Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Squamous cell papilloma of the esophagus is a rare lesion involving less than 60 case reports worldwide. These lesions are generally asymptomatic but may at times grow and spread rapidly. One fatality, a result of massive dissemination, has been reported. Until recently, human papillomavirus had not been identified in association with esophageal papillomas. A second case, to the authors' knowledge, of esophageal papillomas associated with human papillomavirus is reported. The virus has been previously shown to be associated with abnormal squamous epithelium in and adjacent to esophageal carcinoma. The virus was identified from biopsy specimens obtained at endoscopy using DNA in situ hybridization techniques. The strain of human papillomavirus identified is similar to those found in the oropharynx and genital tract, raising the possibility of sexual transmission. This case also differs from the previous case report involving the human papillomavirus because of the patient's benign clinical course. Our case serves to highlight differences that are perhaps unique to the human papillomavirus. Multiple papillomas found in a proximal location within the esophagus seem to favor involvement of the human papillomavirus. Isolated lesions located distally appear more characteristic of chronic gastroesophageal reflux as an etiology. The syndrome of squamous cell papillomas involving the esophagus is reviewed in the article.
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PMID:Squamous papilloma of the esophagus associated with the human papillomavirus. 132 97

Neuroendocrine features and cytogenetic abnormalities of one continuous cell line (MTC-SK) and two long-term cultures (GER, STAH) derived from three sporadic cases of human medullary thyroid carcinomas (MTCs) were studied. Specific neuroendocrine markers (NSE, chromogranins, calcitonin, calcitonin gene-related peptide) were identified by electron microscopy and immunocytochemistry. In situ hybridochemistry and Northern blot analysis confirmed endocrine activity. Cytogenetic studies of the cell line MTC-SK revealed three consistent marker chromosomes, t(3;10), 11p+, and 22p+. Cells of long-term cultures GER and STAH exhibited a consistent translocation t(2;18), a trisomy 7, and two consistent marker chromosomes der3 and 5p+, respectively. Recently, we have isolated 12 stable clones of this MTC-SK cell line, which showed two different growth patterns. Quantitative measurement of mitotic activity flow cytometry and semiquantitative analysis of AgNOR-, Ki67-, and Cyclin/PCNA-(immuno)reactivity showed different DNA composition and duplication rates, indicating at least two subpopulations. Some of our clones developed a new consistent marker (i.e., an unbalanced translocation between mar11p+ and 1q). However, no correlations between chromosome findings, growth rate, and neuroendocrine markers were observed.
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PMID:Biologic and cytogenetic characterization of three human medullary thyroid carcinomas in culture. 148 77

Barrett's esophagus is a condition in which the normal stratified squamous epithelium is replaced by a specialized metaplastic columnar epithelium. It develops as a consequence of chronic gastroesophageal reflux and predisposes to the development of esophageal adenocarcinoma. Adenocarcinoma develops in Barrett's esophagus by a multistep process in which specialized metaplasia progresses to dysplasia, then to early adenocarcinoma, and eventually to deeply invasive and metastatic disease. This neoplastic progression is associated with a process of genomic instability that generates abnormal clones of cells, some of which have aneuploid or increased G2/tetraploid DNA content. A systematic protocol of endoscopic biopsy can detect Barrett's adenocarcinomas at an early stage, when they may be curable.
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PMID:Barrett's esophagus and esophageal adenocarcinoma. 178 15

Barrett's esophagus develops as a complication of chronic gastroesophageal reflux and predisposes patients to the development of dysplasia and adenocarcinoma of the esophagus. Because light microscopy of dysplasia in Barrett's esophagus shows diminished or absent mucus, we used transmission electron microscopy to compare cytoplasmic organelles required for mucus production in dysplastic and nondysplastic esophageal columnar epithelium. These observations of the rough endoplasmic reticulum, Golgi apparatus, and secretory granules were correlated with histologic interpretations and flow cytometric measurements of abnormalities of DNA content. Ultrastructural abnormalities included depletion and alteration of organelles required for mucus biosynthesis. These abnormalities often were accompanied by cells with markedly distended rough endoplasmic reticulum and massive accumulation of cytoplasmic glycogen aggregates. All 9 patients who had Barrett's dysplasia with or without early adenocarcinoma had ultrastructural abnormalities, as did 3 of 8 patients whose biopsy histology was indefinite for dysplasia. Abnormalities measured by flow cytometry correlated well with the presence of these ultrastructural aberrations. All 9 patients with Barrett's dysplasia with or without early adenocarcinoma had abnormalities observed by electron microscopy and aneuploidy or increased G2/tetraploid fractions measured by flow cytometry. Two of the 3 patients whose biopsies were indefinite for dysplasia and who had ultrastructural abnormalities also had aneuploidy or increased G2/tetraploid fractions. Neither ultrastructural nor flow cytometric abnormalities were found in the remaining 5 patients whose biopsies were indefinite for dysplasia, in 19 of 22 patients with Barrett's specialized metaplasia, or in any of the 7 patients with gastroesophageal reflux disease without Barrett's specialized metaplasia. Two of the 22 patients with Barrett's specialized metaplasia had distended rough endoplasmic reticulum in rare cells, and one other had an aneuploid cell population. We conclude that neoplastic progression in Barrett's esophagus is associated with abnormalities of cytoplasmic organelles required for mucus production. With few exceptions, these ultrastructural aberrations correspond to the presence of dysplasia or of aneuploidy or increased G2/tetraploid fractions. Electron microscopy and flow cytometery detect abnormalities associated with the development of dysplasia and cancer in Barrett's esophagus that may be biologically significant.
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PMID:Correlation of ultrastructural aberrations with dysplasia and flow cytometric abnormalities in Barrett's epithelium. 291 Jul 57

Barrett's esophagus is a condition in which metaplastic columnar epithelium replaces squamous esophageal epithelium as a consequence of chronic gastroesophageal reflux. Patients with this condition are at increased risk for the development of adenocarcinoma. To better understand the progression to adenocarcinoma in this disease, we studied abnormalities in DNA content of epithelial cells in Barrett's esophagus. Using flow cytometry, we examined the spatial distribution of abnormal nuclear DNA contents (aneuploidy) in the esophagi of 14 patients with Barrett's adenocarcinoma. Multiple (2 to 14) populations of aneuploid cells were seen in 12 of the 14 cases. Some early carcinomas appeared to be associated with a single aneuploid population of cells. Surrounding dysplastic epithelium often contained multiple, different overlapping aneuploid populations. These data suggest that neoplastic progression in Barret's esophagus is associated with a process of genomic instability which leads to evolution of multiple aneuploid populations, with the ultimate development of a clone of cells capable of malignant invasion. Thus, detection of multiple aneuploid populations of cells in Barrett's esophagus may indicate a high risk of cancer. Barrett's esophagus provides a unique and readily accessible model for the study of neoplastic progression in human epithelial malignancy.
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PMID:Progression to cancer in Barrett's esophagus is associated with genomic instability. 291 Nov 84

A new stimulus for research into the etiology and pathogenesis of Barrett's columnar-lined lower esophagus has been provided by the discovery that Barrett's esophagus has a very high prevalence in the general population and that adenocarcinoma of the esophagus and cardia is the fastest-growing cancer in the United States. Gastroesophageal reflux disease is the single most important factor in the pathogenesis of Barrett's esophagus, and duodenal juices may play a key role in the development of complications of stricture, ulceration, and possibly even malignant degeneration. Treatment is, therefore, aimed at abolishing all forms of reflux. Acid suppression, if used, needs to be given in massive doses to be effective in gastric hypersecretion and has no effect on other constituents of the refluxed material. Antireflux surgery has been shown to be superior to all forms of medical treatment. Regression is rare after any therapy, but continued surveillance is essential, with increased vigilance in patients with dysplasia or DNA abnormalities on flow cytometry. The role of cigarettes and alcohol in malignant degeneration is refuted.
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PMID:Barrett's esophagus. 758 62

Recent studies suggest human immunodeficiency virus (HIV) may be the cause of HIV-associated idiopathic esophageal ulcer (IEU). However, other causes of esophageal disease in HIV-infected patients have not been evaluated for appropriate comparison. Over a 14-month period 13 patients with IEU as determined by clinical, endoscopic, and pathologic criteria were identified. During the same period nine HIV-infected patients with cytomegalovirus (CMV) esophagitis and one HIV-infected patient each with herpes simplex virus esophagitis and gastroesophageal reflux disease (GERD) were also identified. Polymerase chain reaction (PCR) and in situ DNA hybridization (ISH) were performed on paraffin-embedded tissue formed on paraffin-embedded tissue of endoscopic biopsies of ulcer tissue using standard techniques. Eleven of 13 IEU patients (85%) as compared to seven of nine patients (78%) with CMV had HIV detected by PCR (P = 0.38). HIV was also detected in ulcer tissue from biopsy material from the patient with GERD but not herpes simplex virus esophagitis. In PCR-positive patients, ISH confirmed the presence of HIV in four patients (57%) with CMV and eight (73%) with IEU (p = 0.31). HIV was found only in inflammatory cells and not squamous epithelial cells. Given the similar prevalence of detection of HIV by PCR and ISH in ulcer tissue from both groups of HIV-infected patients as well as the location in rare inflammatory cells, we conclude that HIV infection of squamous mucosa does not appear to be the primary cause of IEU.
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PMID:Evaluation of idiopathic esophageal ulceration for human immunodeficiency virus. 767 79

Human papillomavirus infection is important for both the development of papilloma and the progression of the papilloma-carcinoma sequence in the cervix, larynx, lung, and colon. Esophageal squamous cell papilloma is rare but important as a possible precancerous lesion. Esophageal papilloma has previously been thought to develop mainly as a result of chemical irritation by chronic gastroesophageal reflux. However, a few recent studies suggested a role for papillomavirus infection in esophageal tumorigenesis, although the exact route of transmission and invasion of the virus has not been fully elucidated. A case of esophageal squamous papilloma at the site of endoscopic injection sclerotherapy (EIS) for varices is reported. Papilloma development was followed up clinically during a 2-year period, and the papilloma was removed by endoscopic mucosal resection. Histological examination of the tissue confirmed the diagnosis of squamous cell papilloma. DNA analysis of the tumor showed integration of papillomavirus type 16 but not types 18 and 33. The surrounding normal mucosa did not contain any of the three virus types. Injury such as ulceration resulting from EIS may have provided a locus susceptible to the viral infection. The clinical course after EIS should be monitored carefully to detect papilloma formation.
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PMID:Human papillomavirus type 16-positive esophageal papilloma at an endoscopic injection sclerotherapy site. 783 98

Barrett's oesophagus is a condition in which a metaplastic columnar mucosa replaces the normal squamous epithelium of the lower oesophagus. Barrett's oesophagus develops as a complication of gastro-oesophageal reflux and predisposes to the development of oesophageal adenocarcinoma. Most adenocarcinomas arising in Barrett's mucosa are far advanced at the time of diagnosis, and prognosis is consequently poor. Regular endoscopic surveillance of patients with Barrett's oesophagus is recommended to detect the oesophageal malignancy in an early presymptomatic stage. The concept of screening is based on the notion that regular surveillance can reduce the mortality, but there is yet little evidence that this is the case in Barrett's oesophagus. Screening is generally carried out by regular endoscopy with multiple biopsies in an attempt to detect dysplasia. Unfortunately, dysplasia is not an ideal biomarker of malignant potential in Barrett's oesophagus. There is an interest in research into more sensitive and effective predictors of heightened risk for development of malignancy. DNA content flow cytometry and p53 protein expression might be useful in managing the cancer risk in Barrett's patients. However these new techniques need further evaluation before they can be applied to routine clinical investigation.
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PMID:[Barrett esophagus. Current situation of the risk and surveillance policy]. 789 14

In Barrett's esophagus the normal stratified squamous epithelium lining the esophagus becomes replaced by metaplastic columnar epithelium containing goblet cells; it develops as a complication of chronic gastroesophageal reflux disease and predisposes the patient to adenocarcinoma. The frequency with which it leads to adenocarcinoma is not established with certainty, but the reported prevalence averages approximately 10% when the diagnosis of Barrett's esophagus is first made. The estimated incidence of adenocarcinoma varies from one in 152 to one in 441 cases per patient year, or a 30- to 125-fold excess risk. Esophageal adenocarcinoma arises only in patients with metaplastic columnar epithelium. Dysplasia precedes adenocarcinoma in Barrett's esophagus and arises from the metaplastic epithelium; it has been proposed as a marker for detecting patients at high risk for developing carcinoma. Problems with the use of dysplasia as a marker for cancer risk include difficulty in differentiating it from reactive change, variability in diagnosis and grading between observers and when the same observer interprets the sections on different occasions, and lack of understanding of its natural history. Methods other than dysplasia for detecting patients at highest risk for developing carcinoma have been sought, but flow cytometric analysis of DNA content is the only one proven to be valuable to date. Flow cytometric abnormalities correlate well with histological progression in Barrett's esophagus. The prevalence of elevated S phase and G2/tetraploid fractions and of aneuploid cell populations increases with histological progression from metaplasia to indefinite/low grade dysplasia to high grade dysplasia and cancer. Flow cytometric abnormalities in endoscopic biopsy specimens identify those patients with a higher risk of progression to high grade dysplasia or adenocarcinoma.
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PMID:Barrett's esophagus, dysplasia, and adenocarcinoma. 792 21


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