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Abstract
This article has been corrected: Due to errors in image preparation, the separate
red/green images presented for vehicle control and valproate in Figure 6A were incorrect.
In addition, in Figure 9, the graphical panel on the left has been clarified and an
extra sentence and clauses have been added into the figure legend which completely
and accurately describe how the in vivo studies were performed. Both corrected figures
are shown below. The authors declare that these corrections do not change the results
or conclusions of this paper.
Original article: Oncotarget. 2017; 8:90262–90277. 90262-90277 . https://doi.org/10.18632/oncotarget.21660
Figure 6
Figure 6: Neratinib promotes the co-localization of K-RAS with LAMP2 and cathepsin
B, and the disassociation of K-RAS and ERBB1.
(A) PANC-1 cells were treated with vehicle control, sodium valproate (250 μM), neratinib
(0.5 μM) or the drugs combined for 6h. Cells were fixed in place and immunostaining
performed to determine the co-localization of K-RAS with ERBB1 at 60X magnification.
(B) PANC-1 cells were treated with vehicle control, sodium valproate (250 μM), neratinib
(0.5 μM) or the drugs combined for 6h. Cells were fixed in place and immunostaining
performed to determine the co-localization of K-RAS with LAMP2 at 60X magnification.
(C) PANC-1 cells were treated with vehicle control, sodium valproate (250 μM), neratinib
(0.5 μM) or the drugs combined for 6h. Cells were fixed in place and immunostaining
performed to determine the co-localization of K-RAS with cathepsin B at 60X magnification.
(D) PANC-1 cells were treated with vehicle control, sodium valproate (250 μM), neratinib
(0.5 μM) or the drugs combined for 6h. Cells were fixed in place and immunostaining
performed to determine the co-localization of LAMP2 and cathepsin B at 60X magnification.
Figure 6
Figure 9: Neratinib and valproate interact to suppress tumor growth and to opsonize
the surviving tumor cells to checkpoint immunotherapies.
(A) and (B) BALB/c mice were implanted with 4T1 cells in the 4th mammary fat pad and
~30 mm3 tumors permitted to form. Animals were then treated with vehicle control,
neratinib (15 mg/kg QD), valproate (50 mg/kg BID) or the drugs in combination for
3 days. Two days after the cessation of drug exposure mice were injected IP with a
control IgG (100 μg / mouse); an anti-PD-1 antibody (100 μg / mouse); or an anti-CTLA4
antibody (100 μg / mouse). Tumor volumes were measured prior to drug administration
and every three days after the initiation of therapeutic interventions. (n = 10 mice
per group +/-SEM). * p
< 0.05 less than neratinib alone or valproate alone; ** p < 0.05 less than IgG + [neratinib
+ valproate].
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