AN EVALUATION OF THE PHYSICAL RESPONSE OF MALIGNANT TUMOR IMPLANTS TO PULSED LASER RADIATION.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In the experiments on enzymic systems functioning in the metabolism of folic acid and on transplantable tumors in animals the preparation thomizine (chlorohydrate 4-methoxy-6-aminopyrimido (4,5-b) (1,4) thiazine) was worked out. Thomizine, as well as the known antimetabolite of folic acid-methotrexate, suppresses the activity of dihydrofolate reductase, but contrary to it suppresses FAP enzymic system, inhibiting aminopterin in the organism. Thomizine differes from methotrexate by another spectrum of antitumor effect, selective suppression of the tumor tissue growth, compared with the normal in vitro, it does not inhibit leucopoiesis, shows less toxicity and insignificant cumulative properties.
The effect of the cobamide coenzyme (5,6-dimethylbenzimidazolyl-Co-5'-deoxyadenozylcobamide, DBC) on the growth of some forms of rat tumours and on the prolongation of survival of rats with implanted Zajdela ascites hepatoma was compared with that of cyanocobalamine (5,6-dimethylbenzimidazolyl-Co-cyanocobamide, CN-B12). The effect of DBC was shown to differ from that of CN-B12. DBC did not stimulate the growth of the investigated forms of tumours and prolonged survival of rats with implanted Zajdela ascites hepatoma. The rats displayed cancer resistance when DBC or CN-B12 were injected before implantation of tumours or Zajdela ascites hepatoma.
Explore the source record for details and available documents.
Reported are in vivo trials on Friend virus-leukemia (FVL), on methylcholanthren-induced fibrosarcomas of the mouse, and on amelanotic melanoma No. 3 of the Syrian hamster after treatment with halogenated pyrimidines, 5'-bromodeoxyuridine (BUDR) and 5'-iododeoxyuridine (IUDR) as to provoke genuine oncorna viruses. Till now, no prove exists that in tissue culture propagated C-type particles are really oncogenic. From the results demonstrated here the conclusion can be drawn that the chosen in vivo-conditions neither oncogens, possibly located in the cells, will be finished to complete oncogenic viruses, nor a spread and multiplication of dormant viruses will take place due to a provocation treatment of the hosts with halogenated pyrimidines. It seems, therefore, that the requirements to activate oncogens in vitro are absolutely different to those needed under in vivo conditions.
Explore the source record for details and available documents.
Electron microscopy of thin sections of syncytia, formed by fusion of homologous XC cells, clarified that these heterologous cells were simply invaginated by syncytia and that they were clearly separated by the limiting cytoplasmic membranes. The C particles found at the boundary showed no sign of connection with the surrounding syncytial cell membrane, while some were seen budding from the surface of the producer cells. These results strongly suggest that the XC cells, even when cocultured with the C-type virus-producing myeloma cells, fuse homologously among themselves, and the virus-producing heterologous cells do not participate in the event.
Intracisternal viruslike particles were present in outbred Syrian golden and inbred ALB/Mey Pfd hamster blastocysts, embryos, and fetuses. Their morphology was identical to that of the "spoked" viruslike particles found in hamster tumors. They were released in great numbers in the embryonal tissues until day 9 of pregnancy and were found until day 13 in the fetal tissues. Thereafter, these viruslike particles were no longer observed in the fetus. They were never recorded in normal adult hamster tissues.
A series of 15 halogenated hydrocarbons of industrial and environmental importance were tested for carcinogenicity by chronic administration by one or more routes in Ha:ICR Swiss mice. Not all compounds were tested by the four routes of administration used. Allyl chloride, 1,2-dibromo-3-chloropropane, and vinylidene chloride were active as skin tumor initiators in the two-stage carcinogenesis assays; phorbol myristate acetate was used as a promoter. 1,2-Dibromoethane was the only compound that induced a significant incidence (p less than 0.05) of skin papillomas, skin carcinomas, and lung tumors by repeated skin application. 1,2-Dichloroethane, 1,1,2,2-tetrabromoethane, and 1,2-dibromo-3-chloropropane induced lung and/or stomach tumors by repeated skin application. Two compounds showed sarcomagenic activity by sc injection; they were cis-1,3-dichloropropene and 2-chloropropanal. By intragastric intubation, 1-chloropropene and 2-chloropropanal induced significant numbers of stomach tumors. Vehicle, no-treatment, and positive control groups were included in these tests. The following compounds were also tested by one or more of the four routes but were inactive by the criteria used; i.e., they showed P = 0.05 or greater than 0.05: trichloroethylene, tetrachloroethylene, hexachlorobutadiene, chloroacetaldehyde, 1-chloropropene oxide (cis and trans), and trichloroethylene oxide.
5'-DFUR is converted to 5-FU by pyrimidine nucleoside phosphorylase. The activity of this enzyme is higher in tissue tissue than in most normal tissues, leading to a significantly higher conversion to 5-FU and 5-FU concentration in the tumor tissue than in normal tissue and serum. This activation mechanism provides this compound with high tumor selective toxicity. Based on these characteristics, 5'-DFUR has shown significant antitumor activity with less toxicity and immunosuppressive activity in experimental models. In the clinical study, 5'-DFUR has shown antitumor activity in gastric, colo-rectum and breast cancer. Especially in breast cancer, high response was observed including CR cases and also suggested a fast onset of action and long duration of efficacy. In the safety, major adverse reaction was diarrhea but it was controllable. Bone marrow suppression and CNS toxicity were very mild. 5'-DFUR can be a good candidate for the combination regimen and surgical adjuvant chemotherapy.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Mast cells were found to be unique among the peritoneal leukocytes by virtue of their capacity to enhance profoundly the proliferation of a variety of tumors in vitro. This phenomenon occurs at mast cell/tumor ratios which reflect the stoichiometry of host cell/tumor relationships in vivo. The growth factor was found to reside in mast cell granules and was identified as heparin by sequential purification and enzymatic degradation. This cellular interaction was tumor-specific, although isolated granules could enhance fibroblast proliferation. The findings are discussed in relation to previous morphologic studies, reports of in vitro mast-cell-mediated tumor cytotoxicity, and the role of mast cells in angiogenesis and connective tissue proliferation.
The relationship between the macrophage infiltration and the specific growth rate of tumours was studied by the technique of spontaneous migration of lymphoreticular cells from tissue fragments. In the case of dimethylnitrosamine-induced rat kidney tumours and Ehrlich solid tumour in mice the increased migration of activated macrophages was associated with the average specific growth rate. The macrophage infiltration of tumours and systemic immune reactivity to tumour-associated antigens depend probably on tumour cell kinetics.
Explore the source record for details and available documents.