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Review
. 2006 Jan 1;97(1):18-32.
doi: 10.1002/jcb.20634.

Apoptosis evasion: the role of survival pathways in prostate cancer progression and therapeutic resistance

Affiliations
Review

Apoptosis evasion: the role of survival pathways in prostate cancer progression and therapeutic resistance

Shaun McKenzie et al. J Cell Biochem. .

Abstract

The ability of a tumor cell population to grow exponentially represents an imbalance between cellular proliferation and cellular attrition. There is an overwhelming body of evidence suggesting the ability of tumor cells to avoid programmed cellular attrition, or apoptosis, is a major molecular force driving the progression of human tumors. Apoptotic evasion represents one of the true hallmarks of cancer and appears to be a vital component in the immunogenic, chemotherapeutic, and radiotherapeutic resistance that characterizes the most aggressive of human cancers [Hanahan and Weinberg, 2000]. The challenges in the development of effective treatment modalities for advanced prostate cancer represent a classic paradigm of the functional significance of anti-apoptotic pathways in the development of therapeutic resistance.

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Figures

Fig. 1
Fig. 1
Signaling cross-talk between survival and apoptosis pathways in prostate cancer cells. [Color figure can be viewed in the online issue, which is available at www.interscience.wiley.com.]

References

    1. Amantana A, London CA, Iversen PL, Devi GR. X-linked inhibitor of apoptosis protein inhibition induces apoptosis and enhances chemotherapy sensitivity in human prostate cancer cells. Mol Cancer Ther. 2004;3(6):699–707. - PubMed
    1. Arnold JT, Isaacs JT. Mechanisms involved in the progression of androgen-independent prostate cancers: It is not only the cancer cell’s fault. Endocr Relat Cancer. 2002;9:61–73. - PMC - PubMed
    1. Ayala G, Thompson T, Yang G, Frolov A, Li R, Scardino P, Ohori M, Wheeler T, Harper W. High levels of phosphorylated form of Akt-1 in prostate cancer and non-neoplastic prostate tissues are strong predictors of biochemical recurrence. Clin Cancer Res. 2004;10(19):6572–6578. - PubMed
    1. Balkwill F, Coussens LM. An inflammatory link. Nature. 2004;431:405–406. - PubMed
    1. Bello-DeOcampo D, Tindall DJ. TGF-β/Smad signaling in prostate cancer. Curr Drug Targets. 2003;4(3):197–207. - PubMed

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