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Table 2 Summary of PTEN and PIK3CA results

From: Association of phosphatase and tensin homolog low and phosphatidylinositol 3-kinase catalytic subunit alpha gene mutations on outcome in human epidermal growth factor receptor 2-positive metastatic breast cancer patients treated with first-line lapatinib plus paclitaxel or paclitaxel alone

Characteristics

Lapatinib + paclitaxel (n = 222)

Placebo + paclitaxel (n = 222)

Patients with available tumor tissue, n (%)

198 (89)

192 (86)

Tumors available for PTEN a , n (%)

180

175

  PTEN IHC 0

28 (16)

21 (12)

  PTEN IHC 1+

76 (42)

80 (46)

  PTEN IHC 0/1+

104 (58)

101 (58)

  PTEN IHC 2+/3+

76 (42)

74 (42)

Patients consented for PIK3CA b

141

133

Tumors evaluable for PIK3CA a , n (%)

104

106

  PIK3CA mutation

29 (28)

36 (34)

  PIK3CA wild-type

58 (56)

48 (45)

  PIK3CA indeterminate

17 (16)

22 (21)

Tumors with PTEN IHC 0/1+ and/or PIK3CA mutations c,d , n (%)

119/180 (66)

117/175 (67)

Tumors with PTEN IHC 0/1+ and PIK3CA mutation, n (%)

14/104 (13)

20/106 (19)

  1. aNonevaluable findings were due to factors such as insufficient tumor tissue, absence of PTEN staining in stroma and poor DNA quality (PIK3CA). bSomatic mutation analysis was optional. cPIK3CA mutation frequency: 65% (42/65) were H1047R (35 cases are from primary tumor; 5 from metastatic; 2 from unknown site); 25% were E545K/D (14 cases are from primary tumor; 1 from metastatic, 1 from unknown site); 11% were E542K (7 from primary tumor). dDefined as PI3K pathway activation. DNA, deoxyribonucleic acid; IHC, immunohistochemistry; PIK3CA, phosphatidylinositol 3-kinase subunit alpha gene; PTEN, phosphatase and tensin homolog.