MET increases the sensitivity of gefitinib-resistant cells to SN-38, an active metabolite of irinotecan, by up-regulating the topoisomerase I activity.

@article{Sakai2012METIT,
  title={MET increases the sensitivity of gefitinib-resistant cells to SN-38, an active metabolite of irinotecan, by up-regulating the topoisomerase I activity.},
  author={Asao Sakai and Kazuo Kasahara and Tohru Ohmori and Hideharu Kimura and Takashi Sone and Masaki Fujimura and Shinji Nakao},
  journal={Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer},
  year={2012},
  volume={7 9},
  pages={1337-44}
}
INTRODUCTION Most non-small-cell lung cancer tumors with epidermal growth factor receptor mutations are responsive to EGFR tyrosine kinase inhibitors, such as gefitinib and erlotinib, but almost all such tumors ultimately acquire resistance. We previously found that a gefitinib-resistant cell line, PC-9/Met in which MET (MNNG-HOS transforming gene) is amplified, was more sensitive than its parent cell line (PC-9) to 7-ethyl-10-hydroxy-camptothecin (SN-38), an active metabolite of irinotecan… CONTINUE READING
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