P53 Tumor Suppressor Proteins
Mostrando 1-12 de 194 artigos, teses e dissertações.
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1. Leucoplasia oral: tratamento cirúrgico com laser de CO2 e de diodo e análise por imuno-histoquímica da expressão de proteínas relacionadas à carcinogênese (p53, COX-2 e EGFR) / Oral leukoplakia: surgical treatment with CO2 and diode lasers and analysis of the expression of proteins related to carcinogenesis (p53, COX-2 e EGFR) by immunohistochemistry
Oral leukoplakia (OL) is a potentially malignant lesion, defined as a white patch that cannot be characterized as any other disease of the oral mucosa. In general, OL should be treated; however no treatment available has been able to prevent malignant transformation. The aim of this study was to evaluate the efficacy of surgical treatment with CO2 and diode
Publicado em: 2010
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2. Modificadores de penetrância de mutações germinativas no gene TP53 em famílias brasileiras com diagnóstico clínico da síndrome de Li-Fraumeni e Li-Fraumeni like: impacto dos polimorfismos intragênicos do TP53 e de genes / Genetic modifiers of germline TP53 mutation in Brazilian families with Li-Fraumeni and Li-Fraumeni Like syndromes: impact of TP53 intragenic polymorphisms and p53 regulatory genes
Li-Fraumeni syndrome (LFS) and its variant like (LFL) are associated with germline mutations in the TP53 gene and predispose to a variety of cancers at an earlier age. We analyzed 91 LFS/LFL families from southern Brazil for germline mutations in TP53 and polymorphisms in TP53 (PIN2, PIN3, PEX4) and MDM2 (309T-G). The germline TP53 mutation R337H was found i
Publicado em: 2008
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3. Immunohistochemical analysis of cel-cycle related proteins (p53, Ki-67, bcl-2 and c-erbB-2) in the malignant transformation of pleomorphic adenoma of salivary glands / Analise imunoistoquimica de proteinas relacionadas ao ciclo celular (p53, Ki-67, bcl-2 e c-erbB-2) na transformação maligna do adenoma plenomorfico de glandula salivar
O adenoma pleomórfico (AP) é a neoplasia mais freqüente das glândulas salivares e o carcinoma ex-adenoma pleomórfico (CXAP) é a sua forma de transformação maligna mais comum. Os trabalhos da literatura com séries exclusivas de CXAP são poucos e englobam, em sua maioria, carcinomas já em estádios avançados. Raros são os estudos realizados exclus
Publicado em: 2006
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4. ROLE OF Bcl-2 AND Bcl-XL IN ANGIOGENESIS
(...)Angiogenesis is defined as the development of new capillaries from pre-existing blood vessels. The hypothesis that tumor growth is angiogenesis dependent was proposed by Judah Folkman in 1971, and it has been confirmed by many investigators thereafter. We have shown that vascular endothelial growth factor (VEGF) induces Bcl-2 expression in endothelial c
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 2006
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5. Expression of c-erbB-2, p53 and c-myc proteins in male breast carcinoma: Comparison with traditional prognostic factors and survival
There are few data evaluating biological markers for men with breast cancer. The purpose of the present study was to analyze the expression of the oncogenes c-erbB-2 and c-myc and of the suppressor gene p53 by immunohistochemical techniques in archival paraffin-embedded tissue blocks of 48 male breast cancer patients, treated at the A.C. Camargo Cancer Hospi
Brazilian Journal of Medical and Biological Research. Publicado em: 2001-07
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6. Mdm2 Regulates p53 Independently of p19ARF in Homeostatic Tissues
Tumor suppressor proteins must be exquisitely regulated since they can induce cell death while preventing cancer. For example, the p19ARF tumor suppressor (p14ARF in humans) appears to stimulate the apoptotic function of the p53 tumor suppressor to prevent lymphomagenesis and carcinogenesis induced by oncogene overexpression. Here we present a genetic approa
American Society for Microbiology.
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7. Germ-line mutations of the p53 tumor suppressor gene in patients with high risk for cancer inactivate the p53 protein.
Germ-line mutations in the p53 tumor suppressor gene have been observed in patients with Li-Fraumeni syndrome, brain tumors, second malignancies, and breast cancers. It is unclear whether all of these mutations have inactivated p53 and thereby provide an increased risk for cancer. Therefore, it is necessary to establish the biological significance of these g
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8. Expression of wild-type p53 is not compatible with continued growth of p53-negative tumor cells.
Inactivation of the cellular p53 gene is a common feature of Friend virus-induced murine erythroleukemia cell lines and may represent a necessary step in the progression of this disease. As well, frequent loss or mutation of p53 alleles in diverse human tumors is consistent with the view of p53 as a tumor suppressor gene. To examine the significance of p53 g
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9. Proteins of the S100 family regulate the oligomerization of p53 tumor suppressor
S100B protein is elevated in the brains of patients with early stages of Alzheimer's disease and Down's syndrome. S100A4 is correlated with the development of metastasis. Both proteins bind to p53 tumor suppressor. We found that both S100B and S100A4 bind to the tetramerization domain of p53 (residues 325-355) only when exposed in lower oligomerization state
National Academy of Sciences.
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10. Tumor suppressor p53: analysis of wild-type and mutant p53 complexes.
It has been suggested that the dominant effect of mutant p53 on tumor progression may reflect the mutant protein binding to wild-type p53, with inactivation of suppressor function. To date, evidence for wild-type/mutant p53 complexes involves p53 from different species. To investigate wild-type/mutant p53 complexes in relation to natural tumor progression, w
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11. p53-mediated cellular response to DNA damage in cells with replicative hepatitis B virus.
Wild-type p53 acts as a tumor suppressor gene by protecting cells from deleterious effects of genotoxic agents through the induction of a G1/S arrest or apoptosis as a response to DNA damage. Transforming proteins of several oncogenic DNA viruses inactivate tumor suppressor activity of p53 by blocking this cellular response. To test whether hepatitis B virus
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12. Sequence-specific transcriptional activation is essential for growth suppression by p53.
Although several biochemical features of p53 have been described, their relationship to tumor suppression remains uncertain. We have compared the ability of p53-derived proteins to act as sequence-specific transcriptional (SST) activators with their ability to suppress tumor cell growth, using an improved growth-suppression assay. Both naturally occurring an