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 Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Zajchowski, D. Articles by Sager, R. Search for Related Content PubMed Articles by Zajchowski, D. Articles by Sager, R.

Expression of Growth Factors and Oncogenes in Normal and Tumor-derived Human Mammary Epithelial Cells¹

Division of Cancer Genetics, Dana-Farber Cancer Institute, Boston, Massachusetts 02115 [D. Z., V. B., N. P., A. T., R. S.], and Lawrence Berkeley Laboratories, Berkeley, California 94720 [M. S.]

The expression of genes which may be involved in the regulation of human mammary epithelial cell growth [transforming growth factors and ß] and tumorigenesis [c-myc, erbB2, epidermal growth factor receptor (EGFR), Ha-ras, pS2] has been compared in similarly cultured normal cell strains and tumor cell lines. We have found that the normal breast cells produce high levels of EGFR mRNA, which are translated into nearly 10⁵ low affinity epidermal growth factor-binding molecules/cell. In the estrogen receptor-negative lines examined, the EGFR gene was expressed at levels comparable to those in the normal cells. In contrast, EGFR and transforming growth factor mRNAs were reduced in estrogen receptor-positive tumor lines compared to estrogen receptor-negative lines and normal cells. Steady state mRNA levels for transforming growth factor ß, erbB2, c-myc, and Ha-ras in the normal cells were greater than or comparable to those in all of the breast tumor lines. Furthermore, in the absence of gene amplification, only one of the genes examined (i.e., pS2) was overexpressed in a subset of the tumor cells compared to their normal counterparts. Several reports by other investigators have described overexpression of some of these genes in breast biopsies and in tumor lines in studies lacking normal controls. Thus, our results, in which the same genes were not overexpressed compared to normal cells unless amplified, underscore the importance of including appropriate normal controls in studies aimed at defining aberrant patterns of gene expression in tumor cells.

¹ Supported by NIH Grant CA-39814.

² To whom requests for reprints should be addressed, at Division of Cancer Genetics, Dana-Farber Cancer Institute, 44 Binney St., Boston, MA 02115.

Received 5/ 6/88. Revised 8/25/88. Accepted 9/ 1/88.