Journal
CANCER CELL
Volume 17, Issue 6, Pages 547-559Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2010.04.026
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Funding
- DF/HCC [P50 CA127003]
- Dana-Farber-Harvard Cancer Center Lung Cancer Specialized Program of Research Excellence (SPORE) [P50 CA090578, U01CA141576, R01 AG2400401, R01 CA122794, R01 CA140594, 1RC2CA147940-01, CA120060, R01CA137008]
- American Association for Cancer Research
- V Foundation
- American Cancer Society [RSG-06-102-01-CCE]
- Ellison Foundation Scholar
- Novartis
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In mice, Lkb1 deletion and activation of KraS(G12D) results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and metastatic de novo lung cancers with integrated genomic and proteomic profiles, and have identified gene and phosphoprotein signatures associated with Lkb1 loss and progression to invasive and metastatic lung tumors. These studies revealed that SRC is activated in Lkb1-deficient primary and metastatic lung tumors, and that the combined inhibition of SRC, PI3K, and MEK1/2 resulted in synergistic tumor regression. These studies demonstrate that integrated genomic and proteomic analyses can be used to identify signaling pathways that may be targeted for treatment.
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