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Fig. 4 | Breast Cancer Research

Fig. 4

From: 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

Fig. 4

Influence of mutation and phosphatase and tensin homolog (PTEN) status on pathological complete response (pCR) rate by treatment arm using a χ2 test of association. a Influence of PIK3CA mutations in tumours on pCR in patients receiving TCH (docetaxel, carboplatin, trastuzumab) and TCHL (docetaxel, carboplatin, trastuzumab, lapatinib). b Influence of ERBB family mutations in tumours on pCR in patients receiving TCH and TCHL. c Influence of combined PIK3CA and ERBB family mutation status in tumours on pCR in patients receiving TCH and TCHL. d Influence of low PTEN expression in breast tumours on pCR in patients receiving TCH and TCHL. e Influence of tumour phosphatidylinositol 3-kinase (PI3K) activation status on pCR in patients receiving TCH and TCHL. PI3K activation is defined as the presence of one or more of the following in a breast tumour: PIK3CA or ERBB family mutations or low PTEN expression. WT Wild type

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