000			02818na a2200373 4500
999			_c4181 _d4181
003			PC4181
005			20210625062801.0
008			130622s2013 xxx||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_aOrtiz Romero, Pablo Luis _91223 _eDermatología Médico-Quirúrgica y Venereología
245	0	0	_aNIK Controls Classical and Alternative NF-kappa B Activation and Is Necessary for the Survival of Human T-cell Lymphoma Cells. _h[artículo]
260			_bClinical Cancer Research, _c2013
300			_a19(9):2319-30.
500			_aFormato Vancouver: Odqvist L, Sánchez-Beato M, Montes-Moreno S, Martín-Sánchez E, Pajares R, Sánchez-Verde L et al. NIK controls classical and alternative NF-κB activation and is necessary for the survival of human T-cell lymphoma cells. Clin Cancer Res. 2013 May 1;19(9):2319-30.
501			_aPMID: 23536439
504			_aContiene 50 referencias
520			_aPeripheral T-cell lymphomas (PTCL) are a heterogeneous entity of neoplasms with poor prognosis, a lack of effective therapies, and a largely unknown molecular pathology. Deregulated NF-kappa B activity has been associated with several lymphoproliferative diseases, but its importance in T-cell lymphomagenesis is poorly understood. We investigated the function of the NF-kappa B-inducing kinase (NIK), in this pathway and its role as a potential molecular target in T-cell lymphomas. Experimental Design: We used immunohistochemistry to analyze the expression of different NF-kappa B members in primary human PTCL samples and to study its clinical impact. With the aim of inhibiting the pathway, we used genetic silencing of NIK in several T-cell lymphoma cell lines and observed its effect on downstream targets and cell viability. Results: We showed that the NF-kappa B pathway was activated in a subset of PTCLs associated with poor overall survival. NIK was overexpressed in a number of PTCL cell lines and primary samples, and a pivotal role for NIK in the survival of these tumor cells was unveiled. NIK depletion led to a dramatic induction of apoptosis in NIK-overexpressing cell lines and also showed a more pronounced effect on cell survival than inhibitor of kappa B kinase (IKK) knockdown. NIK silencing induced a blockage of both classical and alternative NF-kappa B activation and reduced expression of several prosurvival and antiapoptotic factors. Conclusions: The results of the present study indicate that NIK could be a promising therapeutic target in these aggressive malignancies.
710			_9145 _aServicio de Dermatología Médico-Quirúrgica y Venereología
710			_9625 _aInstituto de Investigación imas12
856			_uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/4/pc4181.pdf _ySolicitar documento
942			_n0 _2ddc _cART