Erratum to: Contribution of tumor endothelial cells to drug resistance: anti-angiogenic tyrosine kinase inhibitors act as p-glycoprotein antagonists

Erratum to: Angiogenesis DOI 10.1007/s10456-017-9549-6

In the original publication of the article, the panel B of Fig. 3 is incorrect. The correct version of the Fig. 3 is provided in this erratum.

Fig. 3

TKI enhance HOC–EC responsiveness to doxorubicin, paclitaxel but not cisplatin. a–c In vitro responsiveness of TEC to chemotherapeutics. HOC–EC or HUVEC were exposed to increasing concentrations of doxorubicin (a), paclitaxel (b) or cisplatin (c) for the duration of the assays (72 h for proliferation and 4 h for migration). Verapamil, sorafenib or sunitinib at the indicated concentrations were added 2 h earlier. Proliferation and migration are expressed as percentage of control (in the absence of chemotherapeutic drugs). Data are representative of at least three independent experiments. d In vivo tumor growth inhibition. A2780-1A9 ovarian cancer cells (10 × 10⁶) were transplanted subcutaneously in nude mice that were randomized to treatments at tumor volume of 150 mm³ (eight mice per group). Vandetanib was administered p.o. at a dose of 50 mg/kg for 5 days. Doxorubicin (8 mg/kg), paclitaxel (20 mg/kg) or cisplatin (5 mg/kg) were administered i.v. as a single bolus (arrowhead). Response is shown as tumor volume over time. P < 0.05 (*), P < 0.01 (**), P < 0.001 (***)