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Métodos Terapéuticos y Terapias MTCI
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1.
Target Oncol ; 15(6): 773-785, 2020 12.
Artículo en Inglés | MEDLINE | ID: mdl-33044683

RESUMEN

BACKGROUND: Inflammation is a long-established hallmark of liver fibrosis and carcinogenesis. Eosinophils are emerging as crucial components of the inflammatory process influencing cancer development. The role of blood eosinophils in patients with hepatocellular carcinoma receiving systemic treatment is an unexplored field. OBJECTIVE: The objective of this study was to analyse the prognostic role of the baseline eosinophil count in patients with sorafenib-treated hepatocellular carcinoma. PATIENTS AND METHODS: A training cohort of 92 patients with advanced- or intermediate-stage sorafenib-treated hepatocellular carcinoma and two validation cohorts of 65 and 180 patients were analysed. Overall survival and progression-free survival in relation to baseline eosinophil counts were estimated by the Kaplan-Meier method. Univariate and multivariate analyses were performed. RESULTS: A negative prognostic impact of low baseline eosinophil counts (< 50*109/L) was demonstrated in all cohorts (training cohort: hazard ratio = 50.1, 95% confidence interval 11.6-216.5, p < 0.0001 for low vs high eosinophil counts; first validation cohort: hazard ratio = 4.55, 95% confidence interval 1.24-16.65, p = 0.022; second validation cohort: hazard ratio = 3.21, 95% confidence interval 1.83-5.64, p < 0.0001). Moreover, low eosinophil counts had a negative prognostic role in patients progressing on or intolerant to sorafenib who received second-line regorafenib, but not capecitabine or best supportive care. CONCLUSIONS: Our analysis identified baseline blood eosinophil counts as a new prognostic factor in patients with sorafenib-treated hepatocellular carcinoma. Concerning second-line therapies, eosinophil counts were associated with survival outcomes only in regorafenib-treated patients, suggesting a possible predictive role in this setting.


Asunto(s)
Carcinoma Hepatocelular/tratamiento farmacológico , Eosinófilos/metabolismo , Neoplasias Hepáticas/tratamiento farmacológico , Sorafenib/uso terapéutico , Adulto , Anciano , Anciano de 80 o más Años , Carcinoma Hepatocelular/mortalidad , Femenino , Humanos , Neoplasias Hepáticas/mortalidad , Masculino , Persona de Mediana Edad , Pronóstico , Sorafenib/farmacología , Análisis de Supervivencia , Adulto Joven
2.
Sci Rep ; 7: 44685, 2017 03 21.
Artículo en Inglés | MEDLINE | ID: mdl-28322221

RESUMEN

Complementary and alternative medicine (CAM) is the term used to describe many kinds of products, practices, and systems that are not part of conventional medicine. Cancer patients usually do everything they can to combat the disease, manage its symptoms, and cope with the side effects of treatment. Unfortunately, patients who use CAM underestimate the risk of interaction with cancer therapy or worse they omit conventional therapy thus reducing the possibility of cancer remission. Herein we analyzed the effects of Vidatox 30 CH (venom extracted from the Junceus Rhopalurus scorpion) on hepatocellular carcinoma (HCC), the second leading cause of cancer-related deaths. We found out that Vidatox increases HCC proliferation and invasion whereas it does not seem to interact with sorafenib, the orally active multikinase inhibitor approved for the treatment of advanced hepatocellular carcinoma. Our results suggest that the concentration of Vidatox used in the present study has not anti-neoplastic effects and care must be taken in hiring Vidatox in patients with HCC.


Asunto(s)
Antineoplásicos/farmacología , Carcinoma Hepatocelular/inducido químicamente , Regulación Neoplásica de la Expresión Génica , Hepatocitos/efectos de los fármacos , Neoplasias Hepáticas/inducido químicamente , Niacinamida/análogos & derivados , Compuestos de Fenilurea/farmacología , Venenos de Araña/toxicidad , Animales , Carcinoma Hepatocelular/tratamiento farmacológico , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/metabolismo , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Línea Celular , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , Citocinas/genética , Citocinas/metabolismo , Dietilnitrosamina , Células Hep G2 , Hepatocitos/metabolismo , Hepatocitos/patología , Humanos , Neoplasias Hepáticas/tratamiento farmacológico , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/metabolismo , Masculino , Niacinamida/farmacología , Ratas Wistar , Escorpiones/química , Escorpiones/patogenicidad , Escorpiones/fisiología , Transducción de Señal , Sorafenib , Venenos de Araña/antagonistas & inhibidores , Venenos de Araña/aislamiento & purificación , Proteína p53 Supresora de Tumor/genética , Proteína p53 Supresora de Tumor/metabolismo , Receptor 2 de Factores de Crecimiento Endotelial Vascular/genética , Receptor 2 de Factores de Crecimiento Endotelial Vascular/metabolismo
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