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 Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Attia, M. A. Articles by Weiss, D. W. Search for Related Content PubMed PubMed Citation Articles by Attia, M. A. Articles by Weiss, D. W.

Immunology of Spontaneous Mammary Carcinomas in Mice

II. Resistance to a Rapidly and a Slowly Developing Tumor¹

( Department of Bacteriology and Department of Zoology and the Cancer Research Genetics Laboratory, University of California, Berkeley, California)

Mice of the C3H/f/Crgl and C3H/Crgl/2 sublines acquired a considerable degree of heightened resistance to the growth of implants of 2 recently arisen spontaneous C3H/Crgl mammary carcinomas as a result of previous exposure to living and killed tumor cells. Pretreatment with normal C3H/2 tissues did not induce tumor resistance, and tumor-resistant mice accepted C3H/2 skin isografts. The mutual isogenicity of the C3H, C3H/f, and C3H/2 sublines was further shown by the permanent acceptance of first and second set reciprocal skin grafts exchanged between randomly chosen pairs of young adult females. The tumor resistance evoked by the previous tumor experience could not be ascribed, therefore, to a residual heterozygosis of normal isoantigenic characteristics among or between the 3 C3H sublines employed, but appears to have evoked by immunogenic properties related to the tumors.

The immunologic nature of the tumor resistance was indicated by a significant enlargement of the lymph nodes of the resistant animals, and by the ability of lymph node and peritoneal washing cells, but not of serum, to passively transfer the resistance to normal isogenic animals. Both tumors developed more rapidly in neonatal than in adult hosts.

The more rapidly developing tumor of the 2 appeared to the more immunogenic. The possible reasons for this are discussed.

¹ This work was supported by grants AI-2309 and CA-05388 from the NIH of the USPHS, E-292 of the American Cancer Society, and by Cancer Research Funds of the University of California.

Received 10/28/64.