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Review
. 2011 Jan;239(1):27-44.
doi: 10.1111/j.1600-065X.2010.00979.x.

Therapeutic cancer vaccines: are we there yet?

Christopher A Klebanoff  1 , Nicolas Acquavella, Zhiya Yu, Nicholas P Restifo
Affiliations
Review

Therapeutic cancer vaccines: are we there yet?

Christopher A Klebanoff et al. Immunol Rev. 2011 Jan.

Abstract

Enthusiasm for therapeutic cancer vaccines has been rejuvenated with the recent completion of several large, randomized phase III clinical trials that in some cases have reported an improvement in progression free or overall survival. However, an honest appraisal of their efficacy reveals modest clinical benefit and a frequent requirement for patients with relatively indolent cancers and minimal or no measurable disease. Experience with adoptive cell transfer-based immunotherapies unequivocally establishes that T cells can mediate durable complete responses, even in the setting of advanced metastatic disease. Further, these findings reveal that the successful vaccines of the future must confront: (i) a corrupted tumor microenvironment containing regulatory T cells and aberrantly matured myeloid cells, (ii) a tumor-specific T-cell repertoire that is prone to immunologic exhaustion and senescence, and (iii) highly mutable tumor targets capable of antigen loss and immune evasion. Future progress may come from innovations in the development of selective preparative regimens that eliminate or neutralize suppressive cellular populations, more effective immunologic adjuvants, and further refinement of agents capable of antagonizing immune check-point blockade pathways.

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Figures

Fig. 1
Fig. 1. Efficacy of therapeutic cancer vaccines in mouse and human
Realistic animal models for the treatment of human cancers have been developed in an attempt to test, improve, and refine immunotherapies for possible clinical translation. In many cases, results in mice have predicted both limitations as well as promising new therapies in man. (A) Treatment of established B16 melanoma in mice with a recombinant viral vector encoding the shared self/tumor antigen gp100 plus recombinant IL-2 causes a statistically significant (P = 0.0029) but modest improvement in overall survival. All mice ultimately expired from uncontrolled tumor growth. (B) Treatment of metastatic castration resistant prostate cancer in humans with autologous peripheral-blood mononuclear cells activated with a recombinant fusion protein consisting of GM-CSF and the self/tumor-associated antigen prostatic acid phoshatase causes a statistically significant (P =0.03) but modest improvement in overall survival. The vast majority of patients expired from uncontrolled tumor growth. Data reproduced with permission from Kantoff P, et al, NEJM 2010.
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