Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostatic adenocarcinomas were induced in 5 out of 20 Wistar rats upon a single administration of 50 mg/kg N-nitroso-N-methylurea (NMU). The rats were pretreated with a daily dose of 50 mg/kg cyproterone acetate for 3 weeks followed by 3 daily injections of 100 mg/kg testosterone. All tumours developed in the dorsolateral prostate and were invasively growing. In 2 cases distant metastases were found. Three proliferative lesions classified as carcinomas in situ were also found in the dorsolateral prostate. A total of 7/20 animals (35%) carried an adenocarcinoma and/or a carcinoma in situ. In addition, 6 epithelial hyperplasias were observed in the dorsolateral and 1 in the ventral prostate of non-tumour-bearing rats. The method described may provide a good animal model for cancer of the prostate and lead to a better understanding of prostatic carcinogenesis.
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PMID:Adenocarcinomas of the prostate induced by N-nitroso-N-methylurea in rats pretreated with cyproterone acetate and testosterone. 621 69

Streptozotocin was administered in a dose of 50 mg/kg body weight intraperitoneally on three consecutive days to 35 8-week old male Syrian golden hamsters. At sacrifice 16-36 weeks later, macroscopic liver tumors had developed in 27 of 29 surviving animals. The majority of animals had multiple hepatic nodules. Some tumors were already large (greater than 1 cm) 16 weeks after streptozotocin. By histologic criteria, five animals (17%) had hepatocellular carcinoma, 23 (79%) had adenomas with varying degrees of atypia, and one (4%) had a normal liver. No metastases to organs outside the liver were noted. No other primary tumors were observed. Sixteen of 29 animals had ascites. Twenty-five age-matched untreated animals showed no evidence of liver tumors. Although sporadic liver tumors due to streptozotocin have been reported in rats and mice, the high incidence of tumors and short latency period to tumor induction seem to be unique to the Syrian hamster. The development of liver carcinoma without the necessity for long-term administration of the carcinogen and without adjunctive procedures such as partial hepatectomy represents a potential improvement over other animal models of hepatic neoplasia.
Carcinogenesis 1984 Oct
PMID:Streptozotocin-induced liver tumors in the Syrian hamster. 623 5

Hepatocellular neoplasms are known to differ in enzyme activity from the surrounding non-neoplastic liver. We have compared histochemically the enzyme activity of spontaneous hepatocellular tumors in mice with tumors induced by diethylnitrosamine and dieldrin. Some neoplasms had increased activity, others had decreased enzyme activity, yet other had the same activity as the surrounding liver. Alkaline phosphatase, glucose-6-phosphatase, succinic dehydrogenase and adenosine triphosphatase, as well as glycogen levels were studied. Carcinomas differed from adenomas in having elevated enzyme activity significantly more often than adenomas. However, the carcinomas showed elevated glycogen levels less frequently than adenomas. Histochemically, pulmonary metastases resembled the primary hepatocellular carcinomas from which they were derived. Tumors of dieldrin animals were notable in having increased activity of all the enzymes which we studied more frequently than tumors of diethylnitrosamine animals or of controls. Differences in enzyme activity between the three mouse strains were slight.
Carcinogenesis 1982
PMID:Enzyme histochemical characteristics of spontaneous and induced hepatocellular neoplasms in mice. 629 95

85 Wistar rats were operated on stomach. Carcinomas in the operated stomach were seen without additional application of a carcinogen 31 and 40 weeks after gastric surgery. Histologically adeno and scirrhous carcinomas were diagnosed. Metastases were observed in rats with gastric cancer. Dysplastic changes and chronic inflammatory reactions of gastric mucosa were seen. The enterogastric reflux is an aetiopathogenic factor in carcinogenesis. Because of reproductivity, high tumor rate, no additional application of a carcinogen and the little operative extent, this experimental model offers to be a model of carcinogenesis in stomach.
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PMID:[Carcinoma in the operated stomach of the rat--a tumor model]. 632 21

The purpose of this investigation was to determine whether cells transformed by herpes simplex virus type 2 (HSV-2) can be stimulated to synthesize prostaglandins (PG). Stimulation was determined by measuring the release of PG into overlay fluids from cell monolayers prelabeled with [3H]arachidonic acid. Results showed that Ca2+ ionophore A-23187 markedly stimulated arachidonic acid release starting 30 min after treatment of HSV-2-transformed and nontransformed rat embryo fibroblast cells. However, only HSV-2-transformed cells were stimulated in production of PG. HSV-2-transformed, nontumorigenic, rat embryo fibroblast, line G, clone 2.0 cells synthesize nearly equal amounts of prostaglandin E2 (PGE2) and prostaglandin F2 alpha, while tumor (rat fibrosarcoma) cells synthesize primarily PGE2. Stimulation of PGE2 synthesis by Ca2+ ionophore A-23187 or 12-O-tetradecanoyl-phorbol-13-acetate decreased as rat fibrosarcoma cells were serially passaged in tissue culture. At low passage of parental rat fibrosarcoma cells, four distinct morphological clonal cell lines were isolated, which varied markedly in their capacity to be stimulated in PG synthesis by 12-O-tetradecanoyl-phorbol-13-acetate. There was correlation between the capacity of clone 1 cells to be stimulated in PGE2 synthesis by serum alone and capacity of the tumors produced by the clone 1 cells to metastasize to the lungs of syngeneic tumor-bearing rats. In summary, cell transformation by HSV-2 appears to be essential for stimulation of PG synthesis in cells. The capacity to be stimulated in arachidonic acid metabolism and PG synthesis may be important in the process of carcinogenesis by a putative human cancer virus.
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PMID:Calcium ionophore A-23187 and 12-O-tetradecanoyl-phorbol-13-acetate stimulation of prostaglandin synthesis in herpes simplex virus type 2-transformed rat cells. 632 82

The mechanism by which dietary cholesterol facilities colon carcinogenesis was investigated in the dimethylhydrazine-induced rat colon cancer model. Fifty female Wistar rats received a standard course of dimethylhydrazine (DMH) injections (40 mg/kg/week subcutaneously for ten weeks) while being fed Vivonex, a cholesterol-free elemental diet. Animals were allocated to one of five dietary regimens. One control group received Vivonex with added cholesterol (10 mg/100 ml Vivonex/rat/day) throughout the experiment, while another group received Vivonex alone. The remaining three groups received added cholesterol exclusively before, during or after the ten week DMH induction period. The experiment continued for over 500 days, and was evaluated by comparing, between groups, the time taken for the development of objective signs of colonic disease (time to tumour presentation or TTP). Animals either died spontaneously or were killed and autopsied. Colon cancers were confirmed histologically in every animal. The results showed that cholesterol feeding throughout the experiment or during the DMH induction period reduced the TTP compared to controls (p less than 0.05). Cholesterol prefeeding had no such effect. In the after group, the TTP was correspondingly delayed (p less than 0.05). Cholesterol-fed controls and groups receiving cholesterol during or after the DMH induction had more colon tumours and/or a greater incidence of metastases than cholesterol-free controls or those pre-fed cholesterol. The findings indicate a direct relationship between timing of cholesterol exposure and signs of colon cancer, and demonstrate that dietary cholesterol has promoter-like characteristics.
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PMID:An investigation into the mechanism of co-carcinogenesis of dietary cholesterol during the induction of colon cancer in rats by 1,2 dimethylhydrazine. 647 81

The subject of chemical carcinogenicity is reviewed with discussions of the involved environmental factors, proposed mechanisms of mutagenesis and carcinogenesis, dose-response considerations, secondary tumor development, and an emphasis on the potential carcinogenicity of antineoplastic agents. Although the causes of various cancers are complex, 70-90% of human cancers are thought to be caused by environmental factors. The factors that have been strongly implicated are excessive cigarette use, heavy alcohol consumption, and disordered dietary practices. Of the minor possible causes of cancer, the administration of prescribed pharmaceutical agents such as the antineoplastic drugs accounts for a suspected 1% of total cancer deaths in the United States. Chemical carcinogenesis involves a multistep process of initiation, promotion, and progression. The development of cancer in man usually takes several years and may be associated with specific tissue susceptibility. Although antineoplastic agents have been recognized for their potential ability to cause cancer, it is difficult to assess from the literature their actual carcinogenic effects in man. Important determinants that modify the ability of the host to deal with carcinogenic substances and the subsequent effects have not been fully evaluated. The control of chemical carcinogenesis must involve reduction of exposure to potential hazards wherever possible. To reduce the risks involved in handling antineoplastic agents, health-care professionals should follow a method of systematic avoidance by adhering to appropriate procedures.
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PMID:Chemical carcinogenicity and the antineoplastic agents. 649 22

Struma maligna raises some questions concerning carcinogenesis, precancerosis, as well as diagnosis, therapy and prognosis. Only little information can be obtained by evaluating morphological criteria. Usually exhibiting modest malignancy papillary carcinoma as well as C-cell-carcinoma of the thyroid deserve particular interest. With regard to the velocity of growth (organoid arrangement of tumour tissue), also folliculoid carcinoma (i.e. Struma Langhans) will differ from so-called 'true' carcinomas characterized by a slower rate of growth. All other types of carcinoma, including sarcoma, represent tumours with rapid growth, accompanied by early formation of metastases.--In this connection all considerations concerning the usefulness of the so-called 'concept of pre-cancerosis' for the thyroid are thought to be very important. Realizing an atypical adenoma seems to be promising in evaluating this concept.
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PMID:[Malignant struma. With remarks on the use of the concept of precancerous conditions in strumas]. 652 26

A total of 18 nickel compounds were tested for carcinogenicity in male Fischer rats by a single i.m. injection at equivalent dosages (14 mg Ni/rat). Within two years, the following incidences of sarcomas occurred at the injection site: nickel subsulfide (alpha Ni3S2), 100%, crystalline nickel monosulfide (beta NiS), 100%; nickel ferrosulfide (Ni4FeS4), 100%; nickel oxide (NiO), 93%; nickel subselenide (Ni3Se2), 91%; nickel sulfarsenide (NiAsS), 88%; nickel disulfide (NiS2), 86%; nickel subarsenide (Ni5AS2), 85%; nickel dust, 65%; nickel antimonide (NiSb), 59%; nickel telluride (NiTe), 54%; nickel monoselenide (NiSe), 50%; nickel subarsenide (Ni11AS8), 50%; amorphous nickel monosulfide (NiS), 12%; nickel chromate (NiCrO4), 6%; nickel monoarsenide (NiAs), 0%; nickel titanate (NiTiO3), 0%, ferronickel alloy (NiFe1.6), 0%; 84 vehicle controls, 0%. Distant metastases were found in 109 of 180 sarcoma-bearing rats (61%). The nickel-induced sarcomas included rhabdomyosarcomas, 52%, fibrosarcomas, 18%, undifferentiated sarcomas, 13%, osteosarcomas, 8%, and miscellaneous and unclassified sarcomas, 9%. Kendall's rank-correlation test showed that the carcinogenic activities of the compounds were correlated (p = 0.02) with their nickel mass-fractions, but not with dissolution half-times in rat serum or renal cytosol, or with phagocytic indices by rat peritoneal macrophages in vitro. Rank-correlation (p less than 0.0001) was found between the carcinogenic activities and the potencies of the compounds to induce erythrocytosis in rats. The discovery that the carcinogenic activities of particulate nickel compounds are correlated with a physical property, namely the nickel mass-fraction, may help to elucidate the mechanisms of nickel carcinogenesis; the observation that nickel stimulation of erythropoiesis is correlated with carcinogenic activity provides a new in vivo screening test for use in determining the carcinogenic risk of nickel compounds.
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PMID:Carcinogenicity of nickel compounds in animals. 653 78

Chromosome studies were done on direct preparations, early passage cultures, and/or cell lines derived from melanocytic lesions of 17 patients. There were 5 nevi (3 dysplastic); 1 early primary melanoma (radial growth phase); 1 advanced primary melanoma (vertical growth phase) with multiple metastases; and 10 metastatic lesions. The 5 nevi had normal karyotypes, while each of the tumors had a predominantly abnormal karyotype. The early melanoma was pseudodiploid, including a 6p;22 translocation. Ten of the 11 advanced melanomas had one or more aberrations involving chromosome #1, with 9 having deletions or translocations of lp that involved the proximal segment 1p12----1p22 9 times in 8 lesions. Six advanced tumors had additional material involving 7q, including extra #7s (4 cases) and 7q+ (2 cases). Nine melanomas, including the early tumor, had alterations in chromosome #6. Three had additional copies of 6p (as iso6p or t6p); the others showed no consistent pattern. In one advanced tumor, the primary lesion and 5 metastases (removed seriatim over an 18-month period) had nearly identical karyotypes, indicating the clonal nature of the neoplasm. The nonrandom cytogenetic changes suggest that genes important in melanoma carcinogenesis are located on the proximal portion of 1p, on 7q, and on chromosome #6. More data on early lesions are needed to identify the relation of these various cytogenetic changes to the different stages of malignant melanoma development.
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PMID:Cytogenetics of human malignant melanoma and premalignant lesions. 658 3


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