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Table 2. Summary of publications investigating EGFR and PIK3CA mutations in pancreatic adenocarcinoma.

# Author Year No. of patients EGFR mutations EGFR mutation type PIK3CA mutations Response to inhibitor Origin
1 Samuels et al. (21) 2004 11 ND ND 0/11 (0%) ND U.S.
2 Kwak et al. (24) 2006 55 2/55 (3.6%) Exon 19 Deletion ND 2/2 disease stabilization U.S.
3 Immervoll et al. (25) 2006 43 0/43 (0%) ND ND Norway
4 Tzeng et al. (26) 2007 31 0/31 (0%)* ND ND U.S.
5 Lee et al. (27) 2007 66 1/66 (1.5%) Exon 20 Substitution (2453G>A, C818Y) ND ND Korea
6 Willmore-Payne et al. (28) 2007 12 0/12 (0%)** ND ND U.S.
7 Morinaga et al. (29) 2008 42 0/42 (0%) ND ND Japan
8 Jimeno et al. (30) 2008 10 0/10 (0%) 1/10 (10%) 1/1 Sensitive U.S./ Europe
9 Iyer et al. (31) 2008 27 0/27 (0%) 0/27 (0%) ND U.S.
10 Ueno et al. (32) 2009 31 0/31 (0%) ND ND Japan
11 Dewald et al. (33) 2009 5 1/5 (20%) Gain ~4n ND ND U.S.
12 Janku et al. (34) 2010 8 ND ND 1/8 (12.5%) NA U.S.
13 Lozano-Leon et al. (35) 2011 34 3/34 (8.8%) R841R, T571T, R831C ND As wild-type Spain
TOTAL 7/347 (2%) 2/56 (3.6%)

ND, not done; NA, not available. *Tzeng et al. found EGFR mutations in 26/31 (83.8%) samples, yet all were silent mutations. 25 patients had 2361G>A in exon 20, and one patient had 2508C>T in exon 21. **Willmore-Payne et al. found no activation mutations. our samples had polymorphism in exon 20