|1.||Schwarz, Margaret A: 16 articles (04/2015 - 01/2004)|
|2.||Li, Zhen: 10 articles (09/2015 - 01/2011)|
|3.||Schwarz, Roderich E: 10 articles (04/2015 - 07/2004)|
|4.||Wang, Ping: 9 articles (09/2015 - 03/2012)|
|5.||Awasthi, Niranjan: 9 articles (04/2015 - 01/2009)|
|6.||Xue, Yi-xue: 6 articles (09/2015 - 01/2011)|
|7.||Liu, Yun-hui: 6 articles (09/2015 - 01/2011)|
|8.||Liu, Li-bo: 6 articles (09/2015 - 01/2011)|
|9.||Xue, Yi-Xue: 5 articles (09/2015 - 03/2010)|
|10.||Liu, Yun-Hui: 5 articles (09/2015 - 03/2010)|
04/15/2010 - "In heterotopic PDAC tumors EMAP II caused a significant reduction (>65%) in tumor growth, accompanied by a >50 and 44% decrease in microvessel density and proliferative activity, respectively. "
07/01/2004 - "This feature enables EMAP II to up-regulate the TNF sensitivity of TNF-resistant tumors, an observation of importance in developing new approaches aimed at improving the efficacy of TNF as an anticancer treatment. "
03/01/2012 - "The purpose of the present study was to determine the potential for RhoA/ROCK signaling to play a role in endothelial-monocyte-activating polypeptide (EMAP) II-induced increase in blood-tumor barrier (BTB) permeability in rat brain microvascular endothelial cells (RBMECs). "
02/15/2015 - "Low-dose endothelial monocyte-activating polypeptide-II increases permeability of blood-tumor barrier via a PKC-ζ/PP2A-dependent signaling mechanism."
06/15/2014 - "Moreover, EMAP-II was found to suppress tumor growth by inducing G2/M arrest in GSCs. "
|2.||Glioblastoma (Glioblastoma Multiforme)
06/15/2014 - "These results suggest that EMAP-II is an effective anticancer agent for glioblastoma therapy, which can induce direct growth suppression in GSCs through defective autophagy and G2/M arrest mediated by the PI3K/Akt/FoxO1 axis."
06/15/2014 - "Anti-neoplastic activity of low-dose endothelial-monocyte activating polypeptide-II results from defective autophagy and G2/M arrest mediated by PI3K/Akt/FoxO1 axis in human glioblastoma stem cells."
11/01/2000 - "To determine whether the production of endothelial-monocyte activating polypeptide II (EMAPII) by tumors confers TNF sensitivity and whether EMAPII expression in glioblastoma can predict the clinical response to TNF therapy, we evaluated EMAPII expression and the efficacy of TNF in patients with glioblastoma. "
11/01/2000 - "Clinical significance of the expression of endothelial-monocyte activating polypeptide II (EMAPII) in the treatment of glioblastoma with recombinant mutant human tumor necrosis factor-alpha (TNF-SAM2)."
01/01/2015 - "This study aims to investigate the effect of endothelial-monocyte activating polypeptide II (EMAP II) on human glioblastoma (GBM) cells and glioblastoma stem cells (GSCs) as well as its possible mechanisms. "
|3.||Pancreatic Neoplasms (Pancreatic Cancer)
09/01/2011 - "Enhancing cytotoxic agent activity in experimental pancreatic cancer through EMAP II combination therapy."
05/01/2010 - "EMAP II-based antiangiogenic-antiendothelial in vivo combination therapy of pancreatic cancer."
04/15/2010 - "Antitumor effects of EMAP II against pancreatic cancer through inhibition of fibronectin-dependent proliferation."
08/01/2009 - "EMAP II had no impact on gemcitabine-induced antiproliferative effects against pancreatic cancer cells in vitro. "
08/01/2009 - "There was a significant extension of survival after EMAP II and gemcitabine combination therapy compared with controls in 2 different pancreatic cancer cell line models at P = .0001 and P = .006, respectively. "
|4.||Sarcoma (Soft Tissue Sarcoma)
09/15/2006 - "In a comparative analysis we found that the overall proEMAP and EMAP-II expression was higher in melanoma as compared to sarcoma cases and measurements in cell lines revealed high proEMAP expression by melanoma cells. "
10/01/2002 - "It has recently been shown that in vivo sensitivity of tumor vasculature to TNF is determined by tumor production of EMAP-II. We measured the level of EMAP-II in a TNF-resistant soft tissue sarcoma. "
10/07/1994 - "A single intra-tumor injection of EMAP II into Meth A sarcomas induced acute thrombohemorrhage and partial tumor regression. "
10/01/2002 - "Improved antitumor response to isolated limb perfusion with tumor necrosis factor after upregulation of endothelial monocyte-activating polypeptide II in soft tissue sarcoma."
02/01/2015 - "We conclude that blockade of EMAP II induces angiogenesis and improves cardiac function following chronic MI, resulting in reduced myocardial fibrosis and scar formation and increased capillary density and preserved viable myocytes in the infarct area."
01/01/2004 - "Six weeks following myocardial infarction, EMAP II protein is elevated above control, changes its location of transcription from the inflammatory cell population to that of the fibroblasts located in the relative avascular scar tissue, and has resumed its perivascular stromal distribution in the viable periinfarct tissue. "
02/01/2015 - "EMAP II AB, compared with vehicle or non-specific antibody, significantly, p<0.05, improved the survival rate after MI, reduced scar size and attenuated the development of heart failure, i.e., left ventricular ejection fraction was significantly higher in EMAP II AB group, fibrosis was reduced by 24%, and importantly, more myocytes were alive in EMAP II AB group in the infarct area. "
01/01/2012 - "Intracellular EMAP II expression is increased during fetal development at epithelial/mesenchymal boundaries and in pathophysiologic fibroproliferative cells of bronchopulmonary dysplasia, emphysema, and scar fibroblast tissue following myocardial ischemia. "
|1.||Tumor Necrosis Factor-alpha (Tumor Necrosis Factor)
|5.||member 1 small inducible cytokine subfamily E
|7.||Protein Kinase C
|8.||Proteins (Proteins, Gene)
|3.||Heterologous Transplantation (Xenotransplantation)
|4.||Homologous Transplantation (Allograft)