Neuroblastoma tumorigenesis and malignant transformation is driven by overexpression and dominance of cell survival
pathways and a lack of normal cellular senescence or apoptosis. Therefore, manipulation of cell survival pathways may decrease the
malignant potential of these tumors and provide avenues for the development of novel therapeutics. This review focuses on the individual
protein tyrosine kinase, focal adhesion kinase (FAK) and its interaction with the transcription factors, MYCN, p53, and Mdm2, and how
their interactions modulate the growth and malignancy of neuroblastomas.
Keywords: FAK, Mdm2, MYCN, neuroblastoma, p53.
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