Atypical fusion among non-malignant cells: Unveiling the link between post-fusion-induced genome chaos and cancer initiation

Background

Atypical cell fusion events can disrupt the normal post-fusion process, initiating genome chaos through the merging of parental genomes accompanied by severe and complex gross structural changes. Consequently, unscheduled fusion events can accelerate tumorigenesis by fostering persistent genomic instability, serving as catalysts in the post-hybrid selection process and decisively contributing to the acquisition of novel and malignant properties. Understanding how hybrid cells survive after fusion and identifying specific transcriptional and phenotypic signatures that characterize hybrids across different fusion phases may provide valuable insights to counteract the evolution of cancer-initiating hybrids.