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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endogenous opioid systems (endogenous opioids and their receptors) are known to participate in the regulation of tumor growth. The present study was conducted to examine whether [Met5]-enkephalin influences the growth of transplanted neuroblastoma, and to explore the role of other opioid peptides in carcinogenesis. A/Jax mice were inoculated with 10(6) S20Y cells and received daily injections of [Met5]-enkephalin. Dosages of 0.5 to 30 mg/kg delayed tumor appearance and prolonged survival of these mice; antitumor effects were blocked by concomitant injections of naloxone. Daily administration (10 mg/kg) of [Leu5]-enkephalin had no effect on neurotumor growth. [D-Ala2, D-Leu5]-enkephalin and ethylketocyclazocine, ligands selective for delta and kappa receptors, respectively, also did not influence neuro-oncogenesis. These results demonstrated the potent growth inhibiting effects of the naturally occurring opioid pentapeptide, [Met5]-enkephalin, and substantiate reports identifying and characterizing an opioid receptor (i.e., zeta) for which [Met5]-enkephalin is the most potent ligand.
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PMID:Endogenous opioids and the growth regulation of a neural tumor. 284 18

Three hundred and forty eight C57Bl mice were killed after diethyl-nitrosamine (DEN) treatment at various time intervals ranging from one day to six months. No esophageal tumors occurred in the first three months after DEN treatment; They occurred, however, at four months and increased in number at six months of DEN treatment. Other groups of animals under the same initial DEN treatment were allowed to survive seven or nine months without treatment. One esophageal tumor was recorded at observations made seven months after one single day of DEN administration. A significant increase in the number of esophageal tumors occurred at seven months in mice treated with DEN for two weeks, and for one, two, three or four months; the highest tumor frequency was found in mice treated for six months and surviving three additional months on a carcinogen-free diet. These results suggest that clones of esophageal cells had been "programmed" for tumor growth at an early stage of DEN treatment. The tumors had, however, remained undetected at macroscopical and microscopical examination several months previously. It is apparent that not only the dose administered, but also the post-carcinogen interval is an important factor in esophageal carcinogenesis in the mouse.
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PMID:The induction of esophageal tumors in mice: dose and time dependency. 297 61

Structural and functional state of erythrocyte surface membrane was studied in C3H and C57B1/6 mice as well as in Wistar rats after 20-methylcholanthrene administration. It is shown that mice genetically susceptible to tumor growth as compared with mice resistant to carcinogenesis are characterized by an increased level of spinous erythrocytes (echinocytosis), higher membrane microviscosity and a tendency to increase polarity of their membrane lipid bilayer in the region of hydrophobic spine sound localization. The growth of chemically induced sarcomas was also accompanied by echinocytosis but with opposite changes in microviscosity and polarity of the erythrocyte membrane lipid bilayer. It is supposed that spinous erythrocyte transformation induced by different causes is based on different physicochemical factors.
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PMID:[Structural and functional state of the erythrocyte membrane in experimental carcinogenesis]. 298 71

Estradiol and other estrogens induce renal carcinoma in male Syrian hamsters. The mechanism of carcinogenesis still remains unclear. Activation of estrogens to catechol metabolites has in the past been postulated to play a role in estrogen-induced carcinogenesis. Therefore, the carcinogenic activity of catechol estrogens was investigated. After 175 days of treatment, 4-hydroxyestradiol was found to be as carcinogenic as estradiol in male Syrian hamsters (4/5 and 4/5 animals with kidney tumors, respectively). Animals treated with 2-hydroxyestradiol (0/5) or 2-methoxyestradiol (0/6) did not develop renal carcinoma. The catechol estrogens failed to be mutagenic in the Ames test (reversions of his- S. typhimurium to histidine prototrophy in the TA 100 strain). The lack of carcinogenic activity of 2-hydroxyestradiol was not due to a failure to stimulate estrogen-dependent tumor growth. Growth of H-301 cells, an estrogen-dependent hamster kidney tumor cell line, was supported in vivo by estrogens in the following order: estradiol greater than 4-hydroxyestradiol greater than 2-hydroxyestradiol. Stimulation of tumor growth by 2-methoxyestradiol was not detected. It was concluded that the carcinogenic activity of 4-hydroxyestradiol was consistent with a role of catechol metabolites in estrogen-induced carcinogenesis. However, the intrinsic carcinogenic or hormonal activity of 2-hydroxyestradiol probably can not be assessed accurately in vivo because of its rapid methylation and metabolic clearance.
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PMID:Carcinogenicity of catechol estrogens in Syrian hamsters. 300 86

Epidemiological data from different populations have suggested positive relationships between the incidence of colon cancer and meat and fat intake and a negative relationship with dietary fiber consumption. Within population comparisons have been less clearcut. Current theories on colonic carcinogenesis in man involve increased concentrations of bile acids and their metabolites, alterations in colonic pH, low Ca++, raised NH3 and long chain fatty acid levels, and alterations in bacterial numbers, type, and metabolic capabilities. The many laboratory studies in rats have been difficult to interpret since powerful initiators of carcinogenesis are always required and this rather than the promotion of spontaneous neoplastic change is the sine qua non for tumor growth in this situation. The current dilemma highlights the lack of knowledge of most aspects of human colonic physiology. Until these issues are more clearly resolved the epidemiological leads would point to low fat diets rich in less processed starchy foods with increased fiber as possible protection. Such advice is in common with the pronouncements of heart foundations, diabetes associations, and recommendations of official bodies to the general public.
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PMID:Cancer risk: possible protective role of high carbohydrate high fiber diets. 302 Sep 71

The effect of combined treatment with D,L-2-difluoromethylornithine (DFMO) and tamoxifen on the growth status, ornithine decarboxylase (ODC) activity and polyamine content of established 1-methyl-1-nitrosourea (MNU)-induced mammary tumors was investigated. DFMO treatment, a 0.125% solution provided as drinking water, inhibited the rate of tumor occurrence and reduced the number of mammary tumors induced by a high dose of MNU (50 mg/kg body weight) during the first 120 days post-carcinogen treatment. Tamoxifen was administered daily via s.c. injection (25 micrograms/100 g body weight) to tumor-bearing rats in both treatment groups, i.e. control and DFMO-treated, for a 30-day period beginning 120 days after carcinogen. Tamoxifen treatment induced tumor regression but the percentage of regressing, static or growing tumors was no different in the presence or absence of DFMO. Whereas the mammary tumors of DFMO-treated rats had reduced ODC activity and lower polyamine concentrations in comparison to the tumors of untreated animals, tamoxifen had no effect on these parameters independent of its effect on tumor growth status. DFMO did not increase the efficacy of tamoxifen in inducing tumor regression.
Carcinogenesis 1986 May
PMID:Effect of tamoxifen and D,L-2-difluoromethylornithine on the growth, ornithine decarboxylase activity and polyamine content of mammary carcinomas induced by 1-methyl-1-nitrosourea. 308 21

Information about effects of protein and amino acid intake on carcinogenesis comes mainly from experiments on laboratory animals. In general, tumor formation and tumor growth are retarded in animals consuming protein- or amino acid-deficient diets, but the effects have been attributed mainly to reduced caloric intake or body weight. Nonetheless, some tumors grow well in animals consuming diets that contain levels of protein that are insufficient to meet their nutritional needs. Induction of tumors by chemical carcinogens or procarcinogens may be enhanced or inhibited in animals consuming a diet containing a particular level of protein, depending upon the responses of enzymes that activate or inactivate the specific compound being tested. The feeding of amino acid-deficient diets or amino acid antagonists has been proposed as an adjunct to chemotherapy. Undoubtedly, tumor development and growth can be influenced by the quantity of protein consumed by an animal, but the responses observed with specific tumors and carcinogens may differ. Therefore, it is not possible to draw general conclusions about effects of protein intake on the incidence of cancer or on the process of carcinogenesis.
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PMID:Proteins and amino acids: effects of deficiencies and specific amino acids. 310 17

The polyamine-biosynthetic pathway represents an inviting target for the development of agents inhibiting carcinogenesis and tumor growth. Polyamines play an essential role in the proliferation and development of mammalian cells. Deranged polyamine metabolism may be an important factor in carcinogenesis. Depletion of polyamines inhibits growth of neoplastic cells in vitro and in animal models. Several different classes of other anticancer agents may under some conditions exert enhanced effects when polyamine levels are depleted. Some suitable inhibitors of polyamine production are currently available and other promising compounds are presently being tested. It should soon prove possible to block polyamine biosynthesis at every step in the pathway. The use of these inhibitors alone and combined either with each other or with other antitumor agents will enable a full examination of the potential of this approach.
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PMID:Polyamine metabolism and its importance in neoplastic growth and a target for chemotherapy. 312 52

Various compounds were screened for antipromoter activity in bladder carcinogenesis in rats with a view to using them clinically to inhibit postoperative intravesical ectopic tumor growth of superficial papillary bladder cancer. Their inhibitions of the effect of sodium saccharin in maintaining increased agglutinability of bladder cells by concanavalin A were examined in 4-week tests. The compounds found to inhibit the effect of saccharin were alpha-tocopherol, ascorbic acid, aspirin, all-trans aromatic retinoid, alpha-difluoromethylornithine, sodium cyanate and p,p'-diamino-diphenylmethane. Considering the toxicities of some of these chemicals, ascorbic acid and alpha-difluoromethylornithine were concluded to be the most promising for future clinical trials.
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PMID:Validity of short-term examination for antipromoters of bladder carcinogenesis. 313 Mar 57

The effect of caloric intake on tumor growth has been recognized for over 70 years. Inhibition of tumor growth depends primarily on the extent of caloric restriction, but tumor type, animal strain, and dietary composition all exert some influence. Caloric restriction is most effective when maintained during both initiation and promotion, but if limited to one of these phases, restriction during promotion appears to be the more effective modality. The types of tumor that have been studied include spontaneous mammary and lung tumors as well as tumors induced by organ-specific carcinogens or irradiation with ultraviolet light. Numerous investigators have studied the effects of fat, and a diet low in calories but high in fat is generally significantly more effective in inhibiting carcinogenesis than is a diet high in calories but low in fat. Mice fed high fat, low calorie diets exhibited 48% fewer chemically induced skin tumors and 61% fewer tumors induced by ultraviolet irradiation than did mice fed low fat, high calorie diets. Mice fed a diet containing 2% fat exhibited a 66% incidence of skin tumors, whereas mice fed an isocaloric diet containing 61% fat showed a 78% incidence. Rats whose diet was restricted in calories by 40% exhibited no mammary tumors (coconut oil as primary dietary fat) or 75% fewer tumors (corn oil as dietary fat) compared to ad libitum-fed controls; they also exhibited 47% fewer colonic tumors. The mechanism by which caloric restriction exerts its tumor-inhibiting effects remains to be elucidated.
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PMID:Influence of caloric intake on experimental carcinogenesis: a review. 329 80


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