965 resultados para p21 ras


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Pós-graduação em Enfermagem (mestrado profissional) - FMB

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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A busca pela identificação de fatores que possam apontar o diagnóstico, a resposta terapêutica e a sobrevida dos pacientes portadores de sarcoma ósseos tem sido incessante. Presumir a agressividade tumoral, capacidade de invasão tecidual, probabilidade de recidiva, propensão ao desenvolvimento de metástases e resposta ao tratamento, poderá ser valioso expediente na escolha da proposta terapêutica. Embora fatores ambientais e dietéticos contribuam para a etiologia do câncer, as neoplasias se originam de um processo de múltiplos passos envolvendo alterações de genes e seleção clonal da progênie variante. Estas mutações ocorrem em classes de genes reguladores da proliferação celular como os oncogenes, genes supressores de tumor, fatores de crescimento, vias de sinalização e genes de reparo de DNA. Os conhecimentos sobre a biologia tumoral melhoraram o entendimento sobre os múltiplos aspectos da carcinogênese. No entanto, embora as perspectivas permaneçam, até agora, há poucos benefícios para prevenção, diagnóstico, tratamento e seguimento dos pacientes com sarcomas ósseos. Este trabalho teve por objetivo detectar e descrever alterações cromossômicas consistentes e recorrentes, através da utilização de análises com a citogenética clássica. Também descreveu o envolvimento dessas alterações com o prognóstico em sarcomas ósseos primários e secundários, na tentativa de contribuir para a realização de estratégias mais eficazes para melhorar as taxas de sobrevida e beneficiar maior número de pacientes portadores de sarcomas ósseos. As lesões ósseas apresentaram alterações citogenéticas clonas e recorrentes, das quais as principais foram: sarcoma pouco diferenciado, o qual apresentou del(7)(p21); osteossarcoma metastático, apresentando del(4)(q32), add(13)(p13), add(14)(p13); tumor de células gigantes com add(14)(p13); ...(Resumo completo, clicar acesso eletrônico abaixo)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Balanced X-autosome translocations are rare, and female carriers are a clinically heterogeneous group of patients, with phenotypically normal women, history of recurrent miscarriage, gonadal dysfunction, X-linked disorders or congenital abnormalities, and/or developmental delay. We investigated a patient with a de novo X;19 translocation. The six-year-old girl has been evaluated due to hyperactivity, social interaction impairment, stereotypic and repetitive use of language with echolalia, failure to follow parents/caretakers orders, inconsolable outbursts, and persistent preoccupation with parts of objects. The girl has normal cognitive function. Her measurements are within normal range, and no other abnormalities were found during physical, neurological, or dysmorphological examinations. Conventional cytogenetic analysis showed a de novo balanced translocation, with the karyotype 46,X,t(X;19)(p21.2;q13.4). Replication banding showed a clear preference for inactivation of the normal X chromosome. The translocation was confirmed by FISH and Spectral Karyotyping (SKY). Although abnormal phenotypes associated with de novo balanced chromosomal rearrangements may be the result of disruption of a gene at one of the breakpoints, submicroscopic deletion or duplication, or a position effect, X; autosomal translocations are associated with additional unique risk factors including X-linked disorders, functional autosomal monosomy, or functional X chromosome disomy resulting from the complex X-inactivation process.

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Evidences suggest a role of renin-angiotensin system (RAS) in the development of chronic allograft injury. We correlated intrarenal angiotensin-converting enzyme, angiotensin II (Angio II) and transforming growth factor β1 (TGFβ1) expression in 58 biopsies-proven chronic allograft nephropathy (CAN) with tissue injury and allograft survival. The biopsies with CAN were graded according to Banff classification as I (22 cases), II (17) and III (19); 27 biopsies also showed a mononuclear inflammatory infiltrate in scarred areas. There were increased expression of angiotensin converting-enzyme (ACE), Angio II and TGFβ1 mainly in tubulointerstitial compartment in the group with CAN; there was no association of Angio II and TGFβ1 expression with interstitial fibrosis. There were no significant differences of ACE, Angio II and TGFβ1 expression between the patients treated and untreated with RAS blockade, and with the graft outcome. Interstitial inflammatory infiltrate had positive correlation with interstitial fibrosis and significant impact on graft survival at 8 years. Our study showed in a group of cases with CAN a high percentage of inflammatory infiltrate that correlated with interstitial fibrosis and graft outcome. The chronic inflammatory changes in these cases did not show significant association with local RAS expression.

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Propolis effect on the growth and apoptosis of human lung adenocarcinoma (A549 cells) was investigated as well as its mechanisms. Cells were incubated with propolis for 72 h, and 3-(4,5- dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assays were employed to assess cell viability and the inhibitory concentration (IC). Apoptosis was detected by Acridine Orange/Ethidium Bromide and 4',6-diamidino-2-phenylindole staining after 24 and 48 h of incubation with ¼ IC50 of propolis by testing the mitochondrial membrane potential (ΔΨm) and the expression of apoptosis-related genes (p53, Caspase-3, Bax, Bcl-2, Bcl-XL , Noxa, Puma and p21) by reverse transcription polymerase chain reaction. Propolis displayed antiproliferative and cytotoxic effects on A549 cells in a dose- and time-dependent manner, but it did not suppress the growth of normal Vero cells. An enhanced apoptosis was seen in A549 propolis-treated cells after 48 h compared with the control cells. Propolis decreased mitochondrial membrane potential by overexpression of pro-apoptotic genes (Bax and Noxa) and reduction of the antiapoptotic gene Bcl-XL . The expression level of other genes remained unchanged (p53, Caspse-3 and Bax), whereas p21 expression was increased. Propolis induced caspase-independent apoptosis through a p53-independent mitochondrial pathway, and cell cycle arrest by upregulation of p21. Although propolis induces apoptosis mainly by p53-independent manner, it may be induced by another pathway, and new insights may arise for preventing or treating lung cancer.