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Table 1 Oncogene addiction in various human cancers

From: Oncogene addiction in gliomas: Implications for molecular targeted therapy

Addicted oncogenes Implications in cancers Contributors
MYC Inactivation of MYC can result in dramatic and sustained tumor regression in various cancers Felsher et al., Genes Cancer. (2010) [6]
cyclin D1 Cell proliferation Lee et al., Cell Cycle. (2010) [7]
Met The MET tyrosine kinase stimulates cell scattering, invasion, protection from apoptosis and angiogenesis Comoglio et al., Nat Rev Drug Discov. (2008) [8]
PDGFRA amplification or mutation Predictive biomarker of drug sensitivity Swanton et al., Cancer Biol Ther. (2009) [9]
NF-kappaB Acquisition of resistance to CPT Togano et al., Biochem Biophys Res Commun. (2009) [10]
FIP1L1-PDGFRalpha Generation sustained activation signaling to maintain a cell malignant phenotype Jin et al., Cancer Sci. (2009) [11]
PDGF-B PDGF-B is required to overcome cell-cell contact inhibition and to confer in vivo infiltrating potential on tumor cells Calzolari et al., Neoplasia. (2008) [12]
EGFR amplification or mutations Increased sensitivity to EGFR small molecule tyrosine kinase inhibitors Rothenberg et al., Proc Natl Acad Sci USA. (2008) [13]
SphK1 SphK1 is involved in the major mechanisms underpinning oncogenesis Vadas et al., Biochim Biophys Acta. (2008) [14]
E2F1 The E2F1 protein functions as a transcription factor that enhances cell proliferation Alonso et al., Cancer Lett. (2008)
[15]
HSP90 Cell proliferation and/or survival Workman et al., Ann N Y Acad Sci. (2007) [16]
Bcr-Abl Chemosensitivity to imatinib Chen et al., Cancer Res. (2006) [17]
mTOR mTOR plays a central role in cell growth, proliferation and survival Choo et al., Cancer Cell. (2006) [18]
microRNA-21 Overexpression of miR-21 leads to a pre-B malignant lymphoid-like phenotype Medina et al., Nature. (2010) [19]