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Elevated Concentrations of Serum -Fetoprotein in Rats with Chemically Induced Liver Tumors¹

National Cancer Institute, NIH, Bethesda, Maryland 20014 [R. K., J. M. S., G. M. W., J. H. W.], and Department of Pathology, San Diego Medical School, University of California, La Jolla, California 92037 [S. S.]

The study was undertaken to determine whether aflatoxin B₁ (AFB₁)-induced liver tumors in rats produced ₁-fetoprotein (AFP) and whether the age of the animals would influence such an appearance, a finding suggested by data seen in man. Other liver carcinogens (N-hydroxy-N-2-fluorenylacetamide, N-2-fluorenylacetamide, and diethylnitrosamine) were tested for their ability to induce liver tumors producing AFP. The presence of AFP in the serum was determined by double diffusion in agarose and by comparison also by quantitative radioimmunoassay.

Using double diffusion, AFP was detected in the majority of tumor-bearing rats that had received either N-2-fluorenylacetamide or N-hydroxy-N-2-fluorenylacetamide. Sera of diethylnitrosamine-treated rats with liver tumors were all positive, whereas sera of rats bearing AFB₁-induced tumors were positive in only a few cases. However, all sera of tumor-bearing rats examined had elevated AFP levels by radioimmunoassay. Nonetheless, the average level of AFP in the sera of rats bearing AFB₁-induced tumors was considerably lower, compared to the sera of rats with tumors caused by diethylnitrosamine, N-2-fluorenylacetamide, or N-hydroxy-N-2-fluorenylacetamide. Rats started on AFB₁ when 6 weeks old had more mixed liver tumors with neoplastic hepatocytes and bile ducts and higher AFP levels than did rats started at 26 weeks of age. However, the histological grade of differentiation of induced tumors did not seem to influence the AFP level.

¹ A portion of this work was presented at the Sixty-fourth meeting of the American Association for Cancer Research (35).

² This work was undertaken during the tenure of a Research Training Fellowship (International Agency for Research on Cancer, Lyon, France) while the recipient was on leave of absence from the Laboratory of Pathology, Rijks Instituut voor de Volksgezondheid, Bilthoven, The Netherlands (present address).

³ This work was undertaken during the tenure of a postdoctoral fellowship awarded by the Damon Runyon Memorial Fund for Cancer Research. To whom reprint requests should be addressed, at Landow Building, Room A-306, National Cancer Institute, Bethesda, Md. 20014.

⁴ Supported in part by Contract I-CP-33404 from the National Cancer Institute.

⁵ Present address: Department of Pathology, Temple University School of Medicine and Fels Research Institute, Philadelphia, Pa. 19140.

⁶ Present address: Naylor Dana Institute for Disease Prevention. American Health Foundation, 2 East End Ave., New York, N. Y. 10021. Supported in part by Grants CA-12376, CA-14298, and CA-15400 from the National Cancer Institute.

Received 11/11/74. Accepted 1/30/75.