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)

Both chronic ulcerative colitis and smoking are associated with colorectal cancer in humans. In the present study, we investigated the effects of cigarette smoke (CS) exposure on inflammation-associated tumorigenesis in the mouse colon. Male balb/c mice were allocated into six groups: control, CS (2%), CS (4%), colitis, colitis + CS (2%) and colitis + CS (4%). They were given water or 3% dextran sulfate sodium (DSS) in drinking water for 7 days to induce colitis, with or without 1 h daily exposure to 2 or 4% CS. They were then allowed to drink water for 14 days. The cycle of 7 day DSS +/- CS/14 day H2O treatments were repeated twice. Mice were killed immediately or 1 month after the three cycles of treatments. Results indicated colonic adenoma was only found in the colitis group (one out of 11), Colitis + CS (2%) group (seven out of 12) and colitis + CS (4%) group (four out of five) 1 month after three cycles of DSS and/or CS treatment. CS exposure dose-dependently increased adenoma formation in mice with inflamed mucosa. CS exposure plus colitis was strongly associated with a high incidence of dysplasia (P < 0.01) and adenocarcinoma formation (P < 0.01) compared with induction of colitis alone. Colitis induced cell proliferation and apoptosis in colonic tissues. Cigarette smoking significantly attenuated the apoptotic effect by DSS probably via the induction of anti-apoptotic protein bcl-2. The ratio of apoptosis over proliferation was also significantly lower in the colitis + CS groups. Vascular endothelial growth factor and angiogenesis in the colon were also increased by cigarette smoking in animals with colitis. In conclusion, CS promotes inflammation-associated adenoma/adenocarcinoma formation in the mouse colon in a dose-dependent manner. This tumor development is associated with the inhibition of cellular apoptosis and supported by increased angiogenesis.
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PMID:Cigarette smoke exposure increases ulcerative colitis-associated colonic adenoma formation in mice. 1280 36

Metanephric metaplasia of the parietal epithelium of the Bowman capsule is a rare pathologic finding of unknown pathogenesis that has occurred in patients with widespread malignant neoplasms of various types. We report this finding in a 25-year-old woman with partial expression of the Carney triad who died of a disseminated gastrointestinal stromal tumor, specifically a gastric stromal sarcoma. The metaplasia involved both kidneys diffusely. It originated in the parietal epithelium of the Bowman capsule, extended into the proximal tubules, and focally surrounded the glomeruli in a semicircular manner Immunohistochemical analysis revealed that the cells of metanephric metaplasia expressed the Wilms tumor gene product, bcl-2 protein, and CD57 and cytokeratin 7 and keratin AE1/AE3 focally, but not CD56. This immunophenotype parallels that of metanephric adenoma, Wilms tumor, and nephrogenic rests and overlaps with antigen expression in certain periods of renal development.
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PMID:An immunophenotypic comparison of metanephric metaplasia of Bowman capsular epithelium with metanephric adenoma, Wilms tumor, and renal development: a case report and review of the literature. 1519 57

The duodenum is the second most frequent site of cancer in patients with familial adenomatous polyposis (FAP). The main objective of this study was to evaluate the cell kinetics in duodenal and ampullary adenomas in FAP. The endoscopic and biopsy findings of duodenal adenomas in 22 FAP subjects and 18 non-FAP subjects were compared. Adenomas in FAP included 15 ampullary adenomas and 17 nonampullary adenomas. The cell kinetics was evaluated by immunohistochemistry for Ki-67, p53, bcl-2, and cyclooxygenase 2 (COX2), and the apoptotic index (AI) as determined by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) method. Any correlations between the indices for cell kinetics and the endoscopic findings were identified. All 50 adenomas were histologically verified to be tubular adenoma with low-grade dysplasia. Neither the expression of Ki-67, p53, bcl-2, and COX2 nor the AI differed substantially between FAP and non-FAP subjects. In patients with FAP, duodenal adenoma tended to have a higher Ki-67-labeling index than the ampullary adenoma (54.3 +/- 11.3 versus 46.8 +/- 12.7; .05 < P < .1). In addition, the Ki-67-labeling index in endoscopically normal or slightly enlarged ampullary adenoma was significantly higher than that in markedly enlarged ampullary adenoma (51.8 +/- 11.4 versus 39.4 +/- 11.3; P < .05). Duodenal adenoma in FAP subjects was not found to have a higher proliferative activity or a smaller degree of apoptosis compared with those in non-FAP subjects. The smaller proliferative activity in larger ampullary adenoma may thus be related to the static nature of ampullary adenoma in FAP.
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PMID:Immunohistochemical characteristics of duodenal adenomas in familial adenomatous polyposis with special reference to cell kinetics. 1571 84

We investigated the case of a 13-year-old male with juvenile polyposis (JP) to determine the extent of intraepithelial neoplasia and associated genetic changes, as well as cellular proliferation, within these polyps using immunohistochemistry with antibodies against p53, bcl-2, and Ki-67. Examination of the total proctocolectomy specimen revealed 70 polyps. The 18 largest polyps were investigated microscopically and disclosed the typical hamartomas with frequent erosions of the surface epithelium and reparative changes. Only one polyp showed focal low-grade intraepithelial neoplasia. The immunohistochemical studies revealed an expression of p53 and an abnormal Ki-67 pattern of the surface epithelium only within the neoplastic area. These findings may hint at a possible pathogenetic mechanism for the evolution of colorectal cancer in JP. As in ulcerative colitis, carcinomas in JP may develop along a dysplasia-carcinoma sequence resulting from permanent mechanical insults, inflammation, and repair rather than from an adenoma-carcinoma sequence as in familial adenomatous polyposis (FAP).
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PMID:Juvenile polyposis coli: a facultative precancerosis with some similarities to ulcerative colitis? 1616 47

Diagnostic criteria for intracapsular carcinoma ex pleomorphic adenoma (CXPA) are subjective and vary among authors. Biomarker analysis, which could provide more objective evaluation of these tumors, has rarely been studied in intracapsular CXPA. Immunohistochemical evaluation of c-erbB-2, p53 protein, bcl-2, and Ki-67 was performed in 8 cases of CXPA at an early phase of malignant transformation (4 intracapsular and 4 minimally invasive) and in 17 pleomorphic adenomas (PA). In all cases of CXPA, p53 and Ki-67 were demonstrated predominantly in luminal cells of benign and malignant areas, significantly more in the latter. Few benign myoepithelial cells were p53 positive. c-erbB-2 reactivity was strongly associated with atypical luminal cells. Bcl-2 expression was weak and focal in malignant areas from 2 cases. In conclusion, both p53 and c-erbB-2 proteins appear to be involved at an early stage of malignization of PA. In PA with atypical cells, evaluation of the expression of these 2 markers provides more objective criteria for the diagnosis of intracapsular CXPA.
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PMID:Biomarker analysis in carcinoma ex pleomorphic adenoma at an early phase of carcinomatous transformation. 1627 89

We describe a hitherto undocumented variant of dimorphic pituitary neoplasm composed of an admixture of neurosecretory cells and profuse leiomyomatous stroma around intratumoral vessels. Radiologically perceived as a macroadenoma of 3.8 cm in diameter, this pituitary mass developed in an otherwise healthy 43-year-old female. At the term of a yearlong history of amenorrhea and progressive bitemporal visual loss, subtotal resection was performed via transsphenoidal microsurgery. Discounting mild hyperprolactinemia, there was no evidence of excess hormone production. Histologically, solid sheets, nests and cords of epithelial-looking, yet cytokeratin-negative cells were seen growing in a richly vascularized stroma of spindle cells. While strong immunoreactivity for NCAM, Synaptophysin and Chromogranin-A was detected in the former, the latter showed both morphological and immunophenotypic hallmarks of smooth muscle, being positive for vimentin, muscle actin and smooth muscle actin. Architectural patterns varied from monomorphous stroma-dominant zones through biphasic neuroendocrine-leiomyomatous areas, to pseudopapillary fronds along vascular cores. Only endothelia were labeled with CD34. Staining for S100 protein and GFAP, characteristics of sustentacular cells, as well as bcl-2 and c-kit was absent. Except for alpha-subunit, anterior pituitary hormones tested negative in tumor cells, as did a panel of peripheral endocrine markers, including serotonin, somatostatin, calcitonin, parathormone and vasoactive intestinal polypeptide. Mitotic activity was absent and the MIB-1 labeling index low (1-2%). While assignment of this lesion to any established neoplastic entity is not forthcoming, we propose it is being considered as a low-grade neuroendocrine tumor possibly related to null cell adenoma.
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PMID:Leiomyomatoid angiomatous neuroendocrine tumor (LANT) of the pituitary: a distinctive biphasic neoplasm with primitive secretory phenotype and smooth muscle-rich stroma. 1652 Sep 66

Aims-To describe the expression of three genes involved in the regulation of cell proliferation and programmed cell death (apoptosis) in normal, dysplastic and malignant large bowel epithelium, and to relate any alterations to important biological and clinical variables.Methods-Immunohistochemistry was used to assess bcl-2, c-myc and p53 gene expression in 70 colorectal carcinomas, 36 adenomas and three samples of normal mucosa.Results-Bcl-2 and c-myc protein were detected in all samples of normal mucosa and most adenomas. P53 was never found in normal mucosa and was expressed in only 5% of adenomas. Sixty nine of 70 carcinomas expressed c-myc protein; p53 was found in 46% and bcl-2 was present in 35%. Bcl-2 expression correlated with a higher degree of tumour differentiation whereas the opposite was true for c-myc. Strong staining for c-myc protein predicted survival in univariate analysis. No correlation was found between p53 and bcl-2 expression.Conclusions-While c-myc and bcl-2 proteins are overexpressed at an early stage of the large bowel adenoma-carcinoma sequence, alterations to the p53 protein level only occur as a late event in large, highly dysplastic adenomas and carcinomas. Bcl-2 may therefore protect the growing adenoma against excessive programmed cell death and mutated p53 may play a similar role in carcinomas. In vitro there is a reciprocal relation between p53 and bcl-2 expression. This could not be confirmed in vivo. Similarly, there was no relation between bcl-2 and c-myc status, despite evidence that these proteins cooperate to cause neoplastic transformation. C-myc may be a prognostic indicator in large bowel cancer. There is no evidence in the present series that bcl-2 status will affect survival.
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PMID:Genes mediating programmed cell death: an immunohistochemical study of bcl-2, c-myc and p53 expression in colorectal neoplasia. 1669 64

The interactions of cigarette smoking with COX-2 on colitis and colitis-associated adenoma formation were studied. Mice were induced with colitis and exposed to cigarette smoke (CS) and/or SC236 (a COX-2 inhibitor). Results indicated that CS did not alter acute colonic inflammation. Addition of SC236 abolished the induction of proliferation and oxidative damage by colitis. Chronic SC236 treatment abolished the promoting effect of CS on colonic adenoma formation, via suppression of COX-2- and VEGF-mediated proliferation and angiogenesis, and reversed bcl-2-mediated inhibition of apoptosis by CS. To conclude, COX-2 inhibitor could be an implication on cancer prevention in smokers with chronic colitis.
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PMID:Interaction of cigarette smoking with cyclooxygenase-2 on ulcerative colitis-associated neoplasia in mice. 1805 73

The aim of the paper was to apply a method for quantitative assessment of proliferation and apoptosis markers, based on their 3D visualization, in cases of parathyroid adenoma and hyperplasia. Material was obtained from 49 patients (32 females and 17 males) with primary hyperparahyroidism. Quantitative immunohistochemistry studies of Ki-67, proliferating cell nuclear antigen (PCNA) and bcl-2 were performed on digital microscopy images with the use of 3D visualization. The use of spatial visualization method allowed us to perform objective quantitative assessment of the studied immunohistochemical markers. The average cell nuclear fraction of Ki67+ was 1.8% in hyperplasia and 1.9% in adenoma cases while 3.5% in the controls. The highest expression of PCNA was found in parathyroid hyperplasia (22.9%) and significantly decreased in adenoma (12.5%) and in the control group (16.8%). The lower expression of bcl-2 in hyperplasia cases (mean area fraction of 0.172 per 1 mum(2), in contrast to 0.643 in adenomas and 0.648 in control) suggested that principal cells can be ready for apoptosis and may confirm the important role of bcl-2 protein in etiopathogenesis of hyperplasia of the parathyroid gland while PCNA might be a useful marker for differentiating adenoma from early hyperplasia in primary hyperparahyroidism cases.
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PMID:Selected markers of proliferation and apoptosis in the parathyroid lesions: a spatial visualization and quantification. 1872 91

Appendiceal mucinous neoplasms have been the focus of considerable debate in recent years. We histologically classified 70 appendiceal mucinous neoplasms into three categories: 32 mucinous adenoma, 23 mucinous neoplasm of uncertain malignant potential, and 15 mucinous adenocarcinomas. Immunohistochemistry was performed for 24 proteins in different functional categories, specifically, oncogenic proteins (bcl-2, beta-catenin, CEA, C-erbB2, c-kit, Cox-2, Cyclin D1, EGFR, Ki-67, NF-kappaB, VEGF), tumor suppressors (E-cadherin, FHIT, hMLH1, p53, p63, smad4), cell-cycle regulators (p21, p27, p16), and mucin proteins (MUC1, MUC2, MUC5AC, MUC6). Our data showed that 9 out of the 24 proteins were more frequently altered in the mucinous adenocarcinoma group than in the mucinous adenoma group (P<0.05), including beta-catenin (13% in mucinous adenoma vs 60% in mucinous adenocarcinoma), CyclinD1 (44 vs 87%), Ki-67 (high labeling index: 31 vs 67%), NF-kappaB (19 vs 60%), VEGF (16 vs 87%), E-cadherin (0 vs 47%), p53 (6 vs 40%), MUC2 (9 vs 67%), and MUC5AC (3 vs 40%). The distinct immunoexpression profile of mucinous neoplasm of uncertain malignant potential was placed between those of mucinous adenoma and mucinous adenocarcinoma (P<0.05). Moreover, the mucinous adenoma, mucinous neoplasm of uncertain malignant potential, and mucinous adenocarcinoma categories displayed differences in terms of the number of altered markers among the nine proteins (P<0.05; mean 1.4 vs 2.6 vs 5.5, respectively). In mucinous adenocarcinoma, the p53 status was related to disease-free survival and overall survival of patients (P<0.05, both). NF-kappaB status and the number of altered protein markers made statistically marginal impacts on disease-free survival; also beta-catenin loss, on overall survival of patients. In conclusion, protein immunoexpression profiles may facilitate the classification of appendiceal mucinous neoplasms. In our study, the three tumor categories of mucinous adenoma, mucinous neoplasm of uncertain malignant potential, and mucinous adenocarcinoma exhibited distinct immunoexpression profiles. Five and more altered protein markers, p53 overexpression, NF-kappaB positivity, and beta-catenin loss were predictive factors of adverse clinical outcomes in appendiceal mucinous adenocarcinomas.
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PMID:Differential protein immunoexpression profiles in appendiceal mucinous neoplasms: a special reference to classification and predictive factors. 1944 92


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