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At least 649 records · Page 36Linked to original sources
PubMed2003

Biopsy of the conjunctiva in dry eye patients establishes a correlation between squamous metaplasia and dry eye clinical severity.

PURPOSE: The aim of this work was to evaluate the different grades of squamous metaplasia of the conjunctiva during the clinical course of dry eye syndrome, detecting the most characteristic morphological and morphometric changes by biopsy in order to provide a diagnostic classification. METHODS: The conjunctiva was studied under light microscopy by conventional histological methods and by morphometric analysis in 165 patients and in 33 controls. Patients were classified according to the Schirmer 1 test, break-up time, rose Bengal staining, osmolarity and impression cytology. The epithelium and connective tissue, with their different cells and other structures, were studied. RESULTS: The conjunctiva in dry eye patients showed progressive stratification, hyperplasia, hypertrophy and cellular flattening, with loss of goblet cell density and mucous layer. We found five pathological grades of squamous metaplasia and one normal grade. Clear nuclear alterations (indentation and binucleation) were found in the early grades of dry eye syndrome, but pyknotic nuclei and anucleated cells were only seen in the most severe grades. The smallest epithelial cells were found in the control group and their size increased with the severity of the dry eye syndrome. From the earliest stages to the most severe cases, increases in cellular separation were observed. There was also an increase in the number of inflammatory cells. Blood and lymphatic vessels showed alterations only in the most severe cases. CONCLUSIONS: This is the first grading system proposed for biopsy evaluation of the ocular surface in dry eye patients. These morphological and morphometric studies alone were able, even in the earliest phases of dry eye, to detect the squamous metaplasia that progresses from the surface of the epithelium to the connective tissue. This degenerative or adaptative cellular process was characterized mainly by marked increases in the stratification, epithelial cellular size and a general loss of goblet cells.

Biopsy↗
PubMed2004

An immunophenotypic comparison of metanephric metaplasia of Bowman capsular epithelium with metanephric adenoma, Wilms tumor, and renal development: a case report and review of the literature.

Metanephric metaplasia of the parietal epithelium of the Bowman capsule is a rare pathologic finding of unknown pathogenesis that has occurred in patients with widespread malignant neoplasms of various types. We report this finding in a 25-year-old woman with partial expression of the Carney triad who died of a disseminated gastrointestinal stromal tumor, specifically a gastric stromal sarcoma. The metaplasia involved both kidneys diffusely. It originated in the parietal epithelium of the Bowman capsule, extended into the proximal tubules, and focally surrounded the glomeruli in a semicircular manner Immunohistochemical analysis revealed that the cells of metanephric metaplasia expressed the Wilms tumor gene product, bcl-2 protein, and CD57 and cytokeratin 7 and keratin AE1/AE3 focally, but not CD56. This immunophenotype parallels that of metanephric adenoma, Wilms tumor, and nephrogenic rests and overlaps with antigen expression in certain periods of renal development.

Adenoma↗
PubMed2000

Gastritis and intestinal metaplasia in Syrian hamsters infected with Helicobacter aurati and two other microaerobes.

Chronic gastritis and intestinal metaplasia associated with naturally occurring colonization by Helicobacter aurati and two other microaerobic species were observed in Syrian hamsters. Thirty-five hamsters, between 7 and 12 months of age, were evaluated from two research and three commercial facilities. Microaerobic bacteria were cultured from the hamster stomachs. These bacteria included H. aurati, a fusiform, urease-positive species; a second novel helical, urease-negative Helicobacter sp.; as well as a smaller, urease-negative Campylobacter sp. Southern blot analysis detected Helicobacter spp. DNA in the gastric tissues of all 35 hamsters; 15 hamsters also had Campylobacter sp. DNA in their gastric tissues. When examined by light microscopy, argyrophilic bacteria consistent with H. aurati or the second Helicobacter sp. were present in antral sections of 12 out of the 15 hamsters where bacteria were seen, while 9 out of the 15 hamsters had bacteria resembling the Campylobacter sp. The presence of Helicobacter spp. but not the presence of Campylobacter sp. was significantly correlated to gastritis severity (P < 0.0001 for Helicobacter spp., P = 0.6025 for Campylobacter sp.) and intestinal metaplasia, as measured by numbers of goblet cells (P = 0.0239 for Helicobacter spp., P = 0.5525 for Campylobacter sp.). Severely affected hamsters also had Giardia sp. within their metaplastic gastric pits. Hamsters with naturally occurring helicobacter-associated gastritis provide a model for studying the development of intestinal metaplasia and gastric giardiasis in H. pylori-infected humans.

Animals↗
PubMed1992

Detection of human papillomavirus DNA in normal epithelium and in squamous metaplasia of the uterine cervix by the polymerase chain reaction.

The presence of human papillomavirus (HPV) 16 was studied by using the polymerase chain reaction (PCR) directly on sections histologically defined as normal squamous epithelium and metaplastic squamous tissue of the uterine cervix. Ten specimens of normal epithelium were obtained at hysterectomy from women with uterine leiomyoma. Six specimens of squamous metaplasia were adjacent to the areas of dysplastic epithelium in which HPV 16 DNA had been detected previously by PCR. HPV 16 DNA was amplified specifically and detected in two of 10 normal cervical epithelium specimens and in all of 6 squamous metaplasia specimens adjacent to dysplastic lesions. However, HPV DNA could not be detected in the metaplasia by in situ hybridization. These results suggest that metaplastic squamous tissue adjacent to dysplastic lesions harbors fewer copies of HPV DNA than the dysplastic area and the carcinoma and that the HPV copy number per cell may be relevant to the pathogenesis of cervical carcinoma.

Base Sequence↗
PubMed2006

Incomplete intestinal metaplasia as an indicator for early detection of gastric carcinoma in the events of helicobacter pylori positive chronic atrophic gastritis.

The aim of the study was to ascertain the existence of intestinal metaplasia in gastric mucosa of patients with gastric carcinoma coupled with H. pylori positive chronic atrophic gastritis and possible connection of IM with the development of gastric carcinoma. The paper presents prospective study that included 50 patients with gastric carcinoma and 50 patients with chronic atrophic H. pylori positive gastritis. All the patients were subjected to gastroscopy as well as biopsy targeted at antrum, lesser curvature and corpus and at the area 1-2 cm removed from tumor lesion. Biopsy samples were sliced by microtome and stained. We analyzed presence, frequency and severity of inflammatory-regenerative, metaplastic and dysplastic changes in the mucosa and evaluated their prognostic value. We typed IM immunohistochemically. This study confirmed responsibility of H. pylori for inflammatory events in gastric mucosa in patients with gastric carcinoma. According to our findings incomplete IM of types IIa and IIb as precancerous lesion is responsible for the development of gastric carcinoma and is associated with chronic atrophic gastritis grade I and II (92% of subjects, p=0.0097, h=1, p=0.01). Thus, the finding of incomplete intestinal metaplasia may be used as an indicator for early gastric carcinoma detection. Patients with patho-histologically verified incomplete intestinal metaplasia associated with active chronic atrophic gastritis of levels I and II represent risk group for the development of gastric carcinoma of intestinal type.

Adult↗
PubMedDate not supplied

Effect of cumulative ozone exposure on ozone-induced nasal epithelial hyperplasia and secretory metaplasia in rats.

Repeated exposure of rats to O3 induces proliferative and secretory metaplastic changes within nasal airway epithelia that may protect against subsequent exposures. Our study assessed the effect of different cumulative exposure times on O3-induced nasal epithelial hyperplasia and secretory metaplasia. Rats were exposed 6 h/day to air or to 0.8 ppm O3 and were sacrificed 18 h after the end of their last exposure. The rats were exposed to either air or 0.8 ppm O3 for 3 or 7 days, or to 0.8 ppm O3 for 3 days followed by a 4-day exposure to air. The effects of the exposures were determined by quantitating the hyperplastic (epithelial nuclei/mm basal lamina) and secretory metaplastic changes (volume densities of acidic and neutral mucosubstances) within the nasal nonciliated cuboidal epithelium (NNCE). There were no significant changes in NNCE cell numeric density, or in the volume density of intraepithelial mucus, compared to air-exposed control rats, in rats exposed to O3 for 3 days and sacrificed 18 h later. Compared to control rats, there was significant epithelial hyperplasia and secretory metaplasia within the NNCE of rats exposed to O3 either for 7 days or for 3 days followed by 4 days of exposure to air. There were no significant differences in NNCE cell hyperplasia or secretory metaplasia between these two experimental groups. Three 6 h/day exposures to 0.8 ppm O3 triggered hyperplastic and metaplastic changes within rat NNCE that were indistinguishable from those produced by seven 6 h/day exposures to the same concentration of O3. The data suggest that O3 is capable of rapidly inducing hyperplastic and metaplastic responses within rat NNCE, and that once initiated, development of the phenotypic changes within the epithelium does not require further O3 exposure.

Animals↗
PubMed2005

Relationship between beta-catenin expression and epithelial cell proliferation in gastric mucosa with intestinal metaplasia.

AIM: To investigate beta-catenin expression in patients with intestinal metaplasia, and to look for a possible relationship between beta-catenin expression and either epithelial proliferation values or Helicobacter pylori (H pylori) infection. METHODS: Twenty patients with complete type intestinal metaplasia were studied. beta-Catenin expression and epithelial cell proliferation in antral mucosa were assessed using an immunohistochemical analysis. H pylori infection was detected by histology and a rapid urease test. RESULTS: Reduced beta-catenin expression on the surface of metaplastic cells was detected in 13 (65%) out of 20 patients. Moreover, in eight (40%) patients intranuclear expression of beta-catenin was found. When patients were analyzed according to H pylori infection, the prevalence of both beta-catenin reduction at the cell surface and its intranuclear localization did not significantly differ between infected and uninfected patients. Cell proliferation was higher in patients with intranuclear beta-catenin expression as compared to the remaining patients, although the difference failed to reach the statistical significance (36+/-8.9 vs 27.2+/-11.4, P = 0.06). On the contrary, a similar cell proliferation value was observed between patients with reduced expression of beta-catenin on cell surface and those with a normal expression (28.1+/-11.8 vs 26.1+/-8.8, P = 0.7). H pylori infection significantly increased cell proliferation (33.3+/-10.2% vs 24.6+/-7.4%, respectively, P = 0.04). CONCLUSION: Both cell surface reduction and intranuclear accumulation of beta-catenin were detected in intestinal metaplasia. The intranuclear localization of beta-catenin increases cell proliferation. H pylori infection does not seem to play a direct role in beta-catenin alterations, whilst it significantly increases cell proliferation.

Aged↗
PubMed1995

[Clinicopathological study of squamous metaplasia in human laryngeal ventricles].

A clinicopathological study was performed to clarify the site of onset of primary cancer of the laryngeal ventricles using larynges resected from 22 individuals with no macroscopic lesions in the laryngeal ventricle, and the following results were obtained. 1) Computer graphics were applied to the laryngeal ventricles based on serial sections, and their complex morphology was displayed. 2) Since the morphology of the laryngeal ventricle is complex, the degree of progression of squamous metaplasia differed considerably depending on the morphology of the laryngeal ventricle, even in the same larynx. According to our classification, the "depressed" part exhibited very highly progressive squamous metaplasia in the laryngeal ventricle, and this appeared to be important as a preliminary stage of carcinogenesis. 3) The "depressed" part of the laryngeal ventricle was distributed anteriorly and posteriorly in the ventricle, and this closely coincided with the clinically preferred site of onset of primary cancer of the laryngeal ventricle. On the other hand, the distribution of the "branching" and "separate" parts, with little squamous metaplasia, was mainly in the center of the laryngeal ventricle, which has a low rate of occurrence of primary cancer of the laryngeal ventricle. 4) The metaplastic area in the epithelial membrane of the laryngeal ventricles has previously been reported to be very narrow, but we found that the area was rather broad in some cases. Moreover, the metaplastic area was significantly broadened by smoking and alcohol drinking, demonstrating that the epithelial membrane of the laryngeal ventricles is influenced by these habits.

Adult↗
PubMed2005

Intestinal metaplasia with a high salt diet induces epithelial proliferation and alters cell composition in the gastric mucosa of mice.

Intestinal metaplasia of the gastric mucosa is an important component in the pathway to adenocarcinoma. The mechanisms that induce the progression from intestinal metaplasia to cancer have not been elucidated. High dietary salt has been known as one of the risk factors for gastric cancer development in humans. Therefore, we investigated the role of high salt diet on gastric epithelial cell proliferation and differentiation, using our mouse model that ectopically expressed Cdx2 homeodomain transcription factor and induced an intestinal metaplastic phenotype in the gastric epithelia. Sixty Cdx2 transgenic and sixty age-matched wild-type littermates were studied. Fifty-percent Cdx2 transgenic and wild type mice were administered a high-salt diet and the other fifty-percent was fed a standard diet starting at 12 weeks after birth. At 10, 20 and 40 weeks after initiation of the diets, histopathological changes were determined by Hemotoxylin and Eosin, alcian blue, and periodic acid-Schiff (PAS) staining. Cell types and cell kinetics were assessed by immunohistochemistry. At 52 weeks, significant alterations in pathology were observed in the Cdx2 transgenic mice fed a high-salt diet, including elongation of gastric pits, reduction of the glandular zone in the gastric corpus, and deepening of glands in the antrum. In the Cdx2 transgenic mice fed a high salt diet, the parietal and chief cells were significantly decreased in the gastric corpus. A significant increase in cell proliferation and apoptosis in the corpus and antrum were observed in Cdx2 transgenic mice fed a high-salt diet as compared to wild-type littermates. Taken together, these data implicate that intestinal metaplasia in concert with a high-salt diet induces epithelial proliferation, apoptosis, and alters cellular types in the gastric mucosa of mice. Alteration in the composition of the gastric epithelium may play a role in influencing the microenvironment to engender susceptibility to carcinogens.

Animals↗
PubMedDate not supplied

[Bladder squamous metaplasia: report of one case and bibliographic review].

OBJECTIVES: We report a new case of squamous metaplasia because of its interest and subtle differential diagnosis with other bladder pathologies. METHODS: We report the case of a male patient with history of previous neoplasia with an exophytic lesion of the bladder wall discovered on follow-up. Pathological diagnosis after TUR was bladder squamous metaplasia. RESULTS: Follow-up is performed by ultrasound, cystoscopy, and urine cytology in adherence to clinical guidelines due to the possibility of transformation into squamous cell carcinoma. CONCLUSIONS: Urothelium is able to develop non neoplastic transformations such as squamous metaplasia. The importance of such transformations depends on proper diagnosis and follow-up due to their ability to transform into a neoplastic process.

Aged↗
PubMed2003

A case of myxoid adrenocortical carcinoma with extensive lipomatous metaplasia.

We report a combination of unusual myxoid change and extensive lipomatous metaplasia of an adrenocortical carcinoma. The patient was a 38-year-old man with hypertension and heart failure. Radiographic examination revealed the presence of a left adrenal tumor, and adrenalectomy was performed. The tumor weighed 380 g and appeared encapsulated. The cut surface was predominantly gelatinous. Histologically, the tumor was composed of atypical round cells with eosinophilic to vacuolated cytoplasm. The tumor was diagnosed as adrenocortical carcinoma. The stroma accumulated copious mucinous material. In addition, individual to nodular mature adipocytes were admixed throughout the tumor. The transition from carcinoma cells to mature adipocytes was recognized. Myxoid change is a very rare phenomenon in adrenocortical carcinoma, and only 10 similar cases have been reported to date. Lipomatous metaplasia is another peculiar feature of adrenocortical lesions that has been reported only in benign conditions. To our knowledge, this is the first reported case of adrenocortical carcinoma with lipomatous metaplasia.

Adipocytes↗
PubMed2005

The genesis of Barrett esophagus: has a histologic transition from gastroesophageal reflux disease-damaged epithelium to columnar metaplasia ever been seen in humans?

Has a histologic transition from gastroesophageal reflux disease-damaged epithelium to columnar metaplasia ever been seen in humans? The answer to this question seems to be that it has but that we either do not readily recognize it or it is not readily recognizable with regular light microscopy. There are at least 3 possible mechanisms for the genesis of Barrett esophagus. The first is ulceration at the gastroesophageal junction with subsequent repair by an epithelium that differentiates into Barrett epithelium. The second is metaplasia through multilayered epithelium. The third is creeping columnar metaplasia at the Z-line proximally followed by intestinalization. These 3 hypotheses may not be mutually exclusive, and all may be operative, depending on the local circumstances, amount of inflammation, erosion, ulcers, healing, acid and alkaline reflux, and use of proton pump inhibitors. Any of the epithelial types involved could be stable and not progress. They might even be reversible, which may also in part explain the mosaic of epithelial types that typify Barrett esophagus, and may be modified by any of the molecular mechanisms that turn protein transcription on and off (eg, promoter methylation, mutations). These mechanisms ultimately may also be involved in the genesis of neoplastic transformation.

Barrett Esophagus↗
PubMed1998

Atrophy, metaplasia and dysplasia: are they reversible?

The eradication of Helicobacter pylori results in the decrease and eventual disappearance of inflammation in the gastric mucosa. An important question with practical implications is whether treatment of H. pylori can promote the resolution of atrophy and intestinal metaplasia. If this happens, then one could infer that even in the presence of established multifocal atrophic gastritis the cure of Helicobacter pylori could reduce the risk of developing gastric cancer. Several investigators have addressed the issue, but the cumulative results remain inconclusive. The great latitude that there exists in the interpretation of the concept of atrophy and the patchy distribution of both atrophic changes and intestinal metaplasia (with resulting inevitable sampling error) are important reasons for the wide discrepancy in the conclusions reached by different authors. Controlled, long-term prospective studies conducted in different ethnic and geographic settings are needed to provide sound evidence-based answers to the question of reversibility of atrophy, intestinal metaplasia, and epithelial dysplasia.

Atrophy↗
PubMed1999

[Intestinal metaplasia of the bladder].

Intestinal metaplasia is a rare condition characterized by the presence of colonic epithelium and mucin-containing goblet cells in the bladder. According to its extension we can distinguish localized from widespread intestinal metaplasia. We describe a case of glandular cystitis intestinal-type in a 58-year-old man whose clinical history and diagnostic work-up are consistent with this proliferative abnormality. We also discuss the pathogenesis and the propensity of intestinal metaplasia to undergo neoplastic transformation.

Cystitis↗
PubMed1999

[Prevalence of cardial or fundic mucosa and Helicobacter pylori in the squamous-columnar mucosa in patients with chronic patological gastroesophageal reflux without intestinal metaplasia comparated with controls].

BACKGROUND: The mucosa distal to the endoscopic mucosal change zone can have easily diagnosed early alterations, in patients with chronic gastroesophageal reflux. AIM: To determine the type of mucosa existent in the zone distal to the squamous-columnar junction in patients with chronic gastroesophageal reflux without intestinal metaplasia. PATIENTS AND METHODS: One hundred thirty four controls and 208 patients with chronic gastroesophageal reflux lasting two years were studied. Forty three of these patients had a normal endoscopy, 54 had an erosive esophagitis and 111 had a short columnar epithelium covering the distal esophagus, without intestinal metaplasia. In all subjects, four biopsies were obtained from a zone distal to the squamous-columnar junction and two from the distal gastric antrum. RESULTS: In 59% of control subjects, fundic mucosa was present in the zone distal to the squamous-columnar junction. Cardial mucosa was present in the rest. In patient with chronic gastroesophageal reflux, cardial mucosa was predominant. Helicobacter pylorii infection decreased along with increasing extension of cardial mucosa covering the distal esophagus. CONCLUSIONS: In patients with chronic gastroesophageal reflux there is a metaplasia of fundic mucosa towards cardial mucosa. On the other hand, Helicobacter pylorii infection decreases gradually.

Adolescent↗
PubMed2000

Duodenal-content reflux esophagitis induces the development of glandular metaplasia and adenosquamous carcinoma in rats.

Recent studies have demonstrated that refluxed duodenal contents cause esophageal carcinoma in rats without exposure to carcinogens. The histopathological spectrum of these carcinomas includes squamous-cell carcinoma, adenocarcinoma and adenosquamous carcinoma. Pure adenocarcinomas are thought to arise in areas of columnar metaplasia adjacent to the anastomosis, similar to Barrett's esophagus in humans. In contrast, the histogenesis of adenosquamous carcinomas is unclear. The purpose here was to investigate the pathogenesis of esophageal adenosquamous carcinomas in a time-course experiment of chronic duodenal-content reflux without carcinogen. Forty-two 8-week-old male Sprague-Dawley rats were divided into seven groups and exposed to duodenal-content esophageal reflux during 10, 15, 20, 25, 30, 35 and 40 weeks, respectively. All animals underwent an esophagojejunostomy with gastric preservation in order to produce chronic esophagitis. The rats received a standard diet without addition of carcinogens. An increasing incidence of glandular metaplasia and carcinoma was observed over the time course, starting at 20 weeks. After 40 weeks of reflux, multiple foci of glandular metaplasia and adenosquamous carcinoma were found in 83 and 50% of the animals, respectively. Most of the carcinomas occurred in the middle and proximal esophagus and had a dual pattern of differentiation, glandular and squamous. These findings confirm that duodenal content reflux alone has a carcinogenic effect. We propose that chronic duodenal reflux induces the development of metaplastic cells with glandular differentiation from the stem cells of squamous epithelium, and that glandular metaplastic foci are the morphological element from which tumors with a dual pattern of differentiation arise.

Anastomosis, Surgical↗
PubMed2001

Cathepsin E and subtypes of intestinal metaplasia in carcinogenesis of the human stomach.

BACKGROUND: Cathepsin E is found mainly over the gastric surface and foveolar epithelial cells, and it also is found in the metaplastic pyloric glands and cancer cells. The exact function of cathepsin E in gastric mucosa remains unclear. The colonic type (type III) of intestinal metaplasia (IM) is strongly associated with intestinal-type gastric carcinoma. IM is considered to be a precancerous lesion. The aim of this study was to find out the role of cathepsin E in IM, dysplasia and cancer of stomach. METHODS: Sixty nine biopsy specimens with IM and dysplasia and 33 gastrectomy specimens with gastric carcinoma were fixed, sectioned and stained with PAS-alcian blue stain, high iron-diamine alcian blue stain to classify IM and immunohistochemical stain to localize cathepsin E. Those patients with dysplastic gastric lesions received regular endoscopic follow-up. RESULTS: Fifteen of 69 patients with gastric dysplasia developed cancer in a median 10.5 months follow-up. Severe dysplasia developed carcinoma significantly higher than mild dysplasia (12/20 vs. 1/25, p < 0.001), and type III intestinal metaplasia seemed to have significantly predilection for severe dysplasia and gastric cancer. Cathepsin E was stained in intestinal metaplasia with dysplastic change in 44/69 specimens (63.8%), and carcinoma in 28/48 (58.3%) specimens, there was no significant difference between intestinal type and diffuse type carcinoma in cathepsin E staining. The positive staining for cathepsin E decreased significantly in severe dysplastic gastric mucosa. CONCLUSIONS: Type III IM is commonly associated with severe dysplasia and cancer; it may be a precancerous lesion. The positive staining of cathepsin E decreased with the severity of gastric dysplasia, representing dedifferentiation of the cells.

Aged↗
PubMed2001

[Oncogene amplification and genetic heterogeneity in the metaplasia-dysplasia-adenocarcinoma sequence of Barrett esophagus].

AIMS: Information about numerical genomic alterations in the tumorigenesis of Barrett's adenocarcinoma (BCA) is still limited. In order to search for gene amplification and ploidy status, a series of locus-specific DNA probes and associated centromere probes was analysed in the metaplasia-dysplasia-adenocarcinoma-sequence. METHODS: Fluorescence in situ hybridisation (FISH) was performed on paraffin sections with locus-specific DNA probes for D7S486, c-myc, cyclin D1, Her-2/neu, 20q13.2 and associated chromosomes 7, 8, 11, 17 and 20. Corresponding areas of intestinal metaplasia (IM, n = 5), low grade dysplasia (LGD, n = 9), high grade dysplasia (HGD, n = 15) and BCA (n = 16) were analysed. RESULTS: Gene amplification of c-myc, Cyclin D1, Her-2/neu and 20q13.2 was observed in 15-35% of BCA. Coincident amplification of genes was also present. Polysomies for all investigated centromere probes were highly prevalent (up to 85%). Gene amplification was also demonstrated in HGD lesions. Polysomies were observed in HGD in high frequency (up to 80%). Extensive genetic heterogeneity was observed in both, BCA and HGD displaying different levels of amplification. None of the samples with LGD showed a locus-specific amplification, but polysomies for all investigated chromosomes were present in 18-48% of LGD. No changes were detected in BCA associated IM and squamous epithelium. CONCLUSIONS: Our data indicate that oncogene amplification of c-myc, cyclin D1, Her-2/neu, and 20q13.2 occurring in BCA and less frequently in HGD is a late event in the tumorigenesis. Polysomies of chromosomes 7, 8, 11, 17 and 20, which were highly prevalent in BCA and HGD occur already at the stage of LGD. This may be a result of an early polyploidization, preceding the later genetic events, such as gene amplification in HGD and BCA. The detection of shared numerical genomic changes and the detected extensive genetic heterogeneity in the metaplasia-dysplasia-carcinoma-sequence in Barrett's esophagus supports the hypothesis of a process of multiclonal expansion underlying this progression.

Adenocarcinoma↗