUR

T1 - Reduction of murine mammary tumor metastasis by conjugated linoleic acid

AU - Hubbard, Neil

AU - Lim, Debora

AU - Summers, Lauri

AU - Erickson, Kent L

PY - 2000/3/13

Y1 - 2000/3/13

N2 - Recent studies have shown that conjugated linoleic acid (CLA) can inhibit the initiation and thus, incidence of mammary tumors in rodents. The concentration of CLA required for these effects was as low as 0.1% of the diet, with no increased effects above 1%. To date, there is little evidence that CLA has any effect on growth or metastasis of mammary tumors. In this report, we demonstrate that CLA, at the concentrations used in previous studies, had a significant effect on the latency, metastasis, and pulmonary tumor burden of transplantable murine mammary tumors grown in mice fed 20% fat diets. The latency of tumors from mice fed CLA was significantly increased when compared with the 0% CLA control diet. The volume of pulmonary tumor burden, as a result of spontaneous metastasis, decreased proportionately with increasing concentrations of dietary CLA. With 0.5 and 1% CLA, pulmonary tumor burden was significantly decreased compared to mice treated with the eicosanoid inhibitor, indomethacin and fed diets containing no CLA. Tumors of mice fed as little as 0.1% CLA and as much as 1% had significantly decreased numbers of pulmonary nodules when compared with diets containing no CLA. The decrease in the number of pulmonary nodules by CLA was nearly as effective as indomethacin, a known suppressor of tumor growth and metastasis in this malignant model. These data suggest that effects of CLA on mammary tumorigenesis may go beyond the reported alterations in tumor incidence and effect later stages, especially metastasis. (C) 2000 Elsevier Science Ireland Ltd.

AB - Recent studies have shown that conjugated linoleic acid (CLA) can inhibit the initiation and thus, incidence of mammary tumors in rodents. The concentration of CLA required for these effects was as low as 0.1% of the diet, with no increased effects above 1%. To date, there is little evidence that CLA has any effect on growth or metastasis of mammary tumors. In this report, we demonstrate that CLA, at the concentrations used in previous studies, had a significant effect on the latency, metastasis, and pulmonary tumor burden of transplantable murine mammary tumors grown in mice fed 20% fat diets. The latency of tumors from mice fed CLA was significantly increased when compared with the 0% CLA control diet. The volume of pulmonary tumor burden, as a result of spontaneous metastasis, decreased proportionately with increasing concentrations of dietary CLA. With 0.5 and 1% CLA, pulmonary tumor burden was significantly decreased compared to mice treated with the eicosanoid inhibitor, indomethacin and fed diets containing no CLA. Tumors of mice fed as little as 0.1% CLA and as much as 1% had significantly decreased numbers of pulmonary nodules when compared with diets containing no CLA. The decrease in the number of pulmonary nodules by CLA was nearly as effective as indomethacin, a known suppressor of tumor growth and metastasis in this malignant model. These data suggest that effects of CLA on mammary tumorigenesis may go beyond the reported alterations in tumor incidence and effect later stages, especially metastasis. (C) 2000 Elsevier Science Ireland Ltd.

KW - Conjugated linoleic acid

KW - Mammary tumor

KW - Metastasis

KW - Murine

UR - http://www.scopus.com/inward/record.url?scp=0034007596&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034007596&partnerID=8YFLogxK

U2 - 10.1016/S0304-3835(99)00379-1

DO - 10.1016/S0304-3835(99)00379-1

M3 - Article

C2 - 10755392

AN - SCOPUS:0034007596

VL - 150

SP - 93

EP - 100

JO - Cancer Letters

JF - Cancer Letters

SN - 0304-3835

IS - 1

ER -