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e-Posters

24P - TGF-?RI contributes to tamoxifen response in luminal B breast cancer with HER2 negative phenotype

Date

06 Oct 2021

Session

e-Posters

Presenters

Nataliya Babyshkina

Citation

Annals of Oncology (2021) 32 (suppl_6): S1345-S1371. 10.1016/annonc/annonc740

Authors

N. Babyshkina1, T. Dronova2, S. Vtorushin3, S. Patalyak3, N. Cherdyntseva3

Author affiliations

  • 1 Tomsk National Research Medical Center, Tomsk/RU
  • 2 Tomsk National Research Medical Center, Russian Academy of Sciences, Cancer Research Institute, 634009 - Tomsk/RU
  • 3 Tomsk National Research Medical Center of the Russian Academy of Sciences, Cancer Research Institute, 634009 - Tomsk/RU
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Abstract 24P

Background

TGF-β signaling is highly important in tumor growth and progression, however, the value of TGF-β family proteins as potential resistance-related markers is not fully understood, especially in breast cancer molecular subtypes. The aim of this study was to examine the contribution of TGF-β family proteins to tamoxifen response in luminal breast cancer patients with different HER2 phenotypes.

Methods

TGF-β, TGF-βRI, TGF-βRII and ERα mRNA and protein expression levels were quantified using quantitative real-time polymerase chain reaction and immunohistochemistry, respectively, in 60 tissue specimens from breast cancer patients with luminal B HER2 negative and luminal HER2 positive phenotype. Flow cytometry was used to evaluate the co-expression of TGF-βRI and CD24 in breast cancer tissue. Association analysis of progression-free survival (PFS) with selected markers was conducted using Kaplan-Meier plots and log-rank test. Tamoxifen resistance was defined as clinical progression during disease treatment or relapse.

Results

High mRNA expression of ESR1 as well as homogeneous ERα expression in tumor were significantly related to favorable tamoxifen response in luminal B breast cancer patients with HER2-negative phenotype (р = 0.046 and p = 0.011; respectively). Furthermore, these patients with high level of TGF-βR1 expression had a significantly better prognosis than those with low TGF-βR1 expression in the tumor (p = 0.021). Luminal B HER2 negative tumors with TGF-βRI-positive expression tended to be closely associated with the homogeneous ERα expression, although this difference was not significant (p = 0.18). The expression of TGF-βRI was significantly correlated with progression-free survival in luminal B HER2-negative patients (log-rank p = 0.010).

Conclusions

The findings of the present study suggest that TGF-βRI may be used as a potential target for the tamoxifen treatment of luminal B breast cancer patients with HER2-negative phenotype. Further study is required to assess the possible relationship between the TGF-β family proteins and tamoxifen responsiveness in luminal HER2 positive breast cancer.

Legal entity responsible for the study

The authors.

Funding

Russian Scientific Foundation, grant #19-75-30016.

Disclosure

All authors have declared no conflicts of interest.

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