Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Localization of alpha-fetoprotein (alpha-FP) has been followed in hepatal tissue and tumors during induction of primary hepatomas with the aid of 0.12% 3'-Me-DAB (3'-methyl-4-dimethylammoazobenzene) in Wistar rats. The indirect immunofluorescence method was used for the localization of alpha-FP positive cells. During the course of carcinogenesis, alpha-FP in serum was detected by means of the crossing over immunoelectrophoresis. This study has yielded the following results: Alpha FP positive cells resembling small hepatocytes occurred dispersed and in groups beginning with the 5th week of a carcinogenic diet until the appearance of tumors. No alpha-FP positive oval cells have been found. Alpha-FP positive cells were always found in rats with alpha-FP positive serum, but they were rarely present in rats with alpha-FP negative serum. From the 10th week, tumors of the cholangiohepatoma type began to be formed in which variously scattered alpha-FP positive cells of the type of small hepatocytes were present, with the serum being negative. Between week 14 and 21 hepatoma nodules began to be formed. At week 21 frequent alpha-FP positive cells close to normal hepatocytes were observed both singly and in groups. These are considered to be the sites of developing tumor nodules. In all the hepatoma nodules, the number of positive tumorous cells and the intensity of fluorescence proved to be directly proportional to alpha-FP concentration in serum.
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PMID:Localization of alpha-fetoprotein by immunofluorescent method during induction of rat liver tumors by 3'-methyl-4-dimethylaminoazobenzene. 7 94

Polyamine concentrations were evaluated in normal human prostatic tissue as well as hyperplastic prostate. Normal tissues had high concentrations of putrescine and spermine with intermediate spermidine concentrations, whereas there was a dramatic increase in the spermine concentration in patients with hypertrophy of the prostate. Although not highly significant, spermidine concentrations were elevated slightly in benign hyperplasia, whereas the putrescine content was decreased compared to normal tissue. Polyamine concentrations were measured also in human kidney tumors and corresponding healthy kidney tissue. The concentration of spermidine in renal carcinomas was significantly elevated when compared to histologically normal areas of the same kidney. The spermine concentration of the tumor was generally lower but not highly significant (p less than 0.01). These data suggest that polyamines are accumulated above normal levels in pathological conditions such as benign hyperplasia of the prostate and renal carcinoma. In both cases, spermidine turnover rate may be influenced by carcinogenesis.
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PMID:Altered polyamine profiles in prostatic hyperplasia and in kidney tumors. 7 57

The concentration of serum alpha-fetoprotein (AFP) was followed in C3H mice having a high incidence of spontaneous liver-cell cancer. No general elevation of serum AFP level with age was seen in mice without tumor. With a single exception, mice bearing hepatocellular carcinomas had increased serum AFP levels. In some mice this increase followed a biphasic course. Mice killed within 1 month of the time when an elevation of serum AFP was first observed had small tumors or no detectable tumor. Premalignant lesions were present in the livers of 11 out of 16 mice that had elevated AFP but no cancer, while only one out of 14 mice with normal AFP had such alterations. Our results strongly suggest that spontaneous hepatocarcinogenesis proceeds through almost the same premalignant lesions as chemically induced carcinogenesis, and that an increase in AFP production occurs early during this process, often preceding macroscopic lesions. Autologous antibodies to AFP were produced in a group of C3H mice by immunization with rat AFP. These anti-AFP antibodies reduced the amount of serum AFP but had no effect on the incidence of spontaneous hepatomas.
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PMID:Early increase of serum alpha-fetoprotein in spontaneous hepatocarcinogenesis in mice. 7 9

Recent findings concerning the significance of alpha 1-fetoprotein (AFP) as a tool for clinical diagnosis and monitoring of tumor diseases are reviewed briefly. The applicability of this protein marker to the early diagnosis of patients at carcinogenic risk is discussed. In addition, experimental data obtained with a model of chemical hepatocarcinogenesis are reported. The increase of proliferative activity in precancerous liver tissue preceded AFP production under experimental conditions with azodyes and aflatoxin B1 as carcinogens. Immunohistochemical analysis of the relation of AFP to changes of cell populations and to liver tissue rearrangement led to the conclusion that AFP-producing cells cannot be precursors of malignant hepatocytes; however, AFP appeared to be linked to dividing hepatocytes at a certain step of cell differentiation regardless of the stages of precancerous development. A decrease in the rate of nuclear RNA synthesis was observed in both precancerous and tumor tissues. A possible analogy between the early phase of AFP production in animal carcinogenesis and that in human carcinogenesis is considered.
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PMID:Clinical aspects of alpha 1-fetoprotein determination in human liver cancer and in humans and experimental animals at carcinogenic risk. 8 99

Carcinogen-induced experimental hepatomas are often characterized by new individually distinct antigens capable of inducing tumor immunity in syngeneic hosts. These antigens arise as a consequence of cell-carcinogen interaction and may result from modification or replacement of normal cell-surface components. Their role in immunosurveillance is not established, but they offer a target for tumor immunotherapy. Reexpressed fetal antigens have also been detected, either as secretory products (alpha 1-fetoprotein) or as common cell-surface components on hepatoma cells. The role of fetal antigens in therapy is doubtful, but they may be important diagnostic indicators of neoplastic change. Possibly associated with these are common antigens initiated early after carcinogen treatment, before malignant cells are detected. Together, the antigens associated with liver carcinogenesis may prove to be powerful tools in understanding the process of liver neoplasia.
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PMID:Antigenic changes associated with liver carcinogenesis. 8

The present study was done to ascertain whether a specific carcinogenic agent has a causal effect on the initial proliferation of only one cell type or whether it acts indiscriminately on all cells in the breast secretory unit. Enzymes histochemistry and electron microscopy were performed on DMBA-induced mammary tumors in female Sprague-Dawley rats and on virus-associated spontaneous mammary tumors in C3H/HEJ mice. The results showed that the chemical carcinogen DMBA affects initial myoepithelial cell proliferation, while virus-associated mammary carcinoma originated from ductular epithelial cell proliferation. To determine whether a specific tumor is composed of a single cell type, tumors were grown in tissue culture. The monolayer was fixed in the usual manner for electron microscopy while in Falcon tissue culture plates. The plates were dissolved in xylene and the monolayer was cut into small pieces and embedded in the plastic media. Electron microscopy performed on the tissue culture and the original tissue from the virus-induced tumors showed the presence of viruses in large numbers. It also suggested the differentiation of basal membrane to form basal lamina and apical plasma membrane into microvilli. This study strongly suggests the presence of selective cell carcinogenesis in the mammary gland.
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PMID:A proposed selective cell carcinogenesis in mammary tumors. 10 7

The classical 2-stage carcinogenesis experiment has been modified in that the carcinogen DMBA was applied to pregnant mother animals at different dose levels and different time intervals during pregnancy. Promotion with the phorbol ester TPA was performed as usual by application of the promoter on the back skin of mice of the F-1 generation. It can be shown that it is possible to initiate fetal epidermal cells by transmaternal route and to promote them to produce visible skin tumors post natum. Tumor promotion by TPA is not restricted to the epidermis, since a broad spectrum of tumors of internal organs can be demonstrated in the initiated and promoted animals. This more general promoting activity of TPA--which implies its absorption and distribution throughout the whole body--has not yet been described. In addition, especially sensitive phases during fetal life with regard to initiation of cells by the carcinogen can be demonstrated. These phases comprise the last third of pregnancy and coincide with a high proliferative activity and the onset of differentiation of the fetal epidermis. The results emphasize the important role of prenatal carcinogenesis and demonstrate the increased risk also to the human organism by either prenatal initiation or postnatal promotion.
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PMID:Transmaternal modification of the Berenblum/Mottram experiment in mice. 10 83

The effect of deoxycholic acid on 7,12-dimethylbenz(a)anthracenecroton oil carcinogenesis in mouse skin was tested. Painting deoxycholic acid in addition to croton oil during promotion resulted in the earlier appearance of tumors, a greater tumor incidence, and a larger number of tumors per animal. DMBA initiation followed by either deoxycholic acid or solvents during the promotion period produced no tumors. Animals receiving deoxycholic acid or solvents alone developed no tumors.
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PMID:Effect of deoxycholic acid on 7,12-dimethylbenz(a)anthracene-induced, two-stage mouse skin carcinogenesis. 10 72

In a modified two-stage carcinogenesis experiment, the effectiveness of the initiator 7,12-dimethylbenz(a)anthracene (DMBA) and the tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) in the epithelium of the forestomach of the mouse has been investigated. Fifty mice were treated intragastrically with a single dose of DMBA (50 mg/kg body weight), followed by repeated intragastric administration of TPA (10 mg/kg body weight) over a period of 35 weeks. In comparison with the corresponding control groups (no treatment, DMBA initiation only, and TPA treatment only), the initiated and promoted group clearly showed the highest tumor incidence in the target organ (45 tumor-bearing animals of 50 animals). No tumors of the forestomach were found in the untreated control group and the TPA-treated group, whereas in the DMBA-initiated group, ten animals had developed tumors of the forestomach. In addition to the mouse skin model for two-stage carcinogenesis, the mouse forestomach appears to respond to DMBA initiation-TPA promotion. This organ provides an additional tissue with which to investigate tumor promotion and further to ascertain specific parameters of the promotion step.
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PMID:Systemic two-stage carcinogenesis in the epithelium of the forestomach of mice using 7,12-dimethylbenz(a)anthracene as initiator and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate as promoter. 10 4

Female Sprague-Dawley rats were fed semipurified diets containing various fats, either alone or in combination, to provide different amounts of dietary fat and linoleic acid. One week before commencing the diets, each rat received an intra-gastric dose of the carcinogen 7,12-dimethylbenz[a]anthracene. Rats fed diets containing mixtures of 3% sunflower seed oil and 17% of either tallow or coconut oil developed twice as many tumors as those fed 3% sunflower seed oil or 20% of either saturated fat alone. Tumor yields in the rats fed these mixed-fat diets were comparable to those in rats fed a 20% lard diet, which provided about the same amount of linoleic acid. No further increase in tumor yield was observed in rats fed a 20% sunflower seed oil diet that contained more than five times as much linoleic acid. These results show that a certain amount of polyunsaturated fat, as well as a high level of dietary fat, is required to promote mammary carcinogenesis.
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PMID:Relationship between amount and type of dietary fat in promotion of mammary carcinogenesis induced by 7,12-dimethylbenz[a]anthracene. 10 58


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