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. Author manuscript; available in PMC: 2021 Dec 30.
Published in final edited form as: Cancer Cell. 2019 May 13;35(5):816. doi: 10.1016/j.ccell.2019.04.011

Inhibition of Nuclear PTEN Tyrosine Phosphorylation Enhances Glioma Radiation Sensitivity through Attenuated DNA Repair

PMCID: PMC8717880  NIHMSID: NIHMS1055076  PMID: 31085179

In the originally published version of this article, a few errors were made in and related to Table S2. We analyzed 44 samples instead of 43 samples. The RPKM value for FGFR2 and FGFR3 were mistakenly copied as the RPMK value of FGFR1. The expression level of PTEN and FGFR2 were determined by mean value instead of median value, which for PTEN is 2.6 and FGFR2 is 2.1. In the legend for Figure 1D, the orange rectangle indicates all radiation sensitive samples in PTEN high group showed low level of FGFR2 expression.

Figure 1. FGFR2-mediated phosphorylation of PTEN tyrosine 240 protects cells from DNA damage by facilitating DNA repair.

(D) 44 patient-derived glioma stem cell lines were evaluated for PTEN and FGFRs expression by RNAseq and for radiation sensitivity by clonogenic assay. Distribution of radiation sensitive and radiation resistant samples in PTEN high versus PTEN low group are shown. Orange rectangle indicates all radiation sensitive samples in PTEN high group showed low level of FGFR2 expression. PTEN high/PTEN low, PTEN expression is higher/lower than the mean value (RNAseq); FGFR2 low, FGFR2 expression is lower than mean value (RNAseq).

We have corrected the information in Table S2, Figure 1D legend, and the “Analysis of patient derived GSC lines” section of the STAR Methods. We apologize for any confusion these errors may have caused.

Supplementary Material

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Supplementary Materials

Ma et al video
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