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PubMedDate not supplied

Telomerase reverse transcriptase expression is increased early in the Barrett's metaplasia, dysplasia, adenocarcinoma sequence.

Barrett's esophagus is a multistage polyclonal disease that is associated with the development of adenocarcinoma of the esophagus and esophagogastric junction. Telomerase activation is associated with cellular immortality and carcinogenesis, and increased expression of the telomerase reverse transcriptase catalytic subunit (hTERT) has been used for the early detection of malignant diseases. To identify biomarkers associated with each stage of the Barrett's process, relative mRNA expression levels of hTERT were measured using a quantitative reverse transcription-polymerase chain reaction method (ABI 7700 Sequence Detector (TaqMan system) in Barrett's intestinal metaplasia (n = 14), Barrett's dysplasia (n = 10), Barrett's adenocarcinoma (n = 14), and matching normal squamous esophagus tissues (n = 32). hTERT expression was significantly increased at all stages of Barrett's esophagus, including the intestinal metaplasia stage, compared to normal tissues from patients without cancer (intestinal metaplasia vs. normal esophagus, P <0.0001; dysplasia, P = 0.001; adenocarcinoma, P = 0.007; all Mann-Whitney U test ). hTERT expression levels were significantly higher in adenocarcinoma tissues than in intestinal metaplasia tissues (P = 0.003), and were higher in dysplasia compared with intestinal metaplasia tissues (P = 0.056). hTERT levels were also significantly higher in histologically normal squamous esophagus tissues from cancer patients than in normal esophagus tissues from patients with no cancer (P = 0.013). Very high expression levels ([hTERT x 100: beta-actin] >20) were found only in patients with cancer. These findings suggest that telomerase activation is an important early event in the development of Barrett's esophagus and esophageal adenocarcinoma, that very high telomerase levels may be a clinically useful biomarker for the detection of occult adenocarcinoma, and that a widespread cancer "field" effect is present in the esophagus of patients with Barrett's cancer.

Adenocarcinoma↗
PubMed2002

Transgenic overexpression of interleukin (IL)-10 in the lung causes mucus metaplasia, tissue inflammation, and airway remodeling via IL-13-dependent and -independent pathways.

To address the complex chronic effector properties of interleukin (IL)-10, we generated transgenic mice in which IL-10 was overexpressed in the lung. In these mice, IL-10 inhibited endotoxin-induced tumor necrosis factor production and neutrophil accumulation. IL-10 also caused mucus metaplasia, B and T cell-rich inflammation, and subepithelial fibrosis and augmented the levels of mRNA encoding Gob-5, mucins, and IL-13. In mice bred to have null mutations of IL-13, IL-4R(alpha), or STAT-6, transgenic IL-10 did not induce mucus metaplasia but did induce inflammation and fibrosis. IL-10 was also a critical mucin regulator of virus-induced mucus metaplasia. Thus, IL-10, although inhibiting lipopolysaccharide-induced inflammation, also causes mucus metaplasia, tissue inflammation, and airway fibrosis. These responses are mediated by multiple mechanisms with mucus metaplasia being dependent on and the inflammation and fibrosis being independent of an IL-13/IL-4R(alpha)/STAT-6 activation pathway.

Animals↗
PubMed2006

Comparative proteomics analysis of Barrett metaplasia and esophageal adenocarcinoma using two-dimensional liquid mass mapping.

Esophageal adenocarcinoma, currently the seventh leading cause of cancer-related death, has been associated with the presence of Barrett metaplasia. The malignant potential of Barrett metaplasia is evidenced by ultimate progression of this condition to invasive adenocarcinoma. We utilized liquid phase separation of proteins with chromatofocusing in the first dimension and nonporous reverse phase HPLC in the second dimension followed by ESI-TOF mass spectrometry to identify proteins differentially expressed in six Barrett metaplasia samples as compared with six esophageal adenocarcinoma samples; all six Barrett samples were obtained from the identical six patients from whom we obtained the esophageal adenocarcinoma tissue. Approximately 300 protein bands were detected by mass mappings, and 38 differentially expressed proteins were identified by microLC-MS/MS. The false positive rates of the peptide identifications were evaluated by reversed database searching. Among the proteins that were identified, Rho GDP dissociation inhibitor 2, alpha-enolase, Lamin A/C, and nucleoside-diphosphate kinase A were demonstrated to be up-regulated in both mRNA and protein expression in esophageal adenocarcinomas relative to Barrett metaplasia. Candidate proteins were examined at the mRNA level using high density oligonucleotide microarrays. The cellular expression patterns were verified in both esophageal adenocarcinomas and in Barrett metaplasia by immunohistochemistry. These differentially expressed proteins may have utility as useful candidate markers of esophageal adenocarcinoma.

Adenocarcinoma↗
PubMedDate not supplied

Morules in cribriform-morular variant of papillary thyroid carcinoma: Immunohistochemical characteristics and distinction from squamous metaplasia.

Morules are a diagnostic clue to the cribriform-morular variant (C-MV) of papillary thyroid carcinoma, and are superficially similar to squamous metaplasia. In order to clarify the histogenesis of morules and differentiate them from squamous metaplasia, we immunohistochemically compared the morules in five cases of C-MV with squamous metaplasia in six cases of diffuse sclerosing variant (DSV) of papillary thyroid carcinoma. The squamous metaplastic cells were immunopositive for low- and high-molecular-weight cytokeratin, whereas the morular cells were negative or focally positive. Vimentin-positive cells were observed focally in the morules and squamous metaplasia, except for one case of CMV that showed intense positivity. The morular cells showed weak cytoplasmic positivity for beta-catenin, and the cell membrane was not highlighted. Some nuclei of the morular cells were also positive for this antibody. Beta-catenin was intensively positive along the cell membrane of the metaplastic cells, and did not react against the nuclei or cytoplasm. Bcl-2 was positive in the morular cells, but negative in the metaplastic cells. S-100 protein-positive dendritic cells were observed in the metaplastic nests, but not in the morules. We argue that morules appear in connection with nuclear and cytoplasmic aberrant localization of beta-catenin, and are not an early form of squamous metaplasia.

Adolescent↗
PubMed2004

Intestinal metaplasia of gastric cardia and carditis in Japanese patients with Helicobacter pylori infection.

AIM: The purpose of this study was to determine the prevalence of intestinal metaplasia of the gastric cardia in Japanese patients with Helicobacter pylori infection. METHODS: One hundred and fifty-seven patients with H. pylori infection participated in this study. Four biopsy specimens were taken from antrum, lesser and greater curvatures of stomach, and cardia for histological examination. The patients were divided into three groups: those < or = 39 years of age (group A), those 40-59 years old (group B), and those > or = 60 years of age (group C). RESULTS: The proportions of the patients with intestinal metaplasia of the gastric cardia in the three groups were 12, 39, and 65%, respectively. Their intestinal metaplasia of gastric cardia scores were 0.2, 0.54, and 0.81, respectively (significant difference among groups A, B, and C: p < 0.05), according to the updated Sydney classification. CONCLUSION: The prevalence of intestinal metaplasia of the gastric cardia and carditis in Japanese patients with H. pylori infection was similar to that of metaplasia of antrum and lesser curvature of the stomach.

Adolescent↗
PubMed1999

Mucous-cell metaplasia and inflammatory-cell recruitment are dissociated in allergic mice after antibody- and drug-dependent cell depletion in a murine model of asthma.

Inflammatory-cell infiltration and epithelial modifications are prominent lesions of the bronchial mucosa in asthma and in experimental allergic bronchopulmonary inflammation. However, the recruitment of inflammatory cells and their relationship to the epithelial modifications and to functional alterations such as bronchopulmonary hyperreactivity (BHR) are less known. We studied the mechanisms of antigen-dependent inflammatory-cell recruitment to the lungs and the associated lesions and their relationship using drug- and antibody-dependent cell-depletion procedures. A single intranasal ovalbumin challenge in BP2 mice was found to induce hyperreactivity within 1 h after challenge, followed by the massive infiltration of immunoglobulin (Ig)E-bearing polymorphonuclear leukocytes (PMN), and eosinophils, and by a mucous-cell metaplasia of the bronchiolar epithelium. Similarly challenged BALB/c mice did not exhibit BHR, despite a moderate recruitment of inflammatory cells and mucous-cell metaplasia. Inflammatory-cell recruitment, mucous-cell metaplasia, and BHR were prevented by prior antibody-dependent depletion of CD3(+) lymphocytes and partially inhibited by the depletion of CD4(+) lymphocytes. Treatment with the granulocytopenic drug vinblastine before challenge completely abolished the recruitment of granulocytes without affecting the antigen-induced mucous-cell metaplasia. In this study two new key elements of the murine model of allergic pulmonary inflammation are described: the recruitment of IgE-bearing PMN between 3 and 72 h after challenge, and the dissociation between granulocytes and mucous-cell metaplasia.

Animals↗
PubMed2003

The utility of cytokeratins 7 and 20 (CK7/20) immunohistochemistry in the distinction of short-segment Barrett esophagus from gastric intestinal metaplasia: Is it reliable?

BACKGROUND: The purpose of the present correlative immunohistochemical study was to assess the utility of cytokeratin (CK7 and CK20) expression in the diagnosis of short-segment Barrett esophagus, particularly its efficacy in differentiating Barrett mucosa from intestinal metaplasia of the gastric cardia and corpus. METHODS: Two groups of endoscopic biopsy specimens were examined, including 20 endoscopic biopsy specimens of short-segment Barrett esophagus (Group A) and equal number exhibiting Helicobacter pylori associated intestinal metaplasia of the gastric cardia and corpus (Group B). All were investigated by immunohistochemistry using the standard ABC method for CK7 and CK20 expression. Fisher's exact test was used for statistical analysis of Barrett CK7/20 and gastric CK7/20 patterns between the groups. RESULTS: The anticipated pattern of reactivity in Barrett mucosa (CK7: strong diffuse positivity in superficial and deep glands; CK20: positivity in surface epithelium and superficial glands) was seen in 2 cases of Group A specimens. The expected gastric pattern (CK7: patchy immunostaining with variable involvement of deep glands; CK20: patchy immunostaining of superficial and deep glands in incomplete intestinal metaplasia / absence of CK7 immunoreactivity with strong CK20 staining in superficial and deep glands in complete intestinal metaplasia) was seen in 8 cases of Group B specimens. The respective sensitivity and false-negativity values of CK7/20 staining for Barrett pattern in Group A were 10% and 90%, respectively. These values for gastric pattern in Group B were 40% and 60%, respectively. The specificity and false-positivity values of both patterns were same (100% and 0%, respectively). There was no statistically significant difference for Barrett pattern between the two groups (P = 0.487), while the observation of gastric pattern was significantly higher in Group B than in Group A (P = 0.02). CONCLUSIONS: We concluded that these hypothesized and recently applied diagnostic criteria involving CK7 and CK20 immunoreactivity are not reliable in distinguishing short-segment Barrett esophagus from intestinal metaplasia as seen in gastric cardia and corpus.

Journal Article↗
PubMed2005

Mucin phenotypic expression and p53 gene abnormality of gastric super-minute well-differentiated adenocarcinoma: re-evaluation with relationship between histogenesis of well-differentiated adenocarcinoma and intestinal metaplasia in distal stomach.

BACKGROUND: Although the gastric well-differentiated adenocarcinoma in the distal stomach has been thought to develop via a intestinal metaplasia-carcinoma sequence, there are some disproofs from new mucin examinations for minute-size lesions in same type carcinoma. The current study was performed and pointed out the new findings for the solution to the problem according to the point described above. METHODS: 12 super-minute lesions (less than 1 mm in maximum diameter) of well-differentiated adenocarcinoma in distal stomach (SMCa), which were detected from the pathological examinations of 210 surgically resected stomach specimens, and the mucosa adjacent to these carcinoma lesions, were examined by immunohistochemical mucin stainings (MUC2 and CD-10: intestinal phenotype, 45M1 and MUC6: gastric phenotype) and p53-overexpression. And the analyses of the replication error of the microsatellites in chromosome 17 related p53 gene (TP53 and D17S786) (RER-p53MS) were performed in SMCa lesions, adjacent mucosa to each lesion and other gastric mucosa with intestinal metaplasia, because all SMCa lesions showed p53-overexpression immunohistochemically, described below. RESULTS: 1. The carcinoma cells in all SMCa lesions were positive for 45M1 and p53. On the other hand, no positive carcinoma cells for MUC6 were seen although the pyloric glands and the remnant pyloric gland in the SMCa lesions in the same slides were positive for MUC6. Ten lesions (83%) had intestinal phenotypic mucin (10 lesions: MUC2 (+), 4 lesions: CD10 (+)). Two lesions (17%) were positive for only 45M1 (gastric phenotypic mucin). 2. All of the mucosa adjacent to SMCa showed intestinal metaplasia (complete type: 7 regions, incomplete type: 5 regions). 3. RER-p53MS was confirmed in 42% (5/12 regions) of SMCa, in 42% (5/12 regions) of the mucosa adjacent to SMCa and 14% (6/42 regions) of the other intestinal metaplasia mucosa. CONCLUSION: Most of the super-minute well-differentiated adenocarcinoma lesions in the distal stomach, which had both gastric and intestinal phenotypic mucin, are considered to develop from the tubular proliferative zone with the incomplete type of the intestinal metaplasia and p53 gene abnormality, while a part of them, which had only gastric phenotypic mucin, may derive from the gastric native tubules (non-metaplastic epithelium) with p53 gene abnormality.

Journal Article↗
PubMed2006

[The characteristics of proliferation activity in squamous metaplasia and reserve cell hyperplasia of uterine cervix].

The aim of our study was to investigate the characteristics of proliferation activity in squamous metaplasia and reserve cell hyperplasia of uterine cervix. Four groups of patients were selected: 1st group--34 reproductive patients with reserve cell hyperplasia, 2nd group--21 reproductive patients with squamous metaplasia, 3rd group--12 postmenopausal patients with reserve cell hyperplasia, 4th group--29 postmenopausal patients with squamous metaplasia. These groups included the patients with and without infections. Cervical biopsies were studied by immunohistochemistry using anti-Ki-67 monoclonal antibody. Ki-67(+) reserve cells were counted in reserve cell hyperplasia. Ki-67(+) squamous cells were counted in squamous metaplasia. The results showed that in both squamous metaplasia and reserve cell hyperplasia the number of Ki-67(+) cells, i.e. the intensity of proliferation is depended on the co-existence of infection, as well as on the age of the patient. These data are important in the complex treatment of cervical pseudoerosions.

Adult↗
PubMed1984

Skin calcium-binding protein in squamous metaplasia of human uterine cervix.

The distribution of skin calcium-binding protein in squamous cell metaplasia of human endocervix, in normal human skin, and in ovarian cancer was determined by the immunofluorescence technique. A rabbit antiserum specific to rat SCaBP was characterized by Ouchterlony immunodiffusion and by immunoprecipitation of 125I-labeled SCaBP. The specificity of antibody labeling was demonstrated by using preimmune rabbit serum and SCaBP antiserum competitively absorbed with purified SCaBP. In normal human skin SCaBP was found exclusively in the basal layer cell cytoplasm. This protein was not detected in normal columnar epithelium of endocervix. Epithelial tissues in the zone of transition between the cylindrical epithelium of the endocervical mucosa and the stratified squamous epithelium of the exocervix were obtained from 14 patients with a wide variety of squamous cell metaplasia. In the early stage of metaplasia SCaBP was detected exclusively in the cytoplasm of reserve undifferentiated cells. In the terminal stage of metaplasia the SCaBP was present only in the basal cell layer. SCaBP was found in several layers of dysplastic tissue, and this distribution appeared to be related to the loss of normal maturation of the epithelium. SCaBP was also present in squamous cell carcinoma of endocervix especially in the least differentiated regions of the tumor. No SCaBP was detected in any ovarian cancer cells. These findings are potentially useful as a means of early detection of squamous metaplasia and of distinguishing premalignant anaplastic lesions from those that are benign and nonproliferative. In addition, the presence of SCaBP in tumors derived from metaplastic epithelia and its absence in the ovarian cancer indicate that immunohistochemical search for this protein might be of value in tumors in which an epidermoid origin is a possibility.

Animals↗
PubMed1983

Induction of squamous metaplasia in organ cultures of hamster trachea by naturally occurring and synthetic fibers.

Asbestos exhibits many properties of classical tumor promoters. These characteristics include the ability to stimulate proliferation and inhibit normal differentiation of cells. In organ cultures of trachea, crocidolite and amosite asbestos stimulate squamous metaplasia, a pathological process in which a rapidly proliferating squamous epithelium replaces the normal epithelium. We hypothesized that the induction of metaplasia depends upon the fibrous nature of asbestos. Accordingly, several naturally occurring and synthetic fibrous materials and their nonfibrous analogues were assessed for their ability to induce metaplastic changes in tracheal mucosa of the Syrian hamster. Exposure to both crocidolite asbestos and fiberglass resulted in significant increases (p less than 0.05) in squamous metaplasia over a range of dosages (1.0, 4.0, 16.0 mg/ml). Attapulgite (palygorskite) and both "long-" and "short-" fiber preparations of chrysotile asbestos had similar but less marked effects. Nonfibrous analogues of each material (riebeckite, antigorite, and glass particles) failed to produce metaplasia. Asbestos, and fibrous materials in general, appear to stimulate squamous metaplasia because of their fibrous geometry.

Animals↗
PubMed1998

Abundant expression of the intestinal protein villin in Barrett's metaplasia and esophageal adenocarcinomas.

Villin is a cytoskeletal protein that is involved in the formation of brush-border microvilli in normal small intestine and colon epithelium. This protein is present in Barrett's metaplasia but is reported not to be expressed in Barrett's adenocarcinoma. In this study, we analyzed villin protein expression in Barrett's metaplasia and in both Barrett's adenocarcinomas and tumors of the gastric cardia. Immunohistochemical analysis was used to evaluate the expression and cellular localization of the villin protein in 21 cases of Barrett's metaplasia, 30 cases of Barrett's adenocarcinoma, 16 cases of gastric cardia adenocarcinoma, and eight cases of adenocarcinoma of the distal esophagus. Southern, northern, and western blot analyses were used to evaluate the potential mechanisms for regulation of villin protein expression. Villin protein expression was observed in 21 of 21 cases (100%) of intestinal-type Barrett's metaplasia and in 28 of 30 cases (93%) of Barrett's adenocarcinoma and was thus highly expressed in these tumors. Northern blot analysis demonstrated villin mRNA (3.5 and 2.7 kb) in both villin-positive Barrett's metaplasia and adenocarcinomas. Western blot analysis with the antibody used for immunohistochemical analysis confirmed the presence of a single villin protein band of 95 kDa. Abundant villin expression also was present in both adenocarcinoma of the gastric cardia (13 of 16 cases; 81%) and distal esophageal adenocarcinomas of unknown origin (six of eight cases; 75%). The intestinal brushborder enzyme sucrase isomaltase was found to be present in only 22 of 46 cases (48%) of the adenocarcinomas that expressed villin. We concluded that the protein villin is highly expressed in Barrett's adenocarcinomas and is well maintained in these and other esophageal tumors.

Adenocarcinoma↗
PubMed1998

Prevalence of gastric metaplasia in the duodenal bulb and distribution of Helicobacter pylori in the gastric mucosa. A clinical and histopathological study in 96 consecutive patients.

BACKGROUND: Consecutive untreated patients with duodenal ulcer (n = 49) or gastric ulcer (n = 47) were compared with regard to the presence of gastric metaplasia in the duodenal bulb, gastric distribution of Helicobacter pylori and histopathological findings to assess differences which may contribute to either duodenal ulcer or gastric ulcer development. METHODS: Serial sections of corpus, antral and duodenal mucosal biopsies were stained by haematoxylin-eosin stain for histopathological evaluation, immunohistochemistry for the detection of Helicobacter pylori, and duodenal biopsies alone by the PAS/Alcian blue stain to assess the presence of gastric metaplasia in the duodenal bulb. RESULTS: Helicobacter pylori was found in 81.6% of duodenal ulcer and in 83.0% of gastric ulcer patients. In duodenal ulcer and gastric ulcer patients, Helicobacter pylori was found in 79.6% and 79.5% of corpus, 77.6% and 72.3% of antral, and 16.7% and 20.0% of duodenal bulb biopsies, respectively. In duodenal ulcer patients, the density of Helicobacter pylori was significantly lower in corpus compared to antrum biopsies (p < 0.001). Furthermore, the Helicobacter pylori density was higher in corpus of gastric ulcer than of duodenal ulcer patients. Inflammatory scores followed the density of Helicobacter pylori infection. In the duodenal bulb of both duodenal ulcer and gastric ulcer patients, the occurrence and extent of gastric metaplasia were comparable. Gastric metaplasia was present in 5 out of 8 Helicobacter pylori positive duodenal biopsies of duodenal ulcer patients and in 3 out of 9 Helicobacter pylori positive duodenal biopsies of gastric ulcer patients. CONCLUSIONS: No evidence was found for a role of gastric metaplasia in the differential pathogenesis of duodenal ulcer or gastric ulcer. Differences in the gastric topography of Helicobacter pylori density and inflammatory scores between duodenal ulcer and gastric ulcer may contribute to differences in development and presentation of both peptic ulcer conditions.

Adult↗
PubMed1996

Inhibition by tunicamycin of mucin synthesis, not morphological changes, in epidermis during retinol-induced mucous metaplasia of chick embryonic cultured skin.

BACKGROUND: Our previous studies have shown that epidermal mucous metaplasia of chick embryonic skin can be induced by culture in medium containing 20 microM retinol for only 8 hr and then in a chemically defined medium without retinol for 2 days and that retinol primarily affects the dermal cells, which then transform the epithelial cells into mucus-secreting cells. METHODS: Tarsometatarsal skin of 13-day-old chick embryo was cultured with 20 microM retinol for 1 day and then without the vitamin but with 0.1 microgram/ml tunicamycin for 5 days. Effect of tunicamycin on epidermal mucous metaplasia was studied biochemically and morphologically. RESULTS: Tunicamycin, which prevents the formation of N-glycans and inhibits maturation or morphological organization of various epithelial cells, irreversibly inhibited the synthesis of sulfated glycoproteins (O-glycans, mucin) in the epidermis only when applied to retinol-pretreated skin. Microvilli on the surface of the cells were well developed, but mucous granules surrounded by a limiting membrane were not observed in the upper cell layer of the epidermis, and many vesicles without electron-dense materials (mucin) and dilated rough endoplasmic reticulum were seen in the intermediate cell layers of the epidermis. When recombinants of 13-day-old normal epidermis and cultured dermis, which had been treated with retinol for 24 hr and with only tunicamycin for 2 days, were cultured without the antibiotic for 5 days, epidermal mucous metaplasia was induced. CONCLUSION: These results suggest that tunicamycin did not prevent morphological changes induced by retinol but inhibited mucin synthesis by a direct action on the epidermis of retinol-pretreated skin. Because in some cell-line mucin precursors contain high mannose N-linked oligosaccharides side chains, tunicamycin may have inhibited mucin synthesis. Interaction between epidermal basal cells and retinol-pretreated dermal fibroblasts is prerequisite for epidermal mucous metaplasia. Thus, the present study suggests that N-linked protein glycosylation is not required for this interaction.

Animals↗
PubMed1996

Numerical aberration and point mutation of p53 gene in human gastric intestinal metaplasia and well-differentiated adenocarcinoma: analysis by fluorescence in situ hybridization (FISH) and PCR-SSCP.

This study examined p53 gene alterations in human gastric mucosa, intestinal metaplasia and well-differentiated (cohesive type) adenocarcinomas to clarify to the role of the p53 gene in gastric tumorigenesis by means of fluorescence in situ hybridization (FISH), polymerase-chain-reaction-single-strand-conformation polymorphism (PCR-SSCP) and immunohistochemistry. Gene alterations were compared with numerical changes of chromosome 17. Samples were obtained from 31 surgically resected stomachs affected with gastric cancer. There was no nuclear p53 protein in cells from normal gastric mucosa. Among 23 specimens of intestinal metaplasia, cells with p53 protein were variably detected in 5 incomplete metaplasias (colonic type). A histological study revealed a mildly dysplastic appearance. PCR-SSCP identified p53-gene mutation in exons 5 and 8 in 2 of the 5 samples. Numerical aberrations of chromosome 17 and the p53 gene were undetectable both in normal mucosa and in intestinal metaplasia. Variable numbers of tumor cells contained p53 protein in 13 (54%) of 24 carcinomas, and PCR-SSCP revealed abnormal bands in 5 of them. Mutations were detected in exons 5, 7, 7, 7 and 8. FISH analysis demonstrated that 6 carcinomas emitted 3 or 4 signals for chromosome 17, and 7 gave one signal for the p53 gene in over 20% of the cells. Ten (77%) of 13 carcinomas examined by FISH appeared to show a p53-gene deletion.

Adenocarcinoma↗
PubMed1982

Intestinal mucinous substances in gastric intestinal metaplasia and carcinoma studied by immunofluorescence.

Immunofluorescent studies using specific antisera against intestinal mucins revealed small intestinal mucin antigen (SIMA) and large intestinal mucin antigen (LIMA) in areas of intestinal metaplasia of the stomach. In 25 gastric carcinomas studied, both these antigens were detected in seven carcinomas, SIMA only was present in four and LIMA in only four cases; the antigens could not be detected in ten of the carcinomas. In 21 of the 25 gastric operation specimens, including the 15 carcinomas positive for intestinal mucin antigens, there was evidence of chronic gastritis and intestinal metaplasia. These immunohistologic observations confirm the results of recent histochemical studies that both small and large intestinal type mucins are present in intestinal metaplasia and gastric carcinomas. Our findings provide further evidence that at least a proportion of gastric carcinomas may supervene on intestinal metaplasia. The absence of one or both antigens in gastric carcinomas may indicate stages of dedifferentiation or alternatively differences in histogenesis.

Adenocarcinoma, Mucinous↗
PubMed1986

Sulphomucin colonic type intestinal metaplasia and carcinoma in the stomach. A histochemical study of 115 cases obtained by biopsy.

One hundred fifteen gastroscopic biopsy specimens (54 cases of carcinoma and 61 of gastritis) were used in this histochemical study. Intestinal metaplasia (IM) was classified into small intestinal type (ST) and colonic type (CT). The former may be a reactive change only. The incidence of sulphomucin colonic type (SCT) metaplasia was higher in gastric carcinomas than in benign lesions (P less than 0.01), and a relation between SCT metaplasia and cancer was demonstrated by both histologic and histochemical procedures. This suggests that SCT IM is correlated with certain precancerous lesions. There was no significant difference in the incidence of O-acetyl sialomucin colonic type (OCT) metaplasia between benign and malignant diseases. Further study is needed to determine why slightly more than half of the SCT IM was accompanied by OCT IM.

Biopsy↗
PubMed1993

Experimental study of the therapeutic effects of folate, vitamin A, and vitamin B12 on squamous metaplasia of the bronchial epithelium.

BACKGROUND: Vitamin deficiency may be related to carcinogenesis. Cytologic examinations of sputum have already found that the administration of folate and vitamin B12 suppressed the development of squamous metaplasia and atypia in smokers' airways. The authors investigated the effect of folic acid, vitamin B12, and vitamin A on the formation of metaplasia and hyperplasia in methylcholanthrene (MCA)-treated rats. METHODS: The SD strain of rats received 10 mg of MCA intratracheally and was divided into six groups as follows: (1) vitamin A; (2) folic acid; (3) vitamin B12; (4) vitamin B12 with folic acid; (5) a combination of vitamin A, folic acid, and vitamin B12; and (6) no vitamins. The Lower respiratory tract epithelia of the rats were examined histologically 20, 32, and 36 weeks after MCA administration and at the end of the experiment. RESULTS: A clear difference was detected between the group receiving folic acid and that receiving vitamin A. In the former group, metaplasia was found in only one rat, atypia was not found, and hyperplasia with marked changes was present in less than 50% of other groups. In the latter group, atypia was found in all of the metaplastic foci. CONCLUSIONS: It was suggested that the epithelial hyperplasia and metaplasia of respiratory tract induced by MCA can be suppressed by the administration of folic acid.

Animals↗