Impact of somatic PI3K pathway and ERBB family mutations on pathological complete response (pCR) in HER2-positive breast cancer patients who received neoadjuvant HER2-targeted therapies

Table 3 Somatic mutation genotyping and phosphatase and tensin homolog immunohistochemistry results by oestrogen receptor and progesterone receptor status and treatment arm

		PTEN low	PIK3CA/ERBB mutated and/or PTEN low^a
Patient group	Total no. of patients	No. of patients (%)	No. of patients (%)
ER status
Negative	19	6 (31.6)	11 (57.9)
Positive	26	8 (30.8)	14 (53.8)
PR status
Negative	29	11 (37.9)	17 (58.6)
Positive	16	3 (18.8)	8 (50)
Treatment arm
TCL	6	2 (33.3)	4 (66.7)
TCH	21	7 (33.3)	13 (61.9)
TCHL	18	5 (31.3)	8 (44.4)

Abbreviations: ER Oestrogen receptor, PR Progesterone receptor, TCH Docetaxel, carboplatin, and trastuzumab, TCHL Docetaxel, carboplatin, trastuzumab, lapatinib, TCL Docetaxel, carboplatin, lapatinib
Association of low PTEN expression and combined low PTEN expression and PIK3CA/ERBB family mutations (i.e., PI3K pathway activation) with ER and PR status. The mutation frequency in each treatment arm is also shown
^aBecause of mutation overlap, these numbers/percentages may not be a sum of PIK3CA and ERBB mutated

ISSN: 1465-542X