Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sterigmatocystin, a mycotoxin produced by Aspergillus versicolor, Aspergillus sydowi, Aspergillus nidulans, and a species of Bipolaris, was given to newborn BALB/c X DBA/2F1 (hereafter referred to as CD2F1) mice by a single s.c. administration in 1% gelatin suspension. In an acute toxicity study, the maximum tolerated dose of sterigmatocystin was 5 mug/g body weight. In a chronic study, a single s.c. injection of 5, 1, or 0.5 mug/g body weight gave rise to high incidences of lung and liver adenomas when the animals were killed at the end of 1 year. The incidence of both tumors in mice at the dose of 5 mug/g body weight was statistically significant, and the incidences of lung tumor in female mice and of liver tumor in male mice at the dose of 1 mug/g body weight were also statistically significant, compared with tumors in control mice. Other tumors also were induced in treated mice (two malignant lymphomas and one adenoma of the submaxillary gland), in contrast to a zero incidence in vehicle control mice. These results confirm that a small quantity of sterigmatocystin induces tumors of lung and liver and that the dose of sterigmatocystin is related to the incidence of tumors in mice.
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PMID:Tumor induction by a single subcutaneous injection of sterigmatocystin in newborn mice. 126 22

We investigated lectin binding patterns on tissue specimens of normal and metaplastic gastric surface mucosae, gastric adenomas, and intestinal and diffuse-type gastric carcinomas. Compared with normal gastric mucosa, metaplastic mucosa exhibited an increase of ConA binding and decreases of WGA, PNA, UEA-1, and DBA binding in the cytoplasm, and decreases of ConA, PNA, and UEA-1 binding at the luminal surface. Intestinal carcinomas were similar to metaplastic gastric surface mucosa in ConA, WGA, and UEA-1 binding in the cytoplasm, while diffuse-type carcinomas were similar to normal gastric mucosa in WGA and UEA-1 binding in the cytoplasm. Adenomas were similar to intestinal carcinomas in ConA and UEA-1 binding in the cytoplasm, but were different from intestinal carcinomas in Con A and UEA-1 binding at the luminal surface. For UEA-1, normal and metaplastic gastric surface mucosae did not show a significant difference between the blood type A, AB, B group and the O group. Intestinal and diffuse carcinomas and adenomas also did not show such a difference between the blood groups. For DBA, normal gastric surface mucosa showed a significant difference between the blood type B, O group and the A, AB group. Normal gastric mucosa of the blood type A, AB group was frequently positive for DBA binding in the cytoplasm and at the luminal surface. Metaplastic mucosa did not show a significant difference between the blood groups. Intestinal and diffuse-type carcinomas and adenomas also did not show a difference between the blood groups. DBA binding in the cytoplasm of intestinal carcinomas and adenomas was more frequently positive than that of normal and metaplastic mucosae, except for normal gastric mucosa of the blood type A, AB group. Compared with diffuse-type carcinomas, intestinal carcinomas were accompanied by a significant increase of ConA binding and decreases of WGA and PNA binding in the cytoplasm.
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PMID:Lectin binding patterns in normal, metaplastic, and neoplastic gastric mucosa. 157 49

The mucin alterations associated with the progress of cellular atypia of the colorectal mucosa were investigated by light and electron microscopy using lectin-histochemical technique with DBA and PNA. The samples showing positive staining in the more than one-third areas of the colonic epithelial mucosa were scored as positive reaction. The DBA positive reaction was found 100%, 95.8% and 45.7% in the normal mucosa, adenoma and carcinoma, respectively. On the other hand, the PNA positive cases increased with the grade of malignancy; 18.2%, 58.5% and 97.1% respectively. The DBA binding sites were found in the mucin of the goblet cells of the normal and adenomatous epithelia. The PNA positive sites were localized in the supranuclear portion of the normal mucosa and adenoma while in the epithelia of the carcinoma the PNA positive areas were found in the intraglandular substance and cell apex. With the electron microscopy the PNA binding sites were detected in the cis cistern of Golgi apparatus in the normal and adenomatous epithelia and in the apical membrane in the epithelia of the carcinoma. It is suggested that the PNA binding activity is a useful marker to detect the adenomas with the high risk of malignant transformation.
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PMID:[A study of binding sites of lectins in colorectal adenomas and carcinomas: the optical and electron microscopical findings]. 165 99

Murine susceptibility to ethyl carbamate-induced carcinogenesis is strain dependent. In vivo sister chromatid exchange (SCE) responses to ethyl carbamate were evaluated in bone marrow cells of gravid adenoma-susceptible (ICR/Jcl), and resistant (C57Bl/6J) and (DBA/2J) murine dams, as well as in liver cells of their respective ICR/Jcl, C57Bl/6J X DBA/2J (BDF1), and DBA/2J X C57Bl/6J (BDF), fetuses following a single intravenous injection of 1.1, 2.2, or 3.3 mmol/kg of ethyl carbamate on gestation day 13/14. Bone marrow tissues of C57Bl/6J and DBA/2J, but not ICR/Jcl dams, demonstrated greater sensitivity to SCE induction than liver cells of their respective fetuses. Furthermore, relative SCE responses in bone marrow among dams indicated greater sensitivity of the more tumor-susceptible ICR/Jcl and C57Bl/6J strains to SCE induction by ethyl carbamate relative to the more tumor-resistant DBA/2J strain. In addition, concurrent alterations (stimulation or inhibition) of bone marrow cell cycle kinetics by ethyl carbamate were consistent with hormone-related, strain-dependent hematopoietic stress during pregnancy.
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PMID:Comparative in vivo sister chromatid exchange induction by ethyl carbamate in maternal and fetal tissues of tumor-susceptible and -resistant murine strains. 197 64

Cytokine effects on permanent cell lines of transformed mouse pancreatic alpha- and beta-cells were compared. The beta-tumor cell 1 (beta TC1) line (from an adenoma created in transgenic mice expressing the SV40 large T-antigen oncogene under control of the rat insulin II promoter) produced insulin predominantly, although small quantities of intracellular glucagon (100:1 insulin to glucagon) were detectable by radioimmunoassay. The alpha TC1 line (from an adenoma created in transgenic mice expressing the SV40 large T-antigen oncogene under control of the rat preproglucagon promoter) produced not only glucagon but also considerable quantities of insulin (4:1 glucagon to insulin) and preproinsulin mRNA. We therefore cloned alpha TC1 cells and obtained 12 glucagon-producing clonal cell lines that did not produce levels of insulin detectable by radioimmunoassay. Analysis by Northern blotting of total RNA from two lines, alpha TC1 clones 6 and 9, confirmed the absence of preproinsulin mRNA. No somatostatin or pancreatic polypeptide was detected by immunohistochemical staining in alpha TC1 clones 6 or 9 or beta TC1 cells. Rat recombinant gamma-interferon (IFN-gamma; 5-250 U/ml) or mouse recombinant interleukin 1 (IL-1; 1-25 U/ml) individually inhibited DNA synthesis in beta TC1 cells after 3 days of treatment. The two cytokines in combination acted synergistically to further depress DNA synthesis and increase cytotoxicity. In contrast, alpha TC1 clone 9 cells were not sensitive to inhibition of DNA synthesis by each cytokine individually, although glucagon synthesis was inhibited. The combination of these cytokines caused marked inhibition of DNA and glucagon syntheses in alpha TC1 clone 9 cells. alpha TC1 clone 9 cells were somewhat more resistant to the cytotoxic action of the combined cytokines than were beta TC1 cells. Incubation with 50 U/ml IFN-gamma induced class II MHC molecules (I-Ab, I-Ad, and I-Ed) and enhanced the constitutive expression of class I molecules (H-2Kb and H-2Kd) on the cell surfaces of beta TC1, uncloned alpha TC1, and alpha TC1 clones 6 and 9. Thus, these cell lines are heterozygous for MHC alleles derived from both parental strains used in the construction of the transgenic mice [C57BL/6J (H-2b) and DBA/2J (H-2d)]. Class II gene transcription induced by IFN-gamma was confirmed in beta TC1 and alpha TC1 clone 9 cells by Northern blot analysis with A alpha-, A beta-, E alpha, and E beta-DNA probes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Comparison of cytokine effects on mouse pancreatic alpha-cell and beta-cell lines. Viability, secretory function, and MHC antigen expression. 210 69

Lectin binding analysis of Con A, SBA, PNA, WGA, HPA, RCA-I, DBA, and UEA-I was performed in two cases of normal human adrenal gland, four cases of adrenocortical hyperplasia, six cases of adrenocortical adenoma, and seven cases of adrenocortical carcinoma to examine the differences of lectin binding properties. No lectins were bound specifically to adrenocortical cells. Binding of RCA-I was observed in some carcinoma cells focally but not in benign counterparts. With WGA and Con A, the cytoplasmic binding became apparent in the cells manifesting hypercorticism. In adrenocortical carcinoma, various WGA and Con A binding patterns were intermingled, but no specific patterns were identified. The focal nature of RCA-I binding, and no specific WGA and Con A binding properties in carcinoma, suggest that diagnosis of malignant neoplasm must still largely rely on clinical, hormonal, and structural criteria in adrenocortical neoplasms.
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PMID:Lectin histochemistry in adrenocortical hyperplasia and neoplasms with emphasis on carcinoma. 291 Feb 29

Intracellular distribution of CEA, lectin binding sites including PNA, DBA and UEA-1, and quantity of nuclear DNA content were examined in 54 adenomas and 29 carcinomas of the colorectum. CEA was found in 40% and 60% of adenomas with mild and moderate dysplasia, and all carcinomas. In particular CEA which was diffusely distributed in the cytoplasm was found in 9% and 26% of adenomas with mild and moderate dysplasia, and in 79% of carcinomas. Both PNA and DBA were shown to have different binding sites in non-tumorous mucosa, adenoma and carcinoma. However, no difference was found in the binding sites of adenomas with different grades of dysplasia. Whereas, the binding sites of UEA-1 were demonstrated to differ with the degree of dysplasia in adenomas and also carcinomas: UEA-1 binding in the brush border was found to be 29%, 63%, and 80% in adenomas with mild and moderate dysplasia, and carcinomas respectively. Nuclear Feulgen DNA content increased in parallel with the grade of cellular dysplasia. All carcinomas exhibited polyploid cell over 4C greater than 8%. Thirty percent of adenomas with moderate dysplasia also showed the same polyploid cells as carcinomas. These results suggest that the changes of CEA distribution, binding sites of lectins and of nuclear Feulgen DNA in adenoma may indicate its malignant potential in the colorectum, and that these changes may occur before any histological malignant transformation.
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PMID:[Immunohistochemical studies on colorectal adenoma and carcinoma--correlation of cellular dysplasia and intracellular CEA distribution, lectin-binding sites and quantities of nuclear Feulgen DNA content]. 320 Feb 38

The experiments were carried out on 60 first generation hybrids. Acute systemic "graft-versus-host" reaction (GVHR) was induced in (CBA X C57B1/6) X 60 X 10(6) hybrids by intravenous administration of spleen cells from C57B1/6 parents. Thyroid glands were examined on the 3rd, 10th and 24th days of GVHR. Chronic GVHR was studied in accordance with routine model. (C57B1/6 X DBA/2) hybrids were given 50 X 10(6) spleen cells from DBA/2 parents. Thyroid glands were investigated 6 months after GVHR induction. On the 10th day of GVHR histological examination revealed that follicular-like adenoma tumours with pronounced cellular abnormalities tended to appear in thyroid gland. In a chronic form of GVHR the histological pattern corresponds to that of follicular cancer.
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PMID:[Possibility of the neoplastic transformation of thyroid gland cells in the graft vs host reaction]. 339 May 91

Binding of FITC conjugated lectins to mucin in benign and malignant colon lesions was studied by fluorescence microscopy. In 145 cases of colonic adenocarcinoma, PNA (peanut agglutinin) was found to be bound to 75% of cases, while DBA (dolichos biflorus agglutinin) to 13% only. By contrast, DBA was bound to 94% of normal colon mucosa, while PNA to 15% only. Chronic colitis, simple adenoma and inflammatory polyps had the same binding pattern as normal mucosa, but villous adenoma, mixed polyps and multiple polyposis which are considered as premalignant lesions in colon had high positive rate of PNA binding and low binding percentage of DBA. These results indicate that an exposed carbohydrate structure Gal B1-2----GlNAc is expressed in the mucin produced by colonic adenocarcinoma. Meanwhile, some normal mucin component disappears from the malignant colonic epithelium. The mechanism of alteration of human colonic mucin present in malignant transformation is briefly discussed.
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PMID:[Histochemical study of colorectal adenocarcinoma by fluorescein isothiocyanate (FITC) conjugated lectins]. 344 60

Fewer lung adenomas were induced by urethan in BALB/cBy mice than in the A/J or SWR/J mouse strains. When BALB mice were crossed with either of these more sensitive strains the response of the progeny to urethan was most easily explained by a single gene which regulates susceptibility, with the more resistant phenotype behaving as a dominant trait. C56BL/6J mice were more resistant to adenoma induction than were BALB mice; progeny obtained when these two strains were crossed resembled the BALB susceptibility phenotype. As an approach to understanding the mechanism of action of this gene, agents that modulate adenoma initiation and tumor promotion were tested in BALB mice and other strains. The number of adenomas in BALB mice were increased severalfold by multiple urethan injections, which presumably affect initiation, and by the use of butylated o-hydroxytoulene as a promoting agent. Tumor incidence in A-mice was increased 50% by each treatment; neither procedure caused tumors to appear in the resistant DBA/2J, C3H/-21BG, or C57BL/6J strains. No relationship was observed between the strain dependency of the lethal effects of multiple injections of these agents and the relative susceptibilities of these strains to adenoma induction. The role of certain host factors in the regulation of tumor susceptibility was also tested. Homozygosity for the beige (bg) mutation had no effect on tumor numbers in C57 mice, suggesting that natural killer cells, deficient in bg/bg mice, played no major role in determining adenoma susceptibility in this strain. No correlation was found between the susceptibility of various sublines to urethan-induced lung adenoma and the reported relative tumoricidal capacities of the peritoneal macrophages from these sublines.
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PMID:Major effect on susceptibility to urethan-induced pulmonary adenoma by a single gene in BALB/cBy mice. 657 37


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