Asunto(s)
Estenosis Esofágica/terapia , Invasividad Neoplásica/patología , Stents/efectos adversos , Estenosis Traqueal/etiología , Estenosis Traqueal/terapia , Adenocarcinoma/complicaciones , Adenocarcinoma/diagnóstico , Adenocarcinoma/cirugía , Neoplasias de los Bronquios/complicaciones , Neoplasias de los Bronquios/diagnóstico , Neoplasias de los Bronquios/cirugía , Cateterismo/métodos , Progresión de la Enfermedad , Estenosis Esofágica/etiología , Estenosis Esofágica/patología , Esofagoscopía/métodos , Resultado Fatal , Humanos , Masculino , Persona de Mediana Edad , Medición de Riesgo , Factores de Tiempo , Tomografía Computarizada por Rayos X , Estenosis Traqueal/diagnóstico por imagenRESUMEN
The detection of IGF-IR signaling in animal models has important implications for determining the role of this receptor in normal physiology and tumor growth. While many reports have correlated changes in plasma IGF-I levels in vivo with biological responses, few have shown that altered IGF-I levels can directly affect signaling within normal or tumor tissue. Here, we present new data that shows how the intravenous (IV) injection of IGF-I can be used to directly examine IGF signaling at the tissue level. Tail-vein IV injection of IGF-I into mice resulted in a rapid and dose-dependent activation of the IGF-I receptor and downstream phosphorylation of Akt and ERK1/2 in liver, kidney, and mammary gland. Similarly, IV IGF-I rapidly stimulated signaling in HT-29 colorectal and in MCF-7 breast cancer xenografts. This study shows how IV IGF injection can be used to examine the signaling mechanisms used by IGF-IR, in both normal mammary tissue and during tumor growth, and may provide a model for the characterization of IGF inhibitors.
