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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]