Immunohistochemical Expression of PD-L1 and CTLA-4 in Triple Negative Breast Cancer and Their Prognostic Associations

Document Type : Research Articles

Authors

1 Department of Pathology, Faculty of Medicine, Mansoura University, Mansoura, Egypt.

2 Medical Oncology Unit, Internal Medicine Department, Professor of Medical Oncology, Faculty of Medicine, Mansoura University, Mansoura, Egypt.

Abstract

Objective: Programmed Death-Ligand 1 (PD-L1) and Cytotoxic T Lymphocyte -Associated Antigen-4 (CTLA-4) are presently considered as prognostic markers and therapeutic targets in numerous human malignancies. The goal of this study was to determine whether PD-L1 and CTLA-4 might be used to predict patients’ survival in Triple Negative Breast Cancer (TNBC). Methods: This retrospective cohort study analyzed 100 primary TNBC cases that had surgical resection at the Oncology Center of Mansoura University (OCMU), Faculty of Medicine, Egypt. Clinicopathological data and survival outcomes were collected, and immunohistochemistry (IHC) was performed for PD-L1 and CTLA-4 expression. Result: In 29% of TNBCs, PD-L1 was expressed. PD-L1 positivity was significantly associated with high tumor grade (P=0.007). PD-L1 did not, however, significantly associate with survival. CTLA-4 was expressed in 45% of TNBCs. CTLA-4 expression was significantly associated with lymph node metastasis (P=0.009), distant metastasis (P=0.001) and advanced TNM stage (P=0.001). In TNBC, multivariate analysis identified CTLA-4 expression as an independent prognostic predictor for both disease-free survival (P=0.002) and overall survival (P=0.003). Conclusion: The selection of patients for immunotherapy and checkpoint-blockade treatment may be guided by CTLA-4, an independent prognostic factor for the overall survival and disease-free survival of TNBC patients.

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Asian Pacific Journal of Cancer Prevention
Volume 26, Issue 1
January 2025
Pages 319-326

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History

  • Receive Date: 28 September 2024
  • Revise Date: 16 November 2024
  • Accept Date: 16 January 2025

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