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At least 631 records · Page 35Linked to original sources
PubMed2000

Basal cell adenocarcinoma of the palate with squamous metaplasia.

Basal cell adenocarcinoma is a rare salivary gland tumour, especially in minor glands. The clinical, histological, and immunohistochemical features of a case involving the palate are described. Formalin fixed, paraffin embedded sections of the tumour were examined in haematoxylin and eosin (H&E) sections and also using immunostaining for cytokeratins 7, 8, 13, 14, 18, 19, vimentin, muscle specific actin (HHF35), and laminin. H&E sections showed that the tumour was composed mainly of basaloid cells and a striking feature was the presence of squamous metaplasia. Neural invasion was also conspicuous. Immunohistochemical reactions indicated that cytokeratin 14 was expressed by all tumour cells and vimentin by all cells except those in the areas of squamous metaplasia. The remaining cytokeratins and actin were present in some of the tumour cells, while laminin showed discreet positivity around cell arrangements. The foci of squamous metaplasia and the immunohistochemical findings are helpful in distinguishing basal cell adenocarcinoma from other salivary gland tumours which show basaloid cells.

Adenocarcinoma↗
PubMed2004

Effects of matrix metalloproteinase inhibitor on LPS-induced goblet cell metaplasia.

Bacterial infections of the lung are known to induce inflammatory responses, which lead to mucus hypersecretion. Moreover, mucin synthesis in the airways has been reported to be regulated by neutrophilic inflammation-induced epidermal growth factor receptor (EGFR) expression and its activation. Furthermore, matrix metalloproteinases (MMPs), especially MMP-9, have been reported to promote the transmigration of activated neutrophils. In this study, we investigated the associations between lipopolysaccharide (LPS)-induced goblet cell (GC) metaplasia and EGFR expression and the effects of MMP inhibitor (MMPI). Various concentrations of LPS were instilled into the tracheas of pathogen-free Sprague-Dawley rats, and airways were examined at different times after LPS instillation. To examine the role of MMP-9, we treated rats 3 days before LPS instillation and daily thereafter with MMPI. Neutrophilic infiltration, Alcian blue/periodic acid-Schiff (AB/PAS) staining, and immunohistochemical staining for MUC5AC, EGFR, and MMP-9 were performed. The instillation of LPS increased AB/PAS and MUC5AC staining in time- and dose-dependent manners, and treatment with MMPI significantly prevented GC metaplasia. The instillation of LPS into the trachea also induced neutrophilic infiltration and EGFR and MMP-9 expression in the airway epithelium, and MMPI was found to significantly prevent neutrophil recruitment, GC metaplasia, and EGFR and MMP-9 expression. This study demonstrates that the MMP-9 and EGFR cascades are associated with LPS-induced mucus hypersecretion.

Animals↗
PubMed2000

Agarose plug instillation causes goblet cell metaplasia by activating EGF receptors in rat airways.

We hypothesized that foreign bodies in airways cause inflammation leading to goblet cell metaplasia. Instilled agarose plugs lodged in the bronchi of pathogen-free rats caused a time-dependent increase in Alcian blue-periodic acid-Schiff staining that was detected within 24 h and markedly increased at 72 h. Control bronchi contained no pregoblet or goblet cells, but plugged bronchi contained many pregoblet and goblet cells and a decrease in nongranulated secretory cells. In situ hybridization showed no expression of MUC5AC in control airways, but plugged airways showed a marked expression. Control bronchi showed sparse staining for epidermal growth factor receptor (EGFR) protein, but plugged bronchi showed intense EGFR staining in the epithelium. Pretreatment with an EGFR tyrosine kinase inhibitor (BIBX1522) prevented Alcian blue-periodic acid-Schiff staining and MUC5AC gene expression in plugged bronchi. Pretreatment with tumor necrosis factor-alpha neutralizing antibody or pretreatment with cyclophosphamide abolished plug-induced EGFR protein expression and goblet cell metaplasia. Thus instillation of agarose plugs induces profound goblet cell metaplasia by causing EGFR expression and activation.

Animals↗
PubMed2001

PAF mediates cigarette smoke-induced goblet cell metaplasia in guinea pig airways.

Goblet cell metaplasia is an important morphological feature in the airways of patients with chronic airway diseases; however, the precise mechanisms that cause this feature are unknown. We investigated the role of endogenous platelet-activating factor (PAF) in airway goblet cell metaplasia induced by cigarette smoke in vivo. Guinea pigs were exposed repeatedly to cigarette smoke for 14 consecutive days. The number of goblet cells in each trachea was determined with Alcian blue-periodic acid-Schiff staining. Differential cell counts and PAF levels in bronchoalveolar lavage fluid were also evaluated. Cigarette smoke exposure significantly increased the number of goblet cells. Eosinophils, neutrophils, and PAF levels in bronchoalveolar lavage fluid were also significantly increased after cigarette smoke. Treatment with a specific PAF receptor antagonist, E-6123, significantly attenuated the increases in the number of airway goblet cells, eosinophils, and neutrophils observed after cigarette smoke exposure. These results suggest that endogenous PAF may play a key role in goblet cell metaplasia induced by cigarette smoke and that potential roles exist for inhibitors of PAF receptor in the treatment of hypersecretory airway diseases.

Animals↗
PubMed2006

Nonsteroidal anti-inflammatory drugs and the esophageal inflammation-metaplasia-adenocarcinoma sequence.

Observational studies suggest that nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the risk of esophageal adenocarcinoma, but it is not known at what stage they may act in the esophageal inflammation-metaplasia-adenocarcinoma sequence. In an all-Ireland case-control study, we investigated the relationship between the use of NSAIDs and risk of reflux esophagitis, Barrett's esophagus, and esophageal adenocarcinoma. Patients with esophageal adenocarcinoma, long-segment Barrett's esophagus and population controls were recruited from throughout Ireland. Esophagitis patients were recruited from Northern Ireland only. Data were collected on known and potential risk factors for esophageal adenocarcinoma and on the use of NSAIDs, including aspirin, at least 1 year before interview. Associations between use of NSAIDs and the stages of the esophageal inflammation-metaplasia-adenocarcinoma sequence were estimated by multiple logistic regression. In total, 230 reflux esophagitis, 224 Barrett's esophagus, and 227 esophageal adenocarcinoma and 260 population controls were recruited. Use of aspirin and NSAIDs was associated with a reduced risk of Barrett's esophagus [odds ratio [OR; 95% confidence interval (95% CI)], 0.53 (0.31-0.90) and 0.40 (0.19-0.81), respectively] and esophageal adenocarcinoma [OR (95% CI), 0.57 (0.36-0.93) and 0.58 (0.31-1.08), respectively]. Barrett's esophagus and esophageal adenocarcinoma patients were less likely than controls to have used NSAIDs. Selection or recall bias may explain these results and the results of previous observational studies indicating a protective effect of NSAIDs against esophageal adenocarcinoma. If NSAIDs have a true protective effect on the esophageal inflammation-metaplasia-adenocarcinoma sequence, they may act early in the sequence.

Acetaminophen↗
PubMed2004

Liver-type fatty acid-binding protein is highly expressed in intestinal metaplasia and in a subset of carcinomas of the stomach without association with the fatty acid synthase status in the carcinoma.

OBJECTIVE: To investigate the relation of liver-type fatty-acid-binding protein (L-FABP) expression to the clinicopathological characteristics or the fatty acid synthase status of gastric cancers. METHODS: L-FABP expression was examined immunohistochemically in 667 gastric cancers, 60 gastric adenomas, and non-neoplastic epithelium contiguous with cancer tissue including normal foveolae, intestinal metaplasia, regenerative epithelium, and gastric glands. RESULTS: L-FABP was positive in 38% (high in 9% and low in 29%) of gastric cancers. It occurred preferentially in papillary carcinomas, female cases, and in patients under 50 years. In gastric cancers, L-FABP expression had no intimate correlation with the FAS status, and it showed no relationship with prognosis and cancer progression as indicated by venous and lymphatic permeation, and nodal or hepatic metastasis. Gastric tubular adenomas mainly revealed low (22%) expression of L-FABP while intestinal metaplasia showed the most frequent (>95%) and intense L-FABP expression. Normal foveolae and gastric glands showed no or less L-FABP expression. CONCLUSIONS: L-FABP is highly and intensely expressed in metaplasia and in a subset of gastric adenocarcinomas, without association with progression, prognosis and fatty acid synthase status of the carcinoma.

Adenocarcinoma↗
PubMed2006

Bladder squamous metaplasia of the urothelium - introductory report.

Seven female patients hospitalized in the Surgery Ward of Warsaw's Hospital for Children are described. Nonspecific abdominal pains, recurrent urinary tract infections, and voiding disorders (difficulty in voiding commencement) were the primary causes of hospitalization. Urodynamics and cystoscopy with a histopathology section of the urothelium achieved the diagnosis of nonkeratizing squamous cell metaplasia of the urothelium. The topic is not new, although the diagnosis is particularly rare in the pediatric patient. Until now, the existing world literature has described only a few cases of this kind of metaplasia in children. These findings may be helpful in differential diagnosis of urinary bladder disease. It is postulated that nonkeratizing squamous cell metaplasia of the urothelium, in the future, may lead to malignant changes in the urothelium. Therefore, the therapeutic process merits close monitoring.

Adolescent↗
PubMed1992

The relationship between large airway and alveolar space inflammation and airway metaplasia.

Bronchoscopy and bronchoalveolar lavage (BAL) yield important information about the lower respiratory tract of subjects who have been exposed to asbestos. Evidence of metaplasia is easily detected with random biopsies in large airways and a relationship with smoking status can be found. A significant finding, however, is that inflammatory cells recovered by late BAL aliquots which presumably reflect alveolar space inflammation are also importantly associated with the presence of metaplasia. Asbestos provides an important stimulus for recruitment of inflammatory cells. These cells release oxidants which can be responsible for direct or indirect mutagenesis. Our data suggest that this inflammatory cell recruitment may be an important additional factor predictive of airway metaplasia and perhaps subsequent carcinogenesis.

Asbestosis↗
PubMedDate not supplied

Apocrine metaplasia in gynecomastia by fine needle aspiration as a possible indicator of anabolic steroid use. A report of two cases.

BACKGROUND: The fine needle aspiration finding of apocrine metaplasia in association with the usual cytologic findings of gynecomastia is distinctly unusual. Previous reports do not mention any historical clinical association. CASES: Two otherwise healthy adult males presented for fine needle aspiration (FNA) of new-onset breast masses. Both showed apocrine metaplasia associated with the typical clinical and cytologic features of gynecomastia on FNA. Additional questioning revealed that both patients reported recent anabolic steroid use as part of their body-building routines. CONCLUSION: The fine needle aspiration finding of apocrine metaplasia in association with the usual cytologic and clinical findings of gynecomastia in otherwise healthy adult males without a medication history may be an indicator of illicit anabolic steroid use. Anabolic steroid use often has serious consequences, so its possibility should prompt further evaluation by the patient's clinician.

Adult↗
PubMed1977

Experimental canine tracheal grafts with reversible squamous metaplasia.

A technique for making bistomal tracheal pedicle grafts in dogs is described. The grafts were placed subcutaneously in the neck, and their mucosa was readily accessible to serial manipulations, endoscopic examinations, and biopsies, without requiring anesthesia. Squamous metaplasia developed in 5 of 8 grafts, or 63 per cent, within 1 week. Within 12 weeks, squamous metaplasia was seen in all grafts, and it was consistently accompanied by basal hyperplasia. After orthotopic reimplantation of the grafts, the squamous metaplasia proved to be reversible within 4 weeks. The preparation used for making these observations is a valuable research tool for sequential studies of the respiratory tract mucosa.

Animals↗
PubMed1984

Emphysema and bronchial secretory cell metaplasia induced in hamsters by human neutrophil products.

Purified human neutrophil elastase (HNE) and a crude extract of human neutrophils (EXT) were administered intratracheally to hamsters, and their effects were determined 21 and 56 days later by measurement of lung statics and dynamics and by light microscopy and morphometry of the lungs. A dose of 450 micrograms of HNE (HNE 450) produced focal emphysema of moderate severity. The combination of HNE 450 and EXT (HNE 450 + EXT) produced no more severe emphysema than HNE 450 alone; EXT alone did not produce emphysema. The HNE 450, HNE 450 + EXT, and EXT all produced persistent secretory cell metaplasia in large intrapulmonary airways. In a second experiment, 40 micrograms of HNE (elastolytic activity equivalent to that in EXT), designated HNE 40, did not produce secretory cell metaplasia. Neither EXT nor EXT treated with the elastase inhibitor suc-ala-ala-pro-val chloromethyl ketone (EXT + CMK), which had a residual elastolytic activity equivalent to 15 micrograms of HNE, produced emphysema; both preparations caused bronchial secretory cell metaplasia 21 days after treatment. Values of maximal expiratory flow, measured 21 days after treatment, were reduced at points between 20 and 50% of vital capacity for HNE 450 and between 30 and 80% of vital capacity for HNE 450 + EXT; maximal expiratory flows were not significantly different from saline controls for HNE 40, EXT, or EXT + CMK.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Interleukin-9 induces mucous cell metaplasia independent of inflammation.

Interleukin-9 (IL-9) has been strongly implicated in the pathogenesis of asthma, including the overproduction of mucus, in humans and in animal models. We evaluated the inflammatory changes associated with the upregulation of mucus production by examining the time course of inflammation after daily intratracheal IL-9 administration to naive C57Bl6 mice for 9 d. IL-9 induced an asthmatic phenotype, which in general took several days to develop, as assessed by the measurement of airway hyperresponsiveness, pulmonary inflammation, and serum immunoglobulin E. However, within 24 h of a single dose of IL-9, muc5ac mRNA upregulation occurred, and increased numbers of periodic acid Schiff/Alcian blue-positive mucous cells appeared. This response occurred before the development of an inflammatory cell influx and was the result of epithelial metaplasia. It seemed that IL-9 evoked mucous cell metaplasia independent of IL-13 because mRNA tissue evaluation indicated that muc5ac upregulation preceded any increase in IL-13 mRNA expression or detectable levels of IL-13 in the brochoalveolar lavage fluid. Therefore, the upregulation of IL-13 by IL-9 may be responsible for the amplification of mucus production but is not required for its initiation. IL-9 seems to directly stimulate mucous cell metaplasia without the requirement of inflammatory cell influx.

Animals↗
PubMed2002

Matrix metalloproteinase-7 is expressed by pancreatic cancer precursors and regulates acinar-to-ductal metaplasia in exocrine pancreas.

In gastrointestinal epithelium, metaplastic conversion between predominant cell types is associated with an increased risk of neoplasia. However, the mechanisms regulating metaplastic transitions in adult epithelia are largely undefined. Here we show that matrix metalloproteinase-7 (MMP-7) is expressed not only in the majority of human pancreatic ductal adenocarcinoma specimens, but also in human pancreatic intraepithelial neoplasia and metaplastic duct lesions in human and mouse. In a mouse model of pancreatic acinar-to-ductal metaplasia, MMP-7 progressively accumulates during the metaplastic transition, resulting in a concomitant increase in solubilization of Fas ligand (FasL). Under identical conditions, mice either deficient in MMP-7 or carrying an inactive FasL gene are severely inhibited in development of progressive metaplasia and acinar cell apoptosis. Thus, MMP-7 and FasL influence the initiation and maintenance of metaplastic events in pancreatic epithelium, explaining the observed link between metaplasia and apoptosis in pancreas and other gastrointestinal tissues.

Animals↗
PubMedDate not supplied

Experimental induction of squamous metaplasia in the dog trachea with cuffed endotracheal tubes.

Clinical reports cite the development of squamous metaplasia in tracheas following tracheostomy, laryngectomy, and cuffed intubation. The purpose of this study was (1) to develop an experimental model using the dog trachea and study the effects of prolonged cuffed intubation and (2) to determine whether squamous metaplasia is produced by prolonged contact of the endotracheal cuff with the tracheal mucosa. Modifications of widely used high-volume, low-pressure 8-mm endotracheal tubes were made with the distal portion of the tube, its cuff, and the inflating catheter attached. This model formed an implantable cuffed tube approximately 8 cm in length. The dogs remained intubated for 14 days, at which time they were killed; seven animals were available for histologic study. Varying degrees of squamous metaplasia were produced in all animals.

Animals↗
PubMed1983

Gastric epithelial dysplasia and sulphomucin-type intestinal metaplasia.

The HID-AB histologic staining technique, which distinguishes sulphomucin from sialomucin types of intestinal metaplasia, was employed in endoscopic gastric mucosal biopsies to evaluate their frequency of association with epithelial dysplasia. Sulphomucin-type intestinal metaplasia was found in 33% of the cases under observation; moderate or severe dysplasia was only associated with this type of intestinal metaplasia. Its precancerous significance can be ascertained only by means of prospective studies.

Adult↗
PubMed1984

Neoplastic colonic polyp with extensive squamous metaplasia. Case report.

Extensive squamous metaplasia in neoplastic colonic polyps is rare. This paper describes extensive squamous metaplasia in an adenomatous polyp evolving into adenocarcinoma. The origin of squamous cell carcinoma and adenocanthoma of the colon is not well understood. This case is the only case reported in the literature that demonstrates the development of squamous metaplasia in dysplastic colonic glands, in situ adenocarcinoma, and finally invasive adenocarcinoma of the colon. The pertinent literature is reviewed.

Adenocarcinoma↗
PubMed2004

Gastric metaplasia and small bowel ulcerogenesis in a case of ulcerative jejunitis not related to celiac disease.

The possible relationship between gastric metaplasia and ulcerative lesions in an unusual case of ulcerative jejunitis not related to celiac disease and with extensive gastric metaplasia is discussed. Previous studies have described gastric metaplasia in duodenal ulcers on the basis of endoscopic data, and some authors maintain that acid secretion in metaplastic mucosa could represent a pathogenetic factor of ulcerogenesis, with a self-amplifying mechanism. In the absence of functional evidence, we could provide data, in a case of ulcerative jejunitis, about morphologic signs of acid secretion in gastric metaplastic epithelium using an antibody against HMFG-1, a good marker of acid-secreting fundic cells. Metaplastic areas demonstrated a focal positivity for HMFG-1, and these finding are suggestive of local acid secretion.

Aged↗