Skip to main content
. Author manuscript; available in PMC: 2010 Sep 15.
Published in final edited form as: Cancer Res. 2009 Aug 25;69(18):7311–7319. doi: 10.1158/0008-5472.CAN-09-1077

Table 1. Genotypes of thyroid cancer cell lines and their sensitivity to the Akt inhibitor perifosine and the mTOR inhibitor temsirolimus.

Cell lines TPC1 C643 Hth7 FTC133 OCUT1 K1 BCPAP SW1736 KAT18 Hth74 WRO TAD2

Derived from PTC ATC ATC FTC ATC PTC PTC ATC ATC ATC FTC Normal
Genetic alterations RET/PTC1 Re-arrangement H-Ras (G13R+/-) N-Ras (Q61R+/-), Akt11 copy gain PTEN (allele deletion and R130+) PIK3CA (H1047R+/+) PIK3CA (E542K+/+) Akt1 copy gain - - - - -

IC50 of Perifosine (μM) 3.58 4.47 4.02 1.71 2.17 10.17 4.92 35.49 >1,000 >1,000 >1,000 >1,000

IC50 of Temsirolimus (nM) 0.11 0.64 3.98 0.01 7.33 0.01 110.46 >1,000 44.55 18.9 0.20 458.74

Footnotes: Ras, PIK3CA and PTEN were analyzed for mutations, and PIK3CA, PIK3CB, PDK1, Akt-1 and -2 were analyzed for copy number as described in Material and Methods. +/-, heterozygous mutation; +/+, homozygous mutation. The IC50 values were calculated using the Reed-Muench method (21).