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Blood, 15 January 2006, Vol. 107, No. 2, pp. 431-434. Prepublished online as a Blood First Edition Paper on September 8, 2005; DOI 10.1182/blood-2005-06-2517. This Article Full Text (PDF) All Versions of this Article: 2005-06-2517v1 107/2/431    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Huff, C. A Articles by Jones, R. J Search for Related Content PubMed PubMed Citation Articles by Huff, C. A Articles by Jones, R. J Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted June 24, 2005 Accepted August 25, 2005 The paradox of response and survival in cancer therapeutics Carol A Huff*, William Matsui, B D Smith, and Richard J Jones Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA * Corresponding author; email: huffca{at}jhmi.edu. Although most cancer patients respond to therapy, few are cured. Moreover, objective clinical responses to treatment often do not even translate into substantial improvements in overall survival. For example, indolent lymphoma patients who achieved a complete remission with conventional-dose therapies in the pre-rituximab era did not experience a survival advantage over similar patients treated with a "watch and wait" approach. Several studies have also shown that neither the magnitude, nor the kinetics, of clinical response has an impact on survival in multiple myeloma. Recent data suggesting many malignancies arise from a rare population of cells that exclusively maintain the ability to self-renew and sustain the tumor (i.e., "cancer stem cells") may help explain this paradox that response and survival are not always linked. Therapies that successfully eliminate the differentiated cancer cells characterizing the tumor may be ineffective against rare, biologically-distinct cancer stem cells. New methods for assessing treatment efficacy must also be developed, as traditional response criteria measure tumor bulk and may not reflect changes in rare cancer stem cell populations. In this article, we discuss the evidence for cancer stem cells in hematologic malignancies and possible ways to begin targeting these cells and measuring clinical effectiveness of such treatment approaches. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: W. Matsui, Q. Wang, J. P. Barber, S. Brennan, B. D. Smith, I. Borrello, I. McNiece, L. Lin, R. F. Ambinder, C. Peacock, et al. Clonogenic Multiple Myeloma Progenitors, Stem Cell Properties, and Drug Resistance Cancer Res., January 1, 2008; 68(1): 190 - 197. [Abstract] [Full Text] [PDF] B. Dekel, S. Metsuyanim, K. M. Schmidt-Ott, E. Fridman, J. Jacob-Hirsch, A. Simon, J. Pinthus, Y. Mor, J. Barasch, N. Amariglio, et al. Multiple Imprinted and Stemness Genes Provide a Link between Normal and Tumor Progenitor Cells of the Developing Human Kidney. Cancer Res., June 15, 2006; 66(12): 6040 - 6049. [Abstract] [Full Text] [PDF]

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