Table 1.

Lapatinib and erlotinib concentrations that achieve IC50 and the corresponding k-Ras, and HER2 molecular status in gastric and esophageal cancer cells

Cell lineLapatinib IC50 (mean ± SE, μmol/L)Erlotinib IC50 growth (mean ± SE, μmol/L)Trastuzumab, growth inhibition (%)HER2 amplification statusK-Ras mutation
N870.01 ± 0.043.32 ± 0.3715.50 ± 6.08AmplifiedWT
OE190.09 ± 0.022.31 ± 0.5034.53 ± 5.20AmplifiedWT
NUGC40.35 ± 0.030.24 ± 0.040Not amplifiedWT
NUGC32.24 ± 0.550.70 ± 0.010Not amplifiedWT
FU974.86 ± 0.344.76 ± 0.960Not amplifiedWT
SNU168.58 ± 0.696.50 ± 1.310Not amplifiedWT
IM95>10>102.80Not amplifiedWT
IM95m>10>107.85Not amplifiedWT
MKN74>10>1010.60Not amplifiedWT
MKN1>100.96 ± 0485.83Not amplifiedWT
KATOIII>105.98 ± 0.984.18Not amplifiedWT
AGS>10>105.01Not amplifiedG12D (exon 1)
SNU1>10>100Not amplifiedG12D (exon 1)
SNU5>10>100Not amplifiedWT

NOTE: Fourteen gastric and esophageal cancer cell lines were treated with lapatinib, erlotinib, and trastuzumab as described. Lapatinib and erlotinib reported as concentrations that achieve IC50 whereas the effects of trastuzumab are reported as a percentage of growth inhibited. HER2 amplification status and k-Ras mutation status of the cell lines as measured by FISH and PCR, respectively.