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Título

Estudio translacional en pacientes con cancer de tiroides diferenciado para evaluar del valor pronostico de biomarcadores metabolicos sobre la progresión tumoral y el proceso angiogénico asociado

AutorSánchez-Ramos, Cristina; García-Quintans, Nieves ; Prieto, Ignacio; Monsalve, María
Fecha de publicación2015
EditorCSIC-UAM - Instituto de Investigaciones Biomédicas Alberto Sols (IIBM)
Citación2nd Symposium on Biomedical Research (2015)
ResumenObesity is considered the worldwide pandemia of the XXI century. It’s association with cardiovascular diseases and type 2 diabetes has been clearly established, more recently it has also being recognized a s relevant risk factor for tumor development, with levels of increased risk being particularly noticeable in some tumor types including: esophagus, pancreas, colon and rectum, breast, endometrium, kidney, thyroid, gallbladder, and hepatocarcinoma. One study, using NCI Surveillance, Epidemiology, and End Results (SEER) data, estimated that in 2007 in the United States, about 34,000 new cases of cancer in men (4 percent) and 50,500 in women (7 percent) were due to obesity. The percentage of cases attributed to obesity varied widely for different cancer types but was as high as 40 percent for some cancers, particularly endometrial cancer and esophageal adeno-carcinoma. Obesity not only increases the incidence, it also worsens prognosis, increasing the risk of metastasis and reducing the effectiveness of therapy. However, the mechanisms that link tumor development to metabolic control are still very poorly understood and the use of metabolic biomarkers or metabolism based therapeutical approaches is very limited in common medical practice. The most generally accepted hypothesis that aims to explain the link between metabolism and tumor development is based on the discoveries of the novel laureated Dr. Otto Warburg in the ‘50s, showing that proliferating cells make a very limited use of mitochondria as source of ATP and use mainly a glycolytic metabolism. This suppression of mitochondrial activity is also observed in obesity and other metabolic disorders, leading to the proposal that some metabolic regulators could also play a relevant physiological role as tumor suppressors. The thyroid is the main responsible for the control of whole body metabolic activity that is not directly regulated by diet, it is also a highly metabolically active organ heavily dependent on mitochondrial activity and with an elevated cellular turnover. Increasing weight has been found to be associated with an increase in the risk of thyroid cancer. However, the underlying mechanisms are still unclear. Thyroid cancer incidence has increased in the last years, but so far how metabolic dysfunction impacts on the origin and development of these tumors has not been investigated. Control of oxidative metabolism, mitochondrial activity and cellular antioxidant capacity are under the regulation of the transcriptional coactivator PGC-1α. PGC-1α activity is induced by caloric restriction and reduced in obesity, and would be expected to be reduced in tumor cells. Importantly, PGC-1α regulates the activity of the tumor suppressors p53 and TLS. PGC-1α activity is particularly high in metabolically active tissues like the thyroid. However, the possible role of PGC-1α activity in tumor suppression has not yet being investigated.
DescripciónResumen del póster presentado al 2nd Symposium on Biomedical Research: "Advances and perspectives in cancer", celebrado en Madrid el 17 de abril de 2015.-- et al.
URIhttp://hdl.handle.net/10261/152713
Aparece en las colecciones: (IIBM) Comunicaciones congresos
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