Specific susceptibility of ddO mice to polyoma virus has been investigated by inoculation of this virus in mice divided into several experimental groups.
1) The newborn mice inoculated with this virus into the salivary glands and the mice inoculated in fetal life (16-18 day gestation) developed salivary gland tumors.
2) Microscopic features of these tumors in salivary glands showed reticular or medullary type rather than glandular type.
3) The newborn mice inoculated with polyoma virus into the back and non-immune adult mice inoculated with virus into the salivary glands after 296r of whole-body X-ray irradiation did not develop salivary gland tumors.
4) Hemagglutination titer of this virus was the lowest in salivary glands of mice inoculated with this virus into the back.
5) The present experiment indicates evidence that ddO mice have partial resistance to polyoma virus.

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Relationship between the extract of mammary tumor in ddO mouse and polyoma virus was examined and following points were found.
1) Polyoma virus propagation in ddO fetal mouse cells was a little prevented compared to that in Swiss fetal mouse cells.
2) In electron microscope two distinct types of particles were present in mammary tumor cells of ddO mouse; one type (70mμ) occured in the cytoplasm and the other type (100mμ) in extracellular region.
3) An important in vitro finding was that polyoma virus and mammary tumor agent were distinguishable by hemagglutination test and appearance of cytopathogenic effect in tissue culture cells.
4) Propagation of polyoma virus was greatly prevented in Swiss mouse fetal cells in vitro previously inoculated with mammary tumor extract.
5) Development of polyoma tumor in hamster was interfered by an extract from mammary tumor of ddO mouse.
6) It was concluded from the present study that the virus-like particle recovered from ddO mouse mammary tumor and propagated in tissue culture in mouse cells has an interaction with polyoma virus in vivo and in vitro.

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Electron microscopic studies were performed on seven cases of human pulmonary carcinoma, which were histologically bronchogenic carcinoma.
These cases were classified into epidermoid and non-epidermoid carcinoma by electron microscopy, and tumor cells of each case were divided into two types, Type A and B. Type A was a relatively undifferentiated cell and type B, a more differentiated cell from submicroscopic features. It is assumed, therefore, that these undifferentiated cells may have the power to differentiate into both epidermoid and non-epidermoid carcinoma.
On the other hand, none of carcinoma cells of these cases had specific intracytoplasmic osmiophilic inclusion, which is found in normal alveolar epithelial cell.

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Two hundred and six cases of human tumors, consisting of 133 malignant and 73 benign tumors, were histochemically examined for the activity of triphosphopyridine nucleotide isocitric dehydrogenase.
The enzymatic activity of epidermoid cancer was confined to the neoplastic epithelium with a low degree and rather high in the diskeratinized portion. The majority of stomach adenocarcinoma exhibited a trace of the activity and rectum adenocarcinoma, a varying intensity from trace to the highest. Mixed tumors of salivary glands, cancer and benign tumors of the thyroid and breast showed a varying intensity of this enzymatic activity. The highest enzymatic activity was present in adenocarcinoma of corpus uteri and adrenocortical adenoma. Tumors of the nervous system showed a rather low activity.

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Spontaneous breast cancer in C3H mouse was histochemically studied for 8 kinds of dehydrogenase, with Nitro-Blue tetrazolium as an electron acceptor.
Activity of succinic and α-glycerophosphate dehydrogenases was high in neoplastic cells, while it was low or none in stromas. Lactic and malic dehydrogenases exhibited a moderate enzymatic activity, and β-hydroxybutyric dehydrogenase showed only a weak activity. Glutamic dehydrogenase activity was lower than other DPN-dependent dehydrogenases. Glucose-6-phosphate dehydrogenase activity was weak to absent, and isocitric dehydrogenase was negative. No definite relationship was observed between histopathological types and their enzymatic histochemical patterns.

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Growth form of Yoshida sarcoma was studied, using the rats transplanted intraperitoneally with 10⁷ cells of this tumor.
1) Yoshida sarcoma cells increased almost exponentially in the period of first 5 days after transplantation. Through this period, the mean generation time of tumor cells was between 12 and 17 hours and mean mitotic time of the cells was about 25 minutes, so far as estimated.
2) Yoshida sarcoma cells growing in ascitic fluid demonstrated a compatible concentration of 200, 000-300, 000/mm³. The total volume of tumor cells was proved to be about 20% of the whole volume of tumor ascites.
3) The rate of tumor cells with abnormal figures among all tumor cells in the constantly growing period was about 3%. Cytological examinations revealed that the most conspicuous findings were fragmentation and aberration of chromosomes in mitotic cells and the ring-shaped nucleus or the fragment nuclei in interphase cells.
4) The mean volume of Yoshida sarcoma cells was 845 μ³ in 3-day-old ascites and it showed a tendency to decrease in later ascites.
5) Inflammatory reaction to the inoculation of tumor cells in ascitic fluid was very slight.

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The rats, intraperitoneally transplanted with 10⁷ Yoshida sarcoma cells, were irradiated with either 200 or 1, 000r of X-rays over the whole body, 72 hours after transplantation. The ascites of these irradiated animals was examined with respect to the total number of tumor cells and their cytological changes caused by radiation. Data so far obtained indicate that:
1) Increase of Yoshida sarcoma cells was inhibited for more than 48 hours by a dose of 1, 000r and for some 24 hours by a dose of 200r.
2) Mitotic time as well as intermitotic time of the tumor cells was prolonged by the radiation.
3) Abnormal figures of tumor cell increased after the radiation, presenting two peaks, the first and second maxima. The first maximum occurred 1 hour after the radiation in mitotic cells, and 6 hours after radiation in interphase cells. The second maximum occurred 24 or 48 hours after the radiation in mitotic and interphase cells.
4) The most conspicuous morphological changes of tumor cells caused by the radiation were the fragmentation and aberration of chromosomes in mitotic cells as well as the fragment nuclei in interphase cells. Some of the irradiated tumor cells showed necrotic changes.
5) The radiation injury of tumor cells in postmitosis was more intensive than that in premitosis period.

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Studies were made, employing 3 different transplant strains of the rat ascites hepatoma, in order to demonstrate the natural resistance of their constituent cells to nitrogen mustard N-oxide after establishing numbers of clonal tumor cell populations from these three ascites hepatomas. Data so far obtained indicate the following facts:
(1) A tumor is not a homogeneous constitution but is a mosaic complex of cells with different grades of drug resistance. The natural drug resistance of a tumor cell population is, therefore, the averaged sum of that of all its constituents which differ from each other in their grade of resistance.
(2) The grade of natural drug resistance of a whole tumor as well as its constituents is not a fixed one but it can naturally fluctuate around a certain level with a range corresponding to the range of variations of cells in the population.

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Chromosomal features in Yoshida sarcoma and its two different sublines, a polyploid clonal subline and a subline highly resistant to nitrogen mustard, were studied. The former two were very sensitive to nitrogen mustard. Although a marked chromosomal difference was detected between the original and resistant strains, it was not proved that the visible change reflected the altered drug susceptibility. Polyploid subline cells including duplicated number of near-diploid chromosomes of the original tumor seemed to have less growth advantage within the predominantly near-diploid tumor cell population.

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Incidence of cancer of the lung induced by 4-nitroquinoline 1-oxide was examined in rats maintained on a diet with or without cigarette tar. Further, effect of cigarette smoke on the induction of lung cancer was examined.
In the rats fed a diet containing cigarette tar, the incidence of lung cancer was only very slightly higher than in those on a basic diet, but the induction of cancer was definitely accelerated in terms of both time and incidence by the inhalation of cigarette smoke. It was noteworthy that only a few adenomas and squamous metaplasias in the lung tissue were induced in the rats when exposed to cigarette smoke alone.
The cigarette smoke, though not carcinogenic in itself, may play an accessory rôle in the induction of cancers in the lung of rats.

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The peptide mapping technique using Ninhydrin coloration was applied to study the structural difference between serum albumin of normal animals and animals bearing tumor.
(1) The characteristic peptide detected as a large yellow spot with intensive positive charge was present in serum albumin of normal rats but not in that of rats bearing Yoshida sarcoma.
(2) A large, positively charged spot which colored intensely purple at first and turned yellow afterward was observed in the tryptic digests of human serum albumin. The characteristic peptide spot of serum albumin of stomach cancer patients was relatively larger than that of serum albumin of normal human.
(3) The corresponding peptides were observed in both the chymotryptic digests of serum albumin of normal human and patients with stomach cancer. However, the differences in size were observed in several peptide spots.
(4) More than 50 peptides were regularly obtained from the tryptic digests of human serum albumin. From the results of amino acid analysis, the number of lysine and arginine residues in the albumin molecule was calculated as 58 and 22, respectively. Therefore, the human serum albumin molecule may possibly consist of considerable numbers of peptides which have the same amino acid sequences.

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