Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Adv Biol Regul ; 52(3): 389-405, 2012 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-22884032

RESUMO

Epidemiological studies have established a positive correlation between cancer and metabolic disorders, suggesting that aberrant cell metabolism is a common feature of nearly all tumors. To meet their demand of building block molecules, cancer cells switch to a heavily glucose-dependent metabolism. As insulin triggers glucose uptake, most tumors are or become insulin-dependent. However, the effects of insulin and of other similar growth factors are not only limited to metabolic control but also favor tumor growth by stimulating proliferation and survival. A key signaling event mediating these metabolic and proliferative responses is the activation of the phosphatidylinositol-3 kinases (PI3K) pathway. In this review, we will thus discuss the current concepts of tumor metabolism and the opportunity of PI3K-targeted therapies to exploit the "sweet tooth" of cancer cells.


Assuntos
Neoplasias/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Animais , Proliferação de Células , Complicações do Diabetes/metabolismo , Dieta/efeitos adversos , Glucose/metabolismo , Humanos , Insulina/metabolismo , Modelos Biológicos , Neoplasias/tratamento farmacológico , Neoplasias/etiologia , Neoplasias/patologia , Inibidores de Fosfoinositídeo-3 Quinase , Transdução de Sinais
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...