1) Cancer cells are present in the blood stream of all rats bearing uuresectable cecal carcinoma. When nitrogen mustard is administered these cells disappear from the blood, but return when fibrinolysin or heparin is administered.
2) With resected cecal carcinoma in the rat (carcinosarcoma Walker 256) liver metastases occurred in 19 of 85 control animals (22%). Nitrogen mustard administered by hepatic artery just before resection reduced this to 15% and when heparin or fibrinolysin was added the incidence was reduced further to 9.5% and 12%, respectively.
The number of pulmonary metastases was also reduced in the treated animals from 8 in the controls to 5 in the nitrogen mustard-treated, and to 3 in those treated with nitrogen mustard and fibrinolysin, or heparin.
The survival time and the number of animals surviving for 9 weeks also increased in the treated animals, the numbers surviving 9 weeks being 15, 25, 29, and 27 animals.
There was no significant change in survival of non-resectable animals.

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Hemorrhage in ascites, its relation to tumor growth, and effect on blood hemoglobin and leucocytic count were examined in Yoshida Sarcoma and 15 different rat ascites hepatomas.
1) Survival time was short when hemorrhage was early and severe.
2) Anemia was a good indicator of the extent of hemorrhage and apparently was an important cause of death in most strains.
3) The level of leucocytosis was positively correlated with the degree of anemia and hemorrhage, and was higher in rats dying early. The leucocytosis appeared late in those showing spontaneous regression, and was absent when tumor did not take.
4) The degree of hemorrhage did not depend on the size of inoculum or tumor cell concentration, or tumor nodule formation in the tissue.

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Donryu rats bearing ascites hepatoma AH-21 were examined microscopically at frequent intervals to study the mechanism of hemorrhage in ascites. A reaction of possibly immunological nature was found in such rats with the appearance of reactive foci showing capillary dilatation within 48 hours from tumor inoculation coinciding with tumor invasion in the mesentery and omentum. Hemorrhage was started from these foci and increased by further injury caused by tumor breakdown. Splenomegaly was also evident. Hemorrhage was slight after treatment with cortisone. The appearance of hemorrhage was found to depend on the dose of tumor inoculum. The importance of hemorrhage as an indicator of the severity of such reaction in ascites tumor was discussed.

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Strain A/Jax mice received a single, subcutaneous injection of 0.04, 0.1, or 0.3mg of 4-nitroquinolin 1-oxide (4-NQO) at birth (less than 24 hours after birth), at 10 or 30 days of age, respectively. The doses of 4-NQO administered caused a slight acute toxicity. Nearly 100% of the treated mice developed multiple pulmonary tumors during one-year observation period. No appreciable different incidence of pulmonary tumors was observed among the newborn, 10-day, and 30-day groups. Eighteen to 25% of the treated mice developed leukemia. Spontaneous occurrence of pulmonary tumors and leukemia was observed in 19.5 and 4.6%, respectively, in the control group. Neither skin tumor nor subcutaneous sarcoma appeared at the site of injection. These results indicate that 4-NQO is capable of inducing pulmonary tumor and leukemia when given to newborn and infant mice. The results obtained on the earliest time that pulmonary tumors or leukemia was observed, average latency of leukemia development, mean count of pulmonary tumor nodules per mouse, number of mice with large and/or numerous pulmonary tumors, and number of mice with thymic type lymphoma, indicate that the carcinogenic response of A/Jax mice treated with 4-NQO is high in newborns, medium in 10-day infants, and low in 30-day-old mice.
The present results are compared with those of previous workers, and the implications of high sensitivity of the lung and lymphoid tissue to the injection of carcinogenic chemicals into newborn and infant mice are discussed.

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Effect of thymectomy performed at 40 days of age on the lymphoid tissues was studied semi-quantitatively in male mice of the AKR strain until 6 months after birth. Histologically, the lymphoid organs of thymectomized mice showed a decrease in small lymphocyte population in the lymphoid follicles. The quantity of lymphocytes referred to as 'lymyphoid mass' reduced significantly in these organs after thymectomy. In the thymectomized mice the lymphoid mass of the spleen averaged 25% and that of the mesenteric lymph node averaged 42% below that of the sham-thymectomized mice. A depression of circulating lymphocyte level was also seen after thymectomy. These changes appeared as early as 3 weeks after thymectomy.
Thymectomy generally prevented spontaneous occurrence of lymphoid tumors in mice of two high-leukemia strains, AKR and SL, and in their F₁ hybrids. The prevention of the disease was the most pronounced in the AKR and was moderate in the other two strains. Of a total of 13 lymphoid tumors developing in the thymectomized mice, 6 were of the reticulum cell type, and 7 of the anaplastic type, none being of the lymphocytic type. Non-lymphoid tumors developed more frequently in the thymectomized mice than in the intact animals.

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Thirty two pre-operatively irradiated lung tumors were studied histologically and changes induced in tumors by irradiation were described as well as healing process of the irradiated tumors. Ionizing radiation affects primarily the individual tumor cells, leading them to degeneration and lysis. Reparative granulomata of various types are formed probably secondarily, in which radiation injured cells and cellular debris play a most important part. The coagulation necrosis of the center of the tumor nests and that involving the tumor stroma are not due to the direct effect of the fractional irradiation.
Clinical impression of the results of radiotherapy was evaluated with the proposed histological grading of irradiated tumors, and paradoxical cases were presented.
Radiation dose required to destroy much of the tumor is larger with increasing size of the tumor and at least 6, 000-7, 000r is necessary for the lung tumors of average size.
Surgical resection of the tumor, if indicated, should be performed within two weeks after completion of radiotherapy, since regrowth of the tumor is most likely to occur with inadequate radiotherapy when surgery is delayed.
Histological structures and other factors influencing the biological effectiveness of radiation have been discussed.

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Comparative studies on three transplant-strains of the ascites hepatoma, AH-41A, AH-41B, and AH-41C, derived from primary tumor ascites and separate hepatoma nodules induced in a single rat by feeding of 3'-methyl-4-dimethylaminoazobenzene, demonstrated that they differed markedly from each other in such aspects as growth pattern and chromosomal composition as well as response to nitrogen mustard Noxide. The characteristics of each tumor in the ascitic form were maintained throughout prolonged animal passages. Data were discussed with emphasis on "the cellular multicentricity" in experimental hepatocarcinogenesis.

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The structure of α₁-glycoprotein isolated from Yoshida ascites tumor was made by electrometric titrations. Acid-base titration curves of Yoshida and normal rat blood serum α₁ glycoprotein confirmed the previous result on the structural differences between these proteins. It was also observed that the enzymic removal of the last terminal residue of the carbohydrate mojety of the molecule determines differential features of the acid-base titration curves for both proteins.

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