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Endocrinology |
Departments of 1 Medicine and 2 Pathology, Divisions of 3 Endocrinology and 4 Oncology, University of Colorado at Denver and Health Sciences Center, Aurora, Colorado
Requests for reprints: Britta M. Jacobsen, Department of Medicine/Endocrinology, University of Colorado School of Medicine, Mail Stop 8106, P.O. Box 6511, Aurora, CO 80045. Phone: 303-724-3942; Fax: 303-724-3920; E-mail: Britta.Jacobsen{at}uchsc.edu.
Adenocarcinoma cells from the pleural effusion of a patient with breast cancer were injected into the mammary glands of nude mice and grown into solid tumors. A cell line derived from these tumors expressed
-smooth muscle actin but not human cytokeratin 7, indicating "activated" stroma of mouse origin. Cells in mitosis exhibited mainly polyploid mouse karyotypes, but 30% had mixed mouse and human chromosomes, among which 8% carried mouse/human translocations. Nuclei of interphase cells were 64% hybrid. Hybrid mouse/human nuclei were also detected in the primary xenograft. Thus, synkaryons formed in the solid tumor by spontaneous fusion between the malignant human epithelium and the surrounding normal host mouse stroma. The transformed stroma-derived cells are tumorigenic with histopathologic features of malignancy, suggesting a new mechanism for tumor progression. (Cancer Res 2006; 66(16): 8274-9)
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R. J. Pelham, L. Rodgers, I. Hall, R. Lucito, K. C. Q. Nguyen, N. Navin, J. Hicks, D. Mu, S. Powers, M. Wigler, et al. Identification of alterations in DNA copy number in host stromal cells during tumor progression PNAS, December 26, 2006; 103(52): 19848 - 19853. [Abstract] [Full Text] [PDF] |
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