Can the co-dependence of the immune system and angiogenesis facilitate pharmacological targeting of tumours?

被引:24
作者
Mortara, Lorenzo [1 ]
Benest, Andrew V. [2 ]
Bates, David O. [2 ]
Noonan, Douglas M. [1 ,3 ]
机构
[1] Univ Insubria, Dept Biotechnol & Life Sci, Immunol & Gen Pathol Lab, Varese, Italy
[2] Univ Nottingham, Sch Med, Queens Med Ctr, Canc Biol,Div Canc & Stem Cells, Nottingham NG2 7UH, England
[3] IRCCS MultiMed, Sci & Technol Pole, Milan, Italy
关键词
INNATE LYMPHOID-CELLS; NATURAL-KILLER-CELLS; CHEMOKINE LIGAND 2; HUMAN MONOCLONAL-ANTIBODY; CARLUMAB CNTO 888; SUPPRESSOR-CELLS; MACROPHAGE POLARIZATION; T-CELLS; IN-VIVO; PHASE-I;
D O I
10.1016/j.coph.2017.05.009
中图分类号
R9 [药学];
学科分类号
100702 [药剂学];
摘要
Tumours elicit a number of mechanisms to induce a reprogramming of innate and adaptive immune cells to their advantage, inducing a pro-angiogenic phenotype. Investigation of these events is now leading to the identification of specific myeloid and lymphoid cell-targeted therapies, as well as of unexplored off-target activities of clinically relevant chemotherapeutic and metabolic drugs. It is also leading to an enhanced understanding of the interplay between angiogenesis and the immune system, and the value of novel co-targeting approaches using both immunotherapy and antiangiogenic therapy. Here, we review recently identified mechanisms and potential pharmacological approaches targeting the crosstalk between cancer cells and the host immune system, providing an overview on novel therapeutic opportunities linking immuno-oncology and anti-angiogenic therapy.
引用
收藏
页码:66 / 74
页数:9
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