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 Ferraz Borin, Mohammad H. Rashid, Iryna Oleksandrivna Lebedyeva, Roxan Ara, Ping-Chang Lin, A. S.M. Iskander, Roni Jacob Bollag, Bhagelu R. Achyut, Ali Syed Arbab

Research output: Contribution to journalComment/debate

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 1 2019

Fingerprint

Glioblastoma
Blood Vessels
Phenotype
Manuscripts
Neoplasms
Neoplastic Stem Cells
Flow Cytometry
Endothelial Cells
corrigendum
Drive
Emotions

ASJC Scopus subject areas

  • Cancer Research

Cite this

@article{1f4e437f61c542798329a078fbf67b4e,
title = "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))",
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.",
author = "Kartik Angara and Borin, {Thaiz Ferraz} and Rashid, {Mohammad H.} and Lebedyeva, {Iryna Oleksandrivna} and Roxan Ara and Ping-Chang Lin and Iskander, {A. S.M.} and Bollag, {Roni Jacob} and Achyut, {Bhagelu R.} and Arbab, {Ali Syed}",
year = "2019",
month = "1",
day = "1",
doi = "10.1016/j.neo.2018.11.001",
language = "English (US)",
volume = "21",
pages = "156--157",
journal = "Neoplasia (United States)",
issn = "1522-8002",
publisher = "Elsevier Inc.",
number = "1",

}

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 Ferraz

AU - Rashid, Mohammad H.

AU - Lebedyeva, Iryna Oleksandrivna

AU - Ara, Roxan

AU - Lin, Ping-Chang

AU - Iskander, A. S.M.

AU - Bollag, Roni Jacob

AU - Achyut, Bhagelu R.

AU - Arbab, Ali Syed

PY - 2019/1/1

Y1 - 2019/1/1

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.

UR - http://www.scopus.com/inward/record.url?scp=85057034728&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85057034728&partnerID=8YFLogxK

U2 - 10.1016/j.neo.2018.11.001

DO - 10.1016/j.neo.2018.11.001

M3 - Comment/debate

VL - 21

SP - 156

EP - 157

JO - Neoplasia (United States)

JF - Neoplasia (United States)

SN - 1522-8002

IS - 1

ER -