Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2016 Nov 9;9:6843–6855. doi: 10.2147/OTT.S117743

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2016 Jeannot et al. This work is published and licensed by Dove Medical Press Limited

The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

PMC Copyright notice

Effects of the gefitinib and vorinostat combination on the growth of H358 or PLC/PRF5 xenografts.

Notes: H358 and PLC/PRF5 cells were grown as subcutaneous tumor xenografts in nude mice. After the tumors were established, the mice were treated with vehicle, gefitinib (5 mg/kg H358 or 50 mg/kg PLC/PRF5), vorinostat (100 mg/kg), or both for 30–35 days. (A, B) The means of body weight and tumor weight at sacrifice and the means of tumor volume ± SEM at the given time points in H358 (A) or PLC/PRF5 (B) xenograft models. *P<0.05; **P<0.01; ***P<0.001 compared to the control group; ^#P>0.05 compared to the single treatment groups. Treatment groups included 8–11 mice, except for the PLC/PRF5 xenograft model in which the vehicle and vorinostat-treated groups included only four to six mice (^♮) because of euthanasia due to tumor size. (C) Tumor size-related death was calculated from the date of the beginning of treatment to the last day of the experiment or tumor size-related death for the PLC/PRF5 tumor-bearing mice. P log-rank =0.0095. (D) Effect of gefitinib and vorinostat on acetylated-tubulin, acetylated-histone H4, p-AKT and active caspase-3 in H358- (tumors 1–8), and PLC/PRF5-xenograft tumors (tumors 9–16) assessed by Western blotting (two mice per condition). (E) Ki67 nuclear protein detected through immunostaining on frozen tumor sections from mice that were treated as indicated. The Ki67 level was determined after counting positive-stained cells in ten randomly selected fields per slide in the tumor sections, and the results are expressed as the mean ± standard deviation and as the rate of staining in the vehicle-treated group (three to six mice per group). *P<0.05; ***P<0.001 compared to the control group; ^#P>0.05 compared to the single treatment groups.

Effects of the gefitinib and vorinostat combination on the growth of H358 or PLC/PRF5 xenografts.

Notes: H358 and PLC/PRF5 cells were grown as subcutaneous tumor xenografts in nude mice. After the tumors were established, the mice were treated with vehicle, gefitinib (5 mg/kg H358 or 50 mg/kg PLC/PRF5), vorinostat (100 mg/kg), or both for 30–35 days. (A, B) The means of body weight and tumor weight at sacrifice and the means of tumor volume ± SEM at the given time points in H358 (A) or PLC/PRF5 (B) xenograft models. *P<0.05; **P<0.01; ***P<0.001 compared to the control group; ^#P>0.05 compared to the single treatment groups. Treatment groups included 8–11 mice, except for the PLC/PRF5 xenograft model in which the vehicle and vorinostat-treated groups included only four to six mice (^♮) because of euthanasia due to tumor size. (C) Tumor size-related death was calculated from the date of the beginning of treatment to the last day of the experiment or tumor size-related death for the PLC/PRF5 tumor-bearing mice. P log-rank =0.0095. (D) Effect of gefitinib and vorinostat on acetylated-tubulin, acetylated-histone H4, p-AKT and active caspase-3 in H358- (tumors 1–8), and PLC/PRF5-xenograft tumors (tumors 9–16) assessed by Western blotting (two mice per condition). (E) Ki67 nuclear protein detected through immunostaining on frozen tumor sections from mice that were treated as indicated. The Ki67 level was determined after counting positive-stained cells in ten randomly selected fields per slide in the tumor sections, and the results are expressed as the mean ± standard deviation and as the rate of staining in the vehicle-treated group (three to six mice per group). *P<0.05; ***P<0.001 compared to the control group; ^#P>0.05 compared to the single treatment groups.