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Human in Vitro System for the Detection of Uterine Cervical Preinvasive Carcinoma¹

Departments of Pathology [S. C., I. K., P. B. P.] and Obstetrics and Gynecology [D. E. R. T.], Temple University Health Sciences Center, Philadelphia, Pennsylvania 19140

The relationship among dysplasia, carcinoma in situ, and invasive carcinoma of the human uterine cervix was investigated by utilizing the in vitro growth properties of epithelial cells and stromal fibroblasts in a series of 25 clinical cases. A close relationship between carcinoma in situ and invasive carcinoma was suggested by the similarity in the primary culture characteristics of epithelial cells. However, a better correlation was obtained by comparing the growth properties of underlying stromal fibroblasts. The stromal fibroblasts underlying a dysplastic area showed a predominantly uniform growth pattern, while the fibroblasts from the stroma underlying carcinoma in situ and invasive carcinoma exhibited a predominantly disorganized growth pattern with criss-crossing. The stromal fibroblasts from sites of carcinoma in situ also had a decreased serum dependency for growth, as compared to dysplasia, and corresponded to that associated with invasive carcinoma.

The optimum pH for growth of epithelial cells and stromal fibroblasts was found to be pH 7.0 and pH 7.6, respectively, but the epithelial cells from all types of lesions were very difficult to maintain for a long period of time. Only one long-time culture of epithelial cells from a case of dysplasia could be obtained. This epithelial cell line was subcultured through 15 transfers and maintained. Fibroblasts, however, could be maintained for a long period of time without any difficulty, and long-time cultures of different stromal fibroblasts were obtained.

Attention was drawn to the progressive changes in mesenchymal cells during evolution of epithelial neoplasia and to the feasibility of using the described alterations of fibroblasts as an additional diagnostic parameter in the management of intraepithelial neoplasia.

¹ This study was supported by USPHS Grants 1 R01 CA13032-01 and 02, Training Grant 5 TO 1 CA05222-05, and Core Grant 5 OP1 CA12923-01.

Received 12/13/73. Accepted 2/25/74.