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. 2010 Apr 24;4(4):335–346. doi: 10.1016/j.molonc.2010.04.008

Figure 1.

Figure 1

Analysis of KIT D816V in mononuclear cells of patients with AML. The presence of KIT D816V was investigated in isolated mononuclear cells by restriction fragment length polymorphism analysis of a 287bp reverse transcriptase polymerase chain reaction product. The arrow indicates the 157bp fragment generated by Hinf I restriction enzyme cleavage in the presence of KIT D816V. The mutation was only detectable in patients with AML and an associated systemic mastocytosis (lanes 2–8). In one patient with AML and associated SM, however, no KIT mutation at codon 816 was detected (lane 9). Lane 10 shows a mutation analysis performed with KIT D816V+ HMC‐1 cells diluted in KIT D816V‐cells at 1:20 (lower limit of detection – control). The Msp I‐digested plasmid pBR322 served as a molecular weight marker (lane 1).