Signal transduction during apoptosis implications for cancer therapy

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Abstract
Programmed cell death is a fundamental aspect of organismal development and stasis through its role in the maintenance of the balance between cell growth and cell death. If the balance is tipped, e.g. by unregulated cell growth, the result can be cancer. If tipped the other direction, e.g. by dysregulated cell death, and the result can again be cancer. The concept of dysregulated cell death, which until recently was not considered by oncologists, has forced a shift in the paradigm of cancer development. Along with this shift in thinking comes the likelihood that radiation and chemotherapy, both major modalities of cancer therapy, can benefit from strategies that modulate programmed cell death. One form of programmed cell death that is distinguished by its morphological features is called apoptosis. This form of programmed cell death is an energy dependent biochemically regulated process that is contingent upon a set of factors: the initial stimulatory event or in some cases a cellular insult, the organism, the cell type, the cellular environment, and other factors. This biochemical process is the result of the expression of a number of genes. In this review, the roles of several genes and gene families considered to be critical to the signal transduction cascade of apoptosis are described. Growth factors and cytokines are also discussed in the context of their interaction with these genes. We also discuss how these genes and their protein products are being used as prognostic indicators for cancer and cancer therapy and/or how they are the focus of strategies that either cause apoptosis or alter a cancer cell's propensity to initiate apoptosis when insulted by chemotherapy agents or radiation in the course of cancer therapy.

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