Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “METAPLASIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources
PubMed1985

Salivary gland components involved in the formation of squamous metaplasia.

Squamous metaplasia is not an uncommon feature of a number of salivary gland lesions. Arterial ligation of rat submandibular and sublingual salivary glands was used for study of the processes and cell types involved in the development of the squamous metaplasia that occurs in ischemic and infarcted portions of gland parenchyma 6 to 8 days following vessel ligation. Light and electron micrographs show that the principal portion of salivary gland tissue undergoing squamous metaplasia is the acinar-intercalated duct cell complex. Early stages of this process involve a gradual dedifferentiation of acinar cells and hyperplasia of acinar, duct luminal cells, and myoepithelium. Subsequently, both luminal and myoepithelial cells have increasing accumulation of tonofilaments and formation of desmosomes, and centrally located cells may undergo keratinization. Immunohistochemical staining of ischemic salivary gland tissue with developing squamous metaplasia was performed with the use of rabbit antisera to human epidermal and Mallory body cytokeratins. The two antisera gave complementary patterns in normal acini and ducts, with antibody to epidermal cytokeratin (ECK) staining only myoepithelial cells and antibody to Mallory body cytokeratin (MBCK) staining mainly luminal epithelial cells. In early phases of squamous metaplasia (6 days after ligation), antibody to ECK stained central and peripheral (myoepithelial) cells, but by 8 days after ligation only central cells were stained. At 6 days after ligation, a proportion of central cells in squamoid clusters stained with antibody to MBCK, and myoepithelial cells were unstained. By 8 days after arterial ligation, cell clusters exhibiting squamous metaplasia were completely unstained with antibody to MBCK, despite the presence ultrastructurally of numerous tonofilament bundles in both types of cells forming these clusters. The propensity for squamous alteration of acinar-intercalated duct complexes has important connotations for salivary gland tumors such as pleomorphic adenoma and mucoepidermoid carcinoma.

Animals↗
PubMed1979

Gastrin and enteroglucagon cells in human antra, with special reference to intestinal metaplasia.

In a consecutive material consisting of 24 stomachs resected due to adenocarcinoma, intestinal metaplasia occurred in 21. Gastrin-producing cells (G-cells) were found to be distributed in a sporadic manner in antra with intestinal metaplasia. Not a single G-cell could be demonstrated in areas with metaplasia, while in the nonmetaplastic areas the distribution of the G-cells corresponded to that of the middle part of the mucosa. This means, that an error can occur when determining the quantity of G-cells, and can explain the previous controversial results regarding the density of G-cells. Enteroglucagon containing cells (GLI-cells) on the contrary were demonstrated in areas with intestinal metaplasia in antra of 19 of the stomachs showing intestinal metaplasia but never in the nonmetaplastic mucosa. This indicated that metaplasia also includes the endocrine cells. The identification of the G-cells and the GLI-cells was carried out by means of indirect immunoperoxidase technique combined with alcian blue pH 2,6-PAS staining.

Adenocarcinoma↗
PubMed1987

Intestinal metaplasia of the stomach in Swedish and Japanese patients without ulcers or carcinoma.

A systematic analysis of the cellular components of intestinal metaplasia (i.e., goblet cells with or without brush border cells and Paneth cells) was performed in endoscopic gastric biopsies from 984 patients without gastric ulcer or carcinoma; 359 Swedish and 625 Japanese patients. The Japanese patients, matched for age and sex, had twice as much intestinal metaplasia as the Swedes. The frequency of goblet cells and columnar cells with brush (absorptive) border increased with increasing age in both ethnic groups. Complete intestinal metaplasia (i.e. the presence of at least two or all three cellular components) was twice as frequent in the Japanese. This may reflect differences in the environment (including food habits) of the gastric mucosa in the two populations. Structural mucosal changes (i.e. pseudo-villus formations) were found more than twice as often in the Japanese. Since pseudo-villus changes occurred as often as goblet cells and brush border cells in both groups, it is suggested that the above-mentioned mucosal structural change should be considered for inclusion among the histological criteria of intestinal metaplasia of the stomach. Incomplete intestinal metaplasia (i.e. the occurrence of goblet cells without the other cellular components) occurred in similar proportions in the two populations. The present findings support the theory that incomplete intestinal metaplasia may be a para- rather than a preneoplastic phenomenon.

Adult↗
PubMed1987

Incidence of squamous metaplasia in large bronchi of Japanese lungs: relation to pulmonary carcinomas of various subtypes.

The incidence of bronchial squamous metaplasia in Japanese lungs was investigated in order to clarify the significance of this lesion for the development of lung cancer of various histological subtypes. The bronchi of 104 and 32 lungs resected, respectively, for primary or metastatic tumors were step-sectioned and examined histologically. The incidence of squamous metaplasia was particularly high (83% of cases, 8-11% of sections) in male lungs bearing primary squamous or small cell carcinoma whereas it was low (43% of cases, 3% of sections) in lungs of both sexes with adenocarcinoma, the latter figures being about the same as those for lungs with secondary metastatic tumors. Although the overall incidence of lung squamous metaplasia in Japanese is much lower than in the U.S., the present data demonstrate a high level in association with squamous or small cell carcinoma, directly comparable to that of Americans. However, atypical metaplasia, or dysplasia, was encountered much less frequently than in the U.S. A topographical study of 7 minute or small squamous cell carcinomas revealed 3 to have adjacent and 2 to have nearby areas of squamous metaplasia. However, 2 cases were found to be completely free of squamous metaplastic lesion. Thus, squamous metaplasia may be associated with the development of squamous cell carcinoma but would appear not to be an obligatory step in the development of this neoplasm.

Bronchi↗
PubMed1987

[Squamous metaplasia of the gastric mucosa associated with an aberrant pancreas].

A squamous metaplasia was found in the superficial regenerative epithelium on the aberrant pancreas tissue (Heinrich type II), situated in the posterior wall of the antrum. The squamous epithelium was positively stained by keratin, according to the PAP method, and intestinal metaplasia also was found surrounding the squamous metaplasia. In this case, it was decided that the squamous metaplasia development was associated with the regenerative change of the superficial ulceration. Squamous metaplasia is extremely rare in the stomach, and thus it was difficult to consider that the adenosquamous cell carcinoma of the stomach had developed from the antecedent squamous metaplasia.

Choristoma↗
PubMed1978

The respiratory epithelium. III. Histogenesis of epidermoid metaplasia and carcinoma in situ in the human.

The histogenesis of epidermoid metaplasia and carcinoma in situ was analyzed in human bronchial epithelium. The conclusion is that epidermoid metaplasia and carcinoma in situ can result from conversion of mucous cells. This implies the direct transformation of one type of fully differentiated cell to another. The study therefore emphasizes the differentiation potentialities of the mucous cells that can divide and undergo goblet cell hyperplasia and epidermoid metaplasia. Epidermoid metaplasia is a common reaction to injury in the bronchus. In our series of cases it was especially frequent in patients without neoplastic disease who had undergone intratracheal intubation or tracheostomy and who had been maintained on a respirator in the Shock Trauma Unit, University of Maryland. Future studies will be required to distinguish the difference, if any, between epidermoid metaplasia destined to become malignant carcinoma and that which is not. One difference noted in this study was the absence of overt cornification in epidermoid metaplasia in patients without neoplastic disease.

Bronchi↗
PubMed1984

On the occurrence of carcinoembryonic antigen (CEA) in different types of intestinal metaplasia of the human stomach.

The occurrence and localization of CEA in mucosa of 15 gastric specimens removed because of adenocarcinoma and 12 gastric specimens removed because of benign ulcer were investigated. CEA occurred in nearly all foci of intestinal metaplasia of the "colonic type" characterized by the secretion of O-acetylated sialo-mucins. In intestinal metaplasia characterized by secretion of sulphomucin a few foci contained CEA. "Small intestinal type" metaplasia, characterized by secretion of non-sulphated acid mucins, and normal gastric epithelium did not contain CEA. These findings may explain some of the discrepancies of earlier published work on the CEA content of intestinal metaplasia. The correlation between CEA and intestinal metaplasia of the "colonic type", known to be associated with gastric adenocarcinoma, may identify a special type of intestinal metaplasia which could be important in the histogenesis of certain types of gastric carcinoma.

Adenocarcinoma↗
PubMed1994

Intestinal metaplasia, atrophic gastritis and stomach cancer: trends over time.

BACKGROUND: The pathogenetic association of chronic atrophic gastritis and intestinal metaplasia with gastric cancer implies that the trends seen in these disorders over time should be similar. Both should similarly decrease in incidence with time, and a time-related relationship should occur between the incidence of gastric cancer and the rate of development of atrophic gastritis in the stomach of Helicobacter pylori-infected subjects. AIMS AND METHODS: We reviewed some recent studies from Finland on the time trends seen in chronic gastritis, atrophic gastritis (and intestinal metaplasia) and gastric cancer over a period of 15 years (1977-1992). In addition, using results from earlier studies from Japan and Finland, we formed hypotheses on how the time-dependent evolution and extension of atrophic gastritis may accord with the occurrence of gastric cancer in the stomach. RESULTS: Our investigations showed that the incidence of gastric cancer and the prevalence of H. pylori-associated gastritis, atrophic gastritis and intestinal metaplasia have decreased similarly in outpatient series during the last 15 years. Correspondingly, gastric cancer, atrophic gastritis and intestinal metaplasia are cohort phenomena in the population, and the prevalence rate of atrophic gastritis is correlated with the cohort-specific incidence of gastric cancer; both are high in cohorts born near the beginning of the century but are quite low in those born in recent decades. Since antral and angular areas of the stomach are primary sites for gastric cancer tumours, the earlier investigations indicate that the time-dependent progression of gastritis in grade (development of atrophic gastritis and intestinal metaplasia) and extent (spreading of gastritis by pylorocardial extension) is well correlated with the rate and predisposition of gastric cancer tumours in the distal and angular stomach. CONCLUSIONS: We conclude that atrophic gastritis (or intestinal metaplasia) and gastric cancer are very much alike in time trends and in course. This parallelism favours suggestions that H. pylori-associated gastritis with atrophic and metaplastic sequelae (atrophic gastritis) contribute to the pathogenesis of gastric cancer.

Finland↗
PubMed1994

Dispersed and acinar forms of pancreatic metaplasia in human gastric mucosa.

Pancreatic acinar cell metaplasia of the gastric mucosa is a newly recognized entity. Its physiological relevance and association with other gastric pathological conditions remains to be elucidated. We studied morphology of pancreatic metaplasia of the gastric mucosa in 15 cases. Two morphological forms of pancreatic metaplasia were noticed: an acinar form and a diffuse form. The diffuse form is characterized by small foci of pancreatic metaplasia dispersed in the gastric mucosa without any separation from the surrounding gastric glands. The acinar form is characterized by acini of pancreatic metaplasia separated from the surrounding gastric mucosa by strands of connective tissue and single smooth muscle cells. Acinar form of pancreatic metaplasia seems to be spared by the chronic atrophic gastritis involving the neighboring gastric mucosa.

Adult↗
PubMed1997

Pancreatic metaplasia of the gastric mucosa in pediatric patients.

UNLABELLED: Antropyloric and intestinal-type metaplasia of gastric columnar epithelial cells occurs commonly in the setting of atrophic gastritis in both adults and pediatric patients. Pancreatic metaplasia of gastric mucosa, although less common, has been reported in a variety of clinical conditions in adult patients, but not in the pediatric population. OBJECTIVES: The aim of this retrospective review was to characterize the clinical and pathological findings in pediatric patients found to have histological and immunohistochemical evidence of pancreatic metaplasia of the gastric mucosa in biopsies taken at the time of upper endoscopy. METHODS: Patients with histological evidence of pancreatic metaplasia of the gastric mucosa were prospectively identified. Their individual medical records were then reviewed for presenting symptoms, pertinent laboratory data, gross findings on endoscopy, radiological features, diagnosis, and subsequent therapy. RESULTS: Of the six children (ages, 8-18 yr; mean, 13.0 yr), with pancreatic metaplasia of the gastric mucosa, two children each had gastroesophageal reflux disease and chronic abdominal pain, whereas one child had a duodenal ulcer and one child had nodular gastritis. Iron deficiency anemia was present in four of six patients; three of four patients with this finding presented with hematemesis. All biopsies were negative for Helicobacter pylori. CONCLUSIONS: Whereas pancreatic metaplasia of the gastric mucosa is strongly associated with chronic atrophic gastritis in adults, its occurrence in children who do not have atrophic gastritis raises the possibility that it may be a developmental phenomenon of gastric mucosal differentiation. The clinical significance of this finding remains to be determined; and its association with iron deficiency in children requires further study.

Abdominal Pain↗
PubMed1997

Effect of Helicobacter pylori eradication on intestinal metaplasia and gastric epithelium proliferation.

Gastric epithelial turnover increase in Helicobacter pylori infection has been demonstrated by interventional and non interventional methods for proliferating cell detection. We have observed a progressive hyperproliferation with the progression of Helicobacter pylori-induced mucosal lesions until the development of intestinal metaplasia. A similar result has been reported in other studies in the succession from normal mucosa to gastric carcinoma even if interventional techniques show less conspicuous differences in comparison to non interventional ones, which give an overestimated picture of proliferation. Later studies show that Helicobacter pylori-related hyperproliferation reverses after eradication. We have observed that this reversibility does not occur in areas of intestinal metaplasia, where the oncoprotein ras p21, involved in early gastric carcinogenesis, is expressed. This finding agrees with that demonstrating that hyperproliferation in intestinal metaplasia or gastric cancer is not affected by Helicobacter pylori. Other oncogenetic changes in intestinal metaplasia (i.e., p53 mutation) may further explain the persistently modified proliferative pattern of the epithelium. Recent studies suggest a lack of reversibility of intestinal metaplasia after Helicobacter pylori eradication, but this problem remains controversial. Our experience suggests that the persistence of the bacterium may increase the extent of this lesion. In conclusion the development of intestinal metaplasia is associated with an impaired regulation of gastric epithelial proliferation. Nevertheless, from the biological point of view, the progression towards carcinoma requires further DNA changes. Moreover, many questions need to be answered in order to establish clear guidelines for the clinical management.

Cell Division↗
PubMed1999

Identification of intestinal-type Barrett's metaplasia by using the intestine-specific protein villin and esophageal brush cytology.

Villin is an actin-binding cytoskeletal protein required for brush-border formation in the normal small intestinal and renal proximal tubule epithelium. Villin is a marker of cell differentiation in small intestinal and renal cell lineages, and recent studies have shown villin to be highly expressed in 100% of intestinal-type Barrett's metaplasias. This epithelium is the single greatest risk factor for developing esophageal adenocarcinoma and arises when the normal esophageal squamous epithelium is replaced by a small intestine-like columnar epithelium after damage by chronic gastroesophageal reflux. In intestinal-type Barrett's metaplasia, the villin protein exhibits a highly characteristic staining pattern in which strong apical, brush-border staining of columnar epithelial cells is observed. In this study, the ability to identify intestinal metaplastic cells by using this distinct villin staining pattern was examined in endoscopic esophageal brushings from patients with confirmed Barrett's metaplasia. Esophageal brushings from 81% (17 of 21) of patients with Barrett's metaplasia demonstrated individual columnar cells with the characteristic villin staining pattern, whereas all normal esophageal squamous cells, blood cells, and gastric columnar cells were negative for villin expression. Northern blot analysis demonstrated villin mRNA expression in Barrett's metaplasia but not in the normal squamous esophagus or gastric mucosa from the same patients. The combined use of villin immunohistochemical analysis and esophageal brush cytology may provide a simple and effective method of detecting intestinal-type Barrett's metaplasia in patients at higher risk for developing this epithelium, such as those experiencing chronic gastroesophageal reflux symptoms.

Barrett Esophagus↗
PubMed2006

An immunohistochemical study of morules in endometrioid lesions of the female genital tract: CD10 is a characteristic marker of morular metaplasia.

PURPOSE: To analyze immunohistochemically morules in endometrioid lesions to show that CD10 is a sensitive marker for morular metaplasia. EXPERIMENTAL DESIGN: Immunohistochemical analysis of 53 instances of morular metaplasia comprising 1 cyclic endometrium and 52 endometrioid lesions associated with focal glandular complexity corresponding to 9 polyps, 4 atypical polypoid adenomyomas, 24 complex endometrial hyperplasias (18 with and 6 without atypia), 12 grade 1 endometrioid adenocarcinomas in early clinical stages of both uterus and ovary, and three ovarian adenofibromas. Immunohistochemistry in paraffin sections was done for CD10, beta-catenin, estrogen and progesterone receptors, and cytokeratins 5-6, 7, 8, 13, 18, 19, 20, and 34beta-E12. RESULTS: Morules were negative for estrogen and progesterone receptors and had beta-catenin-positive nuclei. Cytokeratins 8, 18, 19 were positive; cytokeratins 7 and 20 were negative; and cytokeratins 5-6, 13, and 34beta-E12 were weakly positive. All cases revealed strongly positive membranous CD10 staining in morules, which was absent in glands. CD10 positivity allowed easy identification of morules at low power in various types of surgical specimens and in curettings. CD10 also highlighted early morular metaplasia in glandular epithelium. In cases associated with squamous, keratinizing metaplasia, CD10 discriminated between both types of metaplasia. CONCLUSIONS: CD10 staining represents a useful marker of morules in endometrioid neoplasms of the female genital tract, permitting identification of lesions usually associated with an attenuated malignancy. Considering the immunohistochemical and genetic similarities of morules in tumors of different organs, it is likely that this marker may be also useful to diagnose morular metaplasia in similar neoplasms of extragenital locations.

Adult↗
PubMed2000

Gastric metaplasia of the proximal esophagus associated with esophageal adenocarcinoma and Barrett's esophagus: what is the connection? Inlet patch revisited.

BACKGROUND/AIM: The inlet patch is an area of heterotopic gastric mucosa found in the proximal esophagus at the level of the upper esophageal sphincter. Limited data are available regarding this form of gastric metaplasia and its incidence, significance, and possible association with other esophageal diseases. We report our observations of such gastric metaplasias in patients with esophageal adenocarcinoma or Barrett's esophagus and high-grade dysplasia. METHODS: All patients having Barrett's esophagus and adenocarcinoma referred for photodynamic therapy were included in this study. The patients were prospectively evaluated endoscopically for the presence of gastric metaplasia of the proximal esophagus (salmon-colored area of a least 5 mm in diameter with cardia-type gastric metaplasia on biopsy). RESULTS: A total of 36 patients were included in this study: 11 patients with dysplastic Barrett's esophagus (8 males, mean age 79 years) and 25 adenocarcinoma patients (18 males, mean age 71 years). At endoscopy prior to photodynamic therapy, 11 patients (31%; 8 adenocarcinoma, 3 dysplastic Barrett's esophagus) were noted to have an area of gastric mucosa in the proximal esophagus. In each patient, there was at least 5 cm of normal squamous mucosa between gastric metaplasia and distal esophageal pathology. CONCLUSIONS: In this selected group of patients with high-grade dysplastic Barrett's esophagus or adenocarcinoma referred for photodynamic therapy, gastric metaplasia of the proximal esophagus was found in nearly one third. Prospective studies are under way to test more widely for this association and to determine whether this is a marker of disease severity and the result of similar pathogenetic mechanisms.

Adenocarcinoma↗
PubMed2002

Gastric atrophy and intestinal metaplasia changes 8 years after Helicobacter pylori eradication. A blind, randomised study.

BACKGROUND: Chronic atrophic gastritis and intestinal metaplasia are regarded as predisposing factors for gastric cancer associated with Helicobacter pylori infection, and their severity appears to influence gastric cancer risk. Our purpose was to determine the outcome of chronic gastritis after H. pylori eradication in a long-term follow-up. METHODS: Fifty-four consecutive patients with duodenal ulcer and H. pylori infection were enrolled in the study. Endoscopic examination with antral and corporal biopsy was done at baseline and yearly after conventional eradication therapy (omeprazole 40 mg b.i.d., amoxocyllin 1 g b.i.d and clarithromycin 500 mg b.i.d.). Gastritis, atrophy, and metaplasia were graded according to the updated Sydney System. RESULTS: Twenty-four patients were successfully treated; infection persisted in 14 and 16 dropped out (during the first 5 years of follow-up). Inflammation and mean neutrophil activity significantly decreased in patients in whom H. pylori was eradicated. Glandular atrophy improved in 2 and disappeared in 5/17 patients, whereas intestinal metaplasia improved in 3 and disappeared in 2/12. In the patients in whom H. pylori persisted, inflammatory infiltrate, atrophy and intestinal metaplasia had not significantly decreased during follow-up. In contrast, glandular atrophy worsened in 2 and developed in 5/7 patients. Similarly, intestinal metaplasia did not improve when present and developed in 5/13 cases. CONCLUSIONS: In a long-term follow-up, H. pylori eradication does not affect glandular atrophy, but it seems to prevent the development of precancerous lesions such as intestinal metaplasia.

Journal Article↗
PubMed1983

Morphological lesions of the pancreatic ducts. Significance of pyloric gland metaplasia in carcinogenesis of exocrine and endocrine pancreas.

Morphological lesions of the pancreatic ducts were studied in 113 control autopsy cases, and 84 cases of primary pancreatic carcinoma. The lesions were classified into pyloric gland metaplasia, focal pseudo-proliferation, goblet cell metaplasia, squamous metaplasia, and atypical proliferation. Diabetes mellitus or glycosuria, alcohol intake, and smoking do not seem to have any close associations with these lesions or pancreatic carcinoma. Pyloric-gland and squamous metaplasias were found at nearly comparable incidences both in control and carcinoma cases, but marked atypical proliferations, which were indistinguishable from carcinoma in situ or intraductal spreading of carcinoma, were more frequently observed in the carcinoma cases. Pyloric gland metaplasia was the most common among the various lesions, and considered to represent nonspecific change of the pancreatic duct. However, it was suggested that some of the metaplastic lesions might be transformed into atypical proliferations and further into carcinoma in situ. The expected latent period from the appearance of in situ lesion to overt pancreatic carcinoma may be a clue to early diagnosis and effective surgical treatment, but possible multiplicity of carcinoma in situ or intraductal spreading of carcinoma even at its early stage will burden further problems on its treatment. On rare occasions, argyrophil cells were found in the pyloric gland metaplasia, and its significance was discussed in relation to the genesis of Zollinger-Ellison tumor.

Adult↗
PubMed2024

The Protective Role of DDIT4 in Helicobacter pylori-induced Gastric Metaplasia Through Metabolic Regulation of Ferroptosis.

BACKGROUND & AIMS: Helicobacter pylori (H pylori) infection is a significant factor leading to gastric atrophy, metaplasia and cancer development. Here, we investigated the role of the stress response gene DDIT4 in the pathogenesis of H pylori infection. METHODS: Cell lines, transgenic mice, and human tissue samples were implemented. Proteomics were performed on Ddit4+/+ and Ddit4-/- mice infected with H pylori strain PMSS1. C57BL/6 mice were administered with tamoxifen to induce gastric metaplasia. Stomach tissues were analyzed for histopathologic features, reactive oxygen species, Fe2+, lipid peroxidation, expression of DDIT4, and ferroptosis-related proteins. RESULTS: DDIT4 expression was upregulated at 6 hours but significantly decreased at 24 hours in response to H pylori infection in gastric epithelial cells. Gastric DDIT4 were downregulated in INS-GAS mice at 4 months post H pylori infection. Notably, H pylori infection led to more severe gastric metaplasia lesion in Ddit4-knockout mice. The proteomic profiling revealed an increase in ferroptosis in the gastric tissues of infected Ddit4-deficient mice, compared with infected wild-type mice. Mechanistically, knockout of DDIT4 promoted H pylori-induced ferroptosis through the accumulation of lipid peroxides and ROS levels, and alterations in proteins such as GPX4, ALOX15, and HMOX1. Overexpression of DDIT4 counteracted H pylori-induced stem cell marker CD44V9 through modulation of ferroptosis. Similarly, in another mouse model of gastric metaplasia treated with tamoxifen, as well as in human GIM tissues, we observed the loss of DDIT4 and induction of ferroptosis. CONCLUSIONS: Our results indicate that DDIT4 serves as a protective factor against H pylori-induced gastric metaplasia by metabolic resistance to ferroptosis.

Ferroptosis↗
PubMed1994

Is Barrett's metaplasia the source of adenocarcinomas of the cardia?

OBJECTIVE: To investigate the prevalence of Barrett's esophagus in patients with adenocarcinomas located at the gastroesophageal junction. DESIGN: A case series of patients who underwent esophagogastrectomy for adenocarcinoma was retrospectively reviewed. Tumors were grouped by location as esophageal, cardiac, and subcardiac, and the prevalence of specialized intestinal metaplasia in the histological specimens was determined. SETTING: A university department of surgery that specializes in esophageal diseases. PATIENTS: One hundred patients with adenocarcinoma of the esophagus, cardia, or proximal stomach. MAIN OUTCOME: Cardiac adenocarcinomas were associated with Barrett's esophagus in 42% of the patients. RESULTS: Specialized intestinal metaplasia was identified in the histological sections from the resected specimen in 42% (13/31) of cardiac adenocarcinomas and in 79% (38/48) of esophageal adenocarcinomas but in only 5% (1/21) of subcardiac adenocarcinomas. The preoperative endoscopic biopsy results concurred with the final diagnosis of Barrett's esophagus in 33 of the 38 esophageal tumors, six of the 13 cardiac tumors, and the one subcardiac tumor but failed to detect specialized intestinal metaplasia in 54% (7/13) of cardiac tumors. Cardiac tumors were associated with shorter lengths of Barrett's mucosa than esophageal tumors (2.7 +/- 1.8 cm vs 7.4 +/- 3.4 cm, P < .01). The Barrett's metaplasia was dysplastic in 36 of the 38 esophageal tumors, 10 of the 13 cardiac tumors, but not in the subcardiac tumor. CONCLUSIONS: Adenocarcinomas located at the gastroesophageal junction were associated with Barrett's metaplasia in nearly one half of the patients. The length of the Barrett segment tends to be short and may be missed during endoscopy. The presence of high-grade dysplasia within Barrett's mucosa supports a barrett's origin for half of the adenocarcinomas arising at this location.

Adenocarcinoma↗