Summary
During 1973, 4 new epithelial tumor cell lines were isolated from pleural effusions from breast cancer patients. We describe 3 of these lines: MDA-MB-134, with a mean chromosome number of 43; MDA-MB-175, with a mean chromosome number of 49; and MDA-MB-231, with a mean chromosome number between 65 and 69. We isolated the same cell type from 4 of 10 effusions from MDA-MB-134 and from 6 of 8 effusions from MDA-MB-175. We found that pleural effusions as a source of breast tumor cells to be cultured and studied in vitro have the following advantages: 1) large amounts of material and the possibility of obtaining sequential samples from the same patient; 2) high viability of tumor cells; 3) scarcity or absence of fibroblasts; and 4) the possibility of separating the tumor cells from other “contaminating” cell types by differences in their speed or degree of attachment to the flask. All lines from different patients differed, as seen grossly and microscopically. All lines from sequential pleural effusions from the same patient were apparently alike. No viruses or mycoplasmas were detected in any line.
Nineteen human breast carcinoma cell lines have been established as continuous cultures during the past 6 years in our laboratory. This preliminary report is designed to list the lines by their designated code numbers (MDA-MB) and present a brief summary of their morphological, cytogenetic and biochemical characteristics. Sixteen of our lines were obtained from pleural effusions, two from brain metastases, and one from pericardial fluid. All lines have been shown to be distinct entities and are uncontaminated by HeLa cells or each other. A lq marker chromosome is present in all but one of the lines examined.
Epidermal growth factor (EGF) has been noted to stimulate prolifereation of a variety of normal and malignant cells including those of human breast epithelium. We report here that MDA-468, a human breast cancer cell line with a very high number of EGF receptors, is growth-inhibited at EGF concentrations that stimulate most other cells. The basis for the elevated receptor level is EGF receptor gene amplification and over-expression. An MDA-468 clone selected for resistance to EGF-induced growth inhibition shows a number of receptors within the normal range. The results are discussed in relation to a threshold model for EGF-induced growth inhibition
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