The success of targeted therapies in treating cancer over the last decade has been tempered by acquired drug resistance that follows long-term treatment. There is also emerging evidence for innate mechanisms of cancer cell resistance to targeted therapy that pre-exist as parallel signalling pathways. This aspect is explored by the Alessi group and collaborators from AstraZeneca in this issue of the Biochemical Journal, who identify a subset of breast cancer cell lines that are intrinsically resistant to Akt inhibition through constitutive up-regulation of the related AGC serine/threonine kinase SGK1 (serum- and glucocorticoid-regulated kinase 1). The study could help to profile tumours for sensitivity to Akt inhibitors and once more highlights the therapeutic complexity of cancer and the importance of exploring combination therapies in the clinic.
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June 2013
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Commentary|
May 31 2013
AKT-ing out: SGK kinases come to the fore
Larissa S. Moniz;
Larissa S. Moniz
1
1Centre for Cell Signalling, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, U.K.
1Correspondence may be addressed to either author (email l.moniz@qmul.ac.uk or bart.vanh@qmul.ac.uk).
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Bart Vanhaesebroeck
Bart Vanhaesebroeck
1
1Centre for Cell Signalling, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, U.K.
1Correspondence may be addressed to either author (email l.moniz@qmul.ac.uk or bart.vanh@qmul.ac.uk).
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Publisher: Portland Press Ltd
Received:
May 02 2013
Accepted:
May 07 2013
Online ISSN: 1470-8728
Print ISSN: 0264-6021
© The Authors Journal compilation © 2013 Biochemical Society
2013
Biochem J (2013) 452 (3): e11–e13.
Article history
Received:
May 02 2013
Accepted:
May 07 2013
Connected Content
A commentary has been published:
Elevated SGK1 predicts resistance of breast cancer cells to Akt inhibitors
Citation
Larissa S. Moniz, Bart Vanhaesebroeck; AKT-ing out: SGK kinases come to the fore. Biochem J 15 June 2013; 452 (3): e11–e13. doi: https://doi.org/10.1042/BJ20130617
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