Abstract
Chromosomal rearrangements and recurrent gene fusions were previously presumed to be the primary oncogenic mechanisms of hematological malignancies. However, the discovery of gene fusions in different cancers has opened new horizons to comprehensively investigate how cell type-specific fusion oncoproteins modulate signaling cascades. Prostate cancer (PCa) is a multifaceted and therapeutically challenging disease, and functional genomics have helped us develop a better understanding of the mechanisms underlying prostate carcinogenesis, castration-resistant PCa, and metastasis. Keeping in mind the fact that gene fusions have also been discovered in PCa, there has been rapid expansion in the field of molecular oncology and researchers are uncovering new facets regarding the mechanistic regulation of signaling pathways by fusion oncoproteins.
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