|
|
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.
 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:
|
|
|
|
 
R. L. Wahl, H. Jacene, Y. Kasamon, and M. A. Lodge
From RECIST to PERCIST: Evolving Considerations for PET Response Criteria in Solid Tumors
J. Nucl. Med.,
May 1, 2009;
50(Suppl_1):
122S - 150S.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. A. Lust, M. Q. Lacy, S. R. Zeldenrust, A. Dispenzieri, M. A. Gertz, T. E. Witzig, S. Kumar, S. R. Hayman, S. J. Russell, F. K. Buadi, et al.
Induction of a Chronic Disease State in Patients With Smoldering or Indolent Multiple Myeloma by Targeting Interleukin 1{beta}-Induced Interleukin 6 Production and the Myeloma Proliferative Component
Mayo Clin. Proc.,
February 1, 2009;
84(2):
114 - 122.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
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]
|
|
|
|
|
