The Barrett's esophagus BE is defined as endoscopically visible columnar mucosa at the distal esophagus, of any extension, proved to harbor intestinal metaplasia on biopsy, highlighted by the presence of goblet cells. Therefore, these patients must be on follow-up, in order to diagnose cancer early. BE patients have frequent alterations in esophageal physiologyc studies. Alkaline duodenogastroesophageal reflux seems to have important role. The development BE occurs in steps, initially with formation of cardiac type mucosa subsequent intestinalization.
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The Barrett's esophagus BE is defined as endoscopically visible columnar mucosa at the distal esophagus, of any extension, proved to harbor intestinal metaplasia on biopsy, highlighted by the presence of goblet cells. Therefore, these patients must be on follow-up, in order to diagnose cancer early.
BE patients have frequent alterations in esophageal physiologyc studies. Alkaline duodenogastroesophageal reflux seems to have important role. The development BE occurs in steps, initially with formation of cardiac type mucosa subsequent intestinalization. Futher progression can follow a sequence, from low grade dysplasia, to high grade dysplasia and esophageal adenocarcinoma.
Current follow-up is based on the presence of dysplasia. It has limitations, grouping patients heterogeneously. Different steps of carcinogenesis have been studied looking for an ideal prognostic marker. Uncontrolled proliferative activity, apoptosis inhibition, angiogenesis, tissue invasion and metastases formation are all implicated in cancer origin.
Some cycle cell molecules have been studied in BE, such as retinoblastoma protein, ciclins, kinase dependent ciclins and cell cycle inhibitors.
The P53 protein is one of the most investigated in the metaplasia-adenocarcinoma progression. Growth Factors, apoptotic proteins, telomers and DNA ploidy have also been searched. Increased proliferative activity has been implicated in Barrett's carcinogenesis and the Ki antigen, through imunohistochemical analysis, has become the the method of choice. Present in the nucleus, it is found in proliferative cells only. Some studies suport association between Ki activity and the metaplasia-dysplasia-adenocarcinoma sequence.
The results, however, are inconclusive and research should follow this way. A mortalidade proporcional por ACE foi significativamente maior nos pacientes com EB, especialmente nos com metaplasia intestinal, a qual foi oito vezes maior A displasia significa risco aumentado de ACE. O Ciclo Celular. Marcadores Celulares. Fatores de Crescimento. Ploidia do DNA.
Sua forma normal ou selvagem tem meia-vida curta e rapidamente desaparece do meio celular. Atividade Proliferativa e Ki Hong et al. Feith et al. Polkowski et al. Lauwers et al. Barrett NR.
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