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. 2006 Aug 1;2(3):255-270.
doi: 10.2174/157339406777934681.

Testicular Germ Cell Tumors: A Paradigm for the Successful Treatment of Solid Tumor Stem Cells

Caryl J Giuliano  1 , Sarah J Freemantle  1 , Michael J Spinella  1
Affiliations

Testicular Germ Cell Tumors: A Paradigm for the Successful Treatment of Solid Tumor Stem Cells

Caryl J Giuliano et al. Curr Cancer Ther Rev. .

Abstract

Treatment of testicular germ cell tumors (TGCTs) has been a success primarily due to the exquisite responsiveness of this solid tumor to cisplatin-based therapy. Despite the promise of cure for the majority of TGCT patients, the effectiveness of therapy for some patients is limited by toxicity and the problem of resistance. There is compelling rationale to further understand the biology of TGCTs in order to better treat other solid tumors and to address the shortcomings of present TGCT therapies. TGCTs contain undifferentiated pluripotent stem cells, known as embryonal carcinoma, that share many properties with human embryonic stem cells. The importance of cancer stem cells in the initiation, progression and treatment of solid tumors is beginning to emerge. We discuss TGCTs in the context of solid tumor curability and targeted cancer stem cell therapy.

Keywords: Cisplatin; Nanog; Oct4; cancer stem cell; chemosensitivity; embryonal carcinoma; self-renewal.

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Figures

Fig. (1)
Fig. (1)
Model depicting pluripotent features of embryonal carcinoma that may impact on the pathogenesis and chemosensitivity of testis cancer. Transcriptional plasticity due to stem cell-like chromatin structure, p53, deregulated cell cycle checkpoints, and low DNA repair are highlighted. These features may be lost during in vivo maturation of resistant teratoma. Mechanisms of non-teratoma resistance may or may not be related to mechanisms that confer inherent sensitivity. MSI, microsatellite instability; GST, glutathione-S-transferase.
Fig. (2)
Fig. (2)
Genes on chromosome 12p13.31 with roles or putative roles in regulating stem cell renewal. Genes repressed by retinoic acid in EC and ES during induced differentiation are highlighted with *. Distance between genes is approximate. Cyclin D2 is on 12p13.32 and not depicted here. Cyclin D2 is not downregulated with RA treatment of EC cells (Freemantle unpublished observation). See text for details.
See this image and copyright information in PMC

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