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Stuart Jon Spechler

Publications and source records attributed to Stuart Jon Spechler.

24 records · Page 2Linked to original sources
PubMed2002

Columnar-lined esophagus. Definitions.

Recognition of a columnar-lined esophagus requires precise criteria by which to delimit the esophagus and the stomach. Endoscopically recognizable landmarks such as the squamocolumnar junction (SCJ or Z-line) can be used to identify structures at the gastroesophageal junction. Once the SCJ is located proximal to the gastroesophageal junction, a columnar-lined segment of esophagus is visible. If biopsy specimens from the columnar-lined segment show specialized intestinal metaplasia, then the patient has Barrett's esophagus (BE), and the extent of the columnar lining determines if it is short- or long-segment BE.

Barrett Esophagus↗
PubMed2002

Acid exposure activates the mitogen-activated protein kinase pathways in Barrett's esophagus.

BACKGROUND & AIMS: To explore mechanisms whereby acid reflux might contribute to carcinogenesis in Barrett's esophagus (BE) we studied: (1) the effects of acid on the mitogen-activated protein kinase (MAPK) pathways, cell proliferation, and apoptosis in a Barrett's adenocarcinoma cell line (SEG-1); and (2) the ability of acid to activate the MAPK pathways in vivo in patients with BE. METHODS: SEG-1 cells were exposed to acidic media for 3 minutes, and the activities of 3 MAPKs (ERK, p38, and JNK) were determined. Proliferation was assessed using flow cytometry; cell growth and apoptosis were assessed using cell counts and an apoptosis ELISA assay. MAPK activation was studied in biopsy specimens taken from patients with BE before and after esophageal perfusion for 3 minutes with 0.1N HCl. RESULTS: Acid-exposed SEG-1 cells exhibited a significant increase in proliferation and total cell numbers, and a significant decrease in apoptosis. These effects were preceded by a rapid increase in the activities of ERK and p38, and a delayed increase in JNK activity. PD 98059 abolished the acid-induced increase in G0/G1 and decrease in subG0 phases of the cell cycle. Both SB 203580 and DN-JNK 1/2 inhibited the acid-induced progression from G0/G1 to G2/M. The acid-induced decrease in apoptosis was abolished by inhibition of either ERK or p38. In the patients, acid exposure significantly increased the activity of p38 in the metaplastic epithelium. CONCLUSIONS: Acid increases proliferation and survival, and decreases apoptosis in SEG-1 cells by activating the MAPK pathways. Acid also activates the MAPK pathways in BE in vivo. These findings suggest that acid might contribute to carcinogenesis in BE through activation of MAPK pathways.

Adenocarcinoma↗
PubMed2002

Screening for Barrett's esophagus.

Screening and surveillance for Barrett's esophagus have been proposed as strategies for preventing deaths from esophageal adenocarcinoma. A meaningful discussion on the cost efficacy of screening and surveillance for Barrett's esophagus requires a reasonable estimate of the risk of esophageal cancer in this condition. The primary goal of endoscopic screening for individuals with gastroesophageal reflux disease is to identify patients with Barrett's esophagus who will benefit from an intervention to prevent cancer. There is also indirect evidence to suggest that surveillance for Barrett's esophagus may be beneficial. However, there is much debate over the efficacy of these diagnostic procedures. In the absence of definitive data, investigators have used computer models to study the cost effectiveness of screening and surveillance for Barrett's esophagus. It is important for physicians to recognize that such models do not provide a single, definitive answer.

Adenocarcinoma↗
PubMedDate not supplied

The natural history of dysplasia and cancer in esophagitis and Barrett esophagus.

The natural history of metaplasia and dysplasia in Barrett esophagus is not well defined. Publication bias, the selective reporting of studies that have positive or extreme results, has exaggerated the risk of esophageal adenocarcinoma in this condition. Recent data suggest that patients with Barrett esophagus develop these tumors at the rate of 0.5% per year, a cancer incidence considerably lower than was appreciated just a few years ago. Indirect evidence suggests that aggressive treatment of gastroesophageal reflux might decrease the risk of carcinogenesis, but no therapy yet has been proved to decrease the incidence of cancer in Barrett esophagus. Dysplasia in the metaplastic epithelium clearly is a worrisome finding, but the progression from dysplasia to cancer may take years and may not be inevitable.

Adenocarcinoma↗