This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dairkee, S. H. Articles by Smith, H. S. Search for Related Content PubMed PubMed Citation Articles by Dairkee, S. H. Articles by Smith, H. S.

Selective Cell Culture of Primary Breast Carcinoma¹

Lawrence Berkeley Laboratory, Life Sciences Division, University of California, Berkeley, California 94720 [S. H. D., M. R. S.]; Geraldine Brush Cancer Research Institute, California Pacific Medical Center, San Francisco, California 94115 [S. H. D., G. D., H. S. S.]; and Division of Molecular Cytometry, Department of Laboratory Medicine, University of California, San Francisco, California 94143 [F. M. W.]

We have used culture conditions which simulate the microenvironment of breast tumors for the isolation and propagation of primary breast tumor cells in vitro. In this monolayer setup, the mixture of cells dissociated from primary breast tumors is subjected to self-created gradients of oxygen and nutrients as well as metabolic waste and extracellular pH. The tumor populations isolated under these novel conditions have displayed phenotypic properties characteristic of breast carcinomas, including homogeneous expression of cytokeratin 19, and increased mitochondrial retention of the cationic dye rhodamine 123. Nonmalignant cultures from reduction mammoplasty were unable to survive these conditions. One tumor population which reached passage 10 was aneuploid for chromosomes 15 and 17, and displayed a p53 mutation in exon 8. These studies strongly suggest that the culture conditions described here can suppress the growth of normal breast cells, thereby allowing selective isolation of some populations of slow-growing primary tumor cells in vitro.

¹ This work was supported by U. S. Environmental Protection Agency Grant R813784, National Cancer Institute Grants RO1 CA66998 and PO1 CA 44768, and the Office of Health and Environmental Research, U. S. Department of Energy, Contract DE-AC03-76SF00098.

² To whom requests for reprints should be addressed, at Geraldine Brush Cancer Research Institute, California Pacific Medical Center, 2330 Clay Street, San Francisco, CA 94115.

Received 3/17/95. Accepted 5/ 5/95.

This article has been cited by other articles:

				R. A. Gatenby, E. T. Gawlinski, A. F. Gmitro, B. Kaylor, and R. J. Gillies Acid-mediated tumor invasion: a multidisciplinary study. Cancer Res., May 15, 2006; 66(10): 5216 - 5223. [Abstract] [Full Text] [PDF]

				R. A. Gatenby and E. T. Gawlinski The Glycolytic Phenotype in Carcinogenesis and Tumor Invasion: Insights through Mathematical Models Cancer Res., July 15, 2003; 63(14): 3847 - 3854. [Abstract] [Full Text] [PDF]

				Z. Li, Z. H. Meng, A. Sayeed, R. Shalaby, B.-M. Ljung, and S. H. Dairkee Genome-wide Allelotyping of a New in Vitro Model System Reveals Early Events in Breast Cancer Progression Cancer Res., October 15, 2002; 62(20): 5980 - 5987. [Abstract] [Full Text] [PDF]