Abstract
Over the past two decades, major advances in our understanding of cancer have translated
into only modest increments in survival for the majority of cancer patients. Recent
data suggesting cancers arise from rare self-renewing stem cells that are biologically
distinct from their more numerous differentiated progeny may explain this paradox.
Current anticancer therapies have been developed to decrease the bulk of the tumour
mass (i.e. the differentiated cancer cells). Although treatments directed against
the bulk of the cancer may produce dramatic responses, they are unlikely to result
in long-term remissions if the rare cancer stem cells are also not targeted. Conversely,
treatments that selectively attack cancer stem cells will not immediately eliminate
the differentiated cancer cells, and might therefore be prematurely abandoned if clinical
activity is judged solely by traditional response criteria that reflect changes in
the bulk of the tumour. Re-examining both our pre-clinical and clinical drug development
paradigms to include the cancer stem cell concept has the potential to revolutionize
the treatment of many cancers.
Keywords
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Article info
Publication history
Accepted:
January 23,
2006
Received:
January 23,
2006
Identification
Copyright
© 2006 Elsevier Ltd. Published by Elsevier Inc. All rights reserved.
