. Author manuscript; available in PMC: 2010 Mar 1.

Published in final edited form as: Expert Opin Ther Targets. 2009 Mar;13(3):339–362. doi: 10.1517/14712590902735795

Table 2.

Consequences of activating Kirsten rat sarcoma viral oncogene homolog (KRas) mutations on treatment outcomes in metastatic colorectal cancer (mCRC).

Trial	Size	Treatment	PFS^* (months)/Responses(%)
			KRasWT	KRasMut
CAIRO2 [225]	755	CapOxBev	−C : 10.7 months^†	−C:12.5months
		±Cetuximab(C)	+C: 10.5 months	+C:8.6months,
			p = 0.1	p = 0.044
CRYSTAL [224]	540	1^st line	−C: 8.1 months/43%	−C: 8.7 months/40%
		FOLFIRI	+C:9.9 months/59%	+C:7.6 months/36%
		±Cetuximab(C)	p = 0.017/0.002	p = 0.47
OPUS.[229]	337	1^st line	−C: 7.7 months/37%	−C:8.6 months/49%
		FOLFOX	+C:7.2 months/61%	+C:5.5mo/33%
		±Cetuximab(C)	p = 0.01	p = 1

PFS (progression free survival) here defines time during which no tumor growth was detected radiographically; responses here are the sum of complete and partial responses.

^†

The CAIRO2 study demonstrated no difference in PFS (shown above), response (40.6% versus 43.9%, p = 0.44 ) or median OS (20.4 versus 20.3 months, p = 0.21) upon adding cetuximab to capecitabine, oxaliplatin and bevacizumab. In KRas mutant colon cancer patients, the detrimental effect of the two-antibody combination reached statistical significance. A similar trend was reported in the OPUS study.