TY - JOUR
T1 - Corrigendum to “CXCR2-Expressing Tumor Cells Drive Vascular Mimicry in Antiangiogenic Therapy–Resistant Glioblastoma” (Neoplasia (2018) 20(10) (1070–1082), (S1476558618303798) (10.1016/j.neo.2018.08.011))
AU - Angara, Kartik
AU - Borin, Thaiz F.
AU - Rashid, Mohammad H.
AU - Lebedyeva, Iryna
AU - Ara, Roxan
AU - Lin, Ping Chang
AU - Iskander, A. S.M.
AU - Bollag, Roni J.
AU - Achyut, Bhagelu R.
AU - Arbab, Ali S.
N1 - Publisher Copyright:
© 2018 The Authors
PY - 2019/1
Y1 - 2019/1
N2 - The authors regret to have used incorrect figure legend for Figure 3 in the original manuscript. The incorrect figure legend in the original manuscript and the corrected figure legend have been included here. [Figure presented] Incorrect figure legend in the original manuscript: Figure 3 CXCR2+ tumor cells acquire endothelial and stem cell–like phenotypes following AAT. Quantitative data are expressed in mean ± SEM. *P <.05, **P <.01, and ***P <.001. n = 3. (A) Representative pictorial depiction of the acquisition of endothelial phenotypes by GBM cells. Flow cytometry data in vivo (B) showing different CXCR2 GBM subpopulations and (C) endothelial-like GBM subpopulations in the AAT-treated groups compared to the vehicle. (D) In vitro data showing CXCR2 GBM cells with endothelial cell–like and stem-like phenotypes following AAT treatment compared to control in hypoxic conditions for 24 hours. (E) U251 GBM cells treated with vehicle (control), vatalanib (10 μM), and avastin (100 μg/ml) and cultured in both normoxic (upper panel) and hypoxic (lower panel) conditions for 6 hours. Quantitative data are expressed in mean ± SEM. *P <.05 and ***P <.001. The descriptions for (A), (B), (C), and (D) have been mistakenly included here and do not match with the figures provided in Figure 3. In (E), the term “normoxic” has not been included while describing the treatment conditions. The corrections have been made accordingly, and the corrected figure legend is included here. Corrected figure legend: Figure 3 CXCR2+ tumor cells acquire endothelial and stem cell–like phenotypes following AAT. Quantitative data are expressed in mean ± SEM. *P <.05, **P <.01, and ***P <.001. n = 3. Flow cytometry data in vivo (A) showing different CXCR2 GBM subpopulations and (B) endothelial-like GBM subpopulations in the AAT-treated groups compared to the vehicle. (C) In vitro data showing CXCR2 GBM cells with endothelial cell–like and stem-like phenotypes following AAT treatment compared to control in normoxic and hypoxic conditions for 24 hours. (D) Representative pictorial depiction of the acquisition of endothelial phenotypes by GBM cells. (E) U251 GBM cells treated with vehicle (control), vatalanib (10 μM), and avastin (100 μg/ml) and cultured in both normoxic (upper panel) and hypoxic (lower panel) conditions for 6 hours. Quantitative data are expressed in mean ± SEM. *P <.05 and ***P <.001. The authors would like to apologize for any inconvenience caused.
AB - The authors regret to have used incorrect figure legend for Figure 3 in the original manuscript. The incorrect figure legend in the original manuscript and the corrected figure legend have been included here. [Figure presented] Incorrect figure legend in the original manuscript: Figure 3 CXCR2+ tumor cells acquire endothelial and stem cell–like phenotypes following AAT. Quantitative data are expressed in mean ± SEM. *P <.05, **P <.01, and ***P <.001. n = 3. (A) Representative pictorial depiction of the acquisition of endothelial phenotypes by GBM cells. Flow cytometry data in vivo (B) showing different CXCR2 GBM subpopulations and (C) endothelial-like GBM subpopulations in the AAT-treated groups compared to the vehicle. (D) In vitro data showing CXCR2 GBM cells with endothelial cell–like and stem-like phenotypes following AAT treatment compared to control in hypoxic conditions for 24 hours. (E) U251 GBM cells treated with vehicle (control), vatalanib (10 μM), and avastin (100 μg/ml) and cultured in both normoxic (upper panel) and hypoxic (lower panel) conditions for 6 hours. Quantitative data are expressed in mean ± SEM. *P <.05 and ***P <.001. The descriptions for (A), (B), (C), and (D) have been mistakenly included here and do not match with the figures provided in Figure 3. In (E), the term “normoxic” has not been included while describing the treatment conditions. The corrections have been made accordingly, and the corrected figure legend is included here. Corrected figure legend: Figure 3 CXCR2+ tumor cells acquire endothelial and stem cell–like phenotypes following AAT. Quantitative data are expressed in mean ± SEM. *P <.05, **P <.01, and ***P <.001. n = 3. Flow cytometry data in vivo (A) showing different CXCR2 GBM subpopulations and (B) endothelial-like GBM subpopulations in the AAT-treated groups compared to the vehicle. (C) In vitro data showing CXCR2 GBM cells with endothelial cell–like and stem-like phenotypes following AAT treatment compared to control in normoxic and hypoxic conditions for 24 hours. (D) Representative pictorial depiction of the acquisition of endothelial phenotypes by GBM cells. (E) U251 GBM cells treated with vehicle (control), vatalanib (10 μM), and avastin (100 μg/ml) and cultured in both normoxic (upper panel) and hypoxic (lower panel) conditions for 6 hours. Quantitative data are expressed in mean ± SEM. *P <.05 and ***P <.001. The authors would like to apologize for any inconvenience caused.
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U2 - 10.1016/j.neo.2018.11.001
DO - 10.1016/j.neo.2018.11.001
M3 - Comment/debate
C2 - 30595360
AN - SCOPUS:85057034728
SN - 1522-8002
VL - 21
SP - 156
EP - 157
JO - Neoplasia (United States)
JF - Neoplasia (United States)
IS - 1
ER -