Table A1.
Change | CAF |
---|---|
CAFs that increased during treatment | |
V | VEGF, IL-8, G-CSF, IL-17 |
CP | MCP-1 |
VCP | MCP-1, eotaxin |
CAFs that decreased during treatment | |
V | sVEFGR-2 |
CP | IL-12, IL-1RA, MMP-9, IL-4, IL-10, IL-13, sVEGFR-2, MIP-1α, IP-10 |
VCP | IL-12, IL-1RA, MMP-9 |
CAF increases associated with improved PFS outcome | |
V | ICAM-1, osteopontin, sIL-2R, IL-5 |
CP | IL-13, IL-15, IL-17 |
VCP | IL-12, IP-10, MIP-1α |
CAF increases associated with inferior PFS outcome | |
V | VEGF |
CP | MMP-9, IL-15 |
VCP | IL-8, IFN-α |
CAF changes predictive of PFS benefit from treatment | |
V | ICAM-1 (increase → superior PFS); VEGF (increase → inferior PFS) |
CP | IL-17 (increase → superior PFS) |
VCP | sIL-2R (increase → superior PFS); IL-8 (increase → inferior PFS); IFN-α (increase → inferior PFS) |
Abbreviations: CAF, cytokine and angiogenic factor; V, vandetanib; VEGF, vascular endothelial growth factor; IL, interleukin; G-CSF, granulocyte colony-stimulating factor; CP, carboplatin and paclitaxel; MCP-1, macrophage chemoattractant protein-1; VCP, vandetanib, carboplatin, and paclitaxel; sVEGFR-2, soluble vascular endothelial growth factor receptor 2; IL-1RA, interleukin-1 receptor antagonist; MMP-9, matrix metalloproteinase 9; MIP-1α, macrophage inflammatory protein 1α; IP-10, interferon gamma–induced protein 10; PFS, progression-free survival; ICAM-1, intercellular adhesion molecule 1; sIL-2R, soluble interleukin-2 receptor; IFN-α, interferon alfa.