The antitumor effect of a polysaccharide fraction isolated from bagasse (crushed residue of sugar cane after pressing out the juice) has been tested against sarcoma-180 subcutaneously implanted in mice and the effect was found to be just as marked as that of similar fraction from bamboo leaves. The most significant results were obtained with 100mg/kg doses.
In continued attempts to elucidate the mechanism of this kind of host-mediated antitumor action of the bagasse polysaccharide, the properties of plasma protein was compared between the polysaccharide-treated and normal control mice. There was a considerable increase in circulating protein especially globulin fraction, in the treated mice.
Effect on plasma protein of certain other plant polysaccharides without antitumor effect was determined in the same way as in the case of the bagasse polysaccharide.

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1) A pedicle cross-skin grafting combined with a short-term parabiosis in normal Donryu rats was 92% successful over 100 days. Similar result was obtained in M520/N(F88) rats, a highly inbred American strain, which served as control. Thus, the genetic homogeneity of the Donryu rats was proved to be very high.
2) The Donryu rats have an extremely high susceptibility to Yoshida sarcoma or ascites hepatomas which originated in these rats. However, they show resistance to tumors after various immunization treatments. All of the cross-skin grafts between these resistance-acquired and normal Donryu rats were rejected by each side of their recipients within 100 days. The fact seemed to be dependent on different compatibility between the donor and host, assuming that histocompatibility system of the resistance-acquired rats has been modified through the acquisition of resistance to the tumors.
3) The Donryu rats, in which the grafts from the parabiosed donors resistant to a tumor were rejected, showed resistance to further challenge of the same tumor. A possible mechanism for this fact was discussed from an immunogenetical viewpoint, and transfer of the resistance during the parabiosis seemed to be a main causal factor.

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The growth of Friend virus-induced transplantable tumor cells (referred to as Friend tumor), which originated from the Friend disease spleen of dd/Om mice, was inhibited in mice immunized with live Friend virus. This virus-immune effect was not evident in susceptible dd/Om mice, being only evident in non-susceptible dd/Mk and Swiss mice. This is called a homologous test system in which the Friend virus serially passed in Swiss and dd/Mk mice was inoculated and immunized into Swiss and dd/Mk mice. A given number of days later, Friend tumor cells were intraperitoneally challenged and the temporary growth (take) in days was observed. A definite inhibition in the growth of Friend tumor cells was observed in Friend virus-immune mice by the shortening of average take days which is a significant difference when compared with the control. This effect is seen markedly in long-term surviving mice which escaped death from Friend disease. The mechanism of this immune effect was discussed.

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Effect of several carcinostatic agents on the antitumor activity of sensitized lymphoid cells obtained from Donryu rats immunized with Yoshida sarcoma was examined. The sensitized lymphoid cells were treated with various concentrations of a carcinostatic agent at 37° for 30 minutes. The washed cells were transferred with Yoshida sarcoma cells into recipient animals. The minimum effective concentration (A) of the agent to the sensitized peritoneal exudate cells was defined as the concentration which abolished the antitumor activity of the sensitized peritoneal exudate cells as determined by the death of the recipient animals by the tumor. The minimum effective concentration (B) of the agent to Yoshida sarcoma was examined in a similar manner as above and was defined as the lowest concentration of the agent which protected the recipient animals from death by the tumor.
A and B of each carcinostatic agent in mM were respectively as follows: Nitrogen mustard 0.008 and 0.001, Mitomycin-C 0.05 and 0.01, Actinomycin-D 0.001 and and 0.001, thio-TEPA 1.0 and 0.5, compound No. 838 1.0 and 1.0, and (2-chloroethyl) diethylamine 1.0 and >10. Puromycin and 6-mercaptopurine were ineffective on these cells in the present system. Antitumor activities of sensitized lymph-node cells and spleen cells were also abolished by the same concentration of Actiomycin-D as for the peritoneal exudate cells.
In vitro culture of Yoshida sarcoma cells mixed with sensitized peritoneal exudate cells resulted in a rapid decrease of the tumor cells, whereas cytocidal activity of the peritoneal exudate cells was inhibited by pretreatment of the cells with effective concentration of the carcinostatic agents.
Based on these results possible mechanism for the antitumor effect of sensitized lymphoid cells was discussed.

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The normal mammary gland development of C3H/He and C57BL/6 strains of mice was studied using the virgins of the 30-230 days of age.
The area and DNA content of the mammary gland increased sharply until the 70 and 110 days of age in C3H/He, and 110 and 90 days in C57BL/6, respectively. While only slight changes of these items were found in C3H/He thereafter, DNA content in C57BL/6 seemed to drop temporarily between the 130th and 170th days. DNA content of C3H/He was much larger than that of C57BL/6 in all ages.
The distinct differences were found between the strains in the pattern of relative mammary gland growth to the body growth.
The whole-mount preparations of the gland of C3H/He were distinguished clearly from those of C57BL/6 in showing the bud-alveolar formation after 70 days, the degree and ratio of which increased with age. The hyperplastic alveolar nodules appeared after the 170th day in the gland of C3H/He. The mammary gland development of C57BL/6 was restricted only to the development of the duct system.
It was confirmed that the mammary gland of C3H/He was in a more advanced phase than that of C57BL/6, quantitatively as well as qualitatively in the virginal stage.

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The priming activity for support of DNA-dependent RNA synthesis of chromatin isolated from transplantable rat hepatomas, Morris-5123 and HDEN-10893, from livers of rats bearing these hepatomas and from respective normal control livers was determined. The chromatin from the liver of rats bearing either Morris-5123 or HDEN-10893 showed significantly higher priming activity than that of control liver and that of the tumor tissues, while the chromatin of tumor tissues, irrespective of their growth rate, exhibited almost the same priming activity of that of the normal liver. The effect of Actinomycin-D and ammonium sulfate on the priming activity of these chromatins was also examined.

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The spleen foci of Friend's disease in early stages, which appeared in male DDD mice 3-12 days after the inoculation of diluted virus solution, were histologically examined. The cells of the spleen foci were monotonously large and polygonal, histologically resembling young reticulum cells. They were consistent with the Friend tumor cells of the spleen in the advanced stage. Their first appearance was observed in the periphery of the arterioles in the red pulp, more frequently beneath the splenic capsule, which was followed by their extension to the splenic trabeculae. The earlier spleen foci were usually separate from the erythroblastic cell groups, but a few or several seemingly normal erythroblasts were infrequently found among them.

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Starch, D-glucose, L-leucine, L-glutamic acid, palmitic acid, and stearic acid were heated at 300°, 500°, or 700° in a stream of nitrogen, and the resulting pyrolytic products were analyzed for polycyclic aromatic hydrocarbons by column, paper, and gas chromatography. Nineteen hydrocarbons including those with carcinogenic potency such as benzo[a]pyrene were indentified in the pyrolysis products of the above test compounds heated at 700°. When the same compounds were heated at 500°, the yield of hydrocarbons decreased markedly and no polycyclic aromatic hydrocarbons were formed at 300° in any discernible amount. When heated at 700°, the fatty acids yielded the largest amount of hydrocarbons, and the amino acids the least. When heated at 500°, however, the largest yield was obtained from starch and D-glucose, and a much smaller yield from fatty acids and amino acids.

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Intracellular distribution of NADase (NAD-glycohydrolase, EC 3.2.2.5), β-glucuronidase (β-glucuronide glucuronohydrolase, EC 3.2.1.31), DNase (deoxyribonucleate 3'-nucleotidohydrolase, EC 3.1.4.6.), and acid phosphatase (orthophosphoric monoester phosphohydrolase, EC 3.1.3.2) was investigated with untreated and treated Yoshida sarcoma. Free and total activities of isolated lysosome-rich particles were determined according to the method of de Duve. The results showed that the ratio of free to the total activity of lysosomal enzymes was markedly increased in the Yoshida sarcoma treated with nitrogen mustard N-oxide (HN₂-O) compared with the untreated. Increase of the activity observed with HN₂-O treated Yoshida sarcoma seemed to result from the increase of enzyme content.

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Spleen cells from a BALB/c mouse with splenic Rauscher disease were cultivated in vitro for approximately 3 months. Some of the AKR mice developing Rauscher disease as a result of inoculation of the cell-free culture fluid showed peculiar renal glomerular hyalinization and Feulgen-positive Hematoxylin bodies in the kidneys and lungs.

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Persistent production of deficient particles of Friend virus was demonstrated by combined biological, electron microscopical, and serological studies of an infectious virus-free subline of Friend virus-induced ascites sarcoma of the mouse.

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Friend disease was induced in newborn mice inoculated with X-ray irradiated tumor cells of the variant of Friend virus ascites sarcoma, a subline which is non-infectious and deficient in virus. This phenomenon strongly suggests the possibility of inducing infectious virus synthesis by ionizing radiation.

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The growth of ascites hepatoma AH-13 was inhibited in the early stage of pregnancy, but this was not true in the case of Yoshida sarcoma. Administration of diethylstilbestol or progesterone did not, however, influence the survival period of AH-13-bearing rats.

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The cause of recent increase in lung cancer mortality in Japan may possibly be attributed to "pseudo-increase" by the improvement in diagnosis and discovery besides the "true rise". It is surmised that approximately 30% (or over?) may be due to this "pseudo-increase".

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Induction of lung cancer was demonstrated in mice by the repeated injections of 4-hydroxyaminoquinoline 1-oxide and its hydrochloride in lecithin-water mixture. Incidence of lung cancer was very low when compared with that in mice receiving 4-nitroquinoline 1-oxide in lecithin.

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