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. 2013 Jul 4;139(9):1507–1514. doi: 10.1007/s00432-013-1465-6

Table 1.

Dose of drug that inhibited 50 % growth of human thyroid cancer cell line in vitro

Cell line Mutation/arrangements IC50 (nM) Belinostat IC50 (nM) Panobinostat IC50 (nM) Dasatinib IC50 (μM) Sorafenib IC50 (nM) Pazopanib IC50 Motesanib
Cal62 KRAS 470 ± 36 33 ± 4 35 ± 5 13 ± 1.1 NR NR
Hth7 NRAS 400 ± 56 15 ± 2 NR 6.8 ± 0.8 NR NR
Hth83 HRAS 720 ± 100 34 ± 5 NR 11 ± 1.0 NR NR
C643 HRAS 970 ± 120 71 ± 10 NR 6.5 ± 0.9 NR NR
SW1736 BRAF 380 ± 40 35 ± 8 NR NR NR NR
T241 Nil 750 ± 65 65 ± 7 NR 7.5 ± 0.5 NR NR
T351 Nil 1,100 ± 170 50 ± 10 NR 11 ± 2.0 NR NR
BHP2-7 RET/PTC 770 ± 67 37 ± 6 47 ± 3 5.0 ± 0.8 340 ± 20 NR
T238 PI3 K/BRAF 6,800 ± 740 1,500 ± 200 NR 6.5 ± 1.2 NR NR

Tabulated results of HDACI (belinostat and panobinostat) and tyrosine kinase inhibitor (TKI dasatinib, sorafenib, pazopanib and motesanib)-treated thyroid cancer cell lines at 72 h of drug exposure. Mean 50 % inhibitory concentration (IC50 ± SD) of experiments done in triplicate experiments with each experiment done with triplicate wells using MTT assay. Nil: No mutations detected. NR: IC50 not reached (i.e., pharmacologically relevant IC50 not reached). See “Materials and methods” for details