P16ink4a Expression
Mostrando 13-24 de 89 artigos, teses e dissertações.
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13. Estudo do biomarcador p16 no carcinoma de mama de mulheres submetidas à endocrinoterapia primária de curta duração com tamoxifeno e anastrozol. / Expression of p16 in short term exposition with tamoxifen and anastrozole in postmenopausal women with breast invasive cancer.
Introdução: A endocrinoterapia é uma das principais responsáveis pela redução de mortalidade do câncer de mama. Biomarcadores preditivos de resposta celular precoce vêm sendo estudados com intuito de prever precocemente a hormonioresistência. Freqüentes deleções e mutações têm sido descritas no gene p16 em diversos tipos de tumores, mas pouco
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 25/11/2009
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14. p16INK4 expression in precursor lesions of squamous cell cervical cancer related to the presence of HPV-DNA
The purpose of the present study was to identify the expression of p16INK4 in cervical cancer precursor lesions by immunohistochemistry and to correlate it with lesion grade and presence of human papillomavirus (HPV) infection. Cervical specimens from 144 women seen consecutively at the gynecology outpatient clinic of our institution from December 2003 to Ma
Brazilian Journal of Medical and Biological Research. Publicado em: 2008-07
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15. Expression of p16, cyclin D1, CDK4 and retinoblastoma protein in acral lentiginous melanoma / Expressão da proteína p16, ciclina D1, CDK4 e proteína do retinoblastoma no melanoma acral lentiginoso
INTRODUCTION: Acral lentiginous melanoma (ALM) has an expressive frequency between melanoma cases in our country, and it differs from the others clinical pathological types of cutaneous melanoma, because it does not have sun exposure as a predisposing factor. There are few publications in the literature addressing the expression of tumor suppressor pathway p
Publicado em: 2008
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16. Expression of p16INK4a and of p53 as prognostic markers of cervical intraepithelial neoplasia and their relationship with high risk human papillomavirus / Expressão do p16 POT. INK4a e do p53 como marcadores prognosticos da neoplasia intra-epitelial cervical e sua relação com o papilomavirus humano de alto risco oncogenico
Objetivo: Avaliar a relação da expressão do p53 e do p16INK4a em diferentes graus de neoplasia intra-epitelial cervical (NIC) e suas possíveis relações com a recidiva/persistência da NIC após conização diatérmica e a infecção persistente de papilomavírus humano (HPV) de alto risco oncogênico. Sujeitos e métodos: Este foi um estudo de corte, c
Publicado em: 2007
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17. p16INK4A Participates in a G1 Arrest Checkpoint in Response to DNA Damage
Members of the INK4 protein family specifically inhibit cyclin-dependent kinase 4 (cdk4) and cdk6-mediated phosphorylation of the retinoblastoma susceptibility gene product (Rb). p16INK4A, a prototypic INK4 protein, has been identified as a tumor suppressor in many human cancers. Inactivation of p16INK4A in tumors expressing wild-type Rb is thought to be req
American Society for Microbiology.
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18. Ink4a/Arf expression is a biomarker of aging
The Ink4a/Arf locus encodes 2 tumor suppressor molecules, p16INK4a and Arf, which are principal mediators of cellular senescence. To study the links between senescence and aging in vivo, we examined Ink4a/Arf expression in rodent models of aging. We show that expression of p16INK4a and Arf markedly increases in almost all rodent tissues with advancing age, w
American Society for Clinical Investigation.
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19. Loss of p16INK4a results in increased glucocorticoid receptor activity during fibrosarcoma development
Glucocorticoids inhibit proliferation of many cell types, but the relationship between the glucocorticoid receptor (GR) and the proteins regulating cell cycle progression is not fully understood. We previously found that during fibrosarcoma (FS) progression, GR displays only modest transcriptional activity in the preneoplastic stages, whereas it is highly ac
The National Academy of Sciences.
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20. Mutations and altered expression of p16INK4 in human cancer.
Cell cycle arrest at the G1 checkpoint allows completion of critical macromolecular events prior to S phase. Regulators of the G1 checkpoint include an inhibitor of cyclin-dependent kinase, p16INK4; two tumor-suppressor proteins, p53 and RB (the product of the retinoblastoma-susceptibility gene); and cyclin D1. Neither p16INK4 nor the RB protein was detected
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21. Induced Expression of p16INK4a Inhibits Both CDK4- and CDK2-Associated Kinase Activity by Reassortment of Cyclin-CDK-Inhibitor Complexes
To investigate the mode of action of the p16INK4a tumor suppressor protein, we have established U2-OS cells in which the expression of p16INK4a can be regulated by addition or removal of isopropyl-β-d-thiogalactopyranoside. As expected, induction of p16INK4a results in a G1 cell cycle arrest by inhibiting phosphorylation of the retinoblastoma protein (pRb)
American Society for Microbiology.
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22. p16Ink4a Interferes with Abelson Virus Transformation by Enhancing Apoptosis
Pre-B-cell transformation by Abelson virus (Ab-MLV) is a multistep process in which primary transformants are stimulated to proliferate but subsequently undergo crisis, a period of erratic growth marked by high levels of apoptosis. Inactivation of the p53 tumor suppressor pathway is an important step in this process and can be accomplished by mutation of p53
American Society for Microbiology.
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23. Growth suppression by p16ink4 requires functional retinoblastoma protein.
p16ink4 has been implicated as a tumor suppressor that is lost from a variety of human tumors and human cell lines. p16ink4 specifically binds and inhibits the cyclin-dependent kinases 4 and 6. In vitro, these kinases can phosphorylate the product of the retinoblastoma tumor suppressor gene. Thus, p16ink4 could exert its function as tumor suppressor through
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24. Transcriptional Coactivator Cited2 Induces Bmi1 and Mel18 and Controls Fibroblast Proliferation via Ink4a/ARF
Cited2 (CBP/p300 interacting transactivator with ED-rich tail 2) is required for embryonic development, coactivation of transcription factor AP-2, and inhibition of hypoxia-inducible factor 1 transactivation. Cited2 is induced by multiple growth factors and cytokines and oncogenically transforms cells. Here, we show that the proliferation of Cited2−/− mo
American Society for Microbiology.