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Effect of Serial Passage in Nude Athymic Mice on the Growth Characteristics and Chemotherapy Responsiveness of 13762 and R3230AC Mammary Tumor Xenografts¹

Department of Tumor Biology and Experimental Cancer Therapy, Mason Research Institute, Worcester, Massachusetts, 01608 [A. E. B., D. E. K., W. R. C., T. A. G.], and Tumor Biology Section, Laboratory of Chemical Pharmacology and Experimental Chemotherapy, Drug Research and Development Program, Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland, 20014 [R. K. J.]

Serial passage of the R3230AC and 13762 rat mammary adenocarcinomas for 20 generations in nude athymic mice revealed changes in biological and chemotherapy response characteristics indicating a tumor-host relationship that questions long-term stability of the tumor xenograft-nude mouse test system. Unresponsiveness to L-phenylalanine mustard (NSC 8806), characteristic of the R3230AC tumor, remained stable, but attempts to reestablish progressive growth in previously syngeneic hosts were unsuccessful. Responsiveness to L-phenylalanine mustard, a characteristic of the 13762 tumor marked by oncolysis and many complete remissions in syngeneic hosts, was significantly reduced with no complete remissions after the tenth passage. When tumors were reestablished in syngeneic hosts, tumor growth pattern and responsiveness to L-phenylalanine mustard returned to normal by the second passage. Clearly definable acinar structures typical of the R3230AC and 13762 adenocarcinomas were markedly reduced in the R3230AC and disappeared in the 13762 after serial passage in nude mice. Acini were still absent from the 13762 tumor after being reestablished for three passages in syngeneic females. The chromosomal modes of both tumors were unchanged. These results stress the need for careful monitoring of growth and of biological and chemotherapeutic response characteristics and for periodic replacement of tumor lines to assure long-term stability of the tumor xenograftnude mouse test system.

¹ This work was supported in part by Contract N01-CM-57030 from the Division of Cancer Treatment, National Cancer Institute.

² To whom requests for reprints should be addressed, at Mason Research Institute, 57 Union Street, Worcester, Mass. 01608.

Received 6/27/77. Accepted 9/27/77.