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Irvin M Modlin

Publications and source records attributed to Irvin M Modlin.

41 records · Page 3Linked to original sources
PubMedDate not supplied

Gastroesophageal reflux disease: then and now.

Although Galen first described esophagitis almost 2000 years ago, its relation to acid was only recognized in the 19th century by Rokitansky. Considerably more interest in the symptoms and complications of esophagitis has been evident over the last century, as gastroesophageal reflux disease displaced peptic ulceration and became the principal acid-related disease of our times. Of particular interest has been the recognition of the clinical significance of the previously overlooked extraesophageal manifestations of the disease such as laryngitis, asthma, and sleep disturbance. The evolution of highly effective medical therapy has over the last decade drastically reduced the need for surgical intervention for control of symptoms except under select conditions, especially volume-related reflux and children with refractory symptoms. The proton pump inhibitor class of drugs is indisputably the most effective overall form of management, while individual proton pump inhibitors appear to be equivalent in their efficacy. Issues that remain to be resolved include the management of nonerosive gastroesophageal reflux disease, the long-term dependence of many patients on acid-suppressing medication, and the recognition of atypical manifestations and rare but serious complications of gastroesophageal reflux disease. In this respect, Barrett's esophagus still presents a major biologic and management conundrum for the physicians and scientists alike.

Barrett Esophagus↗
PubMedDate not supplied

Alteration of DNA methylation status induced by epidermal growth factor in gastric cancer cell line, MKN-74.

DNA methylation dynamics are an important key to understanding various biological events, particularly regulation of gene expressions. To test the hypothesis that epidermal growth factor (EGF) signaling may influence DNA methylation status in cancer cells, which will show several altered biological characters compared with those before EGF-stimulation, we evaluated DNA methylation status with/without EGF-stimulation. The specific alteration of biological character in the gastric cancer cell line, MKN-74, by EGF was demonstrated by DNA synthesis, apoptosis and morphology, revealing that high concentrations of EGF (10 nM) altered the morphology accompanying a moderate increase of cell growth with induction of apoptosis, while low concentrations of EGF (0.1 nM) induced a high increase of cell growth without either morphological change or apoptosis. Although DNA synthesis is almost the same between 0.1 nM of EGF (164%) and 10 nM of EGF (172%), 0.1 nM of EGF showed higher methyltransferase activity than 10 nM of EGF did with a significant difference. In addition, the studies for both the methyl-base uptake into DNA incorporated with DNA synthesis and the methyl-base accepting capacity in DNA showed that a high concentration of EGF (10 nM) induced the demethylated status of the DNA compared with that of 0.1 nM EGF. Thus, we demonstrated that DNA methylation status is affected by EGF-stimulation with alteration of cell biological character.

Adenocarcinoma↗
PubMedDate not supplied

In situ RNA-RNA hybridisation of phospholipase C beta 3 shows lack of expression in neuroendocrine tumours.

BACKGROUND: Phospholipase C beta 3 (PLCB3) plays an important role in the signal transduction of the seven transmembrane receptors. The gene is located in the vicinity of the Multiple Endocrine Neoplasia type 1 (MEN1) gene on chromosome 11q13. Transfection of PLCB3 to neuroendocrine cell lines lacking expression suppresses the neoplastic phenotype and affects the gene expression of S100A3 and human mismatch repair protein, suggesting a role for PLCB3 in neuroendocrine tumorigenesis. MATERIALS AND METHODS: We used RNA-RNA in situ hybridisation for PLCB3 on a total of 82 samples including 34 from MEN1 patients. RESULTS: We show that the PLCB3 transcript is missing in 8 out of 14 MEN1-associated neoplasias as well as in 4 out of 10 bronchial carcinoids, 2 out of 10 exocrine pancreatic cancers and one sporadic adrenocortical carcinoma. CONCLUSION: Low or lack of PLCB3 expression in a subset of endocrine tumours, together with earlier published in vitro data on suppressor characteristics upon transfection, indicate that PLCB3 could be involved in the tumorigenesis in a subset of endocrine tumours.

Animals↗