000			nab a22 7a 4500
999			_c17812 _d17812
003			PC17812
005			20240401135804.0
008			240401b xxu||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_93391 _aValeri, Antonio _eHematología y Hemoterapia
100			_9389 _aMartínez López, Joaquín _eHematología y Hemoterapia
245	0	0	_aEvaluation of the potential therapeutic benefits of macrophage reprogramming in multiple myeloma. _h[artículo]
260			_bBlood, _c2016
300			_a128(18):2241-52.
500			_aFormato Vancouver: Gutiérrez González A, Martínez Moreno M, Samaniego R, Arellano Sánchez N, Salinas Muñoz L, Relloso M et al. Evaluation of the potential therapeutic benefits of macrophage reprogramming in multiple myeloma. Blood. 2016 Nov 3;128(18):2241-52.
501			_aPMID: 27625360
504			_aContiene 59 referencias
520			_aTumor-associated macrophages (TAM) are important components of the multiple myeloma (MM) microenvironment that support malignant plasma cell survival and resistance to therapy. It has been proposed that macrophages (MØ) retain the capacity to change in response to stimuli that can restore their antitumor functions. Here, we investigated several approaches to reprogram MØ as a novel therapeutic strategy in MM. First, we found tumor-limiting and tumor-supporting capabilities for monocyte-derived M1-like MØ and M2-like MØ, respectively, when mixed with MM cells, both in vitro and in vivo. Multicolor confocal microscopy revealed that MM-associated MØ displayed a predominant M2-like phenotype in the bone marrow of MM patient samples, and a high expression of the pro-M2 cytokine macrophage migration inhibitory factor (MIF). To reprogram the protumoral M2-like MØ present in MM toward antitumoral M1-like MØ, we tested the pro-M1 cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) plus blockade of the M2 cytokines macrophage colony-stimulating factor or MIF. The combination of GM-CSF plus the MIF inhibitor 4-iodo-6-phenyl-pyrimidine achieved the best reprogramming responses toward an M1 profile, at both gene and protein expression levels, as well as remarkable tumoricidal effects. Furthermore, this combined treatment elicited MØ-dependent therapeutic responses in MM xenograft mouse models, which were linked to upregulation of M1 and reciprocal downregulation of M2 MØ markers. Our results reveal the therapeutic potential of reprogramming MØ in the context of MM.
710			_9297 _aServicio de Hematología y Hemoterapia
856			_uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/1/pc17812.pdf _ySolicitar documento
942			_2ddc _cART _n0