Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0154059 (Esophagus)
 2,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To identify receptors for bombesin-related peptides in the rat esophagus, we measured binding of 125I-Bolton-Hunter neuromedin B (125I-BH-neuromedin B) and 125I-[Tyr4]bombesin to tissue sections from the rat esophagus and compared the results with those for rat pancreas. Esophagus bound both tracers, whereas pancreas bound only 125I-[Tyr4]bombesin. In each tissue binding was saturable, dependent on pH, on time, and on temperature, reversible, and specific. Autoradiography demonstrated binding of both tracers only to the muscularis mucosae of the esophagus and binding of 125I-[Tyr4]bombesin diffusely over pancreatic acini. In the esophagus, the relative potencies for inhibition of binding of both tracers were as follows: neuromedin B greater than bombesin greater than GRP = neuromedin C; similar relative potencies were found for causing contraction of muscle strips from whole esophagus and from the isolated muscularis mucosae. In pancreas tissue sections and dispersed acini, the relative potencies for inhibition of binding of 125I-[Tyr4]bombesin were as follows: bombesin greater than GRP = neuromedin C much greater than neuromedin B. Similar relative potencies were found for stimulation of enzyme secretion from dispersed pancreatic acini. Computer analysis in both tissues demonstrated only a single binding site. The present study demonstrates that rat esophagus muscle possesses specific receptors for bombesin-related peptides. Furthermore, this study shows that the esophageal bombesin receptors represent a previously unidentified class of bombesin receptors in that they have a higher affinity for neuromedin B than for bombesin. In contrast, the pancreatic bombesin receptors have, like all other bombesin receptors described to date, a high affinity for bombesin, but low affinity for neuromedin B.
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PMID:Neuromedin B receptor in esophagus: evidence for subtypes of bombesin receptors. 253 39

We have investigated the effect of bombesin on esophageal motility and explored the mechanism of action of bombesin. Eight healthy subjects were studied in random order during intravenous administration of (1) bombesin, (2) bombesin + vagal cholinergic receptor blockade with atropine and (3) bombesin + somatostatin. Lower esophageal sphincter pressure (LESP) and esophageal body motility were recorded continuously by Dent-sleeve manometry. Bombesin significantly (p < 0.01) increased LESP from 20 +/- 2 mmHg to 43 +/- 6 mmHg. Neither atropine nor somatostatin significantly reduced the bombesin-induced increases in LESP. Bombesin significantly (p<0.05) increased peristaltic wave amplitude (from 61 +/- 4 to 105 +/- 9 mmHg) and duration (from 2.9 +/- 0.2 to 4.8 +/- 0.3 s) in the mid and distal part of the esophagus. Neither atropine nor somatostatin significantly reduced the esophageal body motor response to bombesin. In conclusion (1) bombesin significantly increases LESP and affects esophageal body motility by increasing peristaltic wave amplitude and duration and (2) the effect of bombesin on esophageal motility is not dependent on vagal cholinergic mechanisms and is not mediated by the action of gastrointestinal hormones released by bombesin.
Dis Esophagus 1999
PMID:Effect of bombesin on esophageal motility in humans. 1094 63

Small cell carcinoma arising in the esophagus is a relatively rare disease. In the more common small cell carcinoma of the lung, the diagnostic significance of several new markers has been recently reported. This study used immunohistochemical techniques in addition to clinicopathological analysis, in order to clarify the utility of newer markers as biological parameters or as diagnostic tools. Six patients with small cell carcinoma of the esophagus were clinicopathologically analyzed. Immunohistochemical staining was performed using primary antibodies for bombesin, CD56 and CD57 in addition to conventional endocrine markers chromogranin A, neuron specific enolase and synaptophysin. All patients died within 2 years of surgery due to cancer recurrence, whether or not they had received adjuvant therapy. Pathological stages ranged from IIa to IVb and lymph node metastasis was observed in five cases. Of the six cases, four showed a positive reaction for bombesin and five were positive for CD57. In contrast, no cases revealed a positive reaction for CD56. The one case to survive 24 months after surgery was not shown to express bombesin, CD56 or CD57. Small cell carcinoma of the esophagus demonstrated an unfavorable prognosis. The study suggested that in this disease, bombesin and CD57 (but not CD56) were useful as biological markers, predicting clinical outcome rather than having diagnostic significance.
Dis Esophagus 2003
PMID:Small cell carcinoma of the esophagus; clinicopathological and immunohistochemical analysis of six cases. 1464 20