Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pancreatic tumour-associated monoclonal antibody DD9E7, raised against the GER pancreatic adenocarcinoma cell line, recognises a protein epitope on a novel family of membrane-bound cell surface glycoproteins (Mr 80-115,000). Western blot analysis of SDS/PAGE gels of tumour biopsies and of normal adult pancreas has shown that these glycoproteins are highly expressed in most pancreatic tumours but cannot be detected in normal adult pancreas. Using monoclonal antibodies directed against other antigens that have been associated with pancreatic adenocarcinoma (Du-Pan-2, Ca 19-9, CEA, NCA-95/55, EMA, and FAP), we have been able to show that although some of the antigens are also expressed by the GER pancreatic tumour cell line, the glycoproteins identified by monoclonal antibody DD9E7 are distinct from those other antigens in both molecular weight and antibody binding characteristics. Neuraminidase, periodic acid, and tunicamycin treatment of cultured cells has shown that monoclonal antibody DD9E7 recognises an epitope on the protein core of the antigen. This epitope is also present in NCA-1, but not in CEA, which suggest that there may be an association between DD9-antigen and other members of the NCA/CEA supergene family.
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PMID:The identification of a novel NCA-related pancreatic tumour-associated antigen, DD9-antigen: a comparison with the expression of other tumour antigens by the pancreatic tumour cell line GER. 171 89

The Department of Digestive Surgery was born in 1977. It is a part of the medical surgical unit of gastroenterology and hepatopancreatology. The various developed sectors concern hepatic surgery and liver transplantation (treatment of hepatic tumors and cirrhosis), pancreatic surgery and surgery of the biliary tract (treatment of benign and malignant pancreatic tumors, tumor of the biliary tract, chronic pancreatitis and biliary stones), surgery of morbid obesity (gastroplasty or gastric by-pass), surgery of the upper digestive tract (benign and malignant tumors of the oesophagus or the stomach, treatment of gastroesophageal reflux), surgery of the abdominal wall, colorectal surgery and surgery of the inflammatory bowel diseases (colorectal cancer, familial polyposis, Crohn's disease, ulcerative colitis), proctologic surgery and surgery of anorectal functional disorders, neonatal and paediatric surgery.
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PMID:[The surgical gastroenterology department]. 1258 13

Syndromic and sporadic fundic gland polyps are morphologically indistinguishable but may arise via different pathogenetic mechanisms involving mutations of the adenomatous polyposis coli (APC) and its downstream target beta-catenin genes. Although a higher frequency of dysplasia has been reported in syndromic forms, the risk of developing invasive carcinoma is exceedingly low. The current study was designed to investigate whether syndromic and sporadic fundic gland polyps differ in protein expression of a number of genes that are thought to be important in the control of neoplastic transformation. A total of 262 fundic gland polyps, including 155 syndromic polyps obtained from 35 patients with familial adenomatous polyposis or Gardner's syndrome and 107 sporadic polyps randomly selected from 45 patients with gastroesophageal reflux disease or Barrett's esophagus, were included in this study. Immunohistochemical evaluation showed that loss of immunoreactivity to the antibody against the carboxyl terminus of the APC protein, presumably resulting from APC gene mutations, was more frequent in syndromic than in sporadic cases (40% versus 6.7%, P<0.001). However, immunostaining failed to show aberrant nuclear localization of beta-catenin, a protein regulated by APC, in any of the polyps, irrespective of syndromic or sporadic types. Instead, positive membranous staining for beta-catenin was observed in all the cases. In addition, the expression characteristics of 2 other proteins, c-Myc and cyclin D1, whose genes have been reported to be transcriptionally regulated by the APC/beta-catenin pathway, were similar in these two types of polyps. Furthermore, all cases, including those harboring dysplasia, showed negative nuclear staining for p53 and positive nuclear staining for retinoblastoma (RB). Taken together, these data show a lack of dysregulation in the APC/beta-catenin signaling pathway and in the expression of p53 and RB in fundic gland polyps despite a high frequency of somatic mutations of the APC and beta-catenin genes reported in these polyps. These findings may explain at least in part why fundic gland polyps show a negligible malignant potential even in the presence of dysplasia.
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PMID:Immunohistochemical evaluation of adenomatous polyposis coli, beta-catenin, c-Myc, cyclin D1, p53, and retinoblastoma protein expression in syndromic and sporadic fundic gland polyps. 1501 89

A 58-year-old female with a recurrent history of upper abdominal pain and intermittent dysphagia underwent endoscopic evaluation that demonstrated an irregular and nodular esophago-gastric (EG) junction and grade I erosive esophagitis. Biopsies showed prominent intestinal metaplasia of Barrett's type without dysplasia, chronic inflammation and multiple aggregates of large cells within the mucosal lamina propria, some with spindle shaped nuclei. Immunohistochemistry stains for keratins AE-1/AE-3 were negative, while S-100 and NSE were positive. This, together with routine stains, was diagnostic for mucosal ganglioneuromatosis. The background of chronic inflammation with intestinal type metaplasia was consistent with long-term reflux esophagitis. No evidence of achalasia was seen. Biopsies of gastric antrum and fundus were unremarkable, without ganglioneural proliferation. Colonoscopy was unremarkable. No genetic syndromes were identified in the patient including familial adenomatous polyposis and multiple endocrine neoplasia type IIb (MEN IIb). Iansoprazole (Prevacid) was started by oral administration each day with partial relief of symptoms. Subsequent esophagogastroscopy repeated at 4 mo showed normal appearing EG junction. Esophageal manometry revealed a mild non-specific lower esophageal motility disorder. Mild motor dysfunction is seen with gastro-esophageal reflux disease (GERD) and we feel that the demonstration of localized ganglioneuromatosis was not likely related etiologically. In the absence of findings that might suggest neural hypertrophy, such as achalasia, the nodular mucosal irregularity seen with this instance of ganglioneuromatosis may, however, have exacerbated the patient's reflux.
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PMID:Sporadic ganglioneuromatosis of esophagogastric junction in a patient with gastro-esophageal reflux disorder and intestinal metaplasia. 1720 37