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Abstract
Targeting novel pathways associated with tumor angiogenesis, invasion and immunity, may lead to improvement in patient outcomes for renal cell carcinoma. Chemokines potentiate tumor growth, metastasis, angiogenesis and immune evasion through interactions with stromal cells and neoplastic cells. Further understanding of the mechanisms involved in chemokine-mediated angiogenesis and metastasis may lead to improved therapeutic strategies in this disease. Interactions between chemokine expression and signaling, and the VEGF and hypoxia-inducible factor pathways offer important opportunities to intervene in the process of renal cell carcinoma proliferation, angiogenesis and invasion. Modulation of the CXCR3/CXCR3-ligand or the CXCR4/CXCL12 biologic axis may be potential therapeutic targets for the treatment of renal cell carcinoma. Furthermore, combination treatment with agents targeting chemokine signaling with therapies directed at angiogenesis and tumor immunity may lead to improved outcomes in this disease.
Financial & competing interests disclosure
This review was supported by NCI K12 CA 01727 and Phase One Foundation (Karen L Reckamp); NIH HL66027 and CA87879 (Robert M Strieter). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
Notes
B-TG: β thromboglobulin; CTAP: Connective tissue-activating peptide; ENA: Epithelial neutrophil-activating peptide; GCP: Granulocyte chemotactic protein; GRO: Growth-related oncogene; IP: IFN-inducible protein; ITAC: IFN-inducible T cell chemoattractant; MIG: Monokine induced by IFN-; NAP: Neutrophil-activating peptide; PBP: Platelet basic protein; PF: Platelet factor.
