[Hepatic metastasis of serous cystadenocarcinoma resected 4 years after operation of primary tumors--a case report].
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Cystadenocarcinoma↗
Biomedical subjects
S Sugie
Publications and source records attributed to S Sugie.
Immunohistochemical study of a monoclonal antibody 115D8 against human milk-fat globule membrane (MAM-6) in some histological types of breast cancer.
An antigen, MAM-6, in human milk-fat globule membranes, was detected with a monoclonal antibody 115D8, in paraffin-embedded sections of 148 cases including human breast cancers and other breast diseases with immunoperoxidase technique. There were some differences on the staining portion in the cells among the different types of breast cancers, although we could not find any differences in intensity of reaction with 115D8 among the different histochemical types of breast cancers. MAM-6 was mainly localized in the apical portion of the cells or the cytoplasms of the papillo-tubular carcinoma. The antigen was chiefly localized in the margin of the cells or cytoplasms of the solid- tubular carcinoma and scirrhous carcinoma. Normal mammary glands, sweat glands and sebaceous glands were reacted with 115D8 but epidermis, esophagus, stomach, small intestines, large intestines, pancreas, liver, lung, kidney, urinary bladder, thyroid, adrenal glands, heart, striated and smooth muscles, spleen, lymphnodes and brain were not reacted with 115D8 in this study. Although the antibody was not sufficient for differential diagnosis among the types of breast cancer, it may be useful to detect the breast cancer.
Antibodies, Monoclonal↗
Inhibitory effects of chlorogenic acid, reserpine, polyprenoic acid (E-5166), or coffee on hepatocarcinogenesis in rats and hamsters.
Four different experiments were performed in order to examine the modifying effects of chlorogenic acid (CA), reserpine, polyprenoic acid (E-5166), and coffee on chemical carcinogenesis in rats or hamsters. Experiment 1: The numbers of hyperplastic liver cell foci and the incidence of colon tumors in male and female Syrian golden hamsters given a single intravenous injection of methylazoxymethanol (MAM) acetate and then fed the diet containing 0.025% CA for 24 wk were significantly lower than those of hamsters given MAM acetate alone. Experiment 2: The incidence of altered hepatocellular foci in female ACI/N rats given N-2-fluorenylacetamide (FAA, 0.02% in diet) for 10 wk and reserpine (weekly subcutaneous injections, 1 microgram/g body weight) during or after (17 wk) FAA exposure was significantly lower than that of rats given FAA alone. Experiment 3: The number of hepatocellular foci in male ACI/N rats given 0.02% FAA diet for 13 wk and E-5166 by gavage (40 mg/kg body weight, 3 times/wk) for 16 wk after the end of FAA exposure was significantly smaller than that in rats given FAA diet alone. Experiment 4: Incidences of liver tumors and hepatocellular foci of rats given concurrent dietary administration of aminopyrine (0.01%) and sodium nitrite (0.1%) and coffee solution as a drinking water for 630 da were significantly lower than those of rats given aminopyrine and sodium nitrite. Thus, the tested compounds had inhibitory effects on chemical carcinogenesis in liver or colon.
Animals↗
Fine-needle aspiration cytology of pheochromocytoma-ganglioneuroma of the organ of Zuckerkandl.
Fine-needle aspiration (FNA) cytologic and immunocytochemical findings of a rare combined pheochromocytoma-ganglioneuroma developing in a 48-yr-old Japanese man in the organ of Zuckerkandl are described. This is the first report of a combined pheochromocytoma-ganglioneuroma of the organ of Zuckerkandl. FNA cytology showed typical cytologic findings of these two components similar to those described individually in fine-needle aspirates of these neoplasms. The neoplastic cells showed positive reactions for vasoactive intestinal polypeptide, neuron-specific enolase, and S-100.
Biopsy, Needle↗
Chemoprevention of experimental mammary carcinogenesis by the synthetic organoselenium compound, benzylselenocyanate, in rats.
The effect of the dietary organoselenium compound, benzylselenocyanate (BSC) along with its sulphur analogue, benzylthiocynanate (BTC) and sodium selenite (Na2SeO3), on 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary carcinogenesis was examined in female Sprague-Dawley rats during the initiation phase of carcinogenesis. Semipurified diets containing 25 p.p.m. of BSC and 25 p.p.m. BTC, and 4 p.p.m. Selenium as Na2SeO3 in drinking water were given to 5-week-old rats for 3 weeks starting 2 weeks before, during and until 1 week after carcinogen treatment. At 7 weeks of age animals were given a single dose of DMBA (10 mg) in 1 ml olive oil by oral intubation. One week after DMBA treatment, the groups receiving BSC- and BTC-supplemented diets were transferred to the unsupplemented standard diets and the group of rats receiving Na2SeO3 in drinking water was transferred to regular tap water for the duration of the experiment. The results indicate that the rats receiving BSC in their diet showed a highly significant inhibition of tumor incidence and tumor multiplicity as well as a prolonged latency period when compared to the group fed the control diet. Neither BTC nor Na2SeO3 had any effect on the subsequent development of mammary tumors. These results indicate that dietary BSC inhibits mammary tumor incidence during the initiation phase of carcinogenesis and is a considerably more potent inhibitor than its sulphur analogue BTC and inorganic selenium. This is the first report that demonstrates the inhibition of mammary carcinogenesis by a synthetic organoselenium compound.
9,10-Dimethyl-1,2-benzanthracene↗
Dietary beta-carotene in rat models of gastrointestinal cancer.
The effect of dietary beta-carotene (BC) was investigated in models of gastric and colonic carcinogenesis. Male Wistar rats were fed a diet with 0.4% BC during weaning, then 0.2% BC throughout. Cancer in the stomach and small intestine was induced by giving 80 mg/l N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in drinking water for 52 wk, but BC failed to affect carcinogenesis under these conditions, although the incidence of gastric adenocarcinoma was reduced slightly. Neoplastic and nonneoplastic lesions in the liver, skin, and pancreas were also present to a similar extent with BC feeding and without BC. Colorectal cancer was induced by six 2 mg intrarectal infusions of MNNG per rat over a 3-wk period, with the rats held another 22 wk without an inhibitory effect by BC. Thus, 0.2% dietary BC failed to influence significantly the development of neoplasia induced by a direct-acting carcinogen in the gastrointestinal tract.
Animals↗
Inhibition by dietary benzylselenocyanate of hepatocarcinogenesis induced by azoxymethane in Fischer 344 rats.
The effect of dietary benzylselenocyanate (BSC), a novel organoselenium compound and its sulfur analog, benzylthiocyanate (BTC), on hepatocarcinogenesis induced by azoxymethane (AOM) was investigated in male F344 rats. Eighty-one weanling rats were divided into 3 groups and were raised on a semipurified diet (control diet). Starting from 5 weeks of age, groups of animals consuming the control diet were fed one of the experimental diets containing 25 ppm BSC or BTC. An additional group was continued on the control diet. At 7 weeks of age, animals were given weekly sc injections of AOM (15 mg/kg body weight once weekly for 2 weeks). One week after the second AOM injection, those groups receiving BSC and BTC diets were transferred to the control diet and continued on this diet until termination of the experiment at 34 weeks after the last AOM injection. For quantitative analysis of enzyme-altered liver cell foci, glutathione S-transferase placental form was stained by an immunohistochemical technique. The results indicate that the incidence and the density of the enzyme-altered foci were significantly lower in AOM-treated rats fed the diet containing 25 ppm BSC (foci incidence 56%, foci density 2.43/cm2) than in AOM-treated animals fed the control diet (foci incidence 92%, foci density 4.79/cm2). The incidence of small altered foci was significantly inhibited in rats fed the BTC diet (35%) as compared to those fed the control diet (68%), but the degree of inhibition was more pronounced in animals fed the BSC diet than in those fed the BTC diet.
Animals↗
Effect of voluntary exercise on azoxymethane-induced colon carcinogenesis in male F344 rats.
The effect of voluntary exercise on azoxymethane (AOM; CAS: 25843-45-2)-induced colon carcinogenesis was investigated in male F344 rats. Beginning at 5 wk of age, all animals were divided into two groups (sedentary and exercise) and fed AIN-76A semipurified diet ad libitum. At 7 wk of age, animals were given AOM s.c. at a dose level of 15 mg/kg of body weight, once weekly for 2 wk. Four days after the second dose of AOM, all animals in the exercise group were housed in individual wheel-cage units, and the animals in the sedentary group were housed in plastic cages. The experiment was terminated at 38 wk post-AOM treatment. Body weights of animals in the exercise and sedentary groups were comparable. The incidence (percentage of animals with tumors) and multiplicity (tumors/animal) of colon adenocarcinomas were significantly inhibited in the exercise group, but the incidence and multiplicity of colon adenomas were unaffected by the exercise. The incidence of small intestinal adenocarcinomas and liver foci was also inhibited in the exercise group.
Animals↗
Effect of different levels of omega-3 and omega-6 fatty acids on azoxymethane-induced colon carcinogenesis in F344 rats.
The effect of various levels of dietary Menhaden fish oil containing omega-3 fatty acids plus corn oil containing omega-6 fatty acids fed during the postinitiation phase of colon carcinogenesis was studied in male F344 rats. Starting at 5 weeks of age, groups of animals were fed the 5% corn oil (5% CO) diet. At 7 weeks of age, all animals except the vehicle-treated controls were administered s.c. injections of azoxymethane (15 mg/kg body wt/week for 2 weeks). 4 days after carcinogen or vehicle treatment, groups of animals were transferred to experimental diets containing 4% Menhaden oil + 1% corn oil (4% MO + 1% CO), 23.5% corn oil (23.5% CO), 17.6% corn oil + 5.9% Menhaden oil (17.6% CO + 5.9% MO), 11.8% corn oil + 11.8% Menhaden oil (11.8% CO + 11.8% MO), or 5.9% corn oil + 17.6% Menhaden oil (5.9% CO + 17.6% MO) and fed these diets until termination of the experiment at Week 38 after carcinogen treatment. An additional group consuming a 5% CO diet was continued on these diets. Colon mucosal ornithine decarboxylase activity and microsomal fatty acid composition of colon mucosa were measured in vehicle-treated animals fed experimental diets for 14 weeks. Fatty acids were also analyzed in the microsomal fraction of colon tumors at termination of the experiment. The body weights of animals fed various experimental diets were comparable. Feeding of high fat diets containing 17.6% CO + 5.9% MO, 11.8% CO + 11.8% MO, or 5.9% CO + 17.6% MO significantly inhibited the incidence (percentage of animals with tumors) of colon adenocarcinomas compared to that of 23.5% CO diet. However, the multiplicity (number of tumors/rat) of colon adenocarcinomas was significantly inhibited only in groups fed the 5.9% CO + 17.6% MO compared to those fed the 23.5% CO diet. The incidence and multiplicity of adenocarcinomas were greater in animals fed the 23.5% CO diet compared to those fed the 5% CO diet. Colonic mucosal ornithine decarboxylase activity was lower in animals fed the 11.8% CO + 11.8% MO, 5.9% CO + 17.6% MO, 5% CO, and 4% MO + 1% CO diets compared to the levels in animals fed the 23.5% CO diet. The increasing levels of Menhaden oil in the diet significantly increased the omega-3 fatty acids such as eicosapentaenoic acid and docosahexaenoic acid and decreased the omega-6 fatty acids such as linoleic acid, linolenic acid, and arachidonic acid in microsomal fractions from colonic mucosa and tumors.
Animals↗
Effect of dietary excess of inorganic selenium during initiation and postinitiation phases of colon carcinogenesis in F344 rats.
The effect of supplemental inorganic selenium given during the initiation or postinitiation phase of colon carcinogenesis induced by azoxymethane [(AOM)CAS:25843-45-2] was studied in male F344 rats. Weanling animals were raised on AIN-76A semipurified (control) diet. Starting at 4 wk of age, groups of animals intended for initiation study were fed the semipurified diets containing 0.5 and 2.5 ppm selenium in the form of sodium selenite, and those intended for postinitiation study were continued on the control diet. At 7 wk of age, all animals except the vehicle-treated controls were injected s.c. with AOM (15 mg/kg body weight, once weekly for 2 wk). One wk following AOM treatment, animals in the initiation study receiving the supplemental selenium were transferred to the control diet whereas those in the postinitiation study receiving the control diet were transferred to the diets containing 0.5 and 2.5 ppm selenium. These animals were continued on this regimen until the termination of the experiment at 34 wk post-AOM injection. Tissue and blood glutathione peroxidase activity was measured in vehicle-treated animals fed the control and selenium-supplemented diets. The results indicate that body weights were comparable among the various dietary groups. Feeding of diets containing 0.5 and 2.5 ppm selenium during the initiation phase had no effect on colon tumor incidence, but the multiplicity of adenomas was slightly inhibited in animals fed the 2.5 ppm selenium diet. The incidence and multiplicity of colon adenocarcinomas and the multiplicity of colon adenomas were inhibited in animals fed the 2.5-ppm selenium diet during the postinitiation phase of carcinogenesis. The incidence of small intestinal tumors was higher in animals fed the 2.5-ppm selenium diet during the initiation phase than in animals fed the control diet and 0.5-ppm selenium diet. Selenium-dependent glutathione peroxidase activity was increased in kidneys and small and large intestinal mucosae of animals fed the 2.5-ppm selenium diet compared to those fed the 0.5-ppm selenium and control diets.
Animals↗
Species and sex differences in genotoxicity of heterocyclic amine pyrolysis and cooking products in the hepatocyte primary culture/DNA repair test using rat, mouse, and hamster hepatocytes.
Eleven mutagenic heterocyclic amines, 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]-indole (Trp-P-1), 3-amino-1-methyl-5H-pyrido[4,3]indole (Trp-P-2), 2-amino-6-methyl-dipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1), 2-aminodipyrido[1,2-a:3',2'-d]imidazole (Glu-P-2), 2-amino-9H-pyrido[2,3-b]indole (A alpha C), 2-amino-3-methyl-9H-pyrido[2,3-b]indole (MeA alpha C), 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ), 2-amino-3,8-dimethylimidazo [4,5-f]quinoline (MeIQX), 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (4,8-diMeIQX), and 2-amino-3,7,8-trimethylimidazo[4,5-f]quinoxaline (7,8-diMeIQX), were studied for genotoxicity in the hepatocyte/DNA repair test employing hepatocytes of male rats, male and female mice, and male hamsters. In these four assay systems, all compounds elicited DNA repair in at least three systems, except Trp-P-2, which was uniformly inactive. However, there were several significant differences in the responses of different systems. Rat and hamster hepatocytes responded to nine of the ten genotoxic compounds with the exception of Glu-P-2. Male and female mouse hepatocytes responded to Glu-P-2, whereas female, but not male, mouse hepatocytes responded to MeIQX and 4,8-diMeIQX. These results illustrate species and sex differences in response to these heterocyclic amines and suggest that a number of these compounds are carcinogenic in hamsters, as they have been in rats and mice.
Amines↗
Genotoxicity of epoxy resin hardeners in the hepatocyte primary culture/DNA repair test.
The genotoxicity of 9 chemicals used as epoxy resin hardeners was examined in the DNA repair test with rat hepatocytes. DNA repair synthesis was elicited by 7 chemicals, i.e., 4-aminodiphenyl ether, 4,4-diaminodiphenyl ether, 3,4,4'-triaminodiphenyl ether, 3,3'-dichloro-4,4'-diaminodiphenyl ether, 1,3-phenylenedi-4-aminophenyl ether, 4,4'-diaminodiphenyl methane and 4,4'-methylene-bis(2-chloroaniline). The positive results obtained with 4 epoxy resin hardeners of unknown carcinogenicity, i.e., 4-amino-diphenyl ether, 3,4,4'-triaminodiphenyl ether, 3,3'-dichloro-4,4'-diaminodiphenyl ether and 1,3-phenylene-di-4-aminophenyl ether suggest that they may be carcinogens. The genotoxicity of 1,4-phenylene-di-4-aminophenyl ether, of unknown carcinogenicity, and 4,4'-diaminodiphenyl sulfone, for which there is no sound proof of carcinogenicity, was not confirmed in the DNA repair test. The result with 4,4'-diaminodiphenyl sulfone was in agreement with its lack of mutagenicity in Salmonella typhimurium.
Animals↗
The genotoxicity of a variety of aniline derivatives in a DNA repair test with primary cultured rat hepatocytes.
The genotoxicity of a variety of aniline derivatives was examined by a DNA repair test with rat hepatocytes. Out of 37 aniline derivatives, 6 chemicals, i.e., 2,4,6-trimethylaniline (mesidine), 2,4-xylidine, 3,5-diaminobenzoic acid, 3,4-diaminochlorobenzene, 2-chloro-4-methylaniline and 4-chloro-N-methylaniline, elicited positive DNA repair responses. The results are in agreement with the bacterial mutagenicities with or without norharman of these compounds. Positive compounds of unknown carcinogenicity in the present assay, i.e., 3,5-diaminobenzoic acid, 2-chloro-4-methylaniline and 4-chloro-N-methylaniline are suspected of being potentially carcinogenic.
Aniline Compounds↗
Carcinogenicity of quinoline, 4- and 8-methylquinoline and benzoquinolines in newborn mice and rats.
The relative tumorigenic activity of quinoline, 4-methylquinoline, 8-methylquinoline, and all three isomeric benzoquinolines was evaluated in newborn CD-1 mice and Sprague-Dawley rats. In the newborn-mouse bioassay, 0.25, 0.5 and 1.0 mumol of each compound in dimethylsulphoxide was administered by ip injection on days 1, 8 and 15 of life, respectively. The bioassay was terminated when the mice were 1 yr old. The incidence of liver tumours observed for those male mice treated with either quinoline or 4-methylquinoline was greater than 78%. 8-Methylquinoline, naphthalene, benzo[f]quinoline, benzo[h]quinoline and phenanthridine did not exhibit significant tumorigenic activity in this bioassay. In contrast to these results, none of these compounds induced a significant incidence of liver tumours in female mice. Each of these aza-arenes was administered to newborn Sprague-Dawley rats by supra-scapular injections of 200 mumol/kg body weight in dimethylsulphoxide on the first day of life, 100 mumol weekly at wk 2-7, and 20 mumol at wk 8. This bioassay was terminated when the rats were 78 wk old. No significant difference in tumour incidence was observed between the pups that had been treated with these aza-arenes and the controls. These data indicate that quinoline and 4-methylquinoline are more potent tumorigens than any of the three isomers of benzoquinoline evaluated in this study. In contrast to the potent hepatocarcinogenic activity observed for both quinoline and 4-methylquinoline in newborn mice, no significant tumorigenic activity was observed with these aza-arenes in newborn rats.
Animals↗
Potential carcinogenicity of 5,6-dimethoxysterigmatocystin in rats.
The potential carcinogenic activity of 5,6-dimethoxysterigmatocystin (DMSC) was examined by oral administration in rats. In Experiment I, all of eight effective ACI/N rats given DMSC in the diet at a concentration of 50 p.p.m. developed neoplastic nodules of the liver. Five rats developed hepatocellular carcinomas and four rats had hemangioendothelial sarcomas of the liver. Two other rats developed osteosarcomas. In Experiment II, F344 rats were given DMSC by gavage once every 2 weeks at dose of 2 mg/0.15 ml dimethylformamide. Out of 24 effective animals 19 rats developed neoplastic nodules of the liver, and eight rats had hepatocellular carcinomas. Hemangioendothelial sarcoma of the liver was seen in one rat. Two rats developed osteosarcomas in the upper legs. Proliferative fibrous lesions which were considered to be a preneoplastic change of the bone tumors were seen in the thighbones of four rats. Results obtained from these two experiments indicate that DMSC is hepatocarcinogenic, as is sterigmatocystin, and that the compound is probably weakly carcinogenic for the bone.
Administration, Oral↗
Genotoxicity of a variety of hydrazine derivatives in the hepatocyte primary culture/DNA repair test using rat and mouse hepatocytes.
The genotoxicity of a variety of hydrazine derivatives was examined in the DNA-repair test on rat or mouse hepatocytes. Out of 32 hydrazine derivatives, 6 chemicals, i.e., N'-acetyl-4-(hydroxymethyl)phenylhydrazine, 1,2-dimethylhydrazine.2HCl, 1-hydrazinophthalazine.HCl, methylhydrazine.sulfate, p,p'-oxybisbenzene disulfonylhydrazide and phenylhydrazine.HCl, elicited positive DNA repair responses in the test on rat hepatocytes. In the test on mouse hepatocytes, 4 more hydrazine derivatives, i.e., 1,1-dimethylhydrazine, hydrazine hydrate, hydrazine sulfate and 2-methyl-4-chlorophenoxyacetic acid hydrazide.HCl also generated positive responses, in addition to the 6 positive compounds in the rat assay. These results suggest that mouse hepatocytes are more susceptible to the genotoxicity of hydrazine derivatives, and that the species differences in genotoxicity appear to be in agreement with the in vivo carcinogenicity of these agents.
Animals↗
A case of double cancer (pancreatic and ovarian adenocarcinomas) diagnosed by exfoliative and fine needle aspiration cytology.
A case of double cancer (pancreatic and ovarian adenocarcinomas) in a woman suggested by exfoliative and fine needle aspiration (FNA) cytology is reported. Exfoliative cytology, including immunohistochemical findings of the biliary juice and those of clinical image examinations indicated tubular adenocarcinoma of the pancreatic body. FNA cytologic findings with immunohistochemical observation and those of ultrasound examination showed mucinous adenocarcinoma of the right ovary. As a rare event, pancreatic cancer metastasized to ovarian carcinoma.
Adenocarcinoma↗
Chemoprevention of colon carcinogenesis by dietary organoselenium, benzylselenocyanate, in F344 rats.
The effect of feeding benzylselenocyanate (BSC) and its sulfur analogue, benzylthiocyanate (BTC), 2 wk before, during, and until 1 wk after carcinogen administration (initiation phase) on intestinal carcinogenesis induced by azoxymethane (CAS:25843-45-2) was studied in male F344 rats. Weanling rats were raised on a semipurified diet (AIN-76A diet; control diet). Beginning at 5 wk of age, groups of animals consuming the control diet were fed one of the diets containing 25 ppm BSC or BTC. An additional group was continued on the control diet. At 7 wk of age, all animals in 3 groups, except the vehicle-treated controls, were administered s.c. injections of azoxymethane (15 mg/kg body weight, once weekly for 2 wk). Animals were continued on the control diet and BSC and BTC diets until 1 wk after carcinogen treatment, when those groups receiving BSC and BTC diets were fed the control diet until termination of the experiment. Tissue and blood plasma glutathione peroxidase activity was measured in vehicle-treated animals fed the control diet and BSC and BTC diets for 5 wk. The results indicate that body weights were comparable among the various dietary groups. BSC in the diet significantly inhibited the incidence (percentage of animals with tumors) and multiplicity (tumors/animal) of adenocarcinomas in the colon and multiplicity of adenocarcinomas in the small intestine compared to those fed the control diet. BTC in the diet had no effect on colon and small intestinal tumors. Selenium-dependent glutathione peroxidase activity was significantly increased in kidneys and colon and small intestinal mucosae of animals fed the BSC diet compared to animals fed the BTC and control diets.
Administration, Oral↗