Abstract 1819P
Background
The treatment for breast cancer is determined by its molecular type. CTCs can change their molecular type compared to the primary tumor. This leads to a decrease in the effectiveness of the therapy and worsens the prognosis of the disease. Here we assessed the markers of breast cancer molecular types in metastasis-associated CTC subsets.
Methods
The prospective study included 73 breast cancer patients with stage T1-3N0-3M0, admitted for treatment to Cancer Research Institute, Tomsk NRMC. All patients signed an informed consent for voluntary participation. Markers of breast cancer molecular types (estrogen receptor (ER), progesterone receptor (PR), Her2neu) in metastasis-associated CTC (MA-CTC) subsets with phenotype CD45-EpCAM+CD44-CD24-N-cadherin+ were determined by the flow cytometry. Luminal CTC subsets without Her2neu expression (ER+PR+Her2neu-, ER+PR-Her2neu-, ER-PR+Her2neu-), luminal CTC subsets with Her2neu expression (ER+PR+Her2neu+, ER+PR-Her2neu+, ER-PR+Her2neu+), triple-negative CTCs (ER-PR-Her2neu-) and Her2neu-positive CTCs (ER-PR-Her2neu+) were detected.
Results
Luminal A breast cancer was verified in 41,3% of patients, luminal B breast cancer – in 50% of patients and triple-negative breast cancer – in 8,7% of patients. CTCs was detected only in 46 out 73 patients (63%). The frequency of MA-CTCs didn’t differ in all molecular subtypes of breast cancer. The ER- subset prevailed over the ER+ subset among MA-CTCs (1,66 (0,56-5,81) cells per 1 ml of blood and 1,66 (0,00-3,32) cells per 1 ml of the blood, р=0,0005 and р=0,0003, respectively) in patients with luminal A and B breast cancers. A similar pattern was observed in the Her2neu expression. The count of Her2neu-negative MA-CTCs was more than Her2neu-positive MA-CTCs (1,66 (0,56-6,64) and 1,66 (0,00-4,15) cells per 1 ml of the blood, р=0,0009 and р=0,007, respectively). ER+PR-Her2neu+ cells were not detected among MA-CTCs. ER+PR+Her2neu+ MA-CTCs were absent in patients with triple-negativebreast cancer.
Conclusions
Apparently, the intravasation of MA-CTCs often leads to loss of one or all three markers of the breast cancer molecular subtypes. This should be taken into account in breast cancer therapy. This work was supported by Russian Science Foundation (Grant #19-75-30016).
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
Russian Science Foundation.
Disclosure
All authors have declared no conflicts of interest.