It appears you don't have support to open PDFs in this web browser. To view this file, Open with your PDF reader
Abstract
C–C motif chemokine ligand 2 (CCL2) is a monocyte chemoattractant that promotes metastatic disease and portends a poor prognosis in many cancers. To determine the potential of anti-CCL2 inhibition as a therapy for recurrent metastatic disease in neuroblastoma, a mouse model of minimal residual disease was utilized in which residual disease was treated with anti-CCL2 monoclonal antibody with etoposide. The effect of anti-CCL2 antibody on neuroblastoma cells was determined in vitro with cell proliferation, transwell migration, and 2-dimensional chemotaxis migration assays. The in vivo efficacy of anti-CCL2 antibody and etoposide against neuroblastoma was assessed following resection of primary tumors formed by two cell lines or a patient-derived xenograft (PDX) in immunodeficient NOD-scid gamma mice. In vitro, anti-CCL2 antibody did not affect cell proliferation but significantly inhibited neuroblastoma cell and monocyte migration towards an increasing CCL2 concentration gradient. Treatment of mice with anti-CCL2 antibody combined with etoposide significantly increased survival of mice after resection of primary tumors, compared to untreated mice.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details
1 Children’s Hospital Los Angeles, Division of Pediatric Surgery, Los Angeles, USA (GRID:grid.239546.f) (ISNI:0000 0001 2153 6013)
2 Cedars-Sinai Medical Center, Biostatistics and Bioinformatics Research Center, Los Angeles, USA (GRID:grid.50956.3f) (ISNI:0000 0001 2152 9905)
3 University of Southern California, Division of Hematology, Oncology and Blood and Marrow Transplantation, Keck School of Medicine, Los Angeles, USA (GRID:grid.42505.36) (ISNI:0000 0001 2156 6853)
4 University of Southern California, Division of Hematology, Oncology and Blood and Marrow Transplantation, Keck School of Medicine, Los Angeles, USA (GRID:grid.42505.36) (ISNI:0000 0001 2156 6853); University of Southern California, Department of Pediatrics, Keck School of Medicine, Los Angeles, USA (GRID:grid.42505.36) (ISNI:0000 0001 2156 6853)
5 Children’s Hospital Los Angeles, The Saban Research Institute, Los Angeles, USA (GRID:grid.239546.f) (ISNI:0000 0001 2153 6013)
6 Children’s Hospital Los Angeles, Division of Pediatric Surgery, Los Angeles, USA (GRID:grid.239546.f) (ISNI:0000 0001 2153 6013); University of Southern California, Division of Hematology, Oncology and Blood and Marrow Transplantation, Keck School of Medicine, Los Angeles, USA (GRID:grid.42505.36) (ISNI:0000 0001 2156 6853); University of Southern California, Department of Pediatrics, Keck School of Medicine, Los Angeles, USA (GRID:grid.42505.36) (ISNI:0000 0001 2156 6853); Cedars-Sinai Medical Center, Department of Surgery, Los Angeles, USA (GRID:grid.50956.3f) (ISNI:0000 0001 2152 9905)