Cancer genomes are characterized by the presence of copy number alterations (CNAs), which are recurrent events that increase or decrease the dosage of specific regions of DNA. CNAs can affect up to 30% of a cancer cell genome and are associated with poor clinical outcomes. Among CNAs, genomic deletions are the most recurrent events, yet their functional effects remain largely unknown. This paucity of mechanistic data is due to the complexity of modelling megabase-sized deletions, where most approaches have low efficiency and are not readily scalable.