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Simultaneous Suppression of Epidermal Growth Factor Receptor and c-erbB-2 Reverses Aneuploidy and Malignant Phenotype of a Human Ovarian Carcinoma Cell Line

¹ Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, ² Division of Therapeutic Proteins, Office of Therapeutic Research and Review, Center for Biologics Evaluation and Research, Food and Drug Administration, ³ Genetics Branch, Center for Cancer Research, and ⁴ Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland; ⁵ Institute for Molecular and Human Genetics, ⁶ Laboratory of Pathology, ⁷ Department of Oncology, and ⁸ Department of Biostatistics, Vincent T. Lombardi Cancer Center, Georgetown University Medical School, Washington DC; ⁹ Gynaecological Cancer Center, Royal Hospital for Women, New South Wales, Sydney, Australia; and ¹⁰ Children’s Hospital Informatics Program, Harvard Medical School, Boston, Massachusetts

Coexpression of epidermal growth factor receptor (EGFR) and c-erbB-2 in 47–68% of ovarian cancer cells indicate their strong association with tumor formation. We examined the effects of simultaneous antisense- or immunosuppression of EGFR and c-erbB-2 expression on the invasive phenotype, aneuploidy, and genotype of cultured human ovarian carcinoma cells (NIH:OVCAR-8). We report here that suppression of both EGFR and c-erbB-2 results in regression of aneuploidy and genomic imbalances in NIH:OVCAR-8 cells, restores a more normal phenotype, and results in a more normal gene expression profile. Combined with cytogenetic analysis, our data demonstrate that the regression of aneuploidy is due to the selective apoptosis of double antisense transfected cells with highly abnormal karyotype.

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