Figures & data
Table 1 The most common mutations in c-Kit
Table 2 c-Kit mutation based on their gene location, corresponding cancer, and drug sensitivity
Figure 1 KIT cDNA and protein structure in different cancers and their respective mutations.
Abbreviations: cDNA, complementary DNA; AML, acute myeloid leukemia; GIST, gastrointestinal stromal tumor.
Figure 2 Signal transducer and activator of transcription tyrosine kinase domain c-Kit in normal cell.
Notes: Ras/Erk pathway directs to activate of the proliferation genes. PI3K pathway involves in antiapoptosis gene activation which results in cell survival. JAK/STAT pathway is associated in cell proliferation.
Figure 3 Signal transducer and activator of transcription tyrosine kinase domain c-Kit in cancer cell.
Notes: The Ras-Erk pathway, PI3K/AKT pathway, and Src-signaling pathway have been demonstrated in this schematic picture. Although each of the signaling pathways goes through different ways and has different effects on cell function, the result of all of three pathways is inhibition of the cell apoptosis, resulting in tumorogenesis in different ways, such as inducing of cell proliferation, growth progression, or migration. Moreover, the mechanisms of c-Kit inhibitor drugs have been shown. Each group of c-Kit inhibitor drugs block different targets, which have been highlighted in red.
Table 3 List of the drugs that target c-Kit
Table 4 List of c-Kit inhibitors
Table 5 c-Kit inhibitors classification based on their targets, chemical and structure formulae, and diseases they are tested on