The RNA editing enzyme APOBEC1 induces somatic mutations and a compatible mutational signature is present in esophageal adenocarcinomas

Table 1 List of the non-clonal mutations identified in the BCR-ABL1 fusion gene from imatinib-resistant K562 clones

Samples	Position	AA change	Codon change	Sequence context
	1,503	E495G	GAA > GGA
Control	1,472	R491Q	CGG > CAG	GCCGG
	1,503	Silent	TTT > TTC
	633	G100C	GGC > TGC	GCCTA
AID	395	Silent	AAA > AAG
	568	G190D	GGC > GAC	TGCCA
	633	T212A	ACG > GCG
	987	G155D	GGC > GAC	GGCCA
	607	L203M	CTG > ATG	CCCTG
Rat APOBEC1	613	E205K	GAG > AAG	CTCGG
	764	K255T	AAG > ACG
	987	Silent	GGG > GGT	TTCCC
	1,245	silent	AGC > AGT	AGCCG
	758	R253H	CGC > CAC	TGCGC
	841*	silent	CTG > TTG	AGCTG
	697	H233D	CAT > GAT	TTCAT
Human APOBEC1	699	H233D	CAT > GAC
	1,149*	Silent	GCC > GCA	GCCAT
	1,245*	F415L	TTT > TTG

The region analyzed (encompassing exon 13 of BCR and exon 9 of ABL1) includes the imatinib-binding region of the fusion gene. The asterisk indicates mutations found in the same clone. The local sequence context for the mutations at cytosines is shown. Compared to the AID-induced mutations found in previous reports (mutations in approximately 30% of the sequences) [41],[42], we found approximately one mutation in each of the clones analyzed. This is explained by the different procedures we used to select resistant clones: whereas the other studies focused on competing bulk populations of AID-transfected GFP(+) cells and control GFP(−) cells, we analyzed individual clones arising from the same number of cells plated in the presence of imatinib.

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