UMLS:C0011570 - FACTA Search

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been known that negative signal of natural killer (NK) cells is triggered by HLA-polymorphic determinant (PMD) of target cells. However, it is not clear whether or not the negative signal is triggered by HLA-monomorphic determinant (MMD). In this study, we determined the interaction of NK receptor and MMD by mean of a blocking test. For the blocking, W6/32, which is an antibody to the MMD, was used. As target cells, we used a tumor cell line H42 and several cell lines. The H42 was established from a bladder cancer patient after radiation therapy. This cell line was demonstrated to be PMD negative but MMD positive and showed NK sensitivity. We had established one more cell line, H41, from the same patient before the radiation therapy. However, the H41 possessed both the PMD and MMD and exhibited NK resistance. Thus, the NK sensitivity of the H42 may be due to depression of the PMD. We performed a blocking test against the MMD of these cell lines. When the H42 was pretreated with F(ab')2 fragment of the W6/32, the killing by NK cells increased. Other cell lines, EB33, KMT-1, and HMy2-C1R, which possessed low levels of PMD, were killed moderately after the pretreatment, although the H41 and other cell lines (KO, MT-2, OKM-3T), which possessed high levels of PMD, were killed only slightly. These findings suggest that the negative signal may be triggered not only by the PMD but also by the MMD.
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PMID:Enhancement of tumor cell lysis by natural killer cells after blocking of HLA-monomorphic determinant using F(ab')2 fragment of W6/32. 954 38

In fiscal 1974 and fiscal 1975, $650000 will be spent on contracts for studies of birth control methods and their relationship to birth defects. The effect of oral contraceptives (OCs) on various nutrients is among top interest. It has been shown that OCs increase blood levels of Vitamin-A, copper and iron while they decrease folic acid, zinc and Vitamin-B12 and B6. The decrease of Vitamin-B6 interfers with the tryptophan mechanism and affects glucose tolerance as well as neurotransmitters which can be directly related to reports of depression and a higher rate of bladder cancer. A question arose as to whether dietary supplements would counteract the nutritional depletion. The group of unanswered questions was summed up by a question: "So, the question is, is it the pill or the pill user?"
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PMID:Effects of OCs on various nutrients is among top priority research areas. 1225 42

p-Chloroaniline, a dye and chemical intermediate, was selected for bioassay by the National Cancer Institute because of the high incidence of bladder cancer observed among dye manufacturing industry workers. A bioassay for the possible carcinogenicity of p-chloroaniline was conducted using Fisher 344 rats and B6C3F1 mice. p-Chloroaniline was administered in the feed, at either of two concentrations, to groups of 50 male and 50 female animals of each species. Twenty animals of each sex and species were placed on test as controls. The high and low dietary concentrations of p-chloroaniline were, respectively, 500 and 250 ppm for rats and 5000 and 2500 ppm for mice. The compound was administered in the diet for 78 weeks, followed by an observation period of 24 weeks for rats and 13 weeks for mice. There were no significant positive associations between the dietary concentrations of p-chloroaniline administered and mortality in female rats or in mice of either sex; however, there was a significantly positive association between concentration and mortality in male rats. Adequate numbers of animals in all groups survived sufficiently long to be at risk from late-developing tumors. Mean body weight depression, in relation to controls, was observed in high dose female rats and dosed mice of both sexes, indicating that the concentration of p-chloroaniline administered to these animals may have approximated the maximum tolerated concentrations. Although splenic lesions were observed in male rats, no mean body weight depression relative to controls was associated with administration of p-chloroaniline to these animals. Therefore, it is possible that these animals may have been able to tolerate a higher dietary concentration of the compound. The only neoplastic lesions found that might be related to administration of the compound were mesenchymal tumors in the spleens of male rats and hemangiomatous tumors in mice. In male rats, there was a significant positive association between compound administration and the incidences of fibroma or fibrosarcoma of the spleen. Theincidences of these tumors were not significantly elevated when compared to those in control rats, but the rarity of these tumors in male Fisher 344 rats (0/360 in historical male control rats in this laboratory) strongly suggests a chemically related effect. In addition, three sarcomas of other types were found in high dose male rats. In mice of both sexes, hemangiomas and hemangiosarcomas were found at elevated incidences, when compared to control mice, in the spleen, liver, kidney, and multiple body sites. The increased incidences in dosed mice were statistically related to dose but were not statistically significant when compared directly to matched control animals. In comparison to historical control data, the incidences of hemangiomatous tumors in the dosed mice were elevated, but not greatly. The evidence was considered insufficient to conclusively relate the hemangiomatous tumors in mice to compound administration. Nonneoplastic proliferative and chronic inflammatory lesions were also found in the spleens of dosed rats and mice. The findings of small numbers of fibromas and sarcomas in the spleens of male rats was considered strongly suggestive of carcinogenicity because of the rarity of these tumors in the spleens of control rats. Hemangiomatous tumors in dosed mice may also have been associated with administration of p-chloroaniline. However, it is concluded that, under the conditions of this bioassay, sufficient evidence was not found to establish the carcinogenicity of p-chloroaniline for Fisher 344 rats or B6C3F1 mice. Levels of Evidence of Carcinogenicity: Male Rats: Equivocal Female Rats: Negative Male Mice: Equivocal Female Mice: Equivocal Synonyms: 4-chlorobenzeneamine; 4-chlorophenylamine; 4-chloroaniline; 4-CA; 1-amino-4-chlorobenzene
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PMID:Bioassay of p-Chloroaniline for Possible Carcinogenicity (CAS No. 106-47-8). 1277 90

5-Chloro-o-toluidine, an aromatic amine and dye intermediate, was selected for bioassay by the National Cancer Institute because of the high incidence of bladder cancer observed among dye manufacturing industry workers. A bioassay for the possible carcinogenicity of 5-chloro-o-toluidine was conducted using Fisher 344 rats and B6C3F1 mice. 5-Chloro-o-toluidine was administered in the feed, at either of two concentrations, to groups of 50 male and 50 female animals of each species. Twenty animals of each sex and species were placed on test as controls. The high and low dietary concentrations of 5-chloro-o-toluidine were 5,000 and 2,500 ppm for rats and 4,000 and 2,000 ppm for mice. The compound was administered in the diet for 78 weeks, followed by an observation period of 26 weeks for rats and 13 weeks for mice. There were significant positive associations between the concentrations of 5-chloro-o-toluidine administered and mortality among male and female mice, but not among rats of either sex. Adequate numbers of animals in all groups survived sufficiently long to be at risk from late-developing tumors. Distinct mean body weight depression was apparent when dosed female rats and dosed mice of both sexes were compared to their controls, indicating that the concentrations administered to these animals in this bioassay may have approximated the maximum tolerated concentrations. Since no mean body weight depression, relative to controls, no significantly accelerated mortality, and no signs of toxicity other than fatty metamorphosis of the liver were associated with administration of 5-chloro-o-toluidine to male rats, it is possible that these animals may have been able to tolerate a higher dietary concentration of the compound. There was a significant positive association between the concentration of 5-chloro-o-toluidine administered to male rats and the incidence of adrenal pheochromocytomas in these animals; however, neither of the Fisher comparisons was significant. None of the other statistical tests fortumors at any site in male and female rats indicated a significant positive association between dosage and incidence. In mice of both sexes there were significant positive associations between concentration administered and the incidence of hemangiosarcomas. In addition, the high dose to control Fisher exact comparisons for both sexes were significant. The Cochran-Armitage tests were also significant and positive for the incidences of hepatocellular carcinomas in both sexes of mice. For males and females the high dose to control Fisher exact comparisons were significant, and for females the low dose to control comparison was also significant. Under the conditions of this bioassay, 5-chloro-o-toluidine was carcinogenic to B6C3F1 mice, inducing hemangiosarcomas and hepatocellular carcinomas in both males and females. There was no conclusive evidence of the carcinogenicity of the compound in Fisher 344 rats. Levels of Evidence of Carcinogenicity: Male Rats: Negative Female Rats: Negative Male Mice: Positive Female Mice: Positive Synonyms: 5-chloro-2-methylbenzeneamine; p-chloro-o-aminotoluene; 4-chloro-2-aminotoluene; 2-amino-4-chlorotoluene; o-amino-p-chlorotoluene; 5-chloro-2-methylaniline; 2-methyl-5-chloroaniline; 1-amino-2-methyl-5-chlorobenzene; 1-amino-3-chloro-6-methylbenzene; Fast Red KB Base; Azogene Fast Red KB; Brentamine Fast Red KB Base; Naphthosol Fast Red Base; Naphthanil Red KB Base
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PMID:Bioassay of 5-Chloro-o-toluidine for Possible Carcinogenicity (CAS No. 95-79-4). 1277 91

4,4'-Methylenebis(N,N-dimethyl)benzeneamine, a bicyclic aromatic amine and an intermediate in dye manufacture, was selected for bioassay by the National Cancer Institute because of a high incidence of bladder cancer observed among dye manufacturing industry workers. A bioassay for the possible carcinogenicity of 4,4'-methylenebis-(N,N-dimethyl)benzeneamine was conducted using Fisher 344 rats and B6C3F1 mice. 4,4'-Methylenebis-(N,N-dimethyl)benzeneamine was administered in the feed, at either of two concentrations, to groups of 50 male and 50 female animals of each species. Twenty animals of each sex and species were placed on test as controls. The high and low dietary concentrations of 4,4'-methylenebis-(N,N-dimethyl)benzeneamine were, respectively, 750 and 375 ppm for rats and 2500 and 1250 ppm for mice. The compound was administered for 59 weeks to rats and for 78 weeks to mice. The period of compound administration was followed by an observation period of 45 weeks for rats and 13 weeks for mice. There were no significantly positive associations between the concentrations of 4,4'-methylenebis-(N,N-dimethyl)benzeneamine administered and mortality among rats or mice of either sex. Adequate numbers of animals survived sufficiently long to be at risk from late-developing tumors. There was slight dose-related mean body weight depression among female rats, the mean body weight of high dose male rats was slightly less than that for controls, and the mean body weights of dosed mice were significantly lower than their controls, indicating that the concentrations of 4,4'-methylenebis-(N,N-dimethyl)benzeneamine administered to these animals in this bioassay may have approximated the maximum tolerated concentrations. For both male and female rats, there was a significant positive association between the concentrations of 4,4'-methylenebis-(N,N-dimethyl)benzeneamine administered and the incidences of follicular-cell carcinomas of the thyroid (i.e., 1/18, 4/50, and 21/46 in the control, low dose, and high dose males, respectively; and 0/20, 3/46, and 23/45 in the control, low dose, and high dose females, respectively). The high dose to control Fisher exact comparisons were also significant for each sex. Liver neoplasms were observed among male and female mice. There were elevated incidences of hepatocellular adenomas in dosed mice when compared to controls (i.e., 2/20, 3/50, and 16/48 in control, low dose, and high dose males, respectively; and 1/19, 18/49, and 22/48 in control, low dose, and high dose females). The incidences of hepatocellular carcinomas in dosed mice did not differ greatly from those in controls (i.e., 3/20, 9/50, and 6/48 in control, low dose, and high dose males, respectively; and 0/19, 1/49, and 1/48 in control, low dose, and high dose females). Among both sexes of mice, there was a significant positive association between the concentrations of the chemical administered and the incidences of a combination of hepatocellular adenomas and hepatocellular carcinomas. For male mice, the Fisher exact comparisons were not significant; however, for females, both the high dose to control and the low dose to control comparisons were significant. In both sexes of both species nonneoplastic proliferative lesions of the thyroid occurred in dosed animals but not in any of the controls. Under the conditions of this bioassay, 4,4'-methylenebis-(N,N-dimethyl)benzeneamine was carcinogenic in Fisher 344 rats, inducing thyroid follicular-cell carcinomas in both males and females. Administration of the compound was carcinogenic in female B6C3F1 mice, inducing liver neoplasms. There was no conclusive evidence that 4,4'-methylenebis-(N,N-dimethyl)benzeneamine was carcinogenic in male B6C3F1 mice. Levels of Evidence of Carcinogenicity: Male Rats: Positive Female Rats: Positive Male Mice: Equivocal Female Mice: Positive Synonyms: 4,4'-methylenebis(N,N-dimethyl)aniline; tetramethyldiaminodiphenylmethane; 4,4'-bis(dimethylamino) diphenylmethane; Tetra base; Methane base; Michler's base; Michler's hydride; Michler's methane
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PMID:Bioassay of 4,4'-Methylenebis-(N,N-dimethyl)benzeneamine for Possible Carcinogenicity (CAS No. 101-61-1). 1277 92

Michler's ketone, a dye intermediate and derivative of dimethylaniline, was selected for bioassay by the National Cancer Institute because of the elevated incidence of bladder cancer noted among dye manufacturing industry workers. A bioassay for the possible carcinogenicity of technical-grade Michler's ketone was conducted using Fischer 344 rats and B6C3F1 mice. Michler's ketone was administered in the feed, at either of two concentrations, to groups of 50 male and 50 female animals of each species. Twenty animals of each sex and species were placed on test as controls. The high and low dietary concentrations of Michler's ketone were respectively, 500 and 250 ppm for male rats, 1,000 and 500 ppm for female rats, and 2,500 and 1,250 ppm for mice of both sexes. The compound was administered to rats and mice for 78 weeks. The period of compound administration was followed by an observation period of 28 weeks for male and high dose female rats, 29 weeks for low dose female rats and 13 weeks for mice. There were significant positive associations between the concentrations of Michler's ketone administered and mortality in rats and mice of both sexes. Adequate numbers of animals in all groups survived sufficiently long to be at risk from late-developing tumors. There was distinct dose-related mean body weight depression in female rats and in mice of both sexes, and the mean body weight among dosed male rats was slightly lower than that in controls, indicating that the concentrations of Michler's ketone administered tothese animals in this bioassay may have approximated the maximum tolerated concentrations. There were significant positive associations between the concentrations of Michler's ketone administered and the incidences of hepatocellular carcinomas in both sexes of rats and in female mice and hemangiosarcomas in male mice. In all of these cases the high dose to control Fisher exact comparison was also significant. Under the conditions of this bioassay, dietary administration of Michler's ketone was carcinogenic to male and female Fischer 344 rats and female B6C3F1 mice, causing hepatocellular carcinomas, and to male B6C3F1 mice, causing hemangiosarcomas. Levels of Evidence of Carcinogenicity: Male Rats: Positive Female Rats: Positive Male Mice: Positive Female Mice: Positive Synonyms: bis[4-(dimethylamino)phenyl]methanone; 4,4'-bis(dimethylamino)benzophenone; p,p'-bis(dimethylamino)benzophenone; bis[p-(N,N'-dimethylamino)phenyl]ketone; tetramethyldiaminobenzophenone
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PMID:Bioassay of Michler's Ketone for Possible Carcinogenicity (CAS No. 90-94-8). 1277 96

4-Nitro-o-phenylenediamine, a component of both semipermanent and permanent hair dye formulations, was selected for bioassay by the National Cancer Institute because of the high incidence of bladder cancer reported among workers in the dye manufacturing industry. A bioassay for the possible carcinogenicity of 4-nitro-o-phenylenediamine was conducted using Fischer 344 rats and B6C3F1 mice. 4-Nitro-o-phenylenediamine was administered in the feed, at either of two concentrations, to groups of 50 male and 50 female animals of each species. Twenty animals of each sex and species were placed on test as controls. The high and low dietary concentrations of 4-nitro-o-phenylenediamine were, respectively, 750 and 375 ppm for rats and 7500 and 3750 ppm for mice. The compound was administered for 103 weeks to rats and for 102 weeks to mice. The period of compound administration was followed by an observation period of 2 weeks for rats and mice. There were no significant positive associations between the concentrations of 4-nitro-o-phenylenediamine administered and mortality in rats or mice of either sex. Adequate numbers of animals in all groups survived sufficiently long to be at risk from late-developing tumors. Distinct dose-related mean body weight depression was observed in mice, indicating that the concentrations of 4-nitro-o-phenylenediamine administered to these animals in this bioassay may have approximated the maximum tolerated concentrations. Since no distinct mean body weightdepression relative to controls, no significantly accelerated mortality, and no other manifestations of chronic toxicity were associated with administration of 4-nitro-o-phenylenediamine to male or female rats, it is possible that these animals may have been able to tolerate a higher dietary concentration. None of the statistical tests for any site in rats or in mice of either sex indicated a significant positive association between compound administration and tumor incidence. Under the conditions of this bioassay, dietary administration of 4-nitro-o-phenylenediamine was not carcinogenic in Fischer 344 rats or B6C3F1 mice. Levels of Evidence of Carcinogenicity: Male Rats: Negative Female Rats: Negative Male Mice: Negative Female Mice: Negative Synonyms: 4-nitro-1,2-benzenediamine; 4-nitro-phenylenediamine; 4-nitro-1,2-diaminobenzene; 1,2-diamino-4-nitrobenzene; 2-amino-4-nitroaniline; 4-NO; 4-NOP; 4-NOPD; 4-N-o-PDA; C.I. 76020
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PMID:Bioassay of 4-Nitro-o-phenylenediamine for Possible Carcinogenicity (CAS No. 99-56-9). 1277 97

Multiple genetic alterations such as in Ras or EGFR can result in sustained signaling through PI3K. Our previous experiments have shown that resistance to radiation results from PI3K activity in cells in culture. Here we examined whether inhibition of PI3K in vivo would sensitize tumors to radiation. The human bladder cancer cell line T24 has amplified and mutated H-Ras resulting in sustained PI3K activity and phosphorylation of the downstream target of PI3K, Akt. Nude mice bearing T24 tumor cell xenografts were randomly assigned to one of four groups: control, radiation alone, the PI3K inhibitor LY294002 alone, or combined LY294002 and radiation. The LY294002 was delivered intraperitoneally to the mice. Downregulation of Akt was documented by Western blot analysis of tumor lysates. In vivo sensitization was measured using clonogenic assays or regrowth assays.A dose of 100 mg/kg of LY294002, but not 50 mg/kg, consistently eliminated the phosphorylation of Akt. This inhibition was transient, and Akt activity returned after 30 min. This dose resulted in severe respiratory depression and lethargy resolving without lethality. It is not possible to tell whether these side effects of LY294002 were mechanism-based or idiosyncratic. The PI3K inhibitor LY294002 by itself had minimal antitumor effect. The combination of LY294002 and radiation resulted in significant and synergistic reduction in clonogenicity and growth delay. Inhibition of PI3K by LY294002 can synergistically enhance radiation efficacy. This acts as a proof of principle that inhibition of the Ras to PI3K pathway could be useful clinically.
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PMID:Radiation sensitization of human cancer cells in vivo by inhibiting the activity of PI3K using LY294002. 1278 94

2,4-Dimethoxyaniline hydrochloride, the hydrochloride salt of the dye intermediate 2,4-dimethoxyaniline, was selected for bioassay by the National Cancer Institute because of the increased incidence of bladder cancer among dye manufacturing industry workers. Aromatic amines are one of several classes of chemicals thought to contribute to the increased cancer risk in this industry. A bioassay for the possible carcinogenicity of 2,4-dimethoxyaniline HCl was conducted using Fischer 344 rats and B6C3F1 mice. 2,4-Dimethoxyaniline HCl was administered in the feed, at either of two concentrations, to groups of 50 male and 50 female animals of each species. Twenty animals of each sex and species were placed on test as controls. The high and low dietary concentrations of 2,4-dimethoxyaniline HCl were, respectively, 3,000 and 1,500 ppm for rats and 5,000 and 2,500 ppm for mice. The compound was administered in the diet for 104 weeks to rats and 103 weeks to mice, followed by a 1-week observation period for both species. There were no significant positive associations between the concentrations of 2,4-dimethoxyaniline HCl administered and mortality in rats or mice of either sex. Adequate numbers of animals in all groups survived sufficiently long to be at risk from late-developing tumors. Dose-related mean body weight depression was observed for females of both species, indicating that the concentrations of 2,4-dimethoxyaniline HCl administered to these groups may have approximated the maximum tolerated concentrations. Compound-related mean body weight depression was only slight for male rats and was apparent in male mice only until week 50; however follicular-cell hyperplasias and cystic follicles of the thyroid were observed in dosed male mice, suggesting that the concentrations the male mice received may have approximated the maximum tolerated concentrations. Since no distinct mean body weight depression in relation to controls, no significant accelerated mortality, and no other signs of toxicity were associated with administration of 2,4-dimethoxyaniline HCl to male rats, it is possible that these animals may have been able to tolerate a higher dietary concentration. There was a significant positive trend between concentration of the test chemical and the incidence of a combination of hepatocellular carcinomas and adenomas in male mice and an increase in the combination of these lesions in female mice. However, no statistically significant differences in tumor incidence at any site were observed when dosed rats and mice were compared to their respective controls. Under the conditions of this bioassay there was no convincing evidence for the carcinogenicity of 2,4-dimethoxyaniline HCl in Fischer 344 rats or B6C3F1 mice. Levels of Evidence of Carcinogenicity: Male Rats: Negative Female Rats: Negative Male Mice: Negative Female Mice: Negative Synonyms: 2,4-dimethoxybenzenamine hydrochloride; 4-methoxy-o-anisidine hydrochloride; 2-methoxy-p-anisidine hydrochloride
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PMID:Bioassay of 2,4-dimethoxyaniline hydrochloride for possible carcinogenicity. 1279 92

Hypericum perforatum L. (St. John's wort) is a medicinal plant used for many pathologies, especially for the treatment of mild to moderate depression. In the present study we have investigated the cytotoxic activity of the locally collected (Epirus region) Hypericum perforatum L. against cultured T24 and NBT-II bladder cancer cell lines. The lipophilic extract of the herb, prepared using petroleum ether, induced apoptosis displaying LC(50) values at concentrations as low as 4 and 5 microg/mL. A fraction of this extract displayed 60 % cell growth inhibition at a concentration of 0.95 microg/mL. Evaluating the importance of various biologically active components of the extract, it was found that hypericins (hypericin, pseudohypericin, etc.) were identified only in the methanolic (lipophobic) extract of the herb, and not in the active lipophilic extract. In addition, hyperforin concentrations in the lipophilic extract and its most active fraction, were 0.94 microg/mL, and 0.17 microg/mL, respectively, while the active cytotoxic concentration of pure hyperforin appeared in the range of 1.8 microg/mL - 5.0 microg/mL. Therefore, pure hyperforin does not seem to contribute significantly to the cytotoxicity activity. Chlorophylls were identified in low, not significantly different, concentrations in all extracts and fractions and were not correlated to the biological activity. Owing to the combination of significant cytotoxic activity, natural abundance and low toxicity, the lipophilic extract of Hypericum perforatum holds the promise of being an interesting, new, antiproliferative agent against bladder cancer that deserves further investigation.
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PMID:The lipophilic extract of Hypericum perforatum exerts significant cytotoxic activity against T24 and NBT-II urinary bladder tumor cells. 1632 Feb 4

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