Decreased expression of fas (CD95/AP01)associated with goblet cell metaplasia in barrett's esophagus

Younes, Mamoun; Lechago, Juan; Ertan, Atilla; Finnie, Delia; Younes, Anas

doi:10.1053/hp.2000.6715

Cited by 37 publications

(21 citation statements)

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“…However, there are conflicting data regarding apoptosis, which may relate at least in part to differing methods of quantifying apoptosis (74,75). Fas ligand expression is increased in Barrett's metaplasia associated with dysplasia and adenocarcinoma (76). Normal senescence pathways are circumvented in many cancers through de-repression and activation of telomerase, an enzyme that is responsible for stabilization and maintenance of telomere length.…”

Section: Pathogenesis Of Esophageal Adenocarcinomamentioning

confidence: 99%

Biomarkers of Esophageal Adenocarcinoma and Barrett’s Esophagus

2004

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The rising incidence and poor prognosis of esophageal adenocarcinoma in the Western world have intensified research efforts into earlier methods of detection of this disease and its relationship to Barrett's esophagus. The progression of Barrett's esophagus to adenocarcinoma has been the focus of particular scrutiny, and a number of potential tissue and serum-based disease biomarkers have emerged. The epidemiology and pathogenesis of esophageal adenocarcinoma are outlined. Tissue biomarkers allowing risk stratification of Barrett's are reviewed as well as strategies currently being used to discover novel biomarkers that will facilitate the early detection of esophageal adenocarcinoma. Finally, the uses of biomarkers as predictive tests for targeted treatments and as surrogate endpoints in chemoprevention trials are considered.

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Section: Pathogenesis Of Esophageal Adenocarcinomamentioning

confidence: 99%

Biomarkers of Esophageal Adenocarcinoma and Barrett’s Esophagus

2004

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“…However, Fas-ligand could also be produced to kill lymphoid cells and, thereby, prevent the immune system from recognizing and eliminating the tumor cells [67]. Fas expression seems to compensate for this proapoptotic effect by showing decreased expression in dysplasia and adenocarcinoma [68,69]. Although these data are conflicting, it was recently suggested that Barrett's esophagus is relatively resistant to apoptosis [70], which can promote the outgrowth of mutated esophageal cells.…”

Section: Escape Of Apoptosismentioning

confidence: 99%

Molecular alterations during development of esophageal adenocarcinoma

et al. 2005

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The incidence of esophageal adenocarcinoma has risen significantly over the last decades. During esophageal carcinogenesis many molecular alterations occur that disrupt essential cellular processes, directing the cell to a rapidly proliferating, immortal state. The chronic inflammation that is present in Barrett's esophagus creates an environment in which such molecular alterations are both induced and tolerated. Here, the novel insights in the molecular mechanisms that underlie the development of esophageal adenocarcinoma are reviewed, focusing on the role of inflammation, angiogenesis, apoptosis inhibition, loss of cell cycle control, and loss of cell-cell adhesion. These novel developments will open new perspectives for diagnosis, treatment, and prevention of esophageal adenocarcinoma.

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“…38 Briefly, sections were deparaffinized in xylene, rehydrated with decreasing concentrations of alcohol and finally phosphate-buffered saline (PBS), and subjected to steam-heat epitope retrieval in 10 mM citrate buffer (pH 6.0) for 30 minutes in a commercially available vegetable steamer. The sections were then rinsed in distilled water, washed in PBS for 5 minutes, and incubated for 15 minutes with DAKO protein block (DAKO, Carpenteria, CA).…”

Section: Immunohistochemistrymentioning

confidence: 99%