The antigenic characters of SL-leukemia cells were compared with those of other murine viral leukemia cells by using the transplantation immunity and cytotoxicity tests. Cross reaction was generally demonstrated between SL-leukemia cells and Gross leukemia cells by both tests, but no certain cross reaction was detected between Gross leukemia cells and long-transplanted and cultured SL-leukemia cells. This result was confirmed by the absorption test. The FMR-antigen, which is specific for Friend, Moloney, and Rauscher leukemia, was not detected in SL-leukemia cells by cytotoxicity test.

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Two mutant clones which have lost transplantability were isolated from the cell line of a transplantable ascites tumor, FM3A/B, originating from spontaneous mammary adenocarcinoma of C3H/HeN mice, by treatment with 4-nitroquinoline 1-oxide and subsequent cell-cloning. No difference between the original cells and cells of the mutant produced was seen in their sensitivity to 4-nitroquinoline 1-oxide, rate of cell proliferation, morphology of cell colony, and pattern of lactic dehydrogenase isozyme. Pretreatment with mutant cells induced transplantation resistance to the original cells in syngenic system.

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The activities of β-N-acetylglucosaminidase, β-galactosidase, and α-mannosidase were determined in the serum of normal men and women, and of female patients with genital cancer, using phenyl-β-N-D-acetylglucosaminide, phenyl-β-D-galactoside, and phenyl-α-D-mannoside as the substrate, respectively.
The enzyme activity in the serum of normal adult women was 30.92±3.98μg/ml/hr for β-N-acetylglucosaminidase, 1.14±0.51μg/ml/hr for β-galactosidase, and 0.68±0.39μg/ml/hr for α-mannosidase.
In the serum of female patients with genital cancer, the β-N-acetylglucosaminidase activity was found to be two to three times higher than the normal value. The α-mannosidase activity was slightly increased, but no change was observed on the β-galactosidase activity.
The β-N-acetylglucasaminidase activity in the cases of advanced cancer or cancer with metastasis in regional lymph nodes was higher than that in moderate cases.
The elevated activity of β-N-acetylglucosaminidase in the serum of the patients returned to the normal value by radical operation or radiological treatment.
The β-N-acetylglucosaminidase activity was demonstrated histochemically in metastatic and nonmetastatic lymph node tissues, and the activity in the former tissues was higher than that in the latter.

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Intracranial inoculation of adenovirus type 12 into the newborn hamsters and C3Hf/Bi mice induced tumors in the central nervous system, incidence being 37.2% in hamsters and 30.2% in mice. The period from virus inoculation to death by tumor was 51.1 days in hamsters and 116.2 days in mice on the average.
The predilection sites for tumor development were subependymal region of the ventricular wall of the brain, surrounding area of the central canal of the spinal cord, nerve bundle of the cauda equina, and meninges.
Histologically, the tumors possessed the characteristics of undifferentiated neuroectodermal tumors, and prototype of the cell pattern could be seen even in the ependymal matrix layer of normal embryo. Some tumors which developed in mice resembled human medulloblastoma or some immature types of glioma group.
Histological characteristics of this tumor and peculiar sites of the tumor development indicated that the target cells of adenovirus type 12 in the central nervous system corresponded to medulloblasts or undifferentiated glioblasts.

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Young C57BL mice were irradiated with a leukemogenic dose of X-rays in four fractions, whole-body or thigh shielded. The absolute number of cells of different types in the lymphoid tissue was counted at 34 points after the first irradiation. The marked differences between the two groups were earlier recovery of lymphopoiesis in the lymph nodes and shorter period of lymphopenia in the thigh-shielded animals. The absolute number of primitive cells (target cells) was larger in the shielded group. The number of small lymphocytes in lymph nodes and peripheral blood returned to a normal level 20 days after the 4th irradiation by shielding, whereas it remained below 40% of normal value even 40 days after the last whole-body exposure. The degree of lymphopenia corresponded to the immunological deficiency; production of hemolysin against sheep erythrocytes recovered to a normal level 20 days after the 4th shielded irradiation, but not after whole-body exposure. This earlier recovery of immunological response may account for the elimination of transformed neoplastic cells by irradiation and striking reduction in tumor incidence.

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Histogenesis of urinary bladder tumors in Wistar strain male rats after administration of N-butyl-N-(4-hydroxybutyl)nitrosamine was studied by light microscope, electron microscope, and autoradiography. N-Butyl-N-(4-hydroxybutyl)nitrosamine administration resulted in a selectively high incidence of urinary bladder tumors. Hyperplasia of the urinary bladder epithelium was always observed within 8 weeks and papilloma within 16 weeks, and cancer developed within 20 weeks in 84.7% of the animals. Histologically, the carcinoma, a transitional cell carcinoma, closely resembled those produced in the urinary bladder on administration of other chemical carcinogens. Electron microscopically, tonofibriles were observed in the tumor tissue. Autoradiographically, a good correlation was found between the distribution of cells labeled with tritiated thymidine and the histologic grade of malignancy of the urinary bladder tumors. These results showed that histological changes in the urinary bladder epithelium increase in frequency and extent with the period of N-butyl-N-(4-hydroxybutyl)nitrosamine administration. These results also suggest that papillomas are precursors of bladder cancer in rats administered N-butyl-N-(4-hydroxybutyl)nitrosamine.

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Yokohama Thorotrast sarcoma, originating in the hamster cheek pouch following an administration of Thorotrast, has been maintained in an ascites form as well as in a tissue culture cell line for 3.5 years. Meanwhile, the cells changed some of their characters. Although large and small cells intermingled in earlier generations, large cells predominated in the later generations, both in animal and in vitro passages. At the same time, modal number of chromosomes changed from hypodiploid range to hypotetraploid one. Mean surviving time of animals became shortened and growth rate of cultured cells became rapid. However, while fibrosarcomatous pattern of the original tumor disappeared during in vivo passages and histology of the tumor became irregularly arranged pleomorphic cells at the last generation, the tumors produced by back-transplantation of the cells maintained in vitro retained the original pattern of the initial tumor even in the tumors produced by inoculation of the last generation of cells.

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Three long-term cultured cell lines were established from the human neoplastic lymph nodes. Two were derived from the lymph nodes with an infiltration of acute myeloid leukemia and with a curing process of Hodgkin's disease by chemotherapy, and were designated as RS-2 and RS-3, respectively. Another cell line derived from the lymph node with metastasis from stomach cancer was designated as MC-12. All the cultures grew floating free in suspension and have been successively passaged for 23-41 generations. Doubling time ranged from 24 to 36hr. Both the RS-2 and RS-3 lines appeared to consist of lymphoblastoid and reticulum cells, but the MC-12 line appeared to be a mixed culture of both the cancer cells and lymphoreticular cells. Electron microscopic examination demonstrated the herpes viruslike particles in RS-2 line. The particles appeared identical to those described in Burkitt tumor and other leucocyte cultures.

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Production of immunoglobulins and of herpes-type EB virus in newly established four cell lines, RS-2, RS-3, MC-8, and MC-12, derived from human neoplastic lymph nodes was investigated by means of immunofluorescence. Cells producing at least one of three classes of immunoglobulins, IgG, IgM, and IgA, were demonstrated in all of the four cell lines tested. This finding suggests that lymphoreticular cells are contained in the cell population of these cultures. EB virus antigen was detected in 2-10% of the cells of all the cell lines. Antibody against EB virus as revealed by indirect immunofluorescence method was demonstrated in all of the test sera obtained from the donors of these cultures.

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Molecular species of aldolase in the liver of rats bearing Rhodamine sarcoma was investigated. Activity toward fructose 1, 6-diphosphate or fructose 1-phosphate decreased with the tumor growth. Fructose 1, 6-diphosphate/fructose 1-phosphate aldolase activity ratios and electrophoretic patterns of aldolase in the liver of tumor-bearing animals did not show any deviation from those of the control.

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For the purpose of clarifying whether the adsorption of materials to the cell surface is a necessary prerequiste for phagocytosis, phagocytosis of Ehrlich ascites tumor cells and peritoneal macrophages of mice was examined. The tumor cells. incubated with iron chondroitinsulfate colloid alone in vitro failed to phagocytize the iron colloid, but were stimulated to phagocytize the colloid in the presence of polycationic substances. Electron microscopic observation on the tumor cells incubated with the iron colloid in the presence of polycationic substances revealed the adsorption of colloid particles on the cell surface after a short incubation and their uptake into the phagocytic vesicles after longer incubation. All the polycationic substances so far examined, i.e., methylated albumin, arginine-rich histone, slightly lysine-rich histone, protamine sulfate, poly(L-lysine methyl ester) hydrobromide, and cytochrome c, induced the adsorption of iron colloid particles on the tumor cell surface and then the phagocytosis of colloid particles occurred, but polyanionic substances examined here did not show such an effect. By the pretreatment of the peritoneal macrophages with papain the cells failed to adsorb colloid particles to the cell surface with reduced phagocytic activity. These results indicate that the adsorption of a material to the cell surface is an indispensable prerequisite for phagocytosis. The tumor cell surface should have negative charge and adsorption of negatively charged material may be mediated by the polycationic substances, but the macrophage surface may have some specific groups to bind with this negatively charged colloid particles.

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The levels of two types of aldolase isozyme, aldolase-A (muscle type) and aldolase-B (liver type), were determined in the liver of 49 patients with malignant tumor in stomach or esophagus, and were compared with that of 31 patients without malignancy.
Two methods were used for the differential assay of aldolase isozymes; one was based on the differential inactivation of aldolase-A and -B using the chicken anti-aldolase-A, and the other was based on the different substrate specificity of aldolase-A and -B toward fructose mono- and di-phosphates. A good correlation was obtained between these two assay methods, and the former method was found to be more sensitive than the latter to analyse alterations in the isozyme pattern, especially in the liver.
Compared with the patients without malignant tumor, a significant increase in aldolase-A activity was detected in the liver of patients with malignant tumor, irrespective of its localization and stage.

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Hamster-adenovirus type 12 tumor cell lines were treated with HVJ. In the treated cultures, giant cells with huge pleomorphic nuclei were observed. Giant cells with multinuclei were also found. Some nuclei showed images suggestive of mitosis and the possibility of nuclear fusion in these cells was discussed.

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Glycogen and oligosaccharide contents in Yoshida sarcoma and ascites hepatoma cells markedly increased by treatment with the effective dose of antitumor agents in vivo and in vitro, and the increase was closely correlated to the occurrence of cytomorphological effect.

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