| Literature DB >> 29540494 |
Tobias Hofving1, Yvonne Arvidsson1, Bilal Almobarak1, Linda Inge1, Roswitha Pfragner2, Marta Persson1, Göran Stenman1, Erik Kristiansson3, Viktor Johanson4, Ola Nilsson1.
Abstract
Entities:
Year: 2018 PMID: 29540494 PMCID: PMC8133373 DOI: 10.1530/ERC-17-0445e
Source DB: PubMed Journal: Endocr Relat Cancer ISSN: 1351-0088 Impact factor: 5.678
Figure 6Therapeutic sensitivity of GEPNET cell lines and primary cell cultures. (A) Average Z-score representing the effect on cell viability of individual inhibitors to SINETs (GOT1/P-STS) and PanNETs (BON-1/QGP-1), plotted against each other. Groups of inhibitors that are significantly more potent against SINETs or PanNETs are marked by colour. (B) The effect of all MEKi against SINET cells, PanNET cells and non-tumourigenic cells. MEKi are more potent against PanNET cells, compared to SINET and non-tumourigenic cells. (C) Comparing the sensitivity of PanNET and SINET first-passage primary cells to MEKi trametinib. (D) SINET cell lines are more sensitive to HDACi, compared to PanNET cells and non-tumourigenic cells. (E) First-passage primary SINET cells are seemingly more sensitive than primary PanNET cells to the HDACi vorinostat. (B and D) Bars indicate mean effect, error bars s.d. and P values generated from Wilcoxon signed-rank test. (C and E) Dose–response curves represent a mean of n = 3 and the error bars denote standard deviation (s.d.).