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At least 541 records · Page 30Linked to original sources
PubMed2006

[Bone formation in the ureter. Osseous metaplasia of an obstructed ureter].

Bone formation outside the skeleton is well known. Yet, ossification within the urogenital tract is rare. The case of a patient with distal ureteral obstruction, hydronephrosis, and subsequent circular osseous metaplasia of the ureter is presented. Open transperitoneal right-sided nephrectomy with partial resection of the ureter was performed. Intraoperatively and in histopathologic examination circular bone formation adjacent to the ureteral wall was detected. There was no evidence of malignancy. Early animal experiments in the twentieth century showed that bone metaplasia may be induced by epithelium of the urinary tract under certain conditions such as ischemia, inflammation, necrosis, sclerosis, and trauma. Osseous metaplasia may therefore be considered a differential diagnosis of calcification of the upper urinary tract in the absence of urolithiasis.

Aged↗
PubMed2003

Role of surveillance in intestinal metaplasia of the esophagus and gastroesophageal junction.

This article reviews current concepts of cancer surveillance in esophageal columnar metaplasia (Barrett's esophagus) and intestinal metaplasia at the gastroesophageal junction. An overview is given of the available data on the prevalence of intestinal metaplasia in biopsies from the distal esophagus and from the gastroesophageal junction. Furthermore, special attention is given to the endoscopic detection of dysplasia and early malignancy. Finally, the costs of endoscopic surveillance and its effect on mortality rates from esophageal adenocarcinoma are discussed.

Adenocarcinoma↗
PubMed2004

Immunological and morphogenic basis of gastric mucosa atrophy and metaplasia.

Chronic gastritis with gastric mucosa atrophy, intestinal metaplasia and endocrine cell hyperplasia are alterations with an increased risk for the development of gastric neoplasias. Immunological studies in autoimmune gastritis, in atrophic Helicobacter pylori gastritis and in studies with transgenic mice point to a central role of the parietal cell in the development of gastric mucosa atrophy. Destruction of gastric epithelial cells alone might not be sufficient for the loss of complete gastric glands. Gastric atrophy, endocrine cell hyperplasia and intestinal and pancreatic metaplasia can be regarded as the result of altered morphogenesis within the gastric mucosa. Impaired expression of the gastric morphogenic factor Sonic Hedgehog by parietal cells and increased expression of the transcriptional activators of intestinal and pancreatic differentiation, namely CDX2 and PDX1, seem to be crucial for the development of gastric atrophy and for intestinal, endocrine and pancreatic transdifferentiation processes. Altered expression of these morphogenic factors is partly caused by changes in the gastric milieu. Further studies concerning the normal and pathological morphogenesis of the gastric mucosa and related tissues might give new insight into the pathogenesis of gastric atrophy and metaplasia.

Animals↗
PubMed2001

Sebaceous gland metaplasia in intraductal papilloma of the breast.

We report here the first case of sebaceous gland metaplasia arising within an intraductal papilloma of the breast of a 70-year-old female. Several lobules and nests composed of clear cells closely resembling sebaceous glands of the skin were discovered within an intraductal papilloma of the breast. Squamous metaplasia was also noted in certain areas of the tumor. Immunohistochemically, the cells of the lobules and nests stained positively for monoclonal antibodies anti-cytokeratin 14 and epithelial membrane antigen. This study confirms a novel type of metaplasia of the breast.

Aged↗
PubMed2001

Metaplasia, intraepithelial neoplasia and early cancer of the stomach are related to dedifferentiated epithelial cells defined by cytokeratin-7 expression in gastritis.

Cancer presumably arises from stem cells, preserved in an undifferentiated status since fetal development, or from a dedifferentiation of mature cells that return into a fetal phenotype with the potential for proliferation and renewal. Dedifferentiation in this context could represent a transient phase, passed through by cells, before they switch to redifferentiation, metaplasia or neoplasia. Cytokeratin-7 (CK7) is present in fetal, largely absent in normal adult, and transiently neoexpressed in metaplastic and neoplastic epithelial cells of the stomach according to previous observations. CK7 neoexpression in the stomach could, hence, define a fetal-like, dedifferentiated, cellular phenotype during the development of metaplasia and neoplasia. To test this hypothesis, we investigated CK7 expressions in fetal stomachs, non-neoplastic control stomachs, and neoplastic stomachs exhibiting metaplasia, intraepithelial neoplasia, and early cancer. Proliferation and beta-catenin expression of CK7-positive cells were also evaluated. The chronology of CK7 expression was studied during the experimental gastritis-cancer sequence in Mongolian gerbils. Our results show that metaplastic and neoplastic changes in the gastritis-cancer sequence are related to dedifferentiated epithelial cells which are defined by CK7 expression and can phenotypically be linked to fetal cells at the start of gastric pit development. The dedifferentiated cells exhibit a low proliferation and beta-catenin accumulation, similar to stem cells. Thus, the "stem cell" and "dedifferentiation" hypotheses for cancer origin could complement one another, and dedifferentiation-redifferentiation processes might be decisive for carcinogenesis in the stomach.

Adenocarcinoma↗
PubMed2002

Etiology of intestinal metaplasia at the gastroesophageal junction.

BACKGROUND: Intestinal metaplasia occurs in the esophagus as a consequence of gastroesophageal reflux disease and in the stomach secondary to H. pylori infection. The etiology of intestinal metaplasia limited to the gastroesophageal junction or cardia (CIM) is disputed. We hypothesized that CIM has dual etiologies: gastroesophageal reflux in some, H. pylori infection in others, and that cytokeratin immunostaining can help to differentiate between these two etiologies. METHODS: We defined CIM as the presence of intestinal metaplasia within cardiac mucosa on biopsy from an endoscopically normal-appearing gastroesophageal junction. Thirty patients with CIM who had multiple biopsy specimens taken from the esophagus, gastroesophageal junction, and stomach were identified. Tissue blocks from biopsy specimens taken at the gastroesophageal junction were sectioned and immunostained for cytokeratins 7 and 20. The cytokeratin 7/20 staining of the CIM in each patient was determined to be either a Barrett's or non-Barrett's pattern. H. pylori infection was assessed by Giemsa staining of antral biopsy specimens. RESULTS: H. pylori infection was present in 16 patients. A Barrett's cytokeratin 7/20 staining pattern in the CIM was present in only 46% of the H. pylori-positive patients, as compared to 86% in the 14 patients with CIM and no H. pylori (p = 0.025). Objective evidence of reflux disease was present in 71% of patients with CIM and no H. pylori, as compared to 31% of patients with H. pylori. CONCLUSIONS: The two different patterns of cytokeratin 7/20 staining found in patients with CIM support the concept of dual etiologies for CIM. A Barrett's staining pattern was associated with objective evidence of gastroesophageal reflux and the absence of H. pylori, suggesting that cytokeratin 7/20 immunostaining is useful to determine the likely etiology of CIM.

Biopsy↗
PubMed2005

How to make a Barrett esophagus: pathophysiology of columnar metaplasia of the esophagus.

Barrett esophagus is defined as a specialized intestinal replacing the squamous epithelium of the esophageal mucosa in response to gastroesophageal reflux. Barrett metaplasia is a healing process that develops to protect the esophagus from further damage. Although mechanisms by which Barrett metaplasia evolves toward dysplasia and adenocarcinoma have been extensively studied, the process by which squamous epithelium is replaced by specialized intestinal metaplasia is poorly understood. Barrett esophagus develops when defense mechanisms in the esophageal mucosa (luminal secretion of mucus, bicarbonate, growth factors, etc.) are overwhelmed by an ongoing cycle of mucosal injury and repair. Hydrogen ion, pepsin, trypsin, and bile acids are considered harmful agents that synergistically invade the esophageal mucosa. Areas of destroyed squamous epithelium are then progressively reepithelized by a columnar epithelium that may originate from multipotent stem cells located within the basal layer of the normal esophageal mucosa or in the ducts of submucosal glands.

Barrett Esophagus↗
PubMed1993

Barrett's disease: pathophysiology of metaplasia and adenocarcinoma.

Peptic ulceration arising in the lower esophagus lined by columnar epithelium was described in detail by Tileston in 1906. Although this concept was challenged in 1950 by Barrett, experimental and clinical evidence has now conclusively demonstrated that Barrett's metaplasia is an acquired condition and is a consequence of chronic reflux of gastric or duodenal contents or both. Current concepts suggest that unknown trophic factors present in these secretions stimulate proliferation of multipotential reserve cells located in the esophageal submucosal glands resulting in columnar metaplasia of the normal squamous epithelium with subsequent potential for malignant degeneration. Today, numerous patients are affected by reflux esophagitis, a lesser number by Barrett's metaplasia, and a smaller but ever-enlarging group by adenocarcinoma. Although high-grade dysplasia is considered a precursor to invasive adenocarcinoma, detection of this abnormal mucosa remains controversial and currently requires esophagoscopy with biopsy. Epithelial markers, such as increased activity of mucosal ornithine decarboxylase, sulfomucin production, nuclear DNA aneuploidy, and recently molecular analysis, have also been proposed to identify those paitents at increased risk for malignant degeneration. As more is learned about the pathogenesis of Barrett's disease, perhaps these cancers can ultimately be prevented.

Adenocarcinoma↗
PubMed1977

Alkaline phosphatase isoenzyme in intestinal metaplasia of the stomach.

To investigate the relationship of intestinal metaplasia of the stomach and gastric carcinoma, isoenzymatic analysis of alkaline phosphatase (ALP) of the intestinal metaplasia was studied. Purified human intestinal ALP, and anti-human intestinal ALP antibody were used, and mucosa ALP of the other segments of human gastro-intestinal tract was studied simultaneously. Radioimmunoassay technique, and immunofluorescent staining using anti-human intestinal ALP antibody, were applied to the stomach resected for gastric carcinoma or peptic ulcer, ALP extracted from the mucosa of intestinal metaplasia, and from the mucosa of the other segments of human gastro-intestinal tract, was identical with intestinal ALP in its enzymological and immunological properties.

Alkaline Phosphatase↗
PubMed1987

Antigen reversion of glycogen phosphorylase isoenzyme in carcinoma and proliferative zone of intestinal metaplasia of the human stomach. An immunohistochemical study.

Specific antibodies to three purified glycogen phosphorylase isoenzymes, i.e., brain (or fetal), muscle, and liver types, were used to study the localization of these isoenzymes in carcinoma and the proliferative zone of intestinal metaplasia of the human stomach. Both the malignant cells of well-differentiated adenocarcinoma and the proliferative zone of some intestinal metaplasia of the stomach were stained when the antibrain-type phosphorylase isoenzyme antibody was used, but not when the other two types were used. The results suggest that brain-type phosphorylase in gastric carcinoma could be one example of fetal protein expression in cancer, and that the proliferative zone of some intestinal metaplasia having brain-type phosphorylase may histogenetically relate to well-differentiated adenocarcinoma.

Adenocarcinoma↗
PubMed1977

Squamous metaplasia and invasive epidermoid carcinoma of bladder.

Invasive epidermoid carcinoma of the urinary bladder is described in a young woman with a long history of bladder infections and extensive squamous metaplasia without atypia. The literature on squamous metaplasia and leukoplakia progressing to epidermoid carcinoma of the chronic dysuria, bladder infections, and long histories of squamous metaplasia of the bladder should be followed up very closely. If epidermoid carcinoma of the bladder develops, they should undergo radical surgery.

Adult↗
PubMed2006

Identifying intestinal metaplasia at the squamocolumnar junction by using optical coherence tomography.

BACKGROUND: Optical coherence tomography (OCT) is an optical imaging method that produces high-resolution cross-sectional images of the esophagus. The accuracy of OCT for differentiating tissue types at the squamocolumnar junction (SCJ) has not been established. OBJECTIVE: The purpose of this study was to identify and validate OCT image criteria for distinguishing metaplastic from nonmetaplastic tissue at the SCJ. DESIGN: A total of 196 biopsy-correlated OCT images of the SCJ were acquired from 113 patients undergoing upper endoscopy. A pathologist blinded to the OCT results reviewed each pathology specimen and determined the presence of the following histopathology: gastric cardia, squamous mucosa, pancreatic metaplasia, and intestinal metaplasia. An algorithm for diagnosing specialized intestinal metaplasia (SIM) was created by reviewing a training set of 40 biopsy-correlated OCT images. Two blinded investigators prospectively tested the algorithm on a validation set of 123 images. RESULTS: OCT images of squamous mucosa were characterized by a layered appearance without epithelial glands; gastric cardia, by vertical pit and gland structure, a well-defined epithelial surface reflectivity, and relatively poor image penetration; and SIM by an irregular architecture and good image penetration. The OCT criteria were 85% sensitive and 95% specific for SIM when applied retrospectively to the training set. When applied to the validation set, the algorithm was 81% sensitive for both OCT readers and 66% and 57% specific for diagnosing SIM. The interobserver agreement was good (kappa = 0.53). CONCLUSIONS: OCT imaging can identify SIM at the SCJ with an accuracy similar to that of endoscopy.

Algorithms↗
PubMed2004

Infrequency of microsatellite instability in complete and incomplete gastric intestinal metaplasia.

Chronic inflammation may be associated with microsatellite instability (MSI). To test the hypothesis that MSI frequently occurs in gastric intestinal metaplasia, we examined gastric biopsies from 58 subjects from an area of high risk for gastric cancer. These were selected to have 2 types of intestinal metaplasia: complete (31 subjects) and incomplete or mixed-type (27 subjects). None of the subjects had gastric cancer, but 95% had chronic inflammation with Helicobacter pylori. We used laser capture microdissection to retrieve metaplastic glands to compare with lymphocytes microdissected from the adjacent gastric mucosae in the same subjects. We performed microsatellite analysis using 6 microsatellite loci, including BAT26. None of the cases were found to have reproducible MSI, and only 1 case showed loss of heterozygosity at 1 marker, D3S1067. To test the sensitivity of our assay, we mixed templates to produce bands of different mobility and found that we could detect an aberrant microsatellite pattern if only 2% of the DNA showed that pattern. Our results indicate that MSI is a rare event in intestinal metaplasia in subjects who do not have gastric cancer.

Base Pair Mismatch↗
PubMed2003

Aberrant CpG island hypermethylation of chronic gastritis, in relation to aging, gender, intestinal metaplasia, and chronic inflammation.

Aberrant hypermethylation of promoter CpG islands is an important mechanism for the inactivation of tumor suppressor genes. CpG island hypermethylation occurs in relation to tumorigenesis or aging. Gastric cancer is one of the tumors with a high level of aberrant CpG island methylation. However, the data on the methylation status of normal gastric mucosa has been very limited. The present study attempted to compare the methylation status of nonneoplastic gastric mucosa, using clinicopathological parameters, including age, gender, Helicobacter pylori (H. pylori), acute and chronic inflammation, and intestinal metaplasia. Two hundred sixty-eight nonneoplastic gastric mucosa samples were studied for the methylation status of 11 genes (COX-2, DAP-kinase, E-cadherin, GSTP1, MGMT, hMLH1, p14, p16, THBS1, TIMP3, and RASSF1A), using methylation-specific PCR. CpG island hypermethylation was found in 53.7, 41, 37.7, 23.1, 18.7, 10.9, 10, 4.1, 3.4, 1.7, 0.4% for DAP-kinase, E-cadherin, THBS1, TIMP3, p14, MGMT, p16, COX-2, GSTP1, hMLH1 and RASSF1A, respectively. Five genes (DAP-kinase, E-cadherin, p14, THBS1, and TIMP-3) showed a general progressive increase in the methylation frequency as a function of aging, whereas the other genes (COX-2, GSTP1, MGMT, hMLH1, p16, and RASSF1A) were rarely methylated. Male patients showed higher numbers of methylated genes than females (3.2 vs. 2.1, respectively, P = 0.002). Gastritis samples with marked intestinal metaplasia, showed higher numbers of genes methylated than those without (3.7 vs. 2.6, respectively, P = 0.021). Gastritis samples with marked infiltration of mononuclear cells displayed higher numbers of genes methylated than those with mild or moderate infiltration of mononuclear cells (3.4 vs. 2.5 or 2.5, respectively, P < 0.05). Our results demonstrated that many genes are methylated in the stomach as a function of age, and suggested that male gender, intestinal metaplasia, and chronic inflammation are closely associated with increased methylation in nonneoplastic gastric mucosa samples.

Adolescent↗
PubMed2000

Expression of an intestine-specific transcription factor (CDX1) in intestinal metaplasia and in subsequently developed intestinal type of cholangiocarcinoma in rat liver.

CDX1 is a caudal-type homeobox intestine-specific transcription factor that has been shown to be selectively expressed in epithelial cells in intestinal metaplasia of the human stomach and esophagus and variably expressed in human gastric and esophageal adenocarcinomas (Silberg DG, Furth EE, Taylor JK, Schuck T, Chiou T, Traber PG: Gastroenterology 1997, 113: 478-486). Through the use of immunohistochemistry and Western blotting, we investigated whether CDX1 is also uniquely associated with the intestinal metaplasia associated with putative precancerous cholangiofibrosis induced in rat liver during furan cholangiocarcinogenesis, as well as expressed in neoplastic glands in a subsequently developed intestinal type of cholangiocarcinoma. In normal, control adult rat small intestine, specific nuclear immunoreactivity for CDX1 was most prominent in enterocytes lining the crypts. In comparison, epithelium from intestinal metaplastic glands within furan-induced hepatic cholangiofibrosis and neoplastic epithelium from later developed primary intestinal-type cholangiocarcinoma each demonstrated strong nuclear immunoreactivity for CDX1. CDX1-positive cells were detected in hepatic cholangiofibrotic tissue as early as 3 weeks after the start of chronic furan treatment. We further determined that the percentages of CDX1-positive neoplastic glands and glandular nuclei are significantly higher in primary tumors than in a derived, transplantable cholangiocarcinoma serially-propagated in vivo. Western blotting confirmed our immunohistochemical results, and no CDX1 immunoreactivity was detected in normal adult rat liver or in hyperplastic biliary epithelial cells. These findings indicate that CDX1 is specifically associated with early intestinal metaplasia and a later developed intestinal-type of cholangiocarcinoma induced in the liver of furan-treated rats.

Animals↗
PubMed1979

The prevalence and significance of Brunn's nests, cystitis cystica and squamous metaplasia in normal bladders.

The frequency of Brunn's nests, cystitis cystica and squamous metaplasia was studied by multiple histologic sections in 100 grossly normal bladders obtained at postmortem examination. Of the 100 bladders 93 per cent had at least 1 of the 3 proliferative changes. Brunn's nests and cystitis cystica were seen in 89 and 60 per cent of the bladders, respectively, most often at the bladder neck and trigone. Non-keratinizing squamous metaplasia of the vaginal type was seen almost exclusively on the trigone and bladder neck in 46 per cent of the premenopausal and postmenopausal women but in only 7 per cent of the men. There was no satisfactory evidence that inflammation was casually associated with these changes. These findings suggest that Brunn's nests, cystitis cystica and squamous metaplasia of the vaginal type in women are normal variants of bladder urothelium and have no precancerous potential.

Adolescent↗
PubMed1977

Bladder cancer and squamous metaplasia in spinal cord injury patients.

The influence of long-term indwelling urethral catheterization was studied by random bladder and urethral biopsies in 62 spinal cord injury patients. Six patients (10 per cent) had diffuse squamous cell bladder carcinoma, 4 of whom had no tumor visible endoscopically. Five of the patients with cancer were among 25 patients (20 per cent) managed with an indwelling urethral catheter for more than 10 years (average 21 years, range 15 to 30 years). The other cancer patient had been free of the catheter for 27 years after suprapubic cystotomy for 4 years. Gross and microscopic hematuria was associated with cancer. Squamous metaplasia of the bladder was significantly greater in patients who had been catheterized for more than 10 years (80 per cent), compared to those catheterized for less than 10 years (42 per cent) and patients without catheters (20 per cent). Urethral squamous metaplasia increased slightly in long-term catheterization patients. Urinary infection was universal and did not distinguish patients with inflammation, metaplasia or cancer. Therefore, the duration of indwelling catheterization seems to be the major factor in squamous changes in these patients.

Adult↗
PubMed1983

Intestinal metaplasia of the regenerative epithelia in 549 gastric ulcers.

Histopathologic changes in the regenerative epithelia of 549 foci of gastric ulcer were studied. About 70 per cent of the regenerative epithelia revealed intestinal metaplasia of the so-called complete or incomplete type. Parietal cells and chief cells were occasionally observed in the regenerative epithelia of ulcers located in fundic gland areas or at fundopyloric gland borders. It is possible that the regenerative epithelium frequently reverts to intestinal epithelium during the regenerative process, later redifferentiating into normal gastric mucosa or remaining as intestinal metaplasia and that, thus, only a few foci of intestinal metaplasia are precancerous lesions.

Cicatrix↗