In contrast with cytotoxic agents that do not differentiate between normal proliferating and tumour cells, targeted therapies primarily exert their actions in cancer cells. Initiation and maintenance of tumours are due to genetic alterations in specific loci. The identification of the genes in which these alterations occur has opened new opportunities for cancer treatment. The PI3K (phosphoinositide 3-kinase) pathway is often overactive in human cancers, and various genetic alterations have been found to cause this. In all cases, PI3K inhibition is considered to be one of the most promising targeted therapies for cancer treatment. The present mini-review provides an update on new PI3K inhibitors currently in or entering clinical development. Recent discoveries, challenges and future prospects will be discussed.
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February 2009
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Conference Article|
January 20 2009
PI3K inhibitors for cancer treatment: where do we stand?
Sauveur-Michel Maira;
Sauveur-Michel Maira
1
1Novartis Institutes for Biomedical Research, Oncology Disease Area, Novartis Pharma AG, CH4002 Basel, Switzerland
1To whom correspondence should be addressed (email sauveur-michel.maira@novartis.com).
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Frédéric Stauffer;
Frédéric Stauffer
1Novartis Institutes for Biomedical Research, Oncology Disease Area, Novartis Pharma AG, CH4002 Basel, Switzerland
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Christian Schnell;
Christian Schnell
1Novartis Institutes for Biomedical Research, Oncology Disease Area, Novartis Pharma AG, CH4002 Basel, Switzerland
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Carlos García-Echeverría
Carlos García-Echeverría
1Novartis Institutes for Biomedical Research, Oncology Disease Area, Novartis Pharma AG, CH4002 Basel, Switzerland
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Publisher: Portland Press Ltd
Received:
October 02 2008
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2009 Biochemical Society
2009
Biochem Soc Trans (2009) 37 (1): 265–272.
Article history
Received:
October 02 2008
Citation
Sauveur-Michel Maira, Frédéric Stauffer, Christian Schnell, Carlos García-Echeverría; PI3K inhibitors for cancer treatment: where do we stand?. Biochem Soc Trans 1 February 2009; 37 (1): 265–272. doi: https://doi.org/10.1042/BST0370265
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