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Table 3. Summary of publications investigating EGFR and PIK3CA Mutations in Biliary Tract Carcinoma.

# Author Year No. of patients EGFR mutations EGFR mutation type PIK3CA mutations PIK3CA mutation type Response to inhibitor Origin
1 Gwak et al. (36) 2005 22 3/22 (13.6%) Del Exon 19 ND ND Korea
2 Bekaii-saab et al. (37) 2005 40^ 0/40 (0%) ND ND US
3 Leone et al. (38) 2006 40 *6/40 (15%) ** ND ND Italy
4 Aglietta et al. (39) 2007 49 7/49 (14.3%) *** 5/49 (10.2%) *** ND Italy
5 Riener et al. (40) 2008 68 ND 2/68 (2.9%) E542K, E545K ND Switzerland
6 Iyer et al. (31) 2008 3 0/3 (0%) 0/3 (0%) ND US
7 Lubner et al. (41) 2010 26 3/26 (11.5%) EGFR vIII ND 1/3 CR (NS) US
8 Xu et al. (42) 2010 34 ND 11/34 (32.4%) E545K/D, E542K ND China
TOTAL 19/180 (10.5%) 18/154 (11.7%)

ND, not done; NA, not available; CR, Confirmed Response; NS, not significant. ^Total number of hepatocellular and biliary carcinomas. *Leone et al. found two substitution mutations (C775Y, T790M) in exon 20, two missense point mutations (A864T, E872K) in exon 21, and one patient with two substitution mutations (G882S, V843I) and a silent one (L858R), all in exon 21. **Leone et al. also found silent mutation 787 (Gln; CAG-to-CAA) in exon 20 in 36 of 40 samples. ***Aglietta et al. found five hotspot mutations of PI3K (codon 545, 546, 1048 and 1059) in four cases (10.2%); Mutations of EGFR have been detected in 7 out of 49 samples (14.3%). One of them was a new stop-codon mutation. Lubner et al. found EGFR intron 1 polymorphism and Q787 G > G SNP in 15 and 6 of 26 samples, respectively