Ki67 expression in different epithelial types in columnar lined oesophagus indicates varying levels of expanded and aberrant proliferative patterns

Olvera, Maria; Wickramasinghe, Kumari; Brynes, Russell K.; Bu, Xingyao; Ma, Yanling; Chandrasoma, Parakrama

doi:10.1111/j.1365-2559.2005.02200.x

Cited by 30 publications

(16 citation statements)

References 28 publications

(37 reference statements)

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“…Most interestingly, aberrant Ki67 expression was comparable in cardiac mucosa, intestinal metaplasia without dysplasia and low grade-dysplasia. Aberrant Ki67 expression was absent in oxyntic and oxyntocardiac mucosa [62]. Taken together, these data suggest that when compared to oxyntocardiac mucosa, cardiac mucosa may signify a switch towards "malignant" progression [38,62].…”

Section: Follow Up Of Clementioning

confidence: 80%

“…In contrast to oxyntic mucosa, expanded Ki67 expression from the lower (= normal) towards the middle third of the foveolar pit was detected in different types of CLE, following a step wise increase from oxyntic, onxytocardiac and cardiac mucosa to intestinal metaplasia, low-, high-grade dysplasia and adenocarcinoma [62]. Frequency of aberrant Ki67 expression within surface and foveolar epithelium in cardiac mucosa showed a stepwise increase from cardiac mucosa and intestinal metaplasia towards low-, highgrade dysplasia and adenocarcinoma [62]. Most interestingly, aberrant Ki67 expression was comparable in cardiac mucosa, intestinal metaplasia without dysplasia and low grade-dysplasia.…”

Section: Follow Up Of Clementioning

confidence: 90%

“…presence of goblet cells is paralleled by loss of chief and parietal cell) [8,38,45,46]. Olvera et al [62] recently demonstrated abnormal patterns of Ki67 immunoreactivity, a marker of cell proliferation, in various types of CLE. In contrast to oxyntic mucosa, expanded Ki67 expression from the lower (= normal) towards the middle third of the foveolar pit was detected in different types of CLE, following a step wise increase from oxyntic, onxytocardiac and cardiac mucosa to intestinal metaplasia, low-, high-grade dysplasia and adenocarcinoma [62].…”

Section: Follow Up Of Clementioning

confidence: 99%

“…Olvera et al [62] recently demonstrated abnormal patterns of Ki67 immunoreactivity, a marker of cell proliferation, in various types of CLE. In contrast to oxyntic mucosa, expanded Ki67 expression from the lower (= normal) towards the middle third of the foveolar pit was detected in different types of CLE, following a step wise increase from oxyntic, onxytocardiac and cardiac mucosa to intestinal metaplasia, low-, high-grade dysplasia and adenocarcinoma [62]. Frequency of aberrant Ki67 expression within surface and foveolar epithelium in cardiac mucosa showed a stepwise increase from cardiac mucosa and intestinal metaplasia towards low-, highgrade dysplasia and adenocarcinoma [62].…”

Section: Follow Up Of Clementioning

confidence: 99%

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Diagnosis of Gastroesophageal Reflux Disease (GERD)

et al. 2006

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Section: Follow Up Of Clementioning

confidence: 80%

Section: Follow Up Of Clementioning

confidence: 90%

Section: Follow Up Of Clementioning

confidence: 99%

Section: Follow Up Of Clementioning

confidence: 99%

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Diagnosis of Gastroesophageal Reflux Disease (GERD)

et al. 2006

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“…However, they observed inconsistent results in indefinite for dysplasia samples. Olvera et al 26 found no value for Ki-67 immunohistochemical staining in distinguishing between low-grade dysplastic epithelium and cardiac mucosa or nondysplastic intestinal epithelium. Our study corroborates the results of the study by Hong et al, 25 except that we found lower mitotic counts in indefinite for dysplasia than in low-grade dysplasia.…”

Section: Discussionmentioning

confidence: 99%

Anti-phosphorylated histone H3 expression in Barrett's esophagus, low-grade dysplasia, high-grade dysplasia, and adenocarcinoma

Goodarzi

Correa

Ajani³

et al. 2009

Modern Pathology

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The high interobserver variability in grading dysplasia in Barrett's esophagus demands a biomarker that can be applied in routine surgical pathology practice. Immunohistochemistry for phosphorylated histone H3 is a reliable marker of identifying mitotic figures and has not been evaluated in Barrett's esophagus-associated neoplastic lesions. We retrospectively studied the expression of phosphorylated histone H3 in 88 endoscopic biopsy samples of Barrett's esophagus without dysplasia (n ¼ 19), indefinite for dysplasia (n ¼ 11), low-grade dysplasia (n ¼ 27), high-grade dysplasia (n ¼ 19), or adenocarcinoma (n ¼ 12) from a sample of 54 patients. The samples were included after consensus diagnosis of two gastrointestinal pathologists on the hematoxylineosin (HE)-stained sections. Anti-phosphorylated histone H3-labeled mitotic figures were counted per 10 consecutive high-power fields (HPFs) in three distinct regions: surface epithelium, upper 2/3, and lower 1/3 of the crypts. Anti-phosphorylated histone H3-labeled mitotic counts for the three compartments of the crypts and the total scores for Barrett's esophagus, indefinite for dysplasia, low-grade dysplasia, high-grade dysplasia, and adenocarcinoma were compared using the Mann-Whitney U test. For each compartment, the number of anti-phosphorylated histone H3-positive nuclei was higher in low-grade dysplasia than in Barrett's esophagus without dysplasia or indefinite for dysplasia (Po0.001), but no difference was found between Barrett's esophagus without dysplasia and indefinite for dysplasia. High-grade dysplasia biopsies had significantly more anti-phosphorylated histone H3-labeled mitotic figures in the surface epithelium than the low-grade dysplasia (Po0.001). Adenocarcinoma had higher anti-phosphorylated histone H3-labeled mitotic figures than the highgrade dysplasia (Po0.001). Our data support the previous findings of expansion of the proliferative zone and importance of surface mitotic figure in the progression of Barrett's esophagus-low-grade dysplasia-highgrade dysplasia. In addition, phosphorylated histone H3 is a potential supportive marker to histology in differentiating low-grade dysplasia from indefinite for dysplasia and high-grade dysplasia from adenocarcinoma in the mucosal biopsy samples.

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Barrett's esophagus: The pathomorphological and molecular genetic keystones of neoplastic progression

et al. 2021

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Barrett's esophagus is a widespread chronically progressing disease of heterogeneous nature. A life threatening complication of this condition is neoplastic transformation, which is often overlooked due to lack of standardized approaches in diagnosis, preventative measures and treatment. In this essay, we aim to stratify existing data to show specific associations between neoplastic transformation and the underlying processes which predate cancerous transition. We discuss pathomorphological, genetic, epigenetic, molecular and immunohistochemical methods related to neoplasia detection on the basis of Barrett's esophagus. Our review sheds light on pathways of such neoplastic progression in the distal esophagus, providing valuable insight into progression assessment, preventative targets and treatment modalities. Our results suggest that molecular, genetic and epigenetic alterations in the esophagus arise earlier than cancerous transformation, meaning the discussed targets can help form preventative strategies in at-risk patient groups.

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Ki67 expression in different epithelial types in columnar lined oesophagus indicates varying levels of expanded and aberrant proliferative patterns

Cited by 30 publications

References 28 publications

Diagnosis of Gastroesophageal Reflux Disease (GERD)

Diagnosis of Gastroesophageal Reflux Disease (GERD)

Anti-phosphorylated histone H3 expression in Barrett's esophagus, low-grade dysplasia, high-grade dysplasia, and adenocarcinoma

Barrett's esophagus: The pathomorphological and molecular genetic keystones of neoplastic progression

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