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PubMed2006

Differentiation of the gastric mucosa III. Animal models of oxyntic atrophy and metaplasia.

Gastric cancer in humans arises in the setting of oxyntic atrophy (parietal cell loss) and attendant hyperplastic and metaplastic lineage changes within the gastric mucosa. Helicobacter infection in mice and humans leads to spasmolytic polypeptide-expressing metaplasia (SPEM). In a number of mouse models, SPEM arises after oxyntic atrophy. In mice treated with the parietal cell toxic protonophore DMP-777, SPEM appears to arise from the transdifferentiation of chief cells. These results support the concept that intrinsic mucosal influences regulate and modulate the appearance of gastric metaplasia even in the absence of significant inflammation, whereas chronic inflammation is required for the further neoplastic transition.

Animals↗
PubMed2003

DNA synthesis and Bcl-2 expression during development of mucous cell metaplasia in airway epithelium of rats exposed to LPS.

Exposure of pulmonary airways to environmental toxins and allergens may cause proliferation of airway epithelial cells and mucous cell metaplasia (MCM); however, it is unclear to what extent proliferating cells differentiate into mucus-storing cells and contribute to MCM. Our previous studies demonstrated that Bcl-2, an inhibitor of apoptosis with cell cycle regulatory functions, is expressed in metaplastic mucous cells. The purpose of the present study was to investigate the number of metaplastic mucous cells that are derived from proliferating epithelial cells and whether Bcl-2 has a role in cell cycle entry in these cells. Rats were intratracheally instilled with 100 microg of LPS from Pseudomonas aeruginosa in 500 microl of saline, and proliferating airway cells were labeled with bromodeoxyuridine (BrdU) by implanting a subcutaneous osmotic pump 24 h before instillation. The volume of stored mucosubstance and the number of mucous cells were increased 10- and 3-fold, respectively, from 24-48 h after instillation. The number of total epithelial cells per millimeter of basal lamina increased, and the number of serous cells per millimeter of basal lamina decreased during this time. Approximately 50% of Alcian blue-periodic acid Schiff-stained mucous cells were labeled with BrdU at 48 h after instillation, suggesting that one-half of the secretory cells were derived from proliferating cells. Furthermore, 50% of the Bcl-2-positive mucous cells were BrdU negative and therefore derived from nonproliferating, preexisting cells. Our findings demonstrate that preexisting and proliferating cells differentiate into mucous cells and compose LPS-induced metaplasia and that Bcl-2 does not have cell cycle regulatory function in these cells.

Animals↗
PubMed2005

Hyperplastic gastric tumors with spasmolytic polypeptide-expressing metaplasia caused by tumor necrosis factor-alpha-dependent inflammation in cyclooxygenase-2/microsomal prostaglandin E synthase-1 transgenic mice.

We showed recently that Helicobacter infection induces expression of cyclooxygenase-2 and microsomal prostaglandin E synthase-1 in the mouse stomach, and that transgenic mice expressing both cyclooxygenase-2 and microsomal prostaglandin E synthase-1 (K19-C2mE mice) develop hyperplastic gastric tumors with inflammatory histopathology. To investigate possible roles of proinflammatory cytokines and acquired immunity in the gastric hyperplasia of K19-C2mE mice, we introduced knockout mutations for tumor necrosis factor-alpha (TNF-alpha; Tnf), interleukin-1 receptor-alpha chain (Il1r1), and Rag2 genes, respectively. Among the compound mutants, only the Tnf (-/-) K19-C2mE mice showed significant suppression of hyperplastic tumors with reduced cell proliferation. In contrast, tumorigenesis remained unaffected in either compound mutants of K19-C2mE containing Il1r1 or Rag2 mutation, indicating that neither interleukin-1beta signaling nor T cell/B cell response was required for the development of hyperplastic tumors. Importantly, spasmolytic polypeptide/trefoil factor 2-expressing metaplasia (SPEM) in the K19-C2mE stomach was also suppressed in the Tnf (-/-) K19-C2mE mice, indicating that TNF-alpha-dependent inflammation is responsible for SPEM development. Because gastric metaplasia to the SPEM lineage is considered as a preneoplastic lesion of gastric cancer, it is possible that inhibition of TNF-alpha-dependent inflammation, together with eradication of Helicobacter, can be an effective prevention strategy for gastric cancer.

Animals↗
PubMed2001

Clear cell adenocarcinoma of the male urethra in association with so-called nephrogenic metaplasia.

A clear cell adenocarcinoma of the urethra associated with so-called nephrogenic metaplasia occurring in a 57-year-old male patient is presented. Ten months following total urethrectomy, multiple pulmonary metastases had developed. The patient died 2.5 years after surgery. The possible histogenesis of clear cell adenocarcinoma of the lower urinary tract - reported to develop in the male urethra only in a very few cases - is reviewed briefly. We favor an origin from preexisting nephrogenic metaplasia as one of the possible histogenetic pathways.

Adenocarcinoma, Clear Cell↗
PubMed1994

Adenocarcinoma of the urachus showing extensive calcification and stromal osseous metaplasia.

We report a case of adenocarcinoma of the urachus showing extensive calcification and stromal osseous metaplasia, arising in the bladder dome of a 51-years-old man. The patient underwent partial cystectomy, including in block excision of the entire urachus and umbilicus, and remains well, free from symptoms after a 22-month follow-up period. Main pathologic and clinical characteristics of urachal calcified tumors are reviewed. To our knowledge, this is the first report in the English literature on urachal carcinoma showing both extensive scattered calcification and massive stromal osseous metaplasia.

Adenocarcinoma↗
PubMedDate not supplied

Endometrial hyperplasia with berrylike squamous metaplasia and pilomatrixomalike shadow cells. Report of an intriguing cytohistologic case.

BACKGROUND: The usefulness of endometrial cytology as a diagnostic method in asymptomatic women, especially in postmenopause, in the interpretation of composite pictures characterized by borderline features between atypical hyperplasia and well-differentiated adenocarcinoma, especially if associated metaplastic features are present, is somewhat controversial. CASE: An asymptomatic, 50-year-old, postmenopausal woman underwent a Pap smear and endometrial cytology for routine screening, disclosing three-dimensional, sometimes pseudopapillary groupings of hyperplastic endometrial glandular cells with focal atypia in direct continuity with large, squamoid cells of the keratinizing type and shadow cells. Histologic examination of endometrial tissue was advised, and two subsequent endometrial biopsies and hysteroscopic ablation were performed. The borderline character of the lesion (complex atypical hyperplasia vs. well-differentiated adenocarcinoma) with concomitant squamous metaplasia and pilomatrixomalike shadow cells prevented diagnostic agreement between several pathologists. CONCLUSION: Diagnostic cytology with direct endometrial sampling represents a valuable diagnostic screening tool for the differential diagnosis between normal and pathologic endometrium, a mucosal picture that deserves a subsequent (histologic) diagnostic procedure. In a few cases, as in the one presented above, even histologic examination, especially of so-called borderline lesions, reveals squamous or other types of metaplasia that can lead to interobserver discrepancies.

Adenocarcinoma↗
PubMedDate not supplied

Cystic lesion of the parotid gland with squamous metaplasia mistaken for squamous cell carcinoma. A case report.

BACKGROUND: The diverse range of diseases that affect the salivary glands may lead to problems and pitfalls in cyto-diagnosis. While false negative diagnosis of cystic salivary gland tumors is well known, false positive cytodiagnosis in nonneoplastic salivary cysts is less well documented. CASE: An 85-year-old female presented with a painless left parotid gland swelling of three months' duration. Fine needle aspiration cytology yielded fluid, smears of which showed keratinizing squamous cells with nuclear atypia leading to a cytologic diagnosis of cystic squamous cell carcinoma. A total radical parotidectomy followed. Histopathologic study showed cystic dilatation of many of the salivary ducts, which were lined with metaplastic squamous epithelium that showed atypia. There was no evidence of squamous cell carcinoma. CONCLUSION: Squamous metaplasia is known to occur in benign salivary gland lesions, such as pleomorphic adenoma and Warthin's tumors, as well as in salivary duct cysts and necrotizing sialometaplasia. However, atypical squamous metaplasia of salivary duct cysts mimicking squamous cell carcinoma on cytology is unusual.

Aged↗
PubMedDate not supplied

Apocrine carcinoma vs. apocrine metaplasia with atypia of the breast. Use of aspiration biopsy cytology.

OBJECTIVE: To solve the problem of diagnosing apocrine carcinoma (APCA) through distinguishing it from benign apocrine metaplasia with atypia (APMA). STUDY DESIGN: The study group consisted of five histologically confirmed cases of uncommon infiltrating apocrine carcinoma and a case of noninfiltrating apocrine carcinoma of the breast by aspiration biopsy cytology. The control group consisted of 103 cases of benign apocrine metaplasia with no atypia (APMN), 4 cases of APMA and 34 cases of common-type adenocarcinoma that were encountered in 662 breast aspirations from 1988 to 1992 at Hekinan Municipal Hospital. RESULTS: In APCA the average age of patients (65 +/- 17.7 SD)(mean +/- SD) was more than 20 years older than APMA, and APCA generally measured > or = 2 cm or more in diameter as compared to < or = 2 cm in APMA lesions. In APCA the apocrine cells had high cellularity, with the cells occur singly and with syncytia in the background. Numerous degenerated apocrine cells and characteristic cell detritus were found. APCA was also characterized by apocrine cells with more marked nuclear abnormalities, including hyperchromasia and irregular nuclear shape, frequently with irregular nucleoli; more nuclei measure > or = 12 micron in diameter than in APMA. These findings, however, were present only to a mild degree in APMA, if at all. APMA may coexist with APCA. CONCLUSION: If APMA is diagnosed, an open biopsy should be performed to distinguish it from APCA.

Adult↗
PubMed1992

Covalently linking a peptidyl carbamate elastase inhibitor to a hydrophilic polymer increases its effectiveness in preventing emphysema and secretory cell metaplasia in the hamster.

A peptidyl carbamate, p-nitrophenyl N-(succinyl-L-alanyl-L-alanyl-L-prolyl-methyl)-N-isopropylcarbamate++ + (PCI) was tested for its ability to inhibit the elastolytic activity of human neutrophil elastase (HNE) and to prevent HNE-induced emphysema and secretory cell metaplasia in the hamster. In vitro, 50% of the elastolytic activity of 10 micrograms of HNE was inhibited by 0.9 micrograms of PCI, a molar ratio of PCI to HNE of 4.5. Bronchoalveolar lavage of hamsters receiving PCI intratracheally showed a rapid decrease in HNE inhibitory activity (4 min for 50% decrease), suggesting rapid clearance, binding, or inactivation of the PCI. Instillation of 300 micrograms of HNE combined with 100, 500, or 3,000 micrograms PCI, a 16-, 83-, and 503-fold molar excess of PCI, respectively (molar ratios of 17, 84, and 504), suppressed HNE-induced lung hemorrhage, but it did not moderate HNE-induced emphysema despite the large molar excess of inhibitor. When PCI was covalently bound to a linear hydrophilic polymer of alpha,beta-poly[N(2-hydroxyethyl)-D,L-aspartamide], producing a polymer-bound carbamate inhibitor (PPCI) of HNE, the time for a 50% decrease of PPCI functional activity from the hamster lung lavage was 421 min. Instillation of 100 micrograms of PPCI 1 h before instillation of 300 micrograms HNE resulted in significant amelioration of emphysema; 900 micrograms of PPCI was required to obtain amelioration of bronchial secretory cell metaplasia. The larger dose of PPCI also provided significant amelioration of emphysema when the interval between PPCI and HNE administration was 8 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Effect of varying the time interval between intratracheal administration of eglin-c and human neutrophil elastase on prevention of emphysema and secretory cell metaplasia in hamsters. With observations on the fate of eglin-c and the effect of repeated instillations.

Eglin-c is a naturally occurring polypeptide of 70 amino acids with a molecular mass of 8,100 daltons. It is a strong inhibitor of human neutrophil elastase (HNE) and cathepsin-G, and, when given intratracheally to hamsters 1 h before human neutrophil elastase, it can prevent or ameliorate the emphysema produced by HNE. The present experiments were designed to determine the duration of the effectiveness of eglin-c, prepared by DNA technology from Escherichia coli, in preventing the emphysema and secretory cell metaplasia induced by HNE. Eglin-c (2,000 micrograms in 0.5 ml saline) was effective in ameliorating emphysema, as determined histologically and physiologically, when it was given intratracheally to hamsters 1, 2, 4, and 8 h before the intratracheal instillation of 300 micrograms of HNE. Eglin-c ameliorated bronchial secretory cell metaplasia when given 1 h before HNE but not when the time intervals were 2 h or longer. The clearance of [3H]eglin-c from the lungs was assessed. Four h after intratracheal instillation of 446 micrograms of [3H]eglin-c, 33% of the tritium was found in the lung tissue and bronchoalveolar lavage fluid; 83% of the radioactivity in the lavage fluid supernatant was associated with functionally active eglin-c. No evidence of bronchopulmonary toxicity was seen in hamsters given 4 intratracheal instillations of 2,000 micrograms of eglin-c at 1-wk intervals.

Animals↗
PubMed2001

Lipopolysaccharide Induces Mucus Cell Metaplasia in Mouse Lung.

A murine model of lipopolysaccharide (LPS)-induced airway inflammation and epithelial cell phenotypic change, and the time courses of these events are described. A single intratracheal instillation of Pseudomonas aeruginosa LPS in mice resulted in massive recruitment of neutrophils to the lung 2 d after treatment as assessed by differential cell counts of the inflammatory cells in bronchoalveolar lavage fluid and histologic assessment of hematoxylin and eosin (H&E)-stained lung sections. The LPS-induced neutrophilic inflammation subsided substantially on Day 4 and essentially vanished by Day 7. Airway epithelial mucus cells were not detected by Alcian blue periodic acid-Schiff staining until Day 4 after LPS treatment and became more abundant in number as well as in mucus content on Day 7. The expression of Muc5ac messenger RNA (mRNA) as well as glycoprotein was enhanced on Day 2, peaked on Day 4, and decreased on Day 7, whereas enhanced expression of mucin core 2 beta6 N-acetylglucosaminyltransferase (C2GnT)-M mRNA was not detected until Day 4 and peaked on Day 7. The expression of C2GnT-L mRNA in the lung, a marker for activated leukocytes as well as mucus cells, peaked on Day 2 and remained moderately high until Day 7. C2GnT-L mRNA expression in LPS-treated lung correlated with the presence of neutrophils and the appearance of mucus cells in the airway epithelium. We conclude that mucus cell metaplasia and hyperplasia can be generated in mouse lungs with a single intratracheal instillation of LPS. In addition, C2GnT-M may serve as a marker for mucus cells in mouse lung. This LPS-induced mucus cell metaplasia and hyperplasia model should be useful for the study of Pseudomonas-induced airway mucus hypersecretory diseases.

Animals↗
PubMed1977

Irreversible bronchial goblet cell metaplasia in hamsters with elastase-induced panacinar emphysema.

A single intratracheal instillation of pancreatic elastase in hamsters induces a lesion resembling human panacinar emphysema. This paper reports the occurrence of irreversible goblet cell metaplasia in the bronchial epithelium of hamsters similarly exposed to elastase. The goblet cell change was dose related; a dose of 0.1 mg/100 g body wt or less at 16 days, produced slight or moderate goblet cell metaplasia in fewer than half the animals, whereas 84% of animals treated with a dose between 0.2 and 0.5 mg/100 g body wt developed goblet cell metaplastic lesions, more than half of which were considered to be severe. The percentage of goblet cells in the epithelium of elastase-treated hamsters (32.5) was significantly higher (P less than 0.005) than that of unexposed (12.2) and saline-exposed controls (18.7). All hamsters examined 6 and 12 mo after elastase treatment showed the lesion. The pathogenesis of the changes is unclear but the possibility is raised that the bronchial changes may be due to disturbance of an endogenous protease-antiprotease system. The findings suggest the hypothesis that, under appropriate circumstances, a single pulmonary insult in man could lead to a permanent lung injury demonstrating the anatomic lesions of both chronic bronchitis and panacinar emphysema.

Animals↗
PubMed2005

Mixed gastric- and intestinal-type metaplasia is formed by cells with dual intestinal and gastric differentiation.

We have proposed to divide intestinal metaplasia (IM) into two categories, i.e., a mixed gastric and intestinal (GI) type, and a solely intestinal (I) type, based on the residual gastric phenotype cells. The GI-mixed-type IM can be identified by the presence of both cells with either gastric or intestinal phenotypes in a single gland. This study is conducted to elucidate whether cells in the GI-mixed-type IM glands can simultaneously present both gastric and intestinal phenotypes. MUC5AC, MUC2, CD10 and villin expressions were investigated in 20 samples from five gastric cancer cases, directly using either AlexaFluor 488- or 568-labeled specific monoclonal antibodies and observed by fluorescent microscopy and confocal laser-scanning microscopy. GI-mixed IM glands comprise a population expressing MUC5AC and MUC2, MUC5AC and villin, and MUC5AC and CD10. MUC2 and villin expressions were reciprocally increased with decreasing MUC5AC expression, while CD10 expression was limited to cells with only a residual MUC5AC expression or no expression. These results suggest that a heterogeneous cell population with both gastric and intestinal phenotypes would develop into a single intestinal phenotype, as reflected in the progression of intestinal metaplasia from GI-mixed-type- to I-type IM-type glands.

Animals↗
PubMed1985

Spontaneous vesicular and prostatic gland epithelial squamous metaplasia, hyperplasia, and keratinized nodule formation in rabbits.

Histopathology of the reproductive system of 76 young adult Dutch Belted and 22 young adult or adult male New Zealand White rabbits was conducted as part of fertility studies. Thirty-five (46%) of the Dutch Belted and 11 (50%) of the New Zealand White males had multifocal vesicular gland basal epithelial cell atypia and hyperplasia without metaplasia. The affected cells were taller with pale cytoplasm and a prominent basophilic nucleus longitudinally oriented and increased in number compared to more normal adjacent epithelium. Thirty-one (41%) of the Dutch Belted and 10 (45%) of the New Zealand White males showed one or more nodules of squamous metaplasia in the alveolar epithelial lining or seen occasionally within alveolar walls of the vesicular gland. The prostate was less commonly affected and none of the early cellular atypia or later cornification changes were seen. A few cornified nodules with mitotic figures resembled "carcinoma in situ," but the morphology and available biologic data supported the judgment that the lesion was benign, metaplastic, proliferative, and clinically silent.

Animals↗
PubMedDate not supplied

Goblet cell metaplasia in the pulmonary alveolar epithelium in a rat.

Spontaneous goblet cell metaplasia in the pulmonary alveolar epithelium in a 110-wk-old male Jcl:Wistar rat is described. The rat had a dark red spherical mass in the center of the left lobe of the lung. The mass consisted of distended alveoli and bronchioles filled with mucus and nonciliated epithelial cells with numerous goblet cells lining the alveoli on the periphery of the mass. The goblet cells produced Alcian blue- and high iron diamine-positive sulfated glycoprotein differing from the sialylated glycoprotein seen in the normal rat airway surface epithelium. To the best of this investigator's knowledge, this is the first report dealing with detailed morphological and histochemical features of goblet cell metaplasia in the pulmonary alveolar epithelium resulting in mass formation due to mucous production.

Animals↗
PubMed2006

Expression of histo-blood group antigens in bronchial squamous metaplasia.

The aim of the present study was to evaluate the expression of blood group antigens in squamous bronchial metaplasia in order to determine whether this factor could identify patients at risk of lung cancer. In total, 100 bronchial biopsies were included in the present study. The cases were classified according to the World Health Organization grading system. Immunohistochemical stains for histo-blood groups A and B, and reactivity tests to p53 and the cellular proliferation index were performed. A total of 56 (56%) patients belonged to blood group A. Among them, six (10.7%) patients who did not express antigen in squamous metaplasia, showed carcinoma at the moment of the biopsy (n = 3) or developed synchronous lung carcinoma (n = 3). A total of nine (9%) patients belonged to blood group B. Loss of antigenic expression was observed in five cases. All of them developed synchronous lung carcinoma. The patients with low- and high-grade dysplasia developed lung cancer in 71 and 100% of the cases, respectively. In conclusion, the findings of the present study suggest that the loss of histo-blood antigens expression is an event in the carcinogenesis of bronchial mucosa and it is usually associated with high-grade lesions and hyperproliferative activity.

ABO Blood-Group System↗
PubMed2001

Chondroid metaplasia in a fibroepithelial polyp of the tongue.

This report describes the development of chondroid metaplasia within a fibroepithelial polyp situated on the tongue. Although fibroepithelial polyps in this location are not unusual, chondroid metaplasia in such a lesion in this position has not, as far as the authors are aware, been described previously. The aetiology and the pathogenesis of the lesion are discussed.

Adult↗
PubMed2005

Evaluation of initial and deeper sections of esophageal biopsy specimens for detection of intestinal metaplasia.

There are wide variations in the preparation of histologic sections from endoscopic esophageal biopsy specimens. We evaluated serial step sections from 261 esophageal or gastroesophageal junction biopsies at 4 levels to determine the first level at which goblet cell metaplasia (GCM) was detected. Deeper step sections of 152 paraffin blocks also were obtained to determine whether additional sections are useful in detecting GCM not seen in initial levels. GCM was identified in 95.3% of blocks in 3 levels. GCM was seen at level 4 in 12 blocks (4.7%). In the blocks that did not reveal intestinal metaplasia in the initial 4 levels, deeper sections disclosed GCM in only 1 (0.8%) of 120 blocks. However, deeper sections revealed initially undetected GCM in 4 of 32 blocks from patients with a history of documented Barrett esophagus. We conclude that 4 levels of step sections are adequate in routine processing of esophageal biopsy specimens for demonstration of GCM. Deeper sections may be obtained for patients with known Barrett esophagus to better evaluate for dysplasia or find additional foci of GCM.

Biopsy↗