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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent developments in the field of polyps of the colon are discussed. The WHO classification represents a definite improvement. Apart from standardization, non-neoplastic polypoid changes of varying etiology and hamartomatous polyps are clearly distinguished from neoplastic, non-malignant adenomas. The various changes are outlined briefly in their essential characteristics. Clear-cut differentiation from early invasive cancer is of considerable importance for practical therapeutic purposes. Focal carcinoma within an adenoma is referred to only if invasion through the muscularis mucosae is established, while all other changes confined to the mucosa are termed adenomas with focal epithelial atypia. With regard to the relation between adenoma and cancer of the colon, recent results on topographical distribution of adenomas through the colon are of considerable significance. From serial studies of biopsy and autopsy specimens on the one hand, and from assessment of colon carcinoma incidence compared with mortality rates in carcinomas of different localizations on the other, it is evident that special attention should be given henceforward to adenomas, possible precursors, and carcinomas in the upper segments of the colon.
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PMID:[Pathology of colonic polyps]. 67 94

The role of non-specific cytotoxicity in the pathogenesis of inflammatory bowel disease (IBD) was investigated by assaying the natural killer (NK) and lymphokine-activated killer (LAK) cell activity of lamina propria mononuclear cells (LPMC) from 22 specimens of intestinal mucosa affected by IBD. Only minimal levels of NK activity were detected against K562 cells, as well as colon carcinoma cells, adenoma cells and fibroblasts freshly isolated from the intestinal mucosa. Culture of LPMC from IBD in the presence of interleukin-2 (IL-2) generated LAK cells that mediated high levels of activity against K562 cells and against neoplastic epithelial cells and fibroblasts derived from the intestinal mucosa. A group of 20 histologically normal specimens of intestinal mucosa showed similar levels of LAK activity against the K562 and intestinal cell targets. The minimal mucosal NK activity in IBD suggests that the cytotoxic properties of NK cells are not important in the pathogenesis of IBD. The presence of LAK precursor cells in the inflamed mucosa of IBD and their ability to lyse biologically relevant targets in vitro suggests that LAK cells have the potential to contribute to intestinal mucosal injury in IBD.
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PMID:Intestinal lymphokine-activated killer cells in inflammatory bowel disease. 193 65

The quantity and localization of two lactose-binding lectins with molecular weights of 31,000 and 14,500 in human colorectal carcinoma tissue specimens obtained by surgical resection have been studied using specific polyclonal antibodies. Electrophoretic separation and blotting of detergent extracts of tumor tissues (48 specimens), followed by the binding of an antibody that recognizes both of these lectins, demonstrated that the contents of Mr 31,000 and 14,500 lectins vary from one specimen to another. The Mr 31,000 lectin content was higher in tumor specimens classified as Dukes' stage D than in those from other stages. A significant correlation was found between Mr 31,000 lectin levels and the levels of carcinoembryonic antigen in the patients' sera at the time of surgery. Immunohistochemical staining with antibodies specific for each lectin was performed with 20 colon carcinoma tissues and 5 colonic adenoma tissues. The results showed that the Mr 31,000 lectin localizes in the cytoplasm of colorectal carcinoma cells and normal epithelial cells, whereas antibody binding to Mr 14,500 lectin is observed in a limited number of carcinoma specimens and is mainly associated with luminal surfaces and secretory products. Adenoma cells were reactive with Mr 14,500 anti-lectin antibody at their luminal surfaces or cytoplasms, but they did not stain with Mr 31,000 anti-lectin antibody. These results suggest that a correlation exists among the level of the Mr 31,000 lectin, the serum level of carcinoembryonic antigen, and the stage of progression of colorectal carcinomas.
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PMID:Increased content of an endogenous lactose-binding lectin in human colorectal carcinoma progressed to metastatic stages. 198 99

Colon tumor cells are more responsive to certain growth modulators in their local environment in vivo than are normal colonocytes. Examples of this class of compounds are the fecal diglycerides (DGs)(E. Friedman et al., Cancer Res., 49: 544-548, 1989), which may act as endogenous tumor promoters. At the concentration found in vivo, fecal DGs composed of oleic, myristic, and palmitic fatty acids induced mitogenesis of all classes of benign tumor cells and of half of the resected carcinomas tested in primary culture, but induced no detectable mitogenesis of normal colonocytes. Colon tumor cells also exhibit selective responses to these endogenous modulators as measured by another biological parameter, secretion of urokinase from carcinomas than from normal colonocytes. Fecal DGs also induced a 13-fold increase in urokinase mRNA synthesis in colon carcinoma cells and induced secretion of active urokinase from each of five resected carcinomas. Colon carcinomas, at both the primary site and metastatic to the liver, secreted the Mr 55,000 form of urokinase constitutively and secreted the same form upon treatment with fecal DGs. An increase in the steady-state level of urokinase secretion by saturated-chain DGs exhibited a strong dependency on the chain length of the fatty acid residues, those of 14 and 16 carbons having the greatest activity. Thus, fecal DGs composed of oleic, myristic, and palmitic acid residues induce two biological activities selectively in colon tumor cells, each of which would enhance tumor development. Selective mitogenesis would increase adenoma and carcinoma cell number relative to normal colonocyte number, and induction of the proteolytic enzyme urokinase would aid local invasion of the carcinoma within the bowel wall.
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PMID:Urokinase secretion from human colon carcinomas induced by endogenous diglycerides. 210 72

Autocrine stimulation of the epidermal growth factor receptor (EGF-R), by coexpression of transforming growth factor-alpha (TGF-alpha), causes malignant transformation of some fibroblast cell lines. TGF-alpha and EGF-R are both known to be expressed in colon carcinoma tissue and have been shown coexpressed in colon carcinoma cell lines. TGF-alpha autocrine activation of EGF-R has been suggested as a potential mechanism contributing to abnormal growth control in colon cancer. We now report coexpression of TGF-alpha and EGF-R transcripts in morphologically normal colonic epithelium from five individuals, in colonic adenomas from three individuals, and in a nontumorigenic colon adenoma cell line, VACO-330. Functional studies demonstrate VACO-330 growth is stimulated by exogenous TGF-alpha and is completely abolished by a blocking anti-EGF-R antibody. Autocrine stimulation of EGF-R by TGF-alpha is therefore required for growth of the adenoma cell line. Autocrine stimulation of EGF-R by TGF-alpha does not cause malignant transformation of the colonic epithelial cell. In normal and adenomatous human colon TGF-alpha, via either an autocrine or paracrine mechanism, is likely an important physiologic stimulant of epithelial proliferation.
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PMID:Growth stimulation by coexpression of transforming growth factor-alpha and epidermal growth factor-receptor in normal and adenomatous human colon epithelium. 236 25

CA 72 is a monoclonal antibody (MAb) -defined antigenic determinant expressed on a pancarcinoma antigen (TAG-72) found in more than 85% of human colorectal carcinomas. An immunoradiometric assay has been developed using the murine MAb B72.3 to quantitate CA 72 in human serum. In a simultaneous immunoradiometric assay, the mean CA 72 concentration in 1,099 serum samples from healthy blood donors was 1.83 +/- 2.03 (SD) units/ml. If the upper limit of normal was set at 10 mu/mol of serum, a value including 99% of healthy blood donors, only 4 of 101 serum samples (4%) from patients with benign disease were elevated, whereas 15 of 26 (58%) and 14 of 25 (56%) of rectal and colon carcinoma patient sera, respectively, were positive. Serum samples from 84 benign colorectal disease cases were examined; of these, 0 of 28 (0%) colorectal adenoma, 1 of 39 (3%) ulcerative proctocolitis, 0 of 15 (0%) diverticulosis, and 0 of 2 (0%) irritable bowel disease sera contained more than 10 mu/ml CA 72. At a reference value of 20 mu/ml, 0 of 101 (0%) benign disease and 2 of 1,060 (0.2%) blood donor sera had elevated values, whereas 10 of 26 (38%) and 9 of 25 (36%) rectal and colon patient sera, respectively, remained positive. The majority of patients with pancreatic and ovarian cancer, and a significant fraction of stomach cancer patient sera, also contained elevated levels of CA 72. The ability of this assay to discriminate between malignant and benign diseases suggests its further evaluation for monitoring and diagnosis in groups at risk for development of cancer.
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PMID:Monoclonal antibody immunoradiometric assay for an antigenic determinant (CA 72) on a novel pancarcinoma antigen (TAG-72). 242 34

272 cases of schistosome egg polyp collected from the mass-screening for colon carcinoma in Jiashan County have been divided into 3 groups (i.e. fibrous type, mixed type and epithelial hyperplastic type) according to the amount of fibrous stroma. The epithelial hyperplastic type (E type) was characterized by gland elongation, hypertrophy, variation in size, disorder in arrangement and high percentage of atypical hyperplasia (64.9%). Coexistence and transitional change of hyperplastic and adenomatous glands were noticed. By HID/AB staining, sialomucin increased prominently in E type. CEA and PNA receptors by ABC method were detected in 18/20 and 6/20 of E type respectively. The results of mucin expression were similar to those of adenoma. It is likely that the spectrum of E type polyp, atypical hyperplasia and adenoma exists. The authors suggest that patients with E type polyp of schistosome egg, especially those with atypical hyperplasia, should be treated as "risky" population of colon carcinoma.
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PMID:[Histological classification of schistosome egg polyp and its clinical significance: an analysis of 272 cases]. 251 90

Transformation of normal human colonocytes makes them sensitive to new mitogenic signals. Long-chain diglycerides (LCDGs) found in the human colon are mitogens selective for colon tumor cells, inducing mitogenesis in premalignant cells from each of 13 adenomas and in malignant cells from two of four carcinomas, but having no mitogenic effects on normal colonocytes (E. Friedman, P. Isaksson, J. Rafter, B. Marian, S. Winawer, and H. Newmark, Cancer Res., 49:544-548, 1989). Parallel to this biological activity pattern, LCDGs induce protein phosphorylation only in adenomas and carcinomas. Immunoblotting with an anti-phosphotyrosine monoclonal antibody demonstrated that the LCDG dimyristin, at concentrations found within the body, induced a 6-fold increase of tyrosine phosphorylation of an Mr 63,000 protein found in the particulate fraction of colon carcinoma cells. Tyrosine phosphorylation was maximal 0.5 min after addition of the LCDG, then fell, but remained elevated 40% over constitutive levels for at least 6 h. The Mr 63,000 tyrosine phosphoprotein was found in each of four colon carcinoma cell lines and an adenoma, but not in normal colonocytes, suggesting that the tyrosine kinase is activated only in tumor cells. Constitutive levels of the Mr 63,000 substrate were enhanced 2-fold by incubation of cells for 20 h with sodium orthovanadate, a tyrosine phosphatase inhibitor. This result suggested that carcinoma cells continually phosphorylate and dephosphorylate this tyrosine kinase substrate during growth. Thus, the colon tumor cell mitogen, dimyristin, utilizes a signal transduction pathway, containing the Mr 63,000 tyrosine kinase substrate, which is already in use during cell growth, possibly by other mitogens or growth factors.
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PMID:Tyrosine phosphorylation of a Mr 63,000 protein induced by an endogenous mitogen in human colon carcinoma cells, but not in normal colonocytes. 274 9

The environmental factor, pathogenic factor, host factor and others can be assumed as high-risk factors of colon carcinoma. Histopathologically, in most cases, colon carcinoma is recognized as an adenoma-carcinoma sequence that originates based on the adenoma. In this study, in addition to the adenoma and adenomatosis (familial polyposis, Gardner syndrome, Turcot syndrome), the hamartoma (Peutz-Jeghers syndrome, juvenile polyp), inflammatory bowel diseases (ulcerative colitis, Crohn's disease, fistel ani and others) and the origin of the carcinoma were examined. The oncogenesis based on the tubular adenoma, tubulovillous adenoma, villous adenoma and genetic adenomatosis of the large intestine could be found in many cases, thereby requiring a wide range of examinations and treatments. Concerning the oncogenesis of several kinds of inflammatory bowel diseases, much attention should be paid to diseases such as ulcerative colitis, Crohn's diseases, and fistel ani extending over a period of 10 years. In addition, it is necessary to study the connection and promotion among factors of the environmental, pathogenic and host factors.
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PMID:[High-risk group--colorectal cancer]. 282 Mar 9

Over a period of six years a total of 407 patients with polyps of the gastrointestinal tract were examined by gastroscopy and coloscopy and the findings analysed retrospectively. Among patients with colon polyps 10.5% were found also to have polypoid gastric lesions, among those with adenoma of the colon the prevalence was 11.7%. Only 2.4% of simultaneously diagnosed gastric lesions were found to be malignant or premalignant, a figure similar to the population average. But in patients with more than ten polyps of the colon both the prevalence of polypoid gastric changes and the significance of polyps with respect to precancerous lesions were clearly increased. On the other hand, in patients with epithelial polyps and/or glandular cysts colon polyps were found in 45%, in 42% with precancerous changes (adenoma). Thus patients with epithelial gastric polyps and glandular cysts probably constitute a group with a real additional risk of colon carcinoma. Regular coloscopy will thus reveal precancerous changes (adenoma) in the colon of 42% of such patients; coloscopic polypectomy will be an effective prophylactic measure against carcinoma of the colon.
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PMID:[Are stomach polyps an indicator of colonic carcinoma and colonic polyps an indicator of stomach carcinoma?]. 282 97


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