Tumor microenvironment and therapeutic response

•Tumor microenvironment (TME) influences therapeutic response and clinical outcome.•TME mediated resistance results from continuous crosstalk between tumor cells and stroma.•Targeting TME compartments could improve the effectiveness of current treatment. The tumor microenvironment significantly infl...

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Vydané v:	Cancer letters Ročník 387; s. 61 - 68
Hlavní autori:	Wu, Ting, Dai, Yun
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	Ireland Elsevier B.V 28.02.2017 Elsevier Limited
Predmet:	Angiogenesis Animals Antineoplastic Agents - therapeutic use Apoptosis Bone marrow Cancer Cancer therapies Conflicts of interest Cytokines Dendritic cells Drug resistance Extracellular matrix Fibroblasts Gene expression Hematology, Oncology and Palliative Medicine Humans Hypoxia Immunotherapy Medical prognosis Metastasis Microenvironment Molecular Targeted Therapy Neoplasms - drug therapy Neoplasms - metabolism Neoplasms - pathology Resistance Substance abuse treatment Target therapy Tumor Microenvironment - drug effects Tumorigenesis Tumors Vascular endothelial growth factor SFM-DR CLL TNFα CSF1 Target therapy CXCL1/2 CXCR4 Microenvironment CAFs PI3K TAMs GM-CSF CCL2 SDF1 AML CAM-DR IFNγ MM EM-DR FGF HGF TECs TKIs VEGF MMPs PKC IGF1 MAPK TME bFGF ECM Resistance MDSCs ERK1/2 TGF PDGF ATRA FGFR3 basic fibroblast growth factor platelet-derived growth factor chemokine (C-X-C motif) ligand 1/2 stromal cell-derived factor 1 tumor-associated macrophages fibroblast growth factor colony-stimulating factor 1 matrix metalloproteinases all-trans retinoic acid multiple myeloma cancer-associated fibroblasts soluble factor-mediated drug resistance phosphoinositol 3 kinase granulocyte-macrophage colony-stimulating factor insulin-like growth factor 1 environment-mediated drug resistance tumor necrosis factor α fibroblast growth factor receptor 3 cell adhesion-mediated drug resistance mitogen-activated protein kinase tyrosine kinase inhibitors acute myeloid leukemia chemokine (C-C motif) ligand 2 hepatocyte growth factor interferon γ extracellular signal-regulated kinase 1/2 protein kinase C tumor-associated endothelial cells myeloid-derived suppressor cells chronic lymphocytic leukemia chemokine (C-X-C motif) receptor 4 vascular endothelial growth factor tumor microenvironment transforming growth factor extracellular matrix
ISSN:	0304-3835, 1872-7980
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Popis
Shrnutí:	•Tumor microenvironment (TME) influences therapeutic response and clinical outcome.•TME mediated resistance results from continuous crosstalk between tumor cells and stroma.•Targeting TME compartments could improve the effectiveness of current treatment. The tumor microenvironment significantly influences therapeutic response and clinical outcome. Microenvironment-mediated drug resistance can be induced by soluble factors secreted by tumor or stromal cells. The adhesion of tumor cells to stromal fibroblasts or to components of the extracellular matrix can also blunt therapeutic response. Microenvironment-targeted therapy strategies include inhibition of the extracellular ligand–receptor interactions and downstream pathways. Immune cells can both improve and obstruct therapeutic efficacy and may vary in their activation status within the tumor microenvironment; thus, re-programme of the immune response would be substantially more beneficial. The development of rational drug combinations that can simultaneously target tumor cells and the microenvironment may represent a solution to overcome therapeutic resistance.
Bibliografia:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Article-2 ObjectType-Feature-3 content type line 23 ObjectType-Review-1
ISSN:	0304-3835 1872-7980
DOI:	10.1016/j.canlet.2016.01.043