RESUMEN
The prescription of bone scans (BS) in the initial staging and follow-up of small cell lung carcinoma (SCLC) is a traditional attitude. The availability of the serum neuron-specific enolase (NSE) assay and budget limitations led us to evaluate retrospectively, in 57 patients, the consequences of a more selective attitude, namely to perform BS only in those patients with abnormal serum NSE levels. Both BS and NSE assays were performed in 47 patients referred for initial staging of SCLC; NSE levels were normal in 8 but in 2 of these cases (25%) secondary bone localizations with great clinical significance were discovered at BS. During follow-up, 59 BS were performed in conjunction with NSE assays; 45 NSE levels were in the normal range whereas 17 (38%) corresponding BS were suggestive of bone metastases. In conclusion, due to the frequent occurrence of false-negative results in patients with bone metastases, serum NSE levels proved to be useless in the selection for BS of patients suffering from SCLC.
Asunto(s)
Biomarcadores de Tumor/sangre , Neoplasias Óseas/secundario , Huesos/diagnóstico por imagen , Carcinoma de Células Pequeñas/secundario , Neoplasias Pulmonares/sangre , Proteínas de Neoplasias/sangre , Fosfopiruvato Hidratasa/sangre , Adulto , Anciano , Neoplasias Óseas/sangre , Neoplasias Óseas/diagnóstico , Neoplasias Óseas/diagnóstico por imagen , Carcinoma de Células Pequeñas/sangre , Carcinoma de Células Pequeñas/diagnóstico , Carcinoma de Células Pequeñas/diagnóstico por imagen , Pruebas Diagnósticas de Rutina , Estudios de Evaluación como Asunto , Femenino , Estudios de Seguimiento , Humanos , Neoplasias Pulmonares/patología , Imagen por Resonancia Magnética , Masculino , Persona de Mediana Edad , Estadificación de Neoplasias , Valor Predictivo de las Pruebas , Estudios Retrospectivos , Tomografía Computarizada de Emisión de Fotón ÚnicoRESUMEN
Elevated expression of the integrin-linked kinase (ILK) has been observed in a variety of cancers and has been further correlated with poor clinical outcome. Here, we show that mammary epithelial disruption of ILK results in a profound block in mammary tumor induction. Consistent with these observations, inhibition of ILK function in ErbB2-expressing cells with small molecule inhibitor or RNA interference resulted in profound block in their in vitro invasive properties due to the induction of apoptotic cell death. The rare ILK-deficient tumors that eventually arose overcame this block in tumor induction by an upregulation of ErB3 phosphorylation. These observations provide direct evidence that ILK has a critical role in the initiation phase of ErbB2 tumor induction.