Foveolar type dysplasia in Barrett esophagus

Brown, Ian; Whiteman, David C.; Lauwers, Gregory Y.

doi:10.1038/modpathol.2010.59

Cited by 71 publications

(51 citation statements)

References 47 publications

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“…[5][6][7][8][11][12][13][14][15] Because of its recent description, the gastric variant of Barrett's dysplasia was not separately analyzed in this study. [16][17][18] This omission is unlikely to have affected the reported results; however, because gastric-type Barrett's dysplasia represents a minority of dysplasia cases (B15%). It is also substantially more subtle than intestinal-type dysplasia, leading to under rather than over diagnosis, the subject of this study.…”

Section: Discussionmentioning

confidence: 99%

Overdiagnosis of high-grade dysplasia in Barrett's esophagus: a multicenter, international study

et al. 2015

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Numerous histological mimics of high-grade dysplasia in Barrett's esophagus predispose to overdiagnosis and potential serious mismanagement, including unnecessary esophagectomy. This study investigates the prevalence and sources of this problem. Biopsies from 485 patients diagnosed with Barrett's high-grade dysplasia were screened for a multi-institutional, international Barrett's endoscopic ablation trial. Screening included review of the original diagnostic slides and an additional protocol endoscopy with an extensive biopsy sampling. Observer variability by the study pathologists was assessed through two blinded diagnostic rounds on 437 biopsies from 26 random study endoscopies. Study diagnostic reassessments revealed significantly lower rates of high-grade dysplasia. Only 248 patients (51%) were confirmed to have high-grade dysplasia. The remaining patients had inflamed gastric cardia without Barrett's (n ¼ 18; 7%), Barrett's without dysplasia (n ¼ 35; 15%), indefinite change (n ¼ 61; 26%), low-grade dysplasia (n ¼ 79; 33%), adenocarcinoma (n ¼ 43; 18%), and other (n ¼ 1; o1%), yielding an alarming total of 194 or 40% of patients who were overdiagnosed with Barrett's highgrade dysplasia. Study pathologists achieved a high-level agreement (90% three-way inter-observer agreement per biopsy, Kappa value 0.77) for high-grade dysplasia. Confounding factors promoting overdiagnosis included Barrett's inflammatory atypia (n ¼ 182), atypia limited to the basal metaplastic glands (n ¼ 147), imprecise criteria for low grade neoplasia (n ¼ 102), tangential sectioning artifact (n ¼ 59), and reactive gastric cardiac mucosa (n ¼ 38). A total of 194 patients (40%) were overdiagnosed with Barrett's high-grade dysplasia, as affirmed by the extensive screening process and high-level study pathologist agreement. The multiple diagnostic pitfalls uncovered should help raise pathologists' awareness of this problem and improve diagnostic accuracy.

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Section: Discussionmentioning

confidence: 99%

Overdiagnosis of high-grade dysplasia in Barrett's esophagus: a multicenter, international study

et al. 2015

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“…11,31,36,54 We offer a simple model ( Figure 8B) that encompasses the basic cytological and immunophenotypic features of the transitions we observe and propose the term hybrid metaplasias to identify the transitional states. The name and classification follows established terminology 83,84 in the context of intraepithelial as well as invasive gastric neoplasia, where the mixed patterns of intestinal and gastric phenotypes are referred to as "hybrid-dysplasia" and "hybrid-carcinoma," respectively. 6,7,85 Furthermore, the term "hybrid" avoids temporal connotations and is fitting since it refers to a mixed-lesional pattern in the MIST1 compartment that demonstrates either intestinal (CDX2 ϩ , vertical nuclei, intestinal apical differentiation) or gastric features (ϭ pseudopyloric metaplasia/SPEM: TFF2 ϩ , horizontal nuclei, pyloric apical differentiation).…”

Section: Discussionmentioning

confidence: 99%

The Transcription Factor MIST1 Is a Novel Human Gastric Chief Cell Marker Whose Expression Is Lost in Metaplasia, Dysplasia, and Carcinoma

Lennerz

Kim

Oates

et al. 2010

The American Journal of Pathology

106

148

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The lack of reliable molecular markers for normal differentiated epithelial cells limits understanding of human gastric carcinogenesis. Recognized precursor lesions for gastric adenocarcinoma are intestinal metaplasia and spasmolytic polypeptide expressing metaplasia (SPEM), defined here by ectopic CDX2 and TFF2 expression, respectively. In mice, expression of the bHLH transcription factor MIST1, normally restricted to mature chief cells, is down-regulated as chief cells undergo experimentally induced metaplasia. Here, we show MIST1 expression is also a specific marker of human chief cells. The mainstays of therapy in gastric carcinoma are early recognition, resection, and neoadjuvant or adjuvant therapy. However, gastric cancer remains the second largest cause of cancer-related mortality worldwide, 1 which drastically illustrates our lack of understanding of the sequence and progression of preneoplastic conditions. The traditional linear progression model of cellular changes, such as (Helicobacter-mediated) inflammation, atrophy, intestinal metaplasia (IM), dysplasia, and carcinoma, 2-4 does not apply to all cases and does not allow incorporation of more recently recognized entities. For example, there are distinct types of IMs, not all carrying definitive preneoplastic potential, and some authors have argued that IM in general is a paraneoplastic condition because the earliest gastric carcinomas arise from gasSupported by

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“…In particular, there is an initial upregulation of CDX2 in intestinal metaplasia, followed by progressive decline in its expression from LGD to HGD to adenocarcinoma. However, on the basis of the two different types of dysplasia described in BE (18), related to separate gastric and intestinal pathways of carcinogenesis, in the literature this downward trend of CDX2 upregulation along the neoplastic progression was observed only in cases with adenomatous dysplasia but not in cases with foveolar dysplasia (79). This evidence suggests a role for CDX2 as a tumor suppressor in the metaplasia-dysplasia-carcinoma sequence in the intestinal but not in the gastric pathway.…”

Section: Cox-2 Cdx2 Cdc-2mentioning

confidence: 84%

“…Two patterns of Barrett dysplasia have been recently described (18): adenomatous (type I) and non-adenomatous (type II or foveolar type). The former is said to account for the majority of cases, while the latter is uncommon and it has been less characterized.…”

Section: From Metaplasia To Adenocarcinomamentioning

confidence: 99%

“…Regarding immuphenotype, MUC2, CDX2 and villin are markers of intestinal differentiation and so are useful to diagnose type I dysplasia; by contrast, foveolar type dysplasia commonly expresses MUC5AC. Brown et al (18) placed emphasis on these different pathological entities, highlighting the importance of the morphological subclassification of BE dysplasia into adenomatous and gastric foveolar types. In particular, the foveolar dysplasia should be taken into consideration, as part of a nonintestinal neoplastic pathway.…”

Section: From Metaplasia To Adenocarcinomamentioning

confidence: 99%

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Influence of genetics on tumoral pathologies: The example of the adenocarcinoma arising in Barrett's esophagus

Villanacci

Bassotti

Salemme

et al. 2012

Rev. esp. enferm. dig.

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Barrett's esophagus (BE) refers to an abnormal change (metaplasia) in the cells of the inferior portion of the esophagus. About 10% of patients with symptomatic gastroesophageal reflux disease (GERD) have BE. In some cases, BE develops as an advanced stage of erosive esophagitis. The risk of esophageal cancer appears to be increased in patients with BE. The only way to diagnose BE is by endoscopy and histology. Some studies suggest that intensive treatment of Barrett's esophagus with effective acid suppression can reduce the amount of abnormal lining in the esophagus. It is not clear whether such treatment also prevents esophageal cancer. Generally, the cancer starts out as carcinoma of the esophagus on the surface, and then invades the surrounding tissue. Surgery offers the best chance of long-term survival. There are many events that occur in Barrett's esophagus that lead to the development of cancer and most of them appear to occur early, before high-grade dysplasia or cancer develops. No one knows what the late events are and how cells acquire the ability to leave their normal growth boundaries. It is now widely accepted that the development of most cancers is due to something called genomic or genetic instability. The aim of this review is to show BE pathology in its progression to cancer looking for new biomarkers to distinguish between BE -dysplasia (low grade and high grade)-adenocarcinoma (ADC) and to characterize the ADC, giving more hope for its treatment.

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Foveolar type dysplasia in Barrett esophagus

Cited by 71 publications

References 47 publications

Overdiagnosis of high-grade dysplasia in Barrett's esophagus: a multicenter, international study

Overdiagnosis of high-grade dysplasia in Barrett's esophagus: a multicenter, international study

The Transcription Factor MIST1 Is a Novel Human Gastric Chief Cell Marker Whose Expression Is Lost in Metaplasia, Dysplasia, and Carcinoma

Influence of genetics on tumoral pathologies: The example of the adenocarcinoma arising in Barrett's esophagus

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