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F Carneiro

Publications and source records attributed to F Carneiro.

At least 73 records · Page 4Linked to original sources
PubMed1996

Pattern of pS2 protein expression in premalignant and malignant lesions of gastric mucosa.

The aim of this study was to evaluate the pattern of pS2 protein expression in premalignant and malignant lesions of gastric epithelium. We analysed, by immunohistochemistry, the pS2 expression in six samples of normal gastric mucosa, 18 cases of chronic atrophic gastritis with intestinal metaplasia (IM), 10 hyperplastic polyps, 11 adenomatous polyps and 50 gastric carcinomas, together with the respective samples of adjacent non-neoplastic mucosa. pS2 is expressed throughout foveolar and superficial epithelium of normal gastric mucosa and this pattern is retained in chronic atrophic gastritis out of IM lesions. pS2 expression is confined to goblet cells in complete IM and occurs both in goblet and columnar cells in incomplete IM. Hyperplastic polyps displayed significantly higher pS2 expression than adenomatous polyps. In gastric carcinomas, pS2 expression was observed in 66.0% of cases, being significantly higher in diffuse (88.9%) than intestinal type carcinomas (53.6%). A subset of carcinomas of the latter group displayed pS2 immunoreactivity in a high percentage of cells with a pattern similar to that of hyperplastic polyps. Our results demonstrate there are major changes in pS2 expression, which can be used as a marker of gastric-type differentiation during the process of gastric carcinogenesis, and support the existence of at least two pathways of malignant transformation of gastric mucosa: one via intestinal metaplasia and adenomatous dysplasia, leading to glandular carcinomas with intestinal-type differentiation, the other via hyperplastic changes or de novo changes, leading to diffuse carcinomas and to a subset of glandular carcinomas displaying gastric-type differentiation.

Biomarkers, Tumor↗
PubMed1996

Human trefoil peptides: genomic structure in 21q22.3 and coordinated expression.

Trefoil peptides are small secretory proteins characterized by three intrachain disulfide bonds forming the trefoil motif or P-domain. They are abundantly expressed on mucosal surfaces, especially of the gastrointestinal tract. In pathological conditions such as ulcers, metaplasia and neoplasia, their expression is upregulated. Three human trefoil peptides have been described: the estrogen-inducible pS2 protein, the spasmolytic protein and the intestinal trefoil factor. Recently, their role in the maintenance of surface integrity and ulcer healing was discussed. We already mapped the corresponding three genes (BCEI), SML1, TFF3) to the same genomic region (21q22.3). In this paper, we show that the three genes are clustered in a tandemly orientated fashion within 50 kb on a bacterial artificial chromosome (BAC) recombinant. This cluster is located adjacent to D21S19 and the locus order is cen-D21S212-TFF3-SML1-BCEI-D21S19-tel, whereas transcription of all three genes is directed towards the centromere. The gene structure of SML1 exhibits four exons, two of which encode the two separate trefoil motifs. TFF3 and BCEI, both containing one trefoil motif, are composed of three exons each, suggesting gene duplication and exon-shuffling events during evolution. The 5'-flanking region of SML1 was compared to the corresponding region of other trefoil genes. Two motifs with identical sequence and positions are shared between SML1 and BCEI, thus presenting possible targets for stomach-specific gene regulation. Two other motifs are shared within all known human and rat trefoil genes, suggesting a coordinated regulation and/or a common locus-controlling region. Using RT-PCR, a change in the pattern of trefoil gene expression is detected in tissue samples from normal gastric mucosa, hyperplastic polyps, gastric cancer, and gastric cancer cell lines, respectively.

Amino Acid Sequence↗
PubMed1996

[Family education, a model for allergy prevention].

It is frequent the lack of family adherence toward the therapeutic measures of the allergic diseases. The incidence in the therapeutic non compliance of the asthmatic patients vary from 20 to 80%. In the last decades, the symptomatic expression of the atopic diseases (AD) in the infancy, and in the adolescence of Venezuelans has been transformed into a health care problem, with an inaccessible therapeutic cost for the state and the family. The setup of the first allergic prevention program improved attitudes and perceptions toward bronchial asthma, allergic rhinitis, and atopic dermatitis, by the education of the risk family group, based on the results from previous investigations and adapted to the procedures and customs that govern our current society. A research project, through a multi-disciplinary group included an educational program model for the prevention of allergic diseases in a population from Caracas, Venezuelan allergic pregnant mothers, and their respective couples of a high and middle socioeconomic levels with no helminthic infections (n = 482), group A. Two subgroups were randomly selected for prospective evaluation: A1 (n = 20) without participation in the preventive program or control group, and A2 (n = 15) with participation in the program or intervened group, including strategies to be applied by the family, application of measures and reached goals; immunologic, pediatric, and nutritional sequential control; group B (n = 66), to validate the laboratory tests, and group C (n = 364) to validate immunoclinical diagnoses, in vivo immunodiagnostic tests to the parents and children (clinical history, skin prick tests for cow's milk, egg white, wheat, soybean, cladosporium and Dermatophagoides pteronnysinus), and in vitro tests (total serum IgE, Phadiatop, and Rast to the allergens previously selected). In conclusion, the program permits the identification of atopic risk children, sponsors the systematical application of intervention measures, economic, viable and projected toward the family affected, indicating a positive change through a self-family-management training and new conduct plans, facilitating the participation among the family, the community and the health team, that certifies, an optimistic therapy in the reduction of the clinical manifestations of the atopic diseases in young infants from this tropical population studied.

Asthma↗
PubMed1995

Sporadic gastric carcinomas with microsatellite instability display a particular clinicopathologic profile.

Mutations in recently identified genes on chromosomes 2 and 3 seem to be responsible for repair errors (RER+) throughout the genome. This novel genetic mechanism was first reported in hereditary non-polyposis colorectal cancer syndrome and in cancers that are characteristic of this syndrome, such as carcinomas of the right colon, stomach and endometrium. We investigated the frequency of RER+ phenotype in a series of 34 sporadic gastric carcinomas, in an attempt to see if the RER+ cases displayed any particular morphologic features and/or if they showed distinctive clinicopathologic characteristics. Twelve loci were investigated. We found 23 RER- cases (67.6%) and 11 RER+ cases (32.4%). A significant association was found between RER+ carcinomas and localization of the tumors: 9 of the 11 RER+ carcinomas (81.8%) were located at the antrum whereas all the cardiac tumors were RER-. The RER+ phenotype was also significantly related to the presence of moderate/abundant T-cell lymphoid infiltration within the tumors. The 3-year survival rate of patients with RER+ tumors was suggestively longer than that of patients with RER- tumors. No significant relationship was found between several clinicopathologic characteristics of the cases, including age, sex, staging, histologic type and ploidy, despite a trend towards an association between RER+ phenotype and advanced age of the patients and poorly differentiated, intestinal type of the carcinomas. The high frequency of microsatellite instability in sporadic gastric carcinomas supports the involvement of this genetic mechanism in gastric carcinogenesis. Gastric carcinomas with the RER+ phenotype tend to occur as poorly differentiated adenocarcinomas in the antrum of elderly patients, display abundant T-cell infiltration and carry a relatively good prognosis.

Adult↗
PubMed1995

New elements for an updated classification of the carcinomas of the stomach.

Based upon the results of a thorough study of 213 patients submitted to potentially curative resection we propose the following histologic classification of gastric carcinoma: isolated-cell carcinoma (6.6%), glandular carcinoma (41.8%), solid carcinoma (13.1%) and mixed carcinoma (38.5%). Half of the mixed carcinomas displayed a predominant isolated-cell pattern, whereas in the other half the isolated-cells were a minor component (the predominant component being either glandular, solid, or both). The survival of patients with mixed carcinomas is significantly worse than those of patients with other histologic types of gastric carcinoma regardless of the site of tumors and the inclusion, or not, in the series, of post-operative deaths. The proposed classification keeps its independent prognostic significance in a multifactorial analysis, appearing as the second most important prognostic factor in patients with gastric carcinomas, after the TNM staging and before venous invasion.

Adult↗
PubMed1994

Retinoblastoma gene structure and product expression in human gastric carcinomas.

The role of the retinoblastoma gene (RB1) in human gastric carcinogenesis is yet to be clarified. We report on the analysis of RB1 structure and protein (pRB) expression in gastric carcinomas using Southern blotting, Western blotting and immunohistochemistry. The relationship between pRB expression and cell proliferation was assessed by a proliferation marker (PCNA) in a subset of cases. Non-neoplastic mucosas were studied, as controls, by the same methodology. We found a close relationship between pRB expression and PCNA in non-neoplastic mucosas as well as in gastric carcinomas. All tumours were immunohistochemically positive for pRB, although with a variable proportion of non-immunoreactive cells. Carcinomas of the diffuse type showed absence of pRB expression in a larger proportion of neoplastic cells than carcinomas of the intestinal type (P < 0.05). Analysis of the RB1 structure using probe p68RS2.0 revealed allelic imbalance in 29% of informative cases. No homozygous deletions and/or rearrangements were detected with p68RS2.0 and cDNA probes. Western analysis revealed no abnormal patterns of pRB. Our data therefore suggest that major alterations affecting the RB1 gene are rather infrequent in human gastric carcinomas.

Aged↗
PubMed1994

T (Thomsen-Friedenreich) antigen and other simple mucin-type carbohydrate antigens in precursor lesions of gastric carcinoma.

In a previous report we suggested that T antigen appeared to be associated with gastric carcinoma. To verify this hypothesis and characterize the pattern of expression of simple-mucin type carbohydrate antigens (Tn,sialyl-Tn and T before and after neuraminidase) in normal gastric mucosa and precursor lesions of gastric carcinoma, we studied the mucosa adjacent to 100 cases of gastric carcinoma, gastric biopsies of 60 dyspeptic patients, eight adenomatous polyps and eight hyperplastic polyps. The expression of the antigens was more related to the cell type and underlying lesions than to the coexistence of carcinoma. The most distinctive findings concerned intestinal metaplasia, dysplasia and hyperplastic lesions. In intestinal metaplasia, Tn was found mostly in columnar cells and sialyl-Tn in goblet cells. T was more prevalent in incomplete intestinal metaplasia than in complete. A high prevalence of sialyl-Tn expression and cell membrane immunoreactivity for T antigen, similar to those previously found in gastric carcinomas, were observed in three adenomatous polyps, one hyperplastic polyp, five cases of adenomatous dysplasia in the neighbourhood of intestinal carcinomas and four cases of marked foveolar hyperplasia, three of which were from the mucosa adjacent to diffuse carcinomas. We conclude that adenomatous and hyperplastic lesions share with gastric carcinomas features of aberrant glycosylation, namely the cell membrane expression of T antigen.

Adenocarcinoma↗
PubMed1993

Hyperplastic polyposis and diffuse carcinoma of the stomach. A study of a family.

BACKGROUND: The authors previously described a large pedigree with familial gastric polyposis and a high incidence of gastric cancer and demonstrated the autosomal dominant pattern of inheritance. The current study described the histologic and immunohistologic features of the lesions in an attempt to clarify the mechanisms underlying gastric carcinogenesis in this family. METHODS: The authors studied the histopathologic and histochemical features of several gastric specimens of nine members of this family and searched for the expression of carcinoembryonic antigen (CEA), p21 protein (ras oncogene), p53 protein (p53 suppressor gene), and simple mucin-type carbohydrate antigens (Tn, sialosyl-Tn, and T antigen before and after neuraminidase) and for the presence of Helicobacter pylori. RESULTS: The two carcinomas available for histologic revision were of the diffuse type. One of them apparently originated from a hyperplastic polyp. Hyperplastic polyps were diagnosed in five of seven patients without carcinoma. The remaining two patients had marked foveolar hyperplasia. Chronic atrophic gastritis with complete intestinal metaplasia (IM) was seen in three patients. p53 protein was not expressed in any of the cases. CEA and ras p21 oncoprotein were found in six and eight cases, respectively (mainly in hyperplastic foveolar epithelium). Tn, sialosyl-Tn, and T antigen were expressed in every case. H. pylori colonization was detected in all but the two patients with carcinoma. CONCLUSIONS: The authors concluded that foveolar hyperplasia/hyperplastic polyps play a key role in the development of diffuse carcinoma in this inherited polyposis, confined to the stomach, with hyperplastic phenotype. The genetic and environmental mechanisms underlying this particular situation remain to be clarified.

Adult↗
PubMed1993

Cytogenetic findings in eleven gastric carcinomas.

We describe the results of the cytogenetic study of 10 primary adenocarcinomas of the stomach and one lymph node metastasis of a gastric adenocarcinoma after direct harvesting or short-term in vitro culture. All cases showed a variable number of numerical and/or structural clonal cytogenetic aberrations. Polysomy of chromosomes 2 and 20 were the most common numerical abnormalities. Rearrangements of chromosomes 1, 3, 7, and 13 were each observed in more than half the cases. Chromosomes 3 and 13 were the chromosomes more often exhibiting structural cytogenetic aberrations. In five tumors, rearrangements of chromosome 6 resulting in partial deletion of 6q were noted (common deleted region 6q21-22-->qter). The recurrent markers observed in our series were an i(8q) and an i(17q) in three and two cases, respectively. Double minutes (dmin) or homogeneously staining regions (hsr) were evident in three tumors. Contrary to the recent claim that structural abnormalities affecting 11p13-p15 were specifically involved in gastric cancer, we detected rearrangements of this region in only two cases.

Adenocarcinoma↗