Your browser doesn't support javascript.
loading
Montrer: 20 | 50 | 100
Résultats 1 - 5 de 5
Filtre
1.
Braz. j. med. biol. res ; 43(8): 717-721, Aug. 2010. tab, ilus
Article Dans Anglais | LILACS | ID: lil-554961

Résumé

Gastric cancer is the fourth most frequent type of cancer and the second cause of cancer mortality worldwide. The genetic alterations described so far for gastric carcinomas include amplifications and mutations of the c-ERBB2, KRAS, MET, TP53, and c-MYC genes. Chromosomal instability described for gastric cancer includes gains and losses of whole chromosomes or parts of them and these events might lead to oncogene overexpression, showing the need for a better understanding of the cytogenetic aspects of this neoplasia. Very few gastric carcinoma cell lines have been isolated. The establishment and characterization of the biological properties of gastric cancer cell lines is a powerful tool to gather information about the evolution of this malignancy, and also to test new therapeutic approaches. The present study characterized cytogenetically PG-100, the first commercially available gastric cancer cell line derived from a Brazilian patient who had a gastric adenocarcinoma, using GTG banding and fluorescent in situ hybridization to determine MYC amplification. Twenty metaphases were karyotyped; 19 (95 percent) of them presented chromosome 8 trisomy, where the MYC gene is located, and 17 (85 percent) presented a deletion in the 17p region, where the TP53 is located. These are common findings for gastric carcinomas, validating PG100 as an experimental model for this neoplasia. Eighty-six percent of 200 cells analyzed by fluorescent in situ hybridization presented MYC overexpression. Less frequent findings, such as 5p deletions and trisomy 16, open new perspectives for the study of this tumor.


Sujets)
Humains , Adénocarcinome/génétique , Lignée cellulaire tumorale , Gènes myc/génétique , Tumeurs de l'estomac/génétique , Adénocarcinome/anatomopathologie , Brésil , Analyse cytogénétique , Amplification de gène , Caryotypage , Tumeurs de l'estomac/anatomopathologie
2.
Braz. j. med. biol. res ; 38(6): 901-907, June 2005. tab
Article Dans Anglais | LILACS | ID: lil-402662

Résumé

Mercury is a xenobiotic metal that is a highly deleterious environmental pollutant. The biotransformation of mercury chloride (HgCl2) into methylmercury chloride (CH3HgCl) in aquatic environments is well-known and humans are exposed by consumption of contaminated fish, shellfish and algae. The objective of the present study was to determine the changes induced in vitro by two mercury compounds (HgCl2 and CH3HgCl) in cultured human lymphocytes. Short-term human leukocyte cultures from 10 healthy donors (5 females and 5 males) were set-up by adding drops of whole blood in complete medium. Cultures were separately and simultaneously treated with low doses (0.1 to 1000 æg/l) of HgCl2 and CH3HgCl and incubated at 37°C for 48 h. Genotoxicity was assessed by chromosome aberrations and polyploid cells. Mitotic index was used as a measure of cytotoxicity. A significant increase (P < 0.05) in the relative frequency of chromosome aberrations was observed for all concentrations of CH3HgCl when compared to control, whether alone or in an evident sinergistic combination with HgCl2. The frequency of polyploid cells was also significantly increased (P < 0.05) when compared to control after exposure to all concentrations of CH3HgCl alone or in combination with HgCl2. CH3HgCl significantly decreased (P < 0.05) the mitotic index at 100 and 1000 æg/l alone, and at 1, 10, 100, and 1000 æg/l when combined with HgCl2, showing a synergistic cytotoxic effect. Our data showed that low concentrations of CH3HgCl might be cytotoxic/genotoxic. Such effects may indicate early cellular changes with possible biological consequences and should be considered in the preliminary evaluation of the risks of populations exposed in vivo to low doses of mercury.


Sujets)
Femelle , Humains , Mâle , Lymphocytes/effets des médicaments et des substances chimiques , Composés méthylés du mercure/toxicité , Index mitotique , Tests de mutagénicité
3.
Genet. mol. res. (Online) ; 2(2): 223-228, Jun. 2003.
Article Dans Anglais | LILACS | ID: lil-417606

Résumé

The Canova Method (CM) is a homeopathic medicine indicated for the treatment of patients with cancer and for pathologies that involve a depressed immune system, such as AIDS. This product is composed of homeopathic dilutions of Aconitum napellus, Arsenicum album (arsenic trioxide), Bryonia alba, Lachesis muta venom and Thuya occidentalis. It stimulates the immune system by activating macrophages. Activated macrophages stimulate the lymphocytes so that they increase their cytotoxic action in response to tumoral growth or infection. Given that the CM stimulates and accelerates the activity of macrophages and lymphocytes, we evaluated genotoxic effects induced in human lymphocytes treated with this homeopathic medication in vitro. Structural and numerical chromosomal aberrations were scored for the assessment of induced genotoxic effects, while the variation in mitotic index was considered as a monitor for induced cellular toxicity. The lymphocytes were cultivated for 24, 48 or 72 h in the following final concentrations of the medicinal composite CM: 4, 8 and 12. Treatments with the CM did not affect mitotic indexes, nor did they provoke chromosomal aberrations, when compared with untreated controls. There was no cytotoxicity or genotoxicity at the chromosomal level


Sujets)
Humains , Mâle , Femelle , Adulte , Antinéoplasiques/toxicité , Homéopathie , Techniques in vitro , Lymphocytes/effets des médicaments et des substances chimiques , Aberrations des chromosomes , Analyse cytogénétique , Extraits de plantes/toxicité , Lymphocytes/cytologie , Index mitotique , Tests de mutagénicité
4.
Braz. j. med. biol. res ; 34(8): 1003-1006, Aug. 2001. ilus, tab
Article Dans Anglais | LILACS | ID: lil-290148

Résumé

Twelve breast fibroadenomas were analyzed cytogenetically and only four were found to have clonal alterations. The presence of chromosomal alterations in fibroadenomas must be the consequence of the proliferating process and must not be related to the etiology of this type of lesion. In contrast, the few fibroadenomas that exhibit chromosomal alterations are likely to be those presenting a risk of neoplastic transformation. Clonal numerical alterations involved chromosomes 8, 18, 19, and 21. Of the chromosomal alterations found in the present study, only monosomy of chromosomes 19 and 21 has been reported in breast fibroadenomas. The loss of chromosome 21 was the most frequent alteration found in our sample. The study of benign proliferations and their comparison with chromosome alterations in their malignant counterparts ought to result in a better understanding of the genes acting on cell proliferation alone, and of the genes that cause these cells to exhibit varied behaviors such as recurrences, spontaneous regression and fast growth


Sujets)
Humains , Adolescent , Femelle , Adulte , Tumeurs du sein/génétique , Aberrations des chromosomes/génétique , Analyse cytogénétique , Fibroadénome/génétique , Études de suivi , Caryotypage
5.
Braz. j. med. biol. res ; 33(11): 1325-8, Nov. 2000. tab, ilus
Article Dans Anglais | LILACS | ID: lil-273220

Résumé

Breast cancer in families with germ line mutations in the TP53 gene has been described in the medical literature. Mutation screening for susceptibility genes should allow effective prophylactic and preventive measures. Using single-strand conformational polymorphism, we screened for mutations in exons 5, 6, 7 and 8 of gene TP53 in the peripheral blood of 8 young non-affected members (17 to 36 years old) of families with a history of breast cancer. Studies of this type on young patients (mean age, 25 years) are very rare in the literature. The identification of these mutations would contribute to genetic counseling of members of families with predisposition to breast cancer. The results obtained did not show any polymorphism indicating mutation. In our sample, the familial tumorigenesis is probably related to other gene etiologies


Sujets)
Humains , Femelle , Adolescent , Adulte , Tumeurs du sein/génétique , Gènes p53/génétique , Polymorphisme de conformation simple brin , Facteurs âges , Études cas-témoins , Exons/génétique , Dépistage génétique , Mutation , Réaction de polymérisation en chaîne , Facteurs de risque
SÉLECTION CITATIONS
Détails de la recherche