Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A periodic acid-chromic acid-silver methenamine techniqe for visualizing glycoproteins at the electron microscope level was applied to colonic mucosa taken from areas adjacent to and remote from carcinoma. Normal control mucosa was obtained by biopsy of patients with no known gastrointestinal disease. Non-oxidized control sections were run in parallel. Quantitative and qualitative differences in glycoproteins were detected in the mucosa adjacent to carcinoma ('transitional' mucosa, as we call it) as compared with the normal. Furthermore, the vesicles in both the 'intermediate' and absorptive cells elaborate a glycoprotein product and it seems that a direct relationship exists between the increased vesiculation and the markedly developed 'fuzzy coat' in the 'transitional' mucosa. It is suggested that these findings may represent one of the features of an early stage of carcinogenesis. Histochemical and ultrastructural techniques of the kind used in this study may thus be of value in identifying or predicting malignancy in the colonic epithelium.
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PMID:An ultrastructural application of silver methenamine to the study of mucin changes in the colonic mucosa adjacent to and remote from carcinoma. 5 55

The autoradiographic patterns of the cervical epithelia of 39 virgin C57BL mice after in vivo injection of [3H]cytidine was investigated. Of the 22 animals painted with benzo[a]pyrene for 5 months, 8 developed intraepithelial atypias and 2 had invasive carcinoma. The mean number of silver grains in individual cells increased from histologically normal cervical epithelium through atypical epithelium to invasive carcinoma. It is apparent that the autoradiographic patterns in normal, atypical, and invasive carcinoma cells reflected quantitative differences in cytidine incorporation. These differences may denote increased demand for RNA precursors in the cervical epithelium during carcinogenesis.
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PMID:Behavior of cervical epithelium during carcinogenesis: autoradiography of tritiated cytidine in the C57BL mouse. 28 91

The modifying effects of indole-3-carbinol (I3C) and sinigrin (SIN) on the initiation and post-initiation phases of tongue carcinogenesis induced by 4-nitroquinoline 1-oxide (4-NQO) were investigated in male ACI/N rats. Rats were divided into eight groups: group 1 was given 4-NQO (10 ppm) in the drinking water for 12 weeks, starting at 7 weeks of age; groups 2 and 3 were given 4-NQO and fed the diets containing I3C (1,000 ppm) and SIN (1,200 ppm) for 14 weeks, respectively, starting at 6 weeks of age; groups 4 and 5 were given 4-NQO and then they were fed I3C and SIN containing diets for 23 weeks, respectively, starting one week after 4-NQO exposure; groups 6 and 7 were given I3C and SIN alone, respectively, during the experiment; group 8 served as an untreated control. At the termination of the experiment (week 37), the incidence of tongue neoplasms (squamous cell papilloma and carcinoma) in group 2 (1/15, 7%), group 3 (1/15, 7%), group 4 (3/15, 20%) or group 5 (2/15, 13%) was significantly smaller than that in group 1 (12/17, 71%) (P = 0.0003, P = 0.005 or P = 0.002). No tongue carcinomas developed in rats of groups 2, 3, and 5. Similarly, the incidence of preneoplastic lesions (hyperplasia and dysplasia) of the tongue in group 2 (11/15, 73%), group 3 (10/15, 67%), group 4 (11/15, 73%) or group 5 (10/15, 67%) was significantly lower than that in group 1 (17/17, 100%) (P = 0.04 or P = 0.02). There were no tongue neoplasms in rats of groups 6, 7, and 8. Administration of I3C and SIN also caused significant decreases in the number and area of silver-stained nucleolar organizer regions protein (AgNORs), a new cell proliferation index, of tongue squamous epithelium. Thus, I3C and SIN inhibited rat tongue carcinogenesis in both the initiation and post-initiation phases, when administered in these respective phases together with, or following treatment with, 4-NQO.
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PMID:Inhibitory effects of the natural products indole-3-carbinol and sinigrin during initiation and promotion phases of 4-nitroquinoline 1-oxide-induced rat tongue carcinogenesis. 139 21

Deviations in the pattern of soluble proteins from chemically induced primary rat hepatomas and from transformed, tumorigenic liver cell lines were determined by high resolution two-dimensional gel electrophoresis (2DE). As compared with the protein pattern of normal rat liver with approximately 1300 protein spots visible in silver-stained gels, quantitative and qualitative alterations were found in hepatomas including neoexpression of glutathione-S-transferase P, as described earlier. After correction for proliferation-related changes by comparison with gels of cells from regenerating rat liver, 30 protein variants remained, which were identically up- (n = 6) or down-regulated (n = 18) or were detected as new spots (n = 6) in primary hepatomas and transformed tumorigenic liver cell lines which are devoid of contaminating nonparenchymal cells. Seven of these variants showed a reduced expression in short-term cultured liver cells indicating dedifferentiation processes in the transformed state. Several hepatoma- and transformation-associated variants were found in clusters of similar mol. wt and/or pI, among them a complex of eight protein variants at approximately 33-35.5 kDa and a pI of approximately 6.6-7.4. Spots of this cluster show considerable changes between the investigated experimental groups and might be suited for being studied at the level of posttranslational modification during carcinogenesis.
Carcinogenesis 1992 Jul
PMID:Variant protein patterns in hepatomas and transformed liver cell lines as determined by high resolution two-dimensional gel electrophoresis (2DE). 163 84

The number of silver-stained nucleolar proteins (AgNORs) was enumerated in preneoplastic and neoplastic rat tongue lesions induced by 4-nitroquinoline 1-oxide (4-NQO). Male ACI/N rats were given 0 to 10 p.p.m. 4-NQO for 12, 20 or 36 weeks to induce hyperplasia, dysplasia and neoplasm in tongue. The mean numbers of AgNORs stained by a modified one-step silver colloid method in various epithelial lesions were as follows: normal squamous epithelium (n = 5), 1.52 +/- 0.03; non-lesional squamous epithelium (n = 5), 1.58 +/- 0.04; hyperplasia (n = 20), 1.84 +/- 0.15; dysplasia (n = 20), 2.32 +/- 0.12; papilloma (n = 6), 2.23 +/- 0.10; and squamous cell carcinoma (n = 4), 3.06 +/- 0.26. Thus, the mean number of AgNORs showed a stepwise increase from untreated and treated, histologically normal squamous epithelium through hyperplasia and dysplasia to squamous cell papilloma and carcinoma, although the value of severe dysplasia was between those of papilloma and carcinoma. These results indicate that the mean number of AgNORs may reflect the proliferative nature of tongue lesions, as suggested in carcinogenesis of other organs, and also suggest that severe dysplasia is a direct precursor lesion for squamous cell carcinoma of the tongue induced by 4-NQO.
Carcinogenesis 1991 Feb
PMID:Alterations of the nucleolar organizer regions during 4-nitroquinoline 1-oxide-induced tongue carcinogenesis in rats. 170 23

Gastrin may play a role in gastric carcinogenesis, as indicated by an increased frequency of gastric carcinomas in patients with pernicious anaemia and the fact some human gastric cancer cell lines carry the gastrin receptor. Recently, it has been shown that the acid-stimulatory effect of gastrin may be solely mediated by histamine release from the enterochromaffin-like (ECL) cell, on which gastrin has a specific trophic effect. We therefore found it of interest to examine human gastric carcinomas for the presence of ECL tumour cells by using silver staining and chromogranin immunohistochemistry. We found evidence of ECL cell-derived tumour cells in 40% of the diffuse gastric carcinomas but no such tumour cells in the intestinal type of gastric carcinoma. This may suggest that diffuse gastric carcinomas, like malignant gastric tumours of the mastomys, are in fact malignant ECLomas.
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PMID:Enterochromaffin-like tumour cells in the diffuse but not the intestinal type of gastric carcinomas. 171 Mar 71

BGC-Ha-ras, isolated from the human gastric cancer cell line BGC-823 and activated by point mutation, is a transforming oncogene. To study whether this oncogene can still be located in the original position of chromosome 11 of BGC-823 cell line, chromosomal in situ hybridization method was used. The results showed that 31% silver grains were localized on chromosome 11, 83% of which on the 11p15 region, and in addition, 10% grains on distal end of the short arm of the other abnormal chromosome. Such results are significant in further study of the relation between gene localization and carcinogenesis.
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PMID:[Chromosomal localization of transforming oncogene BGC-Ha-ras in gastric cancer cell line]. 220 54

An in vivo method for assessment of DNA adduct formation and unscheduled DNA synthesis (UDS) in the esophagus of rats was devised. Small ventral incisions were made in the neck and upper abdomen regions of 6 week old F344 rats and ligation of the esophagus with thread at the two extreme ends performed to make an esophageal pouch. For the DNA adduct formation study, a solution (0.5 ml) containing various concentrations of N-[3H]methyl-N-nitrosourea ([3H]MNU) was injected into the pouch. DNA binding levels were calculated from radioactivity of the isolated DNA and dose-dependent DNA adduct formation could be detected 2 h after the treatment with MNU. By HPLC analysis, both 7-methylguanine (7-mGua) and O6-methylguanine (O6-mGua) adducts were identified in the esophageal DNA, the ratio of 7-mGua/O6-mGua being 5.7-12:1. For UDS measurement, a solution containing MNU plus [3H]thymidine (200 microCi/ml) was similarly injected into the pouch. UDS was dose-dependently demonstrated as silver grains over the nuclei of the epithelial cells by autoradiography. The results thus showed that MNU, when injected into the esophageal lumen, can penetrate the surface mucosa, react with the epithelial cell DNA and induce DNA adduct formation and DNA repair synthesis dose-dependently.
Carcinogenesis 1990 Feb
PMID:DNA adduct formation and unscheduled DNA synthesis in rat esophagus in vivo after treatment with N-methyl-N-nitrosourea. 230 50

A silver technique for nucleolar organizer regions (AgNOR) was applied to sections from 156 gastric biopsies and gastrectomy specimens. These included normal controls, normal gastric mucosa from carcinoma-bearing stomachs, intestinal metaplasia types I and III, dysplasia and carcinoma. AgNOR counts gradually increased from normal, through intestinal metaplasia, to carcinoma. This finding supports the chronic atrophic gastritis-intestinal metaplasia-dysplasia-carcinoma sequence concept for gastric carcinogenesis. Normal gastric mucosa was different from all lesions, including normal mucosa from carcinoma-bearing stomachs. Significantly higher AgNOR counts were observed in tumours compared to all other lesions except dysplasia. Dysplasia differed from intestinal metaplasia type I but not from type III. Eighty-five per cent of metaplasia cases overlapped with carcinoma and 19% with normal controls. The spread of AgNOR values in intestinal metaplasia reinforces the concept that this lesion is a heterogeneous entity reflecting a dynamic and continuous process. The AgNOR technique may contribute to the assessment of the stage of evolution of 'borderline' lesions.
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PMID:Nucleolar organizer regions in gastric carcinoma and its precursor stages. 233 11

A large number of human tumor cell lines of various origins have been investigated with respect to expression of glutathione-linked enzymes in the cytosol fraction. The amounts of the different enzymes were estimated by use of activity measurements and by silver staining or immunoblot analysis after electrophoresis of cytosol fractions purified by affinity chromatography on S-hexylglutathione Sepharose. Class Pi glutathione transferase was the most abundant enzyme in most tumor cells; the cell lines HepG2 and Raji were exceptions in not expressing significant amounts of this enzyme. HepG2 cells derive from hepatocytes, which normally do not express the class Pi enzyme, whereas Raji cells originate from B-lymphocytes, which normally do express a class Pi glutathione transferase. The highest level of the class Pi transferase, in terms of protein reacting with antibodies as well as enzyme activity, was noted in the colon carcinoma cell line LS174T. Hu549Pat cells, EBV-transformed B-lymphocytes, also expressed high levels of a protein reacting with antibodies specific for class Pi glutathione transferases, but did not display any significant activity with ethacrynic acid, a substrate characteristic for this class. Class Alpha and class Mu glutathione transferases, in cell lines expressing these isoenzymes, were present in significantly lower concentrations than the class Pi enzyme. Most of the tumor cells contained a class Alpha transferase composed of 27.5 kd subunits, which has the physicochemical and immunological properties of the most basic glutathione transferase found in human skin. In several cell lines, a protein was detected with an apparent subunit Mr value of 30 kd that was tentatively identified as an additional class Alpha glutathione transferase not previously described. In addition, other glutathione-linked enzyme activities, namely glutathione peroxidase, glutathione reductase and glyoxalase I, were assayed with specific substrates in the cytosolic fraction of the tumor cells; glyoxalase I could also be estimated semiquantitatively by silver staining of SDS-PAGE cells after affinity chromatography. Like the glutathione transferases, these enzymes displayed distinctly different levels of expression in the various cell lines. Thus, virtually every cell line was found to have a unique pattern of glutathione-linked enzymes, suggesting that the resistance phenotypes of the cells differ accordingly.
Carcinogenesis 1990 Sep
PMID:Differences among human tumor cell lines in the expression of glutathione transferases and other glutathione-linked enzymes. 240 Oct 46


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