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Publication : Drugging the bad "AKT-TOR" to overcome TKI-resistant lung cancer.

First Author  Settleman J Year  2007
Journal  Cancer Cell Volume  12
Issue  1 Pages  6-8
PubMed ID  17613432 Mgi Jnum  J:122851
Mgi Id  MGI:3715598 Doi  10.1016/j.ccr.2007.06.010
Citation  Settleman J, et al. (2007) Drugging the Bad 'AKT-TOR' to Overcome TKI-Resistant Lung Cancer. Cancer Cell 12(1):6-8
abstractText  EGFR kinase inhibitors constitute an important class of lung cancer treatments. While they produce dramatic responses in a subset of patients-primarily those with activating EGFR mutations-remissions are typically limited to several months due to acquired drug resistance, frequently associated with the secondary T790M mutation in EGFR. In this issue of Cancer Cell, Li et al. report that an irreversible EGFR kinase inhibitor, HKI-272, had limited activity in a mouse lung cancer model driven by an EGFR mutant harboring T790M and an activating mutation. However, combining HKI-272 with rapamycin promoted rapid tumor regression, suggesting a therapeutic strategy to overcome drug resistance.
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