Browsing by Subject "Metaplasia"

Now showing 1 - 6 of 6
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    Characterization of metaplastic and heterotopic epithelia in the human gastrointestinal tract by the expression pattern of acyl-CoA synthetase 5
    (Murcia : F. Hernández, 2005) Gassler, N.; Obermüller, N.; Keith, M.; Schirmacher, P.; Autschbachl, F.
    Metaplastic and heterotopic epithelia are frequently found in the human intestine. The recently cloned human acyl-CoA synthetase 5 (ACS5) is a key enzyme in providing cytosolic acyl-CoA thioesters. The aim of the study was to identify and to locate the expression of ACS5 in the gastric body and the small intestine with metaplasia or heterotopia by different methods. In the normal gastrointestinal tract, ACS5 was predominantly found in the villus epithelium of the small intestine, but not in the gastric mucosa. Of note, strong expression of ACS5 was also detectable in intestinal metaplasia of the stomach. Inversely, ACS5 expression could neither be detected in heterotopic gastric mucosa of the corpus type nor in gastric, pseudopyloric, or antral metaplasia of the small intestine. In conclusion, our data implicate that ACS5 is a suitable differentiating marker molecule in the gastrointestinal tract.
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    Metaplasia of the parietal layer of Bowman's capsule in the human kidney. Incidence in alcoholic liver disease and hypertension
    (Murcia : F. Hernández, 1988) Haensly, William E.
    This report is the second of two surveys to determine the incidence of metaplasia of Bowman's parietal epithelium in the human kidney. Human kidney sections obtained at autopsy at the Department of Pathology, University of Texas Medical Branch, Galveston, Texas, were examined with the light microscope. The kidneys were fixed in neutral formalin, sectioned at 6 pm and stained with hematoxylin and eosin. Autopsy records were consulted after kidney section examination to determine if there was any correlation between clinical disease, histopathological changes in organ systems and metaplasia of Bowman's capsule. The kidney sections represented both sexes in 8 age groups, from less than one year to 80 years. A total of 174 kidneys, representing 174 individuals, were evaluated. One hundred renal corpuscles were counted per section and the parietal layer of Bowman's capsule was classified as normal (squamous) or metaplastic (cuboidal). Of the 174 kidneys examined, 137 (79% )- 79 male and 58 female - had metaplasia of Bowman's capsule. On the average, in the kidneys with the lesion, 6% of the renal corpuscles had metaplasia of Bowman's parietal layer. The lesion was present in both sexes in all age groups. The autopsy records revealed that metaplasia of Bowman's parietal epithelium was usually present with hepatic fatty changes andlor congestion. Alcoholic liver disease and hypertension represented the most frequent clinical diseases in the sample; these conditions had the highest incidence of metaplasia. Twenty-six of the 174 kidney samples were from individuals with alcoholic liver disease, all of whom had metaplasia of Bowman's capsule. In the latter kidneys the mean percentage of glomerular capsules with metaplasia was 14%, with a range of l to 46%. Thirtyeight of the 174 kidney samples were from individuals with hypertension, 29 (76% ) of whom had metaplasia of Bowman's capsule. In these kidneys the mean percentage of glomerular capsules with metaplasia was 6% with a range of 1 to 16%. These observations suggest that metaplasia of Bowman's parietal epithelium is a common occurrence in the human kidney under different pathological conditions, and is especially prominent in alcoholic liver disease and hypertension.
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    Metaplasia of the parietal layer of Bowman's capsule. A histopathological survey of the human kidney
    (Murcia : F. Hernández, 1986) Haensly, William E.; Lee, J.C.
    Human kidney sections taken at autopsy were examined to determine the incidence of metaplasia of the Bowman's parietal epithelium. Autopsy records were consulted to determine if there was any correlation between clinical disease, histopathological changes in organ systems and metaplasia of Bowman's capsule. The sections represented both sexes in 9 age groups from 2 to 87 years. The sections were fixed in neutral formalin, embedded in paraffin, sectioned at 6 pm, and stained with hematoxylin and eosin. A total of 129 kidney sections, representing 129 individuals, were evaluated. One hundred renal corpuscles were counted per section and the parietal layer of Bowman's capsule was classified as normal (squamous) or metaplastic (cuboidal). Of the 129 kidneys examined, 69 (53%) had metaplasia of Bowman's capsule. Of the 87 male kidneys, 51 (59%) exhibited metaplasia of Bowman's capsule. Of the 42 female kidneys examined, 18 (43%) of the kidneys had metaplasia of Bowman's capsule. On average, in kidneys with metaplasia, 4% of the renal corpuscles had metaplasia of Bowman's parietal layer. The lesion was present in both sexes in all age groups. The autopsy records revealed that there was no common clinical condition associated with the metaplastic lesion, but metaplasia of Bowman's parietal epithelium was consistently present with hepatic congestion and/or fatty changes
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    Pericentriolar material analyses in normal esophageal mucosa, Barrett’s metaplasia and adenocarcinoma
    (Murcia : F. Hernández, 2010) Segat, Daniela; Cassaro, Mauro; Dazzo, Emanuela; Cavallini, Lucía; Romualdi, Chiara; Salvador, Renato; Vitale, María Pia; Vitiello, Libero; Fassan, Matteo; Rugge, Massimo; Zaninotto, Giovanni; Ancona, Ermanno; Baroni, Mauricio David
    Barrett’s esophagus metaplasia is a pre-cancerous condition caused by chronic esophagitis. Chromosomal instability (CIN) is common in Barrett’s cells: therefore, we investigated the possible presence of centrosomal aberrations (a main cause of CIN) by centrosomal protein immunostaining in paraffined esophageal samples of patients who developed a Barrett’s adenocarcinoma. In most (55%) patients, alterations of the pericentriolar material (PCM) signals were evident and consistently marked the transition between normal epithelium to metaplasia. The alterations could even be found in adjacent native squamous epithelium, Barrett’s mucosa and submucosal gland cells, as well as in the basal/epibasal layers of the mucosa and submucosal gland duct, which are the regions hosting esophageal stem and progenitor cells. These findings strongly support the hypothesis that the three esophageal histotypes (one being pathological) can have a common progenitor. Surprisingly, PCM defective signal eventually decreased with neoplastic progression, possibly to enhance the genome stability of advanced cancer cells. Importantly, PCM altered signals in Barrett’s mucosa and their apparent evolution in successive histopathological steps were correlated to adenocarcinoma aggressiveness, suggesting PCM as a possible prognostic marker for tumor relapse. Extending our observations in a prospective study might help in the development of new prevention protocols for adenocarcinoma patients
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    Squamous and glandular differentiation in urothelial bladder carcinomas. Histopathology, histochemistry and immunohistochemical expression of carcinoembryonic antigen
    (Murcia : F. Hernández, 1988) López-Beltrán, A.; Martín, J.; García, J.; Toro, Manuel
    This paper reports the itiin~~~nochemical expression of carcinoembryonic antigen in the s c l u a n~o~~glsa.n dular anci mixed clifferrentiation areas ohser\.cd in l90 ~~rothe l iuarli nary bladder carcinomas. Tlic antigen kvas found to occur in 7596 and 81 96 of all papillary and solid infiltrating carcinomas. rcspectivcly. Thc use of thc imm~~nohistochemicdael termination of CEA in improving the niorphological examination of these cliffcrcntiation arcas and their scant nrescnce in thc prognosis of urothelial carcinomas involbing squun~ous andlor glandular focal differentiation are discussed
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    The molecular pathology of Barrett's esophagus
    (Murcia : F. Hernández, 1999) Werner, M.; Mueller, J.; Walch, A.; Hofler, H.
    The incidence of adenocarcinoma of the distal esophagus is rapidly increasing in the Western world. The histopathological sequence of (Barrett's) metaplasia, which develops as a consequence of chronic reflux, to dysplasia and then to carcinoma is well established for these tumors. In Barrett's esophagus a variety of molecular changes have been characterized and correlated with tumor initiation and progression. Among the early changes in premalignant stages of metaplasia are alterations of the transcripts of FHIT, a presumptive tumor suppressor gene which spans the common fragile site FRA3B. Mutations of p53 seem to accumulate mainly in the transition from low to high grade dysplasia. Inactivation of other tumor suppressor genes by mutation (APC, p16) or hypermethylation (p16) as well as amplification of oncogenes such as cerbB2 are relatively late events in the development of adenocarcinoma. Among the phenotypic changes in Barrett's esophagus are an expansion of the Ki67 proliferation compartment which correlates with the degree of dysplasia. Moreover, accumulation of rabll molecules which are involved in membrane trafficking has been reported to be specific for the loss of polarity seen in low grade dysplasia. Reduced expression of the cadherinlcatenin complex as well as increased expression of various proteases develop chiefly in invasive carcinomas. Despite the progress that has been made in the identification of molecular markers in Barrett's carcinoma, to date the histopathogical diagnosis of high grade dysplasia in endoscopic biopsies remains the best predictor of invasive cancer. Immunohistochemistry applying a panel of antibodies including p53, Mib-l or rabll can be helpful to diagnose regenerative metaplastic epithelium or low and high grade dysplasia.