Journal
CANCER CELL
Volume 12, Issue 1, Pages 81-93Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2007.06.005
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Funding
- NCI NIH HHS [P20 CA90578, R01 CA122794, R01 CA90687] Funding Source: Medline
- NIA NIH HHS [K08 AG024004, R01 AG2400401] Funding Source: Medline
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The EGFR T790M mutation has been identified in tumors from lung cancer patients that eventually develop resistance to erlotinib. In this study, we generated a mouse model with doxycycline-inducible expression of a mutant EGFR containing both L858R, an erlotinib-sensitizing mutation, and the T790M resistance mutation (EGFR TL). Expression of EGFR TL led to development of peripheral adenocarcinomas with bronchioloalveolar features in alveoli as well as papillary adenocarcinomas in bronchioles. Treatment with an irreversible EGFR tyrosine kinase inhibitor (TKI), HKI-272, shrunk only peripheral tumors but not bronchial tumors. However, the combination of HKI-272 and rapamycin resulted in significant regression of both types of lung tumors. This combination therapy may potentially benefit lung cancer patients with the EGFR T790M mutation.
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