Poster viewing and lunch

47P - PIK3CA mutational status in tissue & plasma and clinicopathological features in HR+/HER2- breast cancer patients (ID 267)

Lecture Time
12:15 - 12:15
Session Name
Poster viewing and lunch
Exhibition area
Fri, 12.05.2023
12:15 - 13:00
  • Eduardo Terán Brage (Salamanca, Spain)
  • Eduardo Terán Brage (Salamanca, Spain)
  • José Antonio Muñoz León (Salamanca, Spain)
  • Rebeca Lozano Mejorada (Salamanca, Spain)
  • Álvaro López Gutiérrez (Salamanca, Spain)
  • María Mar Abad Hernández (Salamanca, Spain)
  • Magdalena Sancho de Salas (Salamanca, Spain)
  • Luis Figuero Pérez (Salamanca, Spain)
  • Emilio Fonseca Sanchez (Salamanca, Spain)
  • Cesar A. Rodríguez Sanchez (Salamanca, Spain)



Activating mutations of PIK3CA gene are described in around 30-40% of breast cancer (BC) patients. They confer worse prognosis and resistance to endocrine and chemotherapeutic therapy. Concordance between testing methods (tissue & plasma) are not well studied. We aim to compare tissue & plasma assays and to analyze the clinicopathological features and the prognostic value of PIK3CA mutations in HR+/HER2-.


We performed a retrospective and unicentric analysis of PIK3CA mutational status in tissue & plasma samples in patients (p) with HR+/HER2- BC from Feb/21 to Dec/22. PIK3CA test: Cobas®PIK3CA Mutation Kit. We carried out a correlation between both test assays. We used X2 test to compare patients’ features and Kaplan Meier to analyze progression-free survival (PFS) in PIK3CA mutated (PIK3CAm) vs wild-type (wt).


189 samples were analyzed in 155p with HR+/HER2- BC (128 in tissue & 61 in plasma). PIK3CA mutations were detected in 56p (36.1%), of which 39.1% (50p) in tissue and 13.1% (8p) in plasma. Hotspot mutations: H1047X (46%), E545X (20.6%) and E542K (12.7%). Tissue-plasma correlation was available in 34p (M1 stage), with overall correlation rate of 70.6%. 10 cases (29.4%) were positive in tissue but not in plasma. Patient characteristics are described in the table: significant differences were observed in histological type (p=0.005) and grade (p=0.03). 57p received 1L treatment with CDK4/6 inhibitors + endocrine therapy. PFS was significantly shorter in PIK3CAm vs wt (24m [95%CI;3.4-44.6] vs 35.6m [95%CI;19.6-51.6]; p=0.03). A trend towards lower objective response rate (64.7% vs 71.8%, p=0.59) was observed in PIK3CAm patients.

Age (median) 56 [24-91] PIK3CA m PIK3CA wt p-value
Histological type Ductal 45(76.3%) 85(81.7%) P=0.005
Lobular 12(20.3%) 6(5.8%)
Other 2(3.4%) 13(12.5%)
Histological grade 1 19(34.5%) 17(17%) P=0.03
2 30(54.6%) 65(66%)
3 6(10.9%) 18(18%)
Ki67(%) <14% 28(50%) 52(50.9%) P=0.91
≥14% 28(50%) 50(49.1%)
Tumour size <50mm 41(74.5%) 88(85.4%) P=0.09
≥50mm 14(25.5%) 15(14.6%)
Nodes(N) N0 19(41.3%) 29(32,6%) P=0.31
N+ 27(58.7%) 60(67.4%)
Debut M1 Yes 10(34.5%) 21(38.2%) P=0.73
No 19(65.5%) 34(61.8%)
Visceral metastases Yes 24(82.8%) 40 (72.7%) P=0.31
No 5(17.2%) 15(27.3%)


Mutational spectrum and clinical features in PIK3CAm luminal BC in our environment are consistent with those described previously. We observed worse prognosis and resistance to endocrine therapy in PIK3CAm luminal BC. We need larger studies to evaluate the role of liquid biopsy in the detection of PIK3CAm.

Legal entity responsible for the study

The authors.


Has not received any funding.


C.A. Rodríguez Sanchez: Non-Financial Interests, Institutional, Advisory Role: Novartis, Lilly, Pfizer, Roche, Daiichi Sankyo, AstraZeneca, MSD, Veracyte, Gilead. All other authors have declared no conflicts of interest.