Table 1.

In silico prediction of mutations of three NSCLC patients with favorable HLA class I or II binding properties.

Patient	Gene	HLA restriction	Mutated sequencea	Substitution (WT, AA#, Mut)	HLA- I or -IIScoresb
	POLE	B*1502	SRYFHIPIGNLPEYISTFGSDLFFARH	D1663Y	88
	FHL1	A*0206	CFTCSNCKQVIGTVSFFPKGEDFYCVT	G139V	86
	GPM6B	DQA1*0401	TILCFSGVALFCGFGHVALAGTVAILE	C94F	81
	LRP5	B*8101	CSHICIAKGDGTPLCSCPVHLVLLQNL	R1237L	80
P01	DMXL1	B*1502	QLRENFQEKRQWLFKYQSLLRMFLSYC	L2124F	78
	TP53	B*8101	CMGGMNRRPILTIFTLEDSSGNLLGRN	I3123F	70
	TPBG	A*0206	SAPFLASAVSAQPLLPDQCPALCECSE	P57L	84
	HACE1	DRB1*1101	QLNRLTRSLRRARSVELPEDNETAVYT	T20S	70
	COQ3	A*0206	RYPWARLYSTSQTAVDSGEVKTFLALA	T91A	68
	RAB4A	DRB1*1101	ERMGSGIQYGDAAFRQLRSPRRAQAPN	L199F	53
	ITFG1	A*0207	CVFILAIIGILHWLEKKADDREKRQEA	Q591L	39
	OPLAH	DQA1*0501	EGAVFLSFKLVQGDVFQEEAVTEALRA	G890D	49
	BCAR1	DPA1*0202	RQGIVPGNRLKILLVVPTRVGQGYVYE	V64L	31
	TP53	A*3303	TIITLEDSSGNLLVRNSFEVRVCACPG	G266V	32
P02	GBF1	B*1501	SSQHASRGGQSDDYEDEGVPASYHTVS	D1478Y	25
	COP1	B*5801	ILWDGFTGQRSKVSQEHEKRCWSVDFN	Y485S	31
	ATP11B	DQA1*0301	LKNTKEIFGVAVYSGMETKMALNYKSK	T262S	29
	UPF3A	A*3303	GSQDSGAPGEAMETLGRAQRCDDSPAP	R380T	26
	IER5L	A*0207	LHKNLLVSYVLRNTRQLYLSERYAELY	A43T	30
	SNX16	B*5801	QDVWMRSRADNKPYLSFSEPENAVSEI	C318Y	27
	OSBPL6	A*0201	EVLLSASSSENEALDDESYISDVSDNI	S513L	19
	NFE2L2	A*0201	AFFAQLQLDEETGQFLPIQPAQHIQSE	E82Q	18
	SLX4	A*0201	SPTKEAPPGLNDDGQIPASQESVATSV	A1694G	18
	ACAD8	A*0201	QTDVGGSGLSRLDISVIFEALATGCTS	T105I	31
	MTREX	A*0201	EMPKLTEQLAGPLCQMQECAKRIAKVS	R933C	15
P03	BCAR1	A*0201	VLLSWKVLDFSGPVPQGTGQPCSCGHW	G23V	37
	SLC7A1	A*0201	KYAVAVGSLCALSSSLLGSMFPMPRVI	A349S	28
	PLCG1	A*0201	SIEDHCSIAQQRNLAQYFKKVLGDTLL	M425L	23
	PIF1	A*0201	EADLFDKLEAVARGVRQQNKPFGGIQL	A325G	3
	SSH1	A*0201	ILDASKQRHNKLWCQQTDSSLQQPVDD	R470C	2

NSCLC, nonsmall cell lung cancer. ^aMutated residues are highlighted in hold. WT, wide type; AA#, position of mutated amino acid; Mut, mutation. ^bHLA class I and II binding affinity are predicted by netMHCpan 4.0 and netMHCIIpan 3.2, respectively.