Publication: Cell proliferation and apoptosis in prostate cancer. significance in disease progression and therapy
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Date
2000
Authors
Kyprianou, N. ; Bruckheimer, E.M. ; Guo, Y.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Recent biochemical and genetic studies have
substantially increased our understanding of death signal
transduction pathways, making it clear however, that
apoptosis is not a single-lane, one-way street. Rather,
multiple parallel pathways have been identified. For
instance, analysis of bcl-2, bax, p53, and caspase
knockout mice while establishing distinct roles for each
of these apoptotic players, they also provided valuable
information for the design of specific inhibitors of
apoptosis. Thus blocking one pathway, as in caspase
knockout mice, what we observe is not a complete
suppression of apoptosis but rather a delay in apoptosis
induction (Hakem et al., 1998; Kuida et al., 1998). In
view of nature's means of ensuring activation of a
compensatory apoptotic response, when one pathway
fails in developing prostate cancer therapeutic
interventions, the challenge remains to further dissect
individual apoptotic pathways. Advances in our
understanding of the integrated functions governing
prostate cell proliferation and cell death, clearly suggest
that effective prostate cancer therapies are not only
molecularly targeted, but that are also customized to take
into account the delicate balance of opposing growth
influences in the ageing gland. In this review we discuss
the evidence on the significance of molecular
deregulation of the key players of this growth
equlibrium, apoptosis and cell proliferation in prostate
cancer progression, and the clinical implications of
changes in the apoptotic response in disease detection
and therapy.
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