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Establishment and Characterization of Human Renal Cancer and Normal Kidney Cell Lines¹

Laboratory of Human Cancer Immunology, Memorial Sloan-Kettering Cancer Center, and The James Buchanan Brady Foundation, Department of Surgery/Division of Urology, The New York Hospital-Cornell Medical Center, New York, New York 10021

We have reviewed our laboratory's efforts to establish continuous human renal cancer cell lines. During the 16-year period of 1972 through 1987, 498 successive attempts resulted in establishment of 63 renal cancer cell lines. Of these lines, 46 were derived from primary kidney tumors and 17 from metastatic sites (lung, brain, bone, and lymph node). Forty-three of these lines have been characterized with regard to morphology, growth kinetics, anchorage-independent growth, tumorigenicity in athymic nude mice, and expression of kidney cell surface antigens. These results were compared with data from primary short term cultures of normal kidney epithelium. The overall success rate of establishing continuous renal cancer cell lines was 12.7%. In general, no significant difference in success was noted based on whether the specimen was derived from a primary or a metastatic lesion. However, all successfully established lines were derived from tumors exhibiting clinically "aggressive" behavior. All cell lines expressed proximal tubular cell differentiation antigens. Significant morphological heterogeneity was observed among normal kidney as well as kidney cancer cell lines in vitro. No significant difference in doubling time was found between cell lines of renal cancer and passage 1 cultures of normal kidney epithelium. Twenty-one of 30 (70%) lines assayed formed clones on soft agar and 26 of 33 (79%) lines grew in athymic mice. Among the 25 lines which were assayed for both soft agar growth and tumorigenicity in nude mice, this pair of phenotypic traits were concordant in 17 lines (60%). Four lines (16%) grew on agar but not in mice, while four other lines (16%) failed to grow in agar but were tumorigenic in mice.

¹ This work was supported by grants from the Oliver S. and Jennie R. Donaldson Charitable Trust, Inc., The Fred Grossman Fund, The Robert and Iris Chernok Fund, and National Institutes of Health Grants CA-08748 and CA-33049.

² Current address: University of Dusseldorf Medical School, Department of Urology, Moorenstr. 5, 4000 Dusseldorf, FRG.

³ To whom requests for reprints should be addressed, at Division of Urology, Box 94, The New York Hospital-Cornell Medical Center, 525 East 68th Street, New York, N.Y. 10021.

Received 2/ 7/90. Revised 5/ 8/90.

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