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      The retinoid X receptor-selective retinoid, LGD1069, prevents the development of estrogen receptor-negative mammary tumors in transgenic mice.

      Cancer research
      Animals, Anticarcinogenic Agents, pharmacology, Cell Division, drug effects, Female, Gene Expression, Genes, erbB-2, Mammary Glands, Animal, cytology, Mammary Neoplasms, Experimental, genetics, metabolism, pathology, prevention & control, Mammary Tumor Virus, Mouse, Mice, Mice, Transgenic, Receptors, Estrogen, physiology, Receptors, Retinoic Acid, Retinoid X Receptors, Tetrahydronaphthalenes, Transcription Factors, Transgenes

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          Abstract

          Despite the effectiveness of the selective estrogen receptor (ER) modulators in preventing ER-positive breast cancer, chemopreventive agents still need to be developed for the prevention of ER-negative breast cancers. The naturally occurring retinoids are promising agents for the prevention of human cancers but are too toxic for long-term chronic use. We previously demonstrated that the chemopreventive effects of the retinoids could be separated from the toxicity by using an RXR-selective retinoid, LGD1069. The studies described here demonstrate that LGD1069 effectively suppresses ER-negative tumor development in mouse mammary tumor virus-erbB2 transgenic mice with minimal toxicity. These studies suggest that receptor-selective retinoids are promising agents for the prevention of breast cancer and that they may be particularly useful in preventing ER-negative breast cancer.

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