The Dx tumor, an embryonal liposarcoma with reticuloendothelial-like cells and typical intracytoplasmic and intranuclear “vacuoles,” occurred spontaneously in a young adult female BALB/cJax mouse. In the first and second transplant generations it grew in and killed 153 BALB/cJax, without the occurrence of metastases.

The original and the transplant tumors contained an XYZ factor (or factor complex) which could be prepared from fresh or from frozen tumor tissue. The treatment of either hosts or the donor mouse or both with the factor resulted in: (a) significantly larger tumors in a shorter period (at 26 days 7.6 cc., compared with 3.4 cc. for control tumors); (b) a 25-day shortening of the premortality period, of the point of 50 per cent mortality, and of the termination period between the parallel mortality curves for the first and the XYZ-treated second isotransplant generation. The average mortality was 46.3 days for the 34 controls, 38.5 days for the 58 mice treated with fresh and 38.9 days for the 51 mice treated with frozen tumor (diff. = 7.8 ± 2.4 and 7.4 ± 2.4; t = 3, P = 0.01).

Isotransplantation without XYZ treatment in the second generation resulted in a semi-XYZ effect as an altered linear mortality curve in which the beginning was the same as that for XYZ treatment and the termination approximately that of the first transplant generation (the 50 per cent mortality point in the second transplant generation was 37 days for the XYZ-treated groups and 46 days for the untreated controls; it was 61 days in the first generation). It was concluded that the host or donor resistance mechanism after XYZ treatment caused dedifferentiation of more cells in the tumor population than occurred after isotransplantation alone.

The Dx tumor in first and second transplant generations grew in none of 72 C57BR/cdJax and 54 C57BL/6Jax mice with or without XYZ treatment.


The work was aided by grant No. C-2069(C2) from the Division of Research Grants, National Institutes of Health, Bethesda 14, Maryland.

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