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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estradiol receptors and glucose-6-phosphate dehydrogenase, an enzyme induced by estrogens, were measured in both benign and malignant human breast tumors. The mean glucose-6-phosphate dehydrogenase activity was higher in the malignant tumors than in the benign tumors. Tumors containing estradiol receptors contained higher activities of glucose-6-phosphate dehydrogenase than tumors without receptors. In breast carcinomas with and without estradiol receptors glucose-6-phosphate dehydrogenase gave 3 isoenzymes with very similar electrophoretic pattern after polyacrylamide gel electrophoresis. The results showed that although glucose-6-phosphate dehydrogenase was higher in estradiol receptor positive than in estradiol receptor negative tumors there was no significant correlation between the estradiol receptor concentration and glucose-6-phosphate dehydrogenase activity in human breast tumors.
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PMID:Estradiol receptors and glucose-6-phosphate dehydrogenase activity in human breast tumors. 83 20

Forty-six cell lines derived from 31 human melanomas obtained from 28 patients were cultured. Fourteen of 16 lines have produced malignant tumors when injected into nude (thymus-deficient) mice. Tumors in 5 of the nude mice metastasized to distant lymph nodes and/or to the lungs of the mouse host. Extreme variability from line to line was observed for doubling time (34 to 106 hr), plating efficiency (0-86%), and melanin production. All tested lines had type B glucose-6-phosphate dehydrogenase, thereby excluding HeLa cell contamination. HeLa cells have been grown for some time in our laboratory. Our results clearly demonstrated that HeLa cell contamination does not occur invariably in heteroploid lines growing in a laboratory simultaneously with Hela cells, provided that proper care is taken to avoid such occurrence. Multiple cell lines derived from the same tumor had identical phosphoglucomutase enzyme phenotype, which suggested a lack of significant cross-contamination between the lines. Four long-term cultures of normal human uveal embryo melanocytes have also been established and characterized. Although all produced melanin after reaching saturation density, they differed from the melanoma cells morphologically; they were flat, not refringent, and lacked piling up and plating ability. When melanoma cells were exposed to bromodeoxyuridine (BUDR) for long periods, a phenotypic change toward non-neoplastic characteristics was observed. Cells became flat and not refringent and, when injected into nude mice, tumors appeared after a long latent period. These changes were completely reversible in vitro and in vivo. The BUDR-treated cultures were undistinguishable from the untreated mother cultures after 2 to 3 passages. Lines derived from tumors in nude mice (obtained by injection of BUDR-treated cells) were again indistinguishable from the untreated mother line. Normal melanocytes were mostly euploid; all the melanoma cells were aneuploid. All 29 cell lines derived from 14 patients had an average chromosome number higher than 46. Detailed group-by-group chromosome analysis always showed an excess of C chromosomes, which suggested that hyperreduplication of one or more C chromosomes is a specific characteristic of human melanomas.
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PMID:Human neoplastic and normal cells in tissue culture. I. Cell lines derived from malignant melanomas and normal melanocytes. 99 14

The effect of estrogen on synthesis of glucose-6-phosphate dehydrogenase (D-Glucose-6-phosphate:NADP+ 1-oxidoreductase, EC 1.1.1.49) in the R3230AC mammary adenocarcinoma of ovariectomized Fischer rats was investigated. Enzyme synthesis was estimated by techniques using immunochemica precipitation and isolation of enzyme protein from tissues of rats that had been given radioactive leucine prior to sacrifice. The antibody-enzyme complex was dissociated and glucose-6-phosphate dehydrogenase was isolated after electrophoresis on sodium dodecyl sulfate-acrylamide gels. Administration of estradiol-17beta produced a two-fold increase in glucose-6-phosphate dehydrogenase activity, which was preceded by a five-fold increase in specific synthesis of glucose-6-phosphate dehydrogenase in R3230AC tumors. At least a 15-fold increase in enzyme synthesis was observed in the uterus. The rate of enzyme degradation (t 1/2) in the tumor was estimated at 17 h. These data indicate that the estrogen-induced increase in glucose-6-phosphate dehydrogenase activity was due to a de novo increase in enzyme synthesis.
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PMID:Effect of estrogen on synthesis of glucose-6-phosphate dehydrogenase in R3230AC mammary tumors and uteri. 118 4

The genotype of the patient Henrietta Lacks from whose cervical carcinoma the HeLa cell was derived was deduced from the phenotypes of her husband and children, and from studies of the HeLa cell. Hemizygous expression of glucose-6-phosphate dehydrogenase in HeLa, together with the deduced heterozygosity of Mrs. Lacks, is consistent with clonal origin of her neoplasm.
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PMID:Genetic characteristics of the HeLa cell. 124 20

Determination of the glucose-6-phosphate dehydrogenase (G-6-PD) phenotype of a neoplasm occurring in a heterozygous female can be used to trace the cellular origin of the tumor. This technique was performed on 834 individual verrucous subunits from four condylomata acuminata (venereal warts) arising in two patients heterozygous for a B and an A gene at the G-6-PD locus. All four specimens contained both A and B types of G-6-PD. Furthermore, even single verrucous subunits from each specimen occasionally contained both enzyme types. These data indicate that condylomata acuminata have a multicellular origin. The initial number of cells which, after viral infection, developed into a condyloma acuminatum was estimated to be about 4,400 cells, on the basis of statistical analysis of the data in one case.
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PMID:Viral "tumorigenesis" in man: cell markers in condylomata acuminata. 124 1

Cytogenetic investigation of multiple uterine leiomyomas from the same patient revealed karyotypes containing cytogenetically indistinguishable del(7)(q21.2q31.2) in two of the tumors. Since this finding seemed to contradict the conclusion from previous glucose-6-phosphate dehydrogenase studies of multiple uterine leiomyomas in which an independent origin of these tumors was found, we assessed clonal tumor origin by DNA-recombinant X-chromosome inactivation analysis. The two leiomyomas with del(7)(q21.2q31.2) had different inactivated X-chromosomes. This proves that they originated independently and indicates that their cytogenetic similarity was coincidental.
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PMID:Independent origin of uterine leiomyomas with karyotypically identical alterations. 150 17

The cellular origin of estrogen-induced kidney tumors in male Syrian hamsters has been repeatedly the subject of controversy. Several authors have proposed that the tumors arise from proximal tubules, from a combination of tubular and interstitial stromal cells, or solely from interstitial cells. Because of the model character of this tumor for hormone-associated cancer, it was further investigated in this study with respect to morphology, enzyme and intermediate filament pattern, the expression of alpha-smooth muscle actin and the extracellular matrix proteins fibronectin and tenascin. These analyses were carried out with early and late tumors as well as metastases to determine possible changes in expression of biochemical parameters during the development and progression of this neoplasm. The enzyme histochemical and intermediate filament patterns were usually the same as those described previously for proliferative foci and early tumors, i.e. highly elevated activities of glucose-6-phosphate dehydrogenase, adenylate cyclase and alkaline phosphatase, a lack of glucose-6-phosphatase and gamma-glutamyltransferase and coexpression of vimentin and desmin, alpha-smooth muscle actin could not be detected in early lesions. In five of 24 advanced tumors inclusions of kidney tubules were found which showed various degrees of alteration in their morphology and enzyme histochemical pattern, but were often directly connected with tubular segments of normal appearance outside the tumor. Like the normal tubules, the enclosed tubular segments were strongly positive for cytokeratin but never expressed vimentin or desmin. Among the 24 tumors studied, two contained cysts which expressed cytokeratin and sometimes also vimentin but not desmin. The enzyme histochemistry of the cells lining the cysts was similar to that of the surrounding tumor mass, except adenylate cyclase was lacking and alkaline phosphatase was not uniformly distributed. In tumors containing cytokeratin-positive cysts, there often were cytokeratin-positive, vimentin-negative and desmin-negative tumor formations in close contact to these cysts. With the exception of cyst formation, the pattern of metastases were identical to that of the primary tumors. All large tumors and the main component of the metastases expressed vimentin, desmin and fibronectin. Mesothelia surrounding metastatic tumor complexes were positive for vimentin, desmin, alpha-smooth muscle actin, fibronectin, cytokeratin and tenascin. It was concluded from these and previous observations on early stages of tumor development that the estrogen-induced hamster kidney tumor originates from mesenchymal interstitial cells (probably pericytes) which may rarely acquire an epithelial phenotype by metaplastic transformation during tumor progression.
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PMID:Changes in the cellular phenotype and extracellular matrix during progression of estrogen-induced mesenchymal kidney tumors in Syrian hamsters. 171 81

Alpha-glycerophosphate dehydrogenase (alpha-GPD) and succinate dehydrogenase (SD) activities were investigated in lymphocytes from peripheral blood of normal rats and rats bearing the Walker 256 carcinosarcoma. Computer analysis using an original algorithm revealed a hierarchy of biorhythmic patterns of dehydrogenase activities. In all rats, mean SD activity was higher than mean alpha-GPD activity. In rats without tumor, SD and alpha-GPD activities were both higher than in rats with the Walker tumor. Biorhythm spectra for both dehydrogenases were very similar in rats with or without tumor, but tumor implantation resulted in a change of the phase relationship between alpha-GPD and SD.
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PMID:Chronobiological analysis of peripheral lymphocyte dehydrogenase activities in rats with Walker 256 carcinosarcoma. 180 27

Expression of TGF-alpha mRNA, which correlates well with the ability of cells to condition medium with an EGF-like activity, clonally segregates best with tumorigenicity among the several single phenotypes considered in this study. The results of unreported studies in which we have analyzed the quantitative relationships between the expression of selected phenotypes and tumorigenicity, suggest that the elevated expression of myc and TGF-alpha mRNAs interact in their associations with tumor yield. These results suggest that elevated myc expression sensitizes hepatic epithelial cells to the possible tumorigenic action of TGF-alpha. This observation may explain why the correlation between the qualitative expression of TGF-alpha and tumorigenicity, described here, is not perfect. Conventionally applied markers of transformation in hepatocytes in vivo and in cultured liver epithelial cells in vitro that we studied -histochemical expression of GGT, ability to grow in medium containing low levels of calcium, and ability to grow in soft agar- clonally segregated with tumorigenicity poorly in liver epithelial cells transformed in vitro. We conclude that these phenotypes are not adequate markers for determining the lineage of hepatic epithelial neoplasms (including, probably hepatocellular cancers arising in vivo). This study appears to be the first to attempt to analyze clonally the association of these markers with tumorigenicity, and to quantify the sensitivity, specificity, and predictive value of the associations. Our study suggests that the relatively weak associations of these phenotypes with tumorigenicity may be related only to their stronger associations with expression of TGF-alpha, or to some other property that is strongly associated with tumorigenicity. Expression of TGF-alpha is more strongly associated with expression of GLC, for example, than is the GLC phenotype with tumorigenicity. At least for GLC, autocrine stimulation by TGF-alpha is likely, since EGF increases growth of WB cells in low calcium medium. This observation may explain the perfect correlation between expression of TGF-alpha and GLC. EGF also stimulates lactate dehydrogenase, pyruvate kinase, and glucose 6-phosphate dehydrogenase in WB cells. However, quantitative correlation between GGT activity and TGF-alpha is less strong. Thus, our data from these studies suggest that the tumorigenic phenotype of cultured hepatic epithelial cells is intimately dependent on the expression of the TGF-alpha gene, possibly producing autocrine stimulation of growth via the cells' EGF receptors. This is the most simple view of the potential relationship between TGF-alpha expression and tumorigenicity in liver epithelial cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clonal analysis of neoplastic transformation in cultured diploid rat liver epithelial cells. 181 88

To assess the clonality of Wilms' tumor, glucose-6-phosphate dehydrogenase (G6PD) enzymes were studied in normal and tumor tissue from 11 black girls who were heterozygous for G6PD. Normal tissues expressed both A and B type G6PD, whereas only a single G6PD enzyme was found in all tumor specimens. These data support the clonal nature of Wilms' tumor. In the one patient with bilateral disease, type B G6PD was found in both a recurrence and a subsequent tumor in the contralateral kidney. This finding is consistent with either the chance occurrence of the same G6PD in independent tumors or persistence of the original malignant clone. Another patient, who presented with the nephroblastomatosis complex (a precursor of Wilms' tumor), also had only type B enzyme detected. Further studies in patients with bilateral disease or the nephroblastomatosis complex, including the use of molecular biologic probes, are needed to test the hypothesis that Wilms' tumor in these cases arises from a somatic mutation as a second event in persons with an underlying genetic alteration.
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PMID:Evidence for clonal development of Wilms' tumor. 185 99


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