One mechanism by which activated RTKs might cooperatively contribute to tumor cell survival is by engaging overlapping downstream effectors. If this were true, then the inhibition of any one RTK pathway would be insufficient to negate the effector due to inputs from the remaining activated RTKs. Because our data show that the spectrum of co-activated RTKs in tumors varies considerably from patient-to-patient, targeting these node effectors might be a more tenable therapeutic alternative to inhibiting RTKs. Moreover, the identification of these downstream effectors should reveal important novel mechanisms whereby RTKs confer their downstream effects. Our lab is identifying these convergent effectors and characterizing their modes of action through phospho-proteomic profiling, genetic and pharmacogenetic screens, in silico network analyses, and in vivo intracranial tumor generation.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Investigator-Initiated Intramural Research Projects (ZIA)
Project #
1ZIABC011404-02
Application #
8553157
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
2
Fiscal Year
2012
Total Cost
$215,263
Indirect Cost
Name
National Cancer Institute Division of Basic Sciences
Department
Type
DUNS #
City
State
Country
Zip Code