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Towards targeting PD-1/PD-L1 axis in breast cancer, pre-clinical data
  1. Hazem Ghebeh1,
  2. Dilek Colak2,
  3. Asma Tulbah3 and
  4. Abdullah Alsuliman1
  1. Aff1 grid.415310.20000000121914301Stem Cell & Tissue Re-engineering ProgramKing Faisal Specialist Hospital and & Research Centre Takhassusi Road Al-Maathar, Riyadh Saudi Arabia
  2. Aff2 grid.415310.20000000121914301Department of Biostatistics, Epidemiology and Scientific ComputingKing Faisal Specialist Hospital & Research Takhassusi Road Al-Maathar, Riyadh Saudi Arab
  3. Aff3 grid.415310.20000000121914301Department of Pathology and Laboratory MedicineKing Faisal Specialist Hospital & Research Centre Riyadh Saudi Arab

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Meeting abstracts

PD-L1 is a ligand that upon binding to its receptor (PD-1) on T-cells leads to T-cell anergy/and or apoptosis [1, 2]. We have shown that PD-L1 is expressed in breast cancer where its expression correlates with estrogen receptor (ER) negativity [3]. To understand the mechanism of the constitutive expression of PD-L1 in tumor cells of ER negative cells we used gene-in and out approach, large scale bioinformatics and immunohistochemistry. We have demonstrated that epithelial to mesenchymal transition (EMT) upregulates PD-L1 expression while cells expressing ER downregulates PD-L1, in parallel with reversal of EMT process. Bioinformatics analysis of gene expression signatures of breast tumors showed a significant correlation between EMT score and PD-L1 mRNA expression. Strikingly, very strong association were found between PD-L1 expression and claudin low breast cancer, a subset of breast cancer known to have high EMT score. In conclusion, we have characterized the expression of PD-L1 in breast cancer and we have demonstrated a strong association between PD-L1 expression, EMT status and claudin-Low breast cancer. Our finding will be essential for choosing the appropriate subset of breast cancer patients that will likely benefit from anti-PD-L1 targeted therapy and understand biological changes upon anti-PD-L1 therapy.


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