Three chromothripsis-associated mechanisms are thought to be capable of
driving tumorigenesis: 1) disruption or loss of tumor suppressors, 2) generation
of oncogenic fusions, and 3) amplification of oncogenes, with the most prevalent
pathway being through the generation of circular, self-propagating and
oncogene-bearing extrachromosomal DNA (ecDNA). Chromothripsis-affected genes,
identified in patient-derived tumors, are listed for each mechanism.