ABSTRACT
We report a case of successful treatment with erlotinib of a patient with non-small cell lung cancer (stage IV) and meningeal metastasis. Combined treatment with whole brain radiotherapy (WBRT) and erlotinib mitigated neurologic symptoms of the patient. Magnetic resonance imaging showed reduction of the brain metastasis. Partial remission was observed by chest computed tomography (CT) scan after six months of erlotinib therapy.
Reportamos un caso de tratamiento exitoso con el erlotinib de un paciente con cáncer pulmonar de células no pequeñas (fase IV) y metástasis meníngea. El tratamiento combinado con la radioterapia total del cerebro (WBRT) y erlotinib mitigaron los síntomas neurológicos del paciente. Las imágenes de resonancia magnética mostraron una reducción de la metástasis del cerebro. La remisión parcial fue observada mediante CT scan de tórax tras seis meses de terapia con erlotinib.
Subject(s)
Aged , Humans , Male , Carcinoma, Non-Small-Cell Lung/drug therapy , Carcinoma, Non-Small-Cell Lung/radiotherapy , Lung Neoplasms/pathology , Meningeal Neoplasms/drug therapy , Meningeal Neoplasms/radiotherapy , Carcinoma, Non-Small-Cell Lung/secondary , Meningeal Neoplasms/secondary , Protein Kinase Inhibitors/therapeutic use , Quinazolines/therapeutic useABSTRACT
Clear differences exist in the incidence and severity of atherosclerotic plaques that arise in different segments of the arterial tree. Aortic homograft transplant experiments in dogs showed that the greater incidence of plaque formation in the abdominal versus the thoracic aorta was due to intrinsic differences in the cell populations in these two segments rather than to hemodynamic factors. What is the basis for SMC diversity within a common vessel wall? Recent lineage analysis studies in the avian and mammalian embryo indicate that two distinct SMC lineages contribute to the formation of the major elastic outflow arteries including the aorta. A mixture of unique SMC types of diverse developmental lineages within a common vessel wall raises new questions about the potential for SMC type-specific responses to growth factors and cytokines involved in human atherosclerosis and restenosis