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Correction to: Immunotherapy Utilizing the Combination of Natural Killer– and Antibody Dependent Cellular Cytotoxicity (ADCC)–Mediating Agents with Poly (ADP-ribose) polymerase (PARP) Inhibition
  1. Kathleen E. Fenerty1,
  2. Michelle Padget1,
  3. Benjamin Wolfson1,
  4. Sofia R. Gameiro1,
  5. Zhen Su2,
  6. John H. Lee3,
  7. Shahrooz Rabizadeh3,
  8. Patrick Soon-Shiong3 and
  9. James W. Hodge1,i
  1. Aff1 0000 0004 1936 8075grid.48336.3aLaboratory of Tumor Immunology and Biology, Center for Cancer ResearchNational Cancer Institute, National Institutes of Health 10 Center Drive, Room 8B09 20892 Bethesda MD USA
  2. Aff2 0000 0004 0412 6436grid.467308.eEMD Serono Billerica MA USA
  3. Aff3 NantOmics City Culver CA USA
  1. i jh241d{at}nih.gov

Abstract

Following publication of the original article [1], an error was noted in the GAPDH in the western blot depicted in Figure 4b.

The original article can be found online at 10.1186/s40425-018-0445-4

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The original article can be found online at 10.1186/s40425-018-0445-4

Correction to: J ImmunoTher Cancer

https://doi.org/10.1186/s40425-018-0445-4

Following publication of the original article [1], an error was noted in the GAPDH in the western blot depicted in Figure 4b. The GAPDH lanes for the experiment have been updated. The corrected Fig. 4 can be seen below.

Fig. 4

Olaparib treatment enhances ADCC using both cetuximab and avelumab without modulation of mAb targets EGFR and PD-L1. a Treatment with cetuximab (cet) significantly increased NK-induced lysis of olaparib (ola)-treated BRCA mutant prostate carcinoma (22RV1) cells at 12 h. The addition of anti-CD16 antibody neutralized this increase, confirming that the increased lysis is attributable to ADCC. b STING is not expressed in 22RV1 either before or after olaparib treatment. c Olaparib treatment did not result in significant modulation of EGFR expression on 22RV1 cells as measured by flow cytometry. d Treatment with cetuximab increased NK-induced lysis of olaparib-treated BRCA WT prostate carcinoma cells (DU145) cells. Role of anti-CD16 antibody on increased lysis attributable to ADCC. e The PD-L1+ cell line DU145 also underwent NK-induced ADCC in the presence of the anti-PD-L1 antibody avelumab (ave). Lysis of DU145 cells after 12 h in the presence or absence of olaparib and NK, treated with either avelumab or isotype control is shown. f STING was upregulated in DU145 following exposure to olaparib. g Olaparib treatment did not result in significant modulation of EGFR expression in DU145 cells as measured by flow cytometry. h Olaparib treatment did not result in significant modulation of PD-L1 expression in DU145 cells as measured by flow cytometry. These experiments were performed twice with similar results. p < 0.05*, p < 0.0001****

The error does not affect the findings of the experiment.

Reference

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