Myeloid Hyperplasia Brought about in Mice by the Growth of Dibenzanthracene Tumors and its Relation to the Transplantability of the Tumors into Mice of Alien Strains

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Abstract
In 1936 Lewis and Lichtenstein found that the resistance of pure inbred mice of one strain to the transplantation of tumors induced by means of 1:2:5:6-dibenzanthracene in mice of another strain could be broken down by repeated inoculations with tumors from the alien strain mice. As a result of these investigations, tumors from strain A mice were grown in mice of the BA strain, tumors from strain BA mice in those of the C3H strain, and tumors from strain C3H in mice of the BA strain. A total of 101 tumors from one strain of mice were grown in repeatedly inoculated mice of another pure inbred strain, and five of these experimental tumors (PHS 20, C3H 11, BA 6, C3H 4 and C3H 25) were thereafter carried by serial passage through a number of generations in normal mice of more than one strain. Although 54 tumors developed in 19 of the 24 BA strain mice treated with tumors from A strain mice, and 32 tumors appeared in 13 of the 20 C3H mice treated with BA tumors, in some series of BA mice repeatedly grafted with tumors from mice of the C3H strain not a single tumor was produced. Out of a total of 44 BA mice grafted with tumors from the C3H strain, only 11 showed tumors, and the total number of tumors was only 16. Investigations were therefore undertaken to determine, if possible, the reason for this variance in results. Stained sections of the primary tumors (80 in number) failed to reveal any histologic features peculiar to the tumors that developed in treated mice of alien strains. On the other hand, observations made on the growth of the tumor and on the behavior of the host animals disclosed certain differences in biological characteristics of the tumors. The growth or non-growth of tumors in the different series of experimentation could not be attributed to the greater viability of some of the implants or to the so-called cycle of tumor activity, since every one of the implants of these tumors inoculated into normal mice of the same strain grew progressively, and every implant (except some of those of tumor C3H 11) inoculated into normal mice of a different strain grew to some extent and then regressed. The amount of growth was characteristic for the given tumor and graded from the small growth of some of the C3H strain tumors (Nos. 8, 12, 13, 14), through considerable growth of some of the A strain (PHS 9, 14 and 20) and BA strain (Nos. 1, 22, 30, 35 and 54), to culminate in the rapid growth of tumor C3H 11, which in a number of instances failed to regress.

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