Mechanisms of resistance to anti-EGFR monoclonal antibody treatment in metastatic colorectal cancer

Table 1 Significance of KRAS mutations in retrospective single arm studies and randomized prospective trials

Published studies	n	% KRAS mutations	Significant correlations
Retrospective single arm studies
Moroni et al[16]	31	32	None
Lièvre et al[13]	30	43	RR, mOS
Lièvre et al[18]	89	27	RR, PFS, mOS
De Roock et al[17]	66	40	RR, mOS
Randomized prospective trials
Amado et al[12]	427	43	RR, PFS, mOS
Tol et al[22]	256	38	RR, PFS
Van Cutsem et al[19]	277	38	RR, PFS, mOS
Bokemeyer et al[20]	233	42	RR, PFS
Hecht et al[21]	865	40	PFS, mOS
Douillard et al[23]	1096	40	RR, PFS

RR: Response rate; mOS: Median overall survival; PFS: Progression-free survival.

Table 2 Single nuclear polymorphism (SNP) analysis in patients treated with anti-EGFR moAbs

Publication	SNP	n	Variable	Significance
Zhang et al[44]	FcγRIIa H131R, V158F	39	TTP	0.037
Bibeau et al[45]	FcγRIIa H131R, V158F	69	TTP	0.015
Graziano et al[46]	FcγRIIa H131R, V158F	110	RR, OS	NS
Nagashima et al[47]	FcγRIIa H131R, V158F	98	PFS	NS
Graziano et al[46]	EGFR in1 (CA)n repeats	110	RR, OS	0.006, 0.008
Gonçalves et al[52]	EGFR ex 13 R521K	32	PFS	0.020
Graziano et al[46]	EGF 61G/G	110	OS	0.001
Zhang et al[44]	cyclin-D1 870Α>G	39	TTP	0.019
Graziano et al[46]	cyclin-D1 870Α>G	110	RR, OS	NS
Nagashima et al[47]	cyclin-D1 870Α>G	98	PFS	NS

anti-EGFR: Anti-epidermal growth factor receptor; NS: Not significant.