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(A) Phospho-RTK array analysis of MDA1386 cell lysate. The positive (+) controls are the built–in reference spots at the three corners of the array blot. Black arrows pointed to the positions corresponding to the respective RTK on the blot. Noted the strong EGFR and MET phosphorylation signals, the weaker IGF-1R and Axl signals and the absent PDGFR signal. (B) MDA1386 cell response to the MET TKI at three different concentrations (1, 5 and 10 uM, n = 3 at each concentration for each treatment). Tx: treatment; NS: not significant. Error bars represent ±2 standard errors. (C) MDA1386 cell response to the IGF-1R TKI at three different concentrations (1, 5 and 10 uM, n = 3 at each concentration for each treatment). Tx: treatment; NS: not significant. Error bars represent ±2 standard errors. (D) MDA1386 cell response to the dual inhibition of MET and EGFR in comparison to MET or EGFR inhibition alone at three different concentrations (1, 5 and 10 uM, n = 3 at each concentration for each treatment). Noted the increase in cell growth inhibition with dual MET and EGFR TKI at 10 uM. Tx: treatment; NS: not significant. Error bars represent ±2 standard errors.

Journal: International journal of cancer

Article Title: A phosphoarray platform is capable of personalizing kinase inhibitor therapy in head and neck cancers

doi: 10.1002/ijc.31045

Figure Lengend Snippet: (A) Phospho-RTK array analysis of MDA1386 cell lysate. The positive (+) controls are the built–in reference spots at the three corners of the array blot. Black arrows pointed to the positions corresponding to the respective RTK on the blot. Noted the strong EGFR and MET phosphorylation signals, the weaker IGF-1R and Axl signals and the absent PDGFR signal. (B) MDA1386 cell response to the MET TKI at three different concentrations (1, 5 and 10 uM, n = 3 at each concentration for each treatment). Tx: treatment; NS: not significant. Error bars represent ±2 standard errors. (C) MDA1386 cell response to the IGF-1R TKI at three different concentrations (1, 5 and 10 uM, n = 3 at each concentration for each treatment). Tx: treatment; NS: not significant. Error bars represent ±2 standard errors. (D) MDA1386 cell response to the dual inhibition of MET and EGFR in comparison to MET or EGFR inhibition alone at three different concentrations (1, 5 and 10 uM, n = 3 at each concentration for each treatment). Noted the increase in cell growth inhibition with dual MET and EGFR TKI at 10 uM. Tx: treatment; NS: not significant. Error bars represent ±2 standard errors.

Article Snippet: The following small molecular TKIs were purchased (Selleck Chemicals): (1) JNJ-38877605, a highly selective, ATP-competitive inhibitor of c-MET ( 25 ); (2) NVP-AEW541, a potent inhibitor of IGF-1R with IC 50 of 86 nM ( 26 ); (3) OSI-744/erlotinib HCl, a FDA approved EGFR inhibitor and (4) STI-571/imatinib, a multi-target inhibitor of v-Abl, c-Kit and PDGFR.

Techniques: Concentration Assay, Inhibition

Neoadjuvant and adjuvant trials of imatinib in GIST

Journal: Therapeutics and Clinical Risk Management

Article Title: Treatment of gastrointestinal stromal tumor: focus on imatinib mesylate

doi:

Figure Lengend Snippet: Neoadjuvant and adjuvant trials of imatinib in GIST

Article Snippet: This has led to the development of the targeted therapy imatinib mesylate (STI-571; Glivec ® , Novartis, Basel, Switzerland).

Techniques: Adjuvant, Expressing, Mutagenesis