Apoptosis and Nervous System Cancer

Apoptosis and alterations of its regulation clearly play a role in the origin, resistance to therapy, and effectiveness of therapy of nervous system neo-plasia. An understanding of apoptosis and the forces that facilitate and

TABLE 4.1

Proposed Mediators of Tumorigenesis and/or Therapeutic Resistance in Nervous System Neoplasia

Gliomas, Glioblastomas

Mutant P53 protein

Basic fibroblast growth factor

Platelet-derived growth factor

Epidermal growth factor

Protein kinase C

Neuroblastomas

BC1-Xl

Nerve growth factor

P-glycoprotein (multidrug resistance-associated protein)

n-myc

Note: Both the origins of tumors and their resistance to chemotherapy have been hypothesized to be related to resistance to or blocking of apoptosis. The proximate mediators of these phenomena differ from cell type to cell type. This fact makes imperative the individualization of therapeutic approaches aimed at apoptosis-related targets.

Note: Both the origins of tumors and their resistance to chemotherapy have been hypothesized to be related to resistance to or blocking of apoptosis. The proximate mediators of these phenomena differ from cell type to cell type. This fact makes imperative the individualization of therapeutic approaches aimed at apoptosis-related targets.

impair its progress is critical to an understanding of the pathogenesis of neoplasia in the nervous system and elsewhere. Novel targets for overcoming therapeutic resistance and inducing selective apoptosis in nervous system tumors are already being identified as a result of advances in our delineation of the pathways that lead ultimately to apoptotic cell death.

Although it is easy philosophically and useful intellectually to refer to drugs as apoptosis inducers and to cells as targets for apoptosis induction, it has become clear that what that means in particular is dependent both upon the drug and the cell of reference. For example, Table 4.1 lists the molecular species proposed to be involved in blocking glioma or neuroblas-toma cell apoptosis in response to natural and/or pharmacologic stimuli. The differences between these tumors in the proximal pathway that leads downstream to apoptosis demonstrate the probability that selective phar-macologic induction of apoptosis must rely on delineation and targeting of pathways that may be unique to each tumor type. As such, even within a tumor, different cells have different, "hard-wired" propensities and respond to different signals to undergo apoptosis. This heterogeneity at all levels represents a challenge for the future in cancer therapy.

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