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))

Kartik Angara, Thaiz F. Borin, Mohammad H. Rashid, Iryna Lebedyeva, Roxan Ara, Ping Chang Lin, A. S.M. Iskander, Roni J. Bollag, Bhagelu R. Achyut, Ali S. Arbab

Research output: Contribution to journalComment/debatepeer-review

2 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)156-157
Number of pages2
JournalNeoplasia (United States)
Volume21
Issue number1
DOIs
StatePublished - Jan 2019

ASJC Scopus subject areas

  • Cancer Research

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