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At least 433 records · Page 24Linked to original sources
PubMed1994

Lack of any positive effect of intestinal metaplasia on induction of gastric tumors in Wistar rats treated with N-methyl-N-nitrosourea in their drinking water.

The influence of intestinal metaplasia on gastric cancer induction was examined in five-week-old male Wistar:Crj rats. The animals were first treated with two 10 Gy doses of X-rays to the gastric region at a 3-day interval (total 20 Gy) and then, starting two months after the irradiation, received 100 ppm N-methyl-N-nitrosourea (MNU) in their drinking water for 15 weeks. Thereafter they were maintained for 37 weeks with or without a dietary 1% sodium chloride (NaCl) supplement. The incidences of gastric adenocarcinomas in the MNU or MNU plus NaCl groups were significantly higher than in animals receiving X-rays plus MNU with or without NaCl. Intestinal metaplasias and the numbers of alkaline phosphatase (ALP)-positive foci were significantly increased in the X-ray irradiation groups but the numbers of ALP-positive foci were not increased with or without 1% NaCl. An inverse relationship between incidences of gastric tumors and intestinal metaplasias was apparent. The present experiment thus showed that the presence of intestinal metaplasia does not exert a positive influence on induction of gastric neoplasia by MNU in the rat.

Adenocarcinoma↗
PubMed1981

Inappropriate mucin production in gall bladder metaplasia and neoplasia--an immunohistological study.

This study demonstrates the presence of three antigens in glandular metaplasia occurring in patients with cholecystitis and cholelithiasis: specifically carcinoembryonic antigen (CEA), large intestinal mucin antigen (LIMA) and small intestinal mucin antigen (SIMA). These antigens could not be detected in normal gall bladder mucosa or in squamous metaplasia of the gall bladder. The occurrence of the three intestine-associated antigens in three carcinomas was irregular. In one mucinous carcinoma, only SIMA could be demonstrated. In one adenocarcinoma, SIMA was present in small areas of mucinous change, whilst CEA was present in the non-mucinous malignant tissue. In a mixed mucinous and non-mucinous adenocarcinoma with widespread dissemination, the three antigens were present both in the primary tumour and the metastases. These observations suggest that all forms of glandular metaplasia of the gall bladder are intestinal in nature and at least a proportion of gall bladder carcinomas are of an intestinal type. Finally they provide further immunological evidence that glandular metaplasia of the gall bladder should be considered a pre-malignant condition.

Adenocarcinoma↗
PubMed1995

Pancreatic metaplasia of the human gastric mucosa is associated with high expression of transforming growth factor alpha but not of epidermal growth factor.

Pancreatic acinar metaplasia of the gastric mucosa is a newly recognized entity. Its physiological relevance and association with other pathological conditions in the stomach remain to be elucidated. We studied by immunohistochemistry the expression of growth markers in the gastric mucosa in biopsies from 15 patients with recognized pancreatic metaplasia. Pancreatic metaplasia (both acinar and dispersed forms) was found in routine paraffin sections and confirmed by strong lipase immunoreactivity. In parallel paraffin sections we performed immunostaining for epidermal growth factor (EGF), transforming growth factor-alpha (TGF alpha) and epidermal growth factor receptor (EGFr) using a biotin streptavidin method. Strong expression of TGF alpha but only weak expression of EGF was noted within metaplastic mucosa. EGFr was strongly expressed, not only in areas of pancreatic metaplasia but also in the surrounding gastric mucosa.

Antibodies↗
PubMed2005

Metaplasia in the pancreas.

There is currently much interest in the possibility to treat chronic diseases by cell replacement or regenerative therapies. Most of these studies focus on the manipulation of undifferentiated stem cells. However, tissue repair and regeneration can also be achieved by differentiated cells, which, in certain conditions, can even transdifferentiate to other cell types. Such transdifferentiations can lead to tissue metaplasia. The pancreas is an organ wherein metaplasia has been well investigated and for which experimental models have been recently developed allowing to unravel the molecular basis of transdifferentiation. Pancreatic metaplasias studied so far include the conversion of exocrine acinar cells to duct cells, exocrine cells to endocrine islet cells, endocrine cells to duct cells, and acinar cells to hepatocytes. Epitheliomesenchymal transitions have also been described. The available evidence indicates that mature cells can be reprogrammed by specific environmental cues inducing the expression of cell type-specific transcription factors. For example, the glucocorticoid hormone dexamethasone induces pancreatic transdifferentiation to hepatocytes, whereas the combination of epidermal growth factor and leukemia-inhibitory factor induces exocrine-endocrine transdifferentiation in vitro. Further unravelling of the involved signal transduction pathways, transcription factor networks, and chromatin modifications is required to manipulate metaplasia at will and to apply it in tissue repair or regeneration.

Animals↗
PubMed1996

Gastric metaplasia of regenerating duodenal mucosa and deformity of duodenal bulb: a correlative study.

The correlation between the presence and degree of gastric metaplasia of regenerating duodenal mucosa and the deformity of duodenal bulb was studied. Based on the endoscopically morphological patterns of bulb, the duodenal ulcers were divided into three types: type I, with a normal-shaped bulb; type II, with mildly deformed bulb; and type III, with a markedly deformed bulb. A total of 159 patients with active duodenal ulcers were scheduled to be treated with H2-receptor antagonists. Of these patients, 124 proved to have a healed duodenal ulcer 4 weeks after initial treatment upon follow-up endoscopic examinations. Two biopsies were taken from the centre of the ulcer scar when the ulcer was found to be healed for light microscopic study. Histologically, the degree of gastric metaplasia was divided into three grades: grades 0, 1 and 2. The results show that a healed duodenal ulcer with a normal-shaped bulb is not frequently accompanied by gastric metaplasia. However, a healed ulcer with a markedly deformed bulb has a high incidence and degree of gastric metaplasia, which may be easily colonized by Helicobacter pylori and thus develop an environment of easy recurrence. Therefore, a cycle of healing and recurrence may exist in patients with a duodenal ulcer and a markedly deformed bulb. Eradication of H. pylori may be the best way to break this cycle.

Adult↗
PubMed1988

The effects of ranitidine and cysteamine on intestinal metaplasia induced by X-irradiation in rats.

The influence of ranitidine and cysteamine on intestinal metaplasia was examined in 7-month-old male Crj: CD (SD) rats. At the age of 5 weeks, the animals were treated with 10 Gy doses of X-rays at 3-day intervals up to a total of 20 Gy in the gastric region, and 6 months after irradiation, the rats received either ranitidine (0.02% in diet) or cysteamine (0.1% in drinking water) for 2 months. The incidence and number of intestinal metaplasia with alkaline phosphatase-positive foci in rats given X-rays and cysteamine (group 4) were significantly low compared with those in rats given X-rays and ranitidine (group 3) (p less than 0.01). In both the pyloric and the fundic gland mucosae, the average numbers of type C metaplasia (intestinal crypts with Paneth cells) and total numbers of metaplastic foci in rats of group 3 were much higher than those in group 4 (P less than 0.05). The present results showed that the occurrence of intestinal metaplasia was significantly increased after administration of ranitidine and decreased by cysteamine.

Animals↗
PubMed1988

Gastric metaplasia in duodenal ulcer. Histochemical considerations of its pathophysiological significance.

Gastric metaplasia of the duodenal mucosa in biopsy specimens of healed duodenal ulcer and in surgical specimens of perforated duodenal ulcer was investigated using mucin histochemistry and the indirect immunoperoxidase method. Endoscopic methylene blue test was performed prior to biopsy. All specimens from areas showing no dye absorption revealed varying degrees of gastric metaplasia characterized by heterotopic occurrence of gastric-type foveolar cells mainly at the tips of stunted intestinal villi. On average, 31.8% of the total surface length of duodenal mucosa taken from areas showing no dye absorption was occupied by the metaplastic cells. They showed strong reactivities for periodic acid-Schiff (PAS) and galactose oxidase-Schiff sequences, while alcian blue and paradoxical concanavalin A staining, class III, were negative. Immunoperoxidase-PAS double staining revealed a few gastrin and somatostatin cells in foci of gastric metaplasia, but almost no cells containing motilin, secretin, cholecystokinin and gastric inhibitory peptide. Such endocrine cells were scattered in nonmetaplastic mucosa. While such metaplastic change has been regarded as a self-defence mechanism or adaptation of the duodenal mucosa against acid, a local decrease of normal endocrine cells, which allegedly function as acid receptors, may lead to alterations of gastroduodenal interaction. It is suggested that gastric metaplasia is important as one of the pathophysiological mechanisms involved in the recurrence of duodenal ulcer.

Adult↗
PubMed1993

Effects of sex hormones on induction of intestinal metaplasia by X-irradiation in rats.

The influence of sex hormones on induction of intestinal metaplasia was examined in 5 week old Crj: CD (SD) rats of both sexes. At the age of 4 weeks, the animals were gonadectomized and given testosterone or dimethyl estradiol (DES). One week after operation, they were irradiated with two 10 Gy doses of X-rays to the gastric region at a 3 day interval for a total of 20 Gy. At the termination of the experiment, 6 months after the alkaline phosphatase (ALP) positive foci in males was significantly higher than in females, in orchidectomized males or orchidectomized plus DES treated rats (P < 0.01). On the other hand, the incidence of intestinal metaplasia with ALP-positive foci in normal females appeared lower than in ovariectomized females (P < 0.01), and was increased in rats by treatment with testosterone or decreased by DES. Numbers of foci of intestinal metaplasias with Paneth cells and total numbers appeared to increase in males treated with DES. The results suggested a promoting role for testosterone in the development of ALP positive lesions and indicated considerable heterogeneity between intestinal metaplasia subtypes.

Alkaline Phosphatase↗
PubMed1995

Peutz-Jeghers syndrome with osseous metaplasia of the intestinal polyps.

A case of Peutz-Jeghers syndrome (PJS) with osseous metaplasia in three of 15 hamartomatous polyps of the small intestine is reported. At 35 years of age, the patient was diagnosed as having PJS by cutaneous pigmentation around the mouth and polyposis of the stomach, duodenum and intestine. Fifty-two polys of the large intestine were resected, which were characteristic of those of PJS. Three of them showed adenomatous and carcinomatous changes, but there was no osseous metaplasia in any of the resected polyps. At age 40, he had surgery under the diagnosis of intestinal obstruction. There were 15 polyps in the resected jejunum. These polyps were also characteristic of those of PJS. Additionally, three of these polyps were accompanied by osseous metaplasia. Histologically, mature bone formation and calcification were found close to the hyperplastic glands in the submucosa or in the propriate muscle. Malignant transformation was not observed. Osseous metaplasia is extremely rare in benign polyps, and it has not been reported in hamartomatous polyps of PJS to date. The knowledge of this association may be helpful in the clinical diagnosis of this benign lesion in PJS.

Adult↗
PubMed1983

The incidence and significance of vaginal metaplasia of the bladder trigone in adult women.

One hundred and six bladders were removed at autopsy from adult women dying of diseases unrelated to the urinary tract. A fixative solution had been introduced into the bladder as soon as possible after death. The naked-eye appearances were recorded before and after application of Lugol's iodine solution and the trigones then submitted to histological examination. Vaginal metaplasia of the trigone was present in the majority (72%) of bladders, a similar incidence being found in both pre-menopausal and post-menopausal age groups. Histological evidence of chronic inflammation was found significantly more frequently in bladders showing vaginal metaplasia and it is suggested that vaginal metaplasia is not a consequence of chronic inflammation but that its surface characteristics may predispose to chronic infection. Its purported hormonal aetiology does not explain all observed features. Prominent venous channels within the tunica propria around the urethral orifice were a constant feature in all bladders studied. Two of the 76 bladders showing vaginal metaplasia also displayed atypical hyperplasia of this squamous epithelium, a previously unrecorded observation. The possible implications of such atypical hyperplasia are briefly discussed.

Adult↗
PubMed2005

The interplay between Helicobacter pylori, gastro-oesophageal reflux disease, and intestinal metaplasia.

Helicobacter pylori infection and gastro-oesophageal reflux disease (GERD) account for most upper gastrointestinal pathologies with a wide spectrum of clinical manifestations. The interplay of both conditions is complex, in part intriguing, and has become a matter of debate because of conflicting results. The cardia is an area where both H pylori and abnormal GERD exert their damaging potential, inducing inflammation and its consequences, such as intestinal metaplasia. While the role of intestinal metaplasia within columnar lined epithelium (Barrett's oesophagus) in the context of GERD is well established as a risk for neoplasia development, the role of intestinal metaplasia at the cardia in the context of H pylori infection is unclear. A particular challenge is the distinction of intestinal metaplasia as a consequence of GERD or H pylori if both conditions are concomitant. Available data on this issue, including follow up of a small patient series, are presented, but more studies are required to shed light on this issue because they will help to identify those patients that need surveillance.

Barrett Esophagus↗
PubMed1989

Clinical importance of squamous metaplasia in invasive transitional cell carcinoma of the bladder.

One hundred cases of transitional cell carcinoma of the bladder were studied to determine whether squamous metaplasia and other histological features within the bladder can be of value in predicting outcome of treatment with radiotherapy. Sixty cases showed the changes of squamous metaplasia, and of this group 46 (78%) failed to respond to radiotherapy. A significant response rate of 90% was seen in the 40 tumours without squamous metaplasia. It is concluded that transitional cell carcinomas of the bladder showing squamous metaplasia are mainly resistant to radiotherapy and alternative treatment methods should be sought.

Adult↗
PubMed2003

Helicobacter pylori babA2, cagA, and s1 vacA genes work synergistically in causing intestinal metaplasia.

AIMS: To determine any associations between the Helicobacter pylori genes babA2, oipA, cagA and the s and m alleles of vacA. In addition, to verify whether these genes work synergistically or independently in causing gastritis, peptic ulcer, and intestinal metaplasia. METHODS: One hundred and sixty seven H pylori positive patients were studied (52 antral gastritis, 41 diffuse gastritis, 41 peptic ulcer, and 33 duodenitis). Helicobacter pylori virulence genes were amplified by means of the polymerase chain reaction. RESULTS: Significant associations were found between babA2 and the other H pylori genes studied. When considered singly, all the genes were associated with disease diagnosis, inflammation, and intestinal metaplasia. Four H pylori groups were defined. Group A: cagA-, s2m2, babA2-; group B: cagA+, s1m1, babA2+; group C: cagA+, s1m2, babA2+; group D: cagA+, s1m2, babA2-. Group A infecting strains were associated with less severe endoscopic and inflammatory conditions, whereas group B strains were associated with the worst endoscopic and inflammatory findings. Intestinal metaplasia was a rare finding in group A infected patients (< 10%), whereas it was frequent in those infected with group B strains (48%). CONCLUSIONS: The H pylori genes cagA, oipA "on", s1 and m1 vacA, and babA2 are associated with each other, possibly as a result of shared selective pressure. When coexpressed by the same H pylori strain, cagA, s1 and m1 vacA, and babA2 work synergistically in worsening inflammation. Infections caused by strains coexpressing cagA, s1m1 vacA, and babA2 are those at higher risk for intestinal metaplasia.

Adhesins, Bacterial↗
PubMed2004

Neutrophil elastase induces mucus cell metaplasia in mouse lung.

Goblet cell hyperplasia in the superficial airway epithelia is a signature pathological feature of chronic bronchitis and cystic fibrosis. In these chronic inflammatory airway diseases, neutrophil elastase (NE) is found in high concentrations in the epithelial lining fluid. NE has been reported to trigger mucin secretion and increase mucin gene expression in vitro. We hypothesized that chronic NE exposure to murine airways in vivo would induce goblet cell metaplasia. Human NE (50 microg) or PBS saline was aspirated intratracheally by male Balb/c (6 wk of age) mice on days 1, 4, and 7. On days 8, 11, and 14, lung tissues for histology and bronchoalveolar lavage (BAL) samples for cell counts and cytokine levels were obtained. NE induced Muc5ac mRNA and protein expression and goblet cell metaplasia on days 8, 11, and 14. These cellular changes were the result of proteolytic activity, since the addition of an elastase inhibitor, methoxysuccinyl Ala-Ala-Pro-Val chloromethylketone (AAPV-CMK), blocked NE-induced Muc5ac expression and goblet cell metaplasia. NE significantly increased keratinocyte-derived chemokine and IL-5 in BAL and increased lung tissue inflammation and BAL leukocyte counts. The addition of AAPV-CMK reduced these measures of inflammation to control levels. These experiments suggest that NE proteolytic activity initiates an inflammatory process leading to goblet cell metaplasia.

Actins↗
PubMed2005

Immunohistochemical analysis of morules in colonic neoplasms: morules are morphologically and qualitatively different from squamous metaplasia.

Morules develop in several neoplasms and have been considered as a type of squamous metaplasia despite the absence of keratinization and intercellular bridges. The objective of this study was to clarify the pathological significance of morules and to distinguish morules from squamous metaplasia in colonic neoplasms. Ten cases of morule-associated colonic neoplasms (4 adenocarcinomas, 1 adenoma with carcinoma in situ, and 5 adenomas), and 3 cases of squamous metaplasia in colonic adenocarcinoma were examined morphologically and immunohistochemically. Morules were well-defined structures composed of small, oval to short-spindled cells with bland nuclei, and frequently associated with intranuclear inclusions that were positive for biotin and biotin-binding enzymes (pyruvic acid carboxylase and propionyl CoA carboxylase). On immunohistochemical examination, morules characteristically showed nuclear overexpression of beta-catenin, cyclin D1 and p63, low Ki-67 labeling index (<1%), cytoplasmic overexpression of CD10, and no expression of cytokeratin 20. These molecules were useful for the differentiation of morules. Furthermore, p63 and 34betaE12 positivities in morules suggested that they have a basal/stem cell phenotype. Thus, morules were morphologically and qualitatively different from squamous metaplasia. We consider that morules in colonic neoplasms are cell clusters with a basal/stem cell phenotype, and have less proliferative and less invasive potential than other cancer cells.

Adenocarcinoma↗
PubMed1983

Human papillomavirus: detection of viral DNA sequences and evidence for molecular heterogeneity in metaplasias and dysplasias of the uterine cervix.

Colposcopic-directed biopsies of the uterine cervix from 22 patients were analyzed for the presence of human papillomavirus (HPV) DNA and structural antigens. 11 of the biopsies were classified microscopically as mild dysplasia, 3 as moderate dysplasia, 1 as severe dysplasia, and 7 as squamous metaplasia. Nonstringent hybridization with a bovine papillomavirus type 1 DNA probe and immunocytochemical analysis with an antiserum against papillomavirus genus-specific structural antigens were performed on all specimens. Of the 11 mild dysplasias, both HPV DNA and structural antigens were detected in 5, only HPV antigens in 3, only HPV DNA in 1, and neither DNA nor structural antigens in 2. Both HPV DNA and structural antigens were present in the 3 cases of moderate dysplasia. Only HPV DNA sequences were detected in the single case of severe dysplasia. HPV DNA was detected in 2 cases of squamous metaplasia. The 5 remaining cervical biopsies showing squamous metaplasia, tissue from 3 placentas, and 6 cervical carcinomas were negative for HPV DNA and structural antigens. Restriction enzyme cleavage patterns of HPV DNA in the dysplasias suggested that there are multiple virus types or subtypes associated with cervical dysplasia. Stringent hybridization with a HPV type 11 (HPV-11) probe revealed that only 1 of 10 dysplasias contained sequences with homology to the probe. Of the remaining 9 dysplasias, 5 contained HPV sequences detected under nonstringent hybridization. 2 of 4 squamous metaplasias contained viral sequences which hybridized to the HPV-11 probe as well as 1 of 6 cervical carcinomas.

Adolescent↗
PubMed1987

Immunoelectron microscopic study on the histogenesis of epidermoid metaplasia in respiratory epithelium.

To elucidate the histogenesis of epidermoid metaplasia with an immunoelectron microscopic method, we studied the localization of secretory component (SC), a differentiation marker of the epithelial cell, in human bronchial epithelium. In the area of normal epithelium, SC was synthesized by mucous cells, particularly by small mucous granule cells. It was also found with small mucous granules in both superficial columnar or cuboidal cells in the area of stratification and superficial, less flattened cells in the area of epidermoid metaplasia, but SC was not identified in polygonal cells under the superficial SC-positive cells in both of the above areas. These superficial cells containing SC and small mucous granules possessed increasing number of tonofilaments parallel with the degree of flattening of the surface cells. On the other hand, in the advanced epidermoid metaplasia, in which surface cells were composed of very flattened cells, SC and small mucous granules were not found in the bronchial epithelium. Tonofilaments increased in number in the cytoplasm parallel to morphologic changes from basal cells to outermost flattened cells, via polygonal cells. These findings suggest that small mucous granule cells containing SC could gradually change to flattened cells through a quantitative change of a cytoplasmic component, such as SC or tonofilaments, and constitute the superficial cells of initial epidermoid metaplasia, in which surface cells are composed of less flattened cells. Moreover, these findings suggested that basal cells play an important role in epidermoid differentiation.

Epidermis↗
PubMed1998

Expression of the Bcl-2 protein in nasal epithelia of F344/N rats during mucous cell metaplasia and remodeling.

Exposure to ozone induces mucous cell metaplasia in rat airway epithelia. During the regeneration process, apoptotic mechanisms may be responsible for eliminating metaplastic cells. Therefore, the present study investigated expression of Bcl-2, a regulator of apoptosis, in ozone-induced mucous cell metaplasias. Adjacent metaplastic mucous cells in nasal airway epithelia that were exposed to ozone were heterogeneous in their expression of Bcl-2; some cells expressed high levels, whereas others expressed low levels or no Bcl-2. On Western blot analysis, Bcl-2 was detected in protein extracts from nasal epithelia of rats exposed to 0.5 ppm ozone for 1 mo but not in control rats exposed to filtered air. The number of metaplastic mucous cells in transitional epithelia of rat nasal airways was increased from 0 to about 200 after 3 and 6 mo of exposure to ozone; only 0 to 10 metaplastic mucous cells remained after a recovery period of 13 wk in rats exposed to ozone for 3 mo. The number of mucous cells of the respiratory epithelium lining the midseptum did not change after ozone exposure or recovery. The percentage of Bcl-2-positive cells lining the midseptum increased from 7 to 14% after a 3- and 6-mo ozone exposure, respectively. In transitional epithelia of the lateral wall and the nasoturbinates and maxilloturbinates, 35 to 55% of cells were Bcl-2-positive after a 1-mo exposure and 10 to 18% after both a 3- and a 6-mo exposure to ozone. Bcl-2 reactivity decreased to 0 to 8% after a recovery period of 13 wk. These observations suggest that Bcl-2 plays a role in the development and resolution of mucous cell metaplasias. This model may be useful in uncovering the role of Bcl-2 during the development and maintenance of metaplastic mucous cells. Disregulation of Bcl-2 expression may be responsible for the sustained mucous cell metaplasia in asthmatics or may allow cells to accumulate and become more susceptible to transformation leading to neoplasia.

Animals↗