Strategies for co-targeting the PI3K/AKT/mTOR pathway in NSCLC

Heavey, Susan, O'Byrne, Kenneth J., & Gately, Kathy (2014) Strategies for co-targeting the PI3K/AKT/mTOR pathway in NSCLC. Cancer Treatment Reviews, 40(3), pp. 445-456.

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The PI3K/AKT/mTOR pathway regulates cell growth and proliferation and is often dysregulated in cancer due to mutation, amplification, deletion, methylation and post-translational modifications. We and others have shown that activation of this pathway in non-small cell lung cancer (NSCLC) leads to a more aggressive disease which correlates to poor prognosis for patients. A multitude of selective inhibitors are in development which target key regulators in this pathway, however the success of PI3K targeted inhibition has been hampered by a high rate of innate and acquired resistance. Response to PI3K inhibition may be improved by co-targeting potential mediators of resistance, such as related cell surface receptors or other intracellular signaling pathways which cross-talk with the PI3K pathway. Inhibition of the PI3K pathway may also overcome radioresistance, chemoresistance and immune evasion in NSCLC. The identification of appropriate patient cohorts who will benefit from PI3K co-targeted inhibition strategies will be key to the success of these inhibitors.

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39 citations in Web of Science®
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ID Code: 67773
Item Type: Journal Article
Refereed: Yes
Keywords: Chemoresistance, Co-targeted inhibition, Lung cancer, MEK, MTOR, NSCLC, PI3K, PI3K inhibition, PIK3CA, Radioresistance
DOI: 10.1016/j.ctrv.2013.08.006
ISSN: 03057372
Subjects: Australian and New Zealand Standard Research Classification > MEDICAL AND HEALTH SCIENCES (110000) > ONCOLOGY AND CARCINOGENESIS (111200)
Divisions: Current > Schools > School of Biomedical Sciences
Current > QUT Faculties and Divisions > Faculty of Health
Current > Institutes > Institute of Health and Biomedical Innovation
Copyright Owner: Copyright 2013 Elsevier Ltd.
Deposited On: 24 Feb 2014 23:49
Last Modified: 12 Mar 2014 03:47

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