Abstract

Protein kinase C (PKC) comprises a family of serine/threonine kinases that are involved in the transduction of signals for cell proliferation, differentiation, apoptosis and angiogenesis. Unsurprisingly, disruption of PKC regulation is implicated in tumorigenesis and drug resistance. PKC function is complex in this context owing to the differing roles of individual isozymes within the cell and across tumour types. Therapeutically targeting PKC isozymes is not new; however, with many of the early PKC inhibitor cytotoxic drug combinations being discarded at the phase II level, and recent phase III studies in non-small-cell lung cancer proving negative, what's going wrong?

Author affiliations

1. Helen J. Mackay is at the University of Toronto, Department of Medical Oncology and Hematology, Princess Margaret Hospital, 610 University Avenue, Toronto, Ontario, Canada.
2. Christopher J. Twelves is at the Institute of Cancer Therapeutics, University of Bradford, West Yorkshire, BD7 1DP, UK.

Correspondence to: Christopher J. Twelves² Email: c.twelves@Bradford.ac.uk

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