Table 1.

Candidate genes from a transposon mutagenesis screen for resistance to afatinib in the EGFR-mutant PC9 lung adenocarcinoma cell line

Gene name	Predicted functional effect of insertions	No. of distinct insertion sites	No. of independent transfections with insertions	Total no. of clones with insertions
MET	Activating	19	12	129
YES1	Activating	15	8	109
FYN	Activating	14	9	30
GSK3B	Inactivating	7	4	8
SOS1	Activating	6	12	37
DNM3	Inactivating	4	8	24
NAV2	Inactivating	4	5	15
EPS8	Activating	4	2	6
KRAS	Activating	4	2	5
MYOF	Inactivating	3	4	19
RABGAP1L	Activating	3	3	15
RAF1	Activating	3	3	6
RABGAP1	Activating	3	3	4

Candidate genes from a transposon mutagenesis screen for resistance to afatinib in the EGFR-mutant PC9 lung adenocarcinoma cell line. A total of 1,927 distinct transposon insertion sites were identified in 188 afatinib-resistant PC9 clones from 13 independent transfections. Insertions were predicted to be activating if a transposon was situated near the transcription start site or first intron of a known human gene and was correctly oriented to drive expression of that gene. Genes that were found to be disrupted by insertions in both orientations or throughout the body of the gene were predicted to be inactivated.