RAS-MAPK in ALK targeted therapy resistance
G Hrustanovic, TG Bivona - Cell Cycle, 2015 - Taylor & Francis
G Hrustanovic, TG Bivona
Cell Cycle, 2015•Taylor & FrancisThe clinical success of ALK targeted therapy is limited by resistance. To identify rational co-
targeting strategies to enhance clinical outcomes, we explored the molecular basis of ALK
oncogene dependence in ALK gene rearrangement positive (ALK+) lung adenocarcinoma.
We discovered that the RAS-RAF-MEK-ERK pathway is the critical downstream pathway
necessary for ALK+ tumor cell survival. Upfront co-targeting of ALK plus MEK enhanced
response and forestalled resistance in preclinical ALK+ tumor models, providing rationale …
targeting strategies to enhance clinical outcomes, we explored the molecular basis of ALK
oncogene dependence in ALK gene rearrangement positive (ALK+) lung adenocarcinoma.
We discovered that the RAS-RAF-MEK-ERK pathway is the critical downstream pathway
necessary for ALK+ tumor cell survival. Upfront co-targeting of ALK plus MEK enhanced
response and forestalled resistance in preclinical ALK+ tumor models, providing rationale …
The clinical success of ALK targeted therapy is limited by resistance. To identify rational co-targeting strategies to enhance clinical outcomes, we explored the molecular basis of ALK oncogene dependence in ALK gene rearrangement positive (ALK+) lung adenocarcinoma. We discovered that the RAS-RAF-MEK-ERK pathway is the critical downstream pathway necessary for ALK+ tumor cell survival. Upfront co-targeting of ALK plus MEK enhanced response and forestalled resistance in preclinical ALK+ tumor models, providing rationale for a new approach the treatment of ALK+ patients.
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