Immunity was observed in the DBA₁ inbred strain of mouse against the S-91 tumor which recently originated in this strain. This immunity contained specific components which inhibited tumor development and made possible transference by means of spleen and lymph node cell transplantation. Much immunity was transferred through the lymphatic cells of tumor-bearing animals. However, attempts to induce tumor immunity in this inbred strain failed. Immunization with dead cells accelerated tumor development in the isologous host, whereas in the homologous host, tumor development was depressed. Natural resistance inherent in this strain of mice was discussed.

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Evidence was obtained for the transfer of a murine leukemia virus across extraembryonic membranes. Pregnant A/LN and BALB/c mice were inoculated intravenously with a mouse-derived Moloney leukemia virus preparation. The periods of inoculation ranged from the first through the 18th day of gestation, based on time of detection of the vaginal plug. Immediately after birth the offspring of the viremic mothers were given to normal, untreated BALB/c or Swiss female mice for nursing. These animals were then observed for the development of leukemia. The data obtained indicate that the virus will infect the embryos prior to the formation of the placenta. Similarly, the virus will cross the placental barrier and infect the fetus. It is interesting that several of the mothers remained free of the disease through the period of observation, whereas their offspring died with the virus-inducedn eoplasm.

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Chromosome studies were made in 8 cases of benign giant-cell tumors and 6 cases of human bone sarcomas. All of the giant-cell tumors showed a sharp chromosome-number mode at 46 with a superficially normal diploid karyotype. The sarcomas were characterized by having aneuploid modal numbers with a rather wide variation ranging from 58 to 92.
Six out of 8 giant-cell tumors were maintained successivelyin culture for a period ranging from 4 months to 3 years. Cells from early subculture passages showed a modal number of 46, with a higher proportion of tetraploid cells than that of the original tumors in vivo. In general, frequencies of polyploid and aneuploid cells increased with the accretion of in vitro generations. Two cell lines of giantcell tumors were successfully maintained in in vitro culture for more than 850 days; they showed a striking morphological change of cells. The modal chromosome number of these two lines fell in a range of hypotriploidy.

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An attempt was made by the use of a single injection to compare 4-hydroxyaminoquinoline 1-oxide with 4-nitroquinoline 1-oxide and 4-aminoquinoline 1-oxide in the potency of carcinogenic activity. An equivalent mole of the chemicals suspended in a mixture of peanut oil and cholesterol was introduced subcutaneously into the right groin of a rat. Fibrosarcomas were induced in 2 out of 8 effective rats in the group administered 2mg of 4-hydroxyaminoquinoline 1-oxide hydrochloride, while no tumor was found in rats given the same mole of 4-nitroquinoline 1-oxide or 4-aminoquinoline 1-oxide hydrochloride.
The carcinogenic mechanism of 4-nitroquinoline 1-oxide was discussed from these results.

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Carcinostatic action in vitro of the liver factor was found to be mainly due to pH decrease in the incubation media during incubation of the tumor cells and the liver factor. The pH decrease in question is assumed to be partly due to the glycolytic production of lactic acid, for it was found that a large amount of reducing sugars were contained in the liver factor, and lactic acid was formed during incubation of the tumor cells with the liver factor.
Possibilities other than the role of pH in the incubation medium in the carcinostatic action of the liver factor still remain to be studied are also discussed.

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The ultrastructure of pulmonary adenomas in mice was studied, using tumors induced by isonicotinic acid hydrazide or by urethan plus 4-nitroquinoline 1-oxide. Electron-microscopically, there was no difference between pulmonary adenomas in mice induced by isonicotinic acid hydrazide or urethan plus 4-nitroquinoline 1-oxide.
Klärner's "virus-like particles" were present within the cytoplasm and nuclei of the induced adenoma cells. It seems safe to regard them as non-viral.
A lamellar or lattice-like substance was observed in adenomas induced by isonicotinic acid hydrazide or urethan plus 4-nitroquinoline 1-oxide. This substance was mainly located extracellularly, being apparently derived from osmiophilic bodies which had been released from tumor cells. It is assumed that tumors bearing the extracellular lamellar or lattice-like substance may be of alveolar cell origin, even if these tumor cells are devoid of intracellular lamellar osmiophilic bodies.

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Newly established tissue culture strain JTC-14 from actinomycin-induced ascites sarcoma of mice is reported.
1) The cells have been kept in vitro for more than 2 years, 93 transfer generations to date, and have the ability to produce tumor in ddO mice.
2) The cells that had undergone animal passage can grow in vitro with ease even after 27 serial transfer generations. This character is different from that of the original actinomycin-induced ascites sarcoma cells, which can grow only after a very long period of culture.

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The effect of 4-nitroquinoline 1-oxide and 4-hydroxyaminoquinoline 1-oxide, known to be carcinogenic and mutagenic in several biological systems, were investigated in a pure line culture of a ciliate protozoon, Tetrahymena pyriformis strain GL, in which the synchronous cell division is inducible by cyclic temperature changes.
4-Nitroquinoline 1-oxide produced nuclear inclusions at sublethal concentration (10-20γ/ml) and protected the nucleus from karyolysis at lethal concentration. In the system of the synchronous cell division, sublethal concentration of the substance applied at a certain specific stage inhibited cell division and induced abnormal nuclear and cell divisions of such nature as to indicate that karyokinesis and cytokinesis may be independent in their mechanism.
4-Hydroxyaminoquinoline 1-oxide was relatively less active than 4-nitroquinoline 1-oxide, but it produced perfect cellular lysis. In the synchronous system its effects were similar to those of 4-nitroquinoline 1-oxide.
The non-carcinogenic 4-aminoquinoline 1-oxide produced none of these changes.

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A microspectrophotometric study was made on the DNA content of the splenic cells from Friend virus-infected mice and of cells from a transplantable strain of tumors derived from the spleen of a mouse with Friend's disease. The normal mouse splenic cells showed DNA content corresponding to the basic diploid value with a limited degree of variation from cell to cell. The spleen cells in Friend's disease showed a much larger scatter in distribution of DNA values and their average DNA values were higher than the control DNA amount. A deviation of the same order was observed in the transplantable tumor cells.
The differences were statistically significant and began to be observed between the 3rd and 5th day of inoculation with the Friend's virus.

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A polymorphous cell sarcoma which developed under the skin on the back of a Friend virus-infected mouse was established as a transplantable strain. The growth of the transplants does not produce generalized Friend disease in mice carrying them, though the sarcoma tissue can be shown to contain a small amount of the virus. The sarcoma, when it invades the peritoneal cavity, easily takes the ascites form spontaneously. No Friend virus inactivating substance was demonstrated in the sarcoma tissue.

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Water-soluble fraction of crude toxohormone (ethanol precipitate) was adsorbed on calcium phosphate gel at pH 7.0, eluted with 0.2M Na₂HPO₄ and the eluate was dialysed against deionized water. Specific activity of liver catalase-depressing activity of this purified fraction was enhanced 3 times with almost complete recovery.

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