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      Metastatic progression and gene expression between breast cancer cell lines from African American and Caucasian women

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          Abstract

          African American (AA) women have a lower overall incidence of breast cancer than do Caucasian (CAU) women, but a higher overall mortality. Little is known as to why the incidence of breast cancer is lower yet mortality is higher in AA women. Many studies speculate that this is only a socio-economical problem. This investigation suggests the possibility that molecular mechanisms contribute to the increased mortality of AA women with breast cancer. This study investigates the expression of 14 genes which have been shown to play a role in cancer metastasis. Cell lines derived from AA and CAU patients were analyzed to demonstrate alterations in the transcription of genes known to be involved in cancer and the metastatic process. Total RNA was isolated from cell lines and analyzed by RT-PCR analysis. Differential expression of the 14 targeted genes between a spectrum model (6 breast cancer cell lines and 2 non-cancer breast cell lines) and a metastasis model (12 metastatic breast cancer cell lines) were demonstrated. Additionally, an in vitro comparison of the expression established differences in 5 of the 14 biomarker genes between African American and Caucasian breast cell lines. Results from this study indicates that altered expression of the genes Atp1b1, CARD 10, KLF4, Spint2, and Acly may play a role in the aggressive phenotype seen in breast cancer in African American women.

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          Most cited references49

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          Cancer metastasis and angiogenesis: an imbalance of positive and negative regulation.

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            Metabolism of neoplastic tissue. IV. A study of lipid synthesis in neoplastic tissue slices in vitro.

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              Functional analysis of secreted and transmembrane proteins critical to mouse development.

              We describe the successful application of a modified gene-trap approach, the secretory trap, to systematically analyze the functions in vivo of large numbers of genes encoding secreted and membrane proteins. Secretory-trap insertions in embryonic stem cells can be transmitted to the germ line of mice with high efficiency and effectively mutate the target gene. Of 60 insertions analyzed in mice, one-third cause recessive lethal phenotypes affecting various stages of embryonic and postnatal development. Thus, secretory-trap mutagenesis can be used for a genome-wide functional analysis of cell signaling pathways that are critical for normal mammalian development and physiology.
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                Author and article information

                Journal
                J Carcinog
                Journal of Carcinogenesis
                BioMed Central (London )
                1477-3163
                2007
                1 May 2007
                : 6
                : 8
                Affiliations
                [1 ]Department of Arts and Sciences, Coppin State University, Baltimore, MD, 21216, USA
                [2 ]Department of Microbiology, College of Medicine, Howard University, Washington, D.C. 20059, USA
                [3 ]Department of Physiology, Howard University, Washington, D.C. 20059, USA
                [4 ]Division of Pathology, Walter Reed Army Institute for Research, Silver Spring, MD 20910, USA
                Article
                1477-3163-6-8
                10.1186/1477-3163-6-8
                1876212
                17472751
                99b372b1-7194-480f-ab41-d86eb340791d
                Copyright © 2007 Yancy et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 18 August 2006
                : 1 May 2007
                Categories
                Short Paper

                Oncology & Radiotherapy
                Oncology & Radiotherapy

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