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Programmed Death Ligand 1 Expression Among 700 Consecutive Endometrial Cancers: Strong Association With Mismatch Repair Protein Deficiency
  1. Zaibo Li, MD, PhD*,
  2. Amy S. Joehlin-Price, MD,
  3. Jennifer Rhoades,
  4. Martins Ayoola-Adeola§,
  5. Karin Miller, MD,
  6. Anil V. Parwani, MD, PhD, MBA*,
  7. Floor J. Backes, MD,
  8. Ashley S. Felix, PhD and
  9. Adrian A. Suarez, MD*
  1. * Department of Pathology, The Ohio State University, Columbus, OH;
  2. Department of Pathology, University of California San Francisco, San Francisco, CA;
  3. Division of Epidemiology, College of Public Health,
  4. § College of Medicine, The Ohio State University, Columbus, OH;
  5. Department of Pathology, Johns Hopkins University, Baltimore, MD; and
  6. Department of Obstetrics and Gynecology, The Ohio State University, Columbus, OH.
  1. Address correspondence and reprint requests to Adrian A. Suarez, MD, Department of Pathology, Wexner Medical Center, The Ohio State University, E414 Doan Hall, 410 West 10th Ave, Columbus, OH 43210. E-mail: Adrian.Suarez{at}osumc.edu.

Abstract

Objective This study aims to determine the prevalence of programmed death ligand 1 (PD-L1) expression in endometrial carcinoma (EC) and determine clinical and pathological associations.

Methods Immunohistochemistry for PD-L1 was performed on sections of a triple-core tissue microarray of 700 ECs. Positive PD-L1 expression, defined as 1% of cells staining positive, was evaluated in tumor and stromal compartments. Using age-adjusted logistic regression, we estimated odds ratios and 95% confidence intervals for associations between PD-L1 expression (overall and by staining compartment) with clinical and tumor characteristics. Kaplan-Meier plots and log-rank tests were used to evaluate associations between PD-L1 expression and EC-specific survival.

Results PD-L1 expression was observed in 100 cases (14.3%), including 27 (3.9%) with expression in tumor cells only, 35 (5.0%) with expression in both tumor cells and stroma, and 38 (5.4%) with expression in stroma only. Expression was observed in ECs of different histologic types. Tumors characterized by loss of mismatch repair proteins were significantly associated with tumoral PD-L1 expression (P < 0.0001), but not with stromal PD-L1 expression. Both tumoral and stromal PD-L1 expressions were associated with high-grade endometrioid histology, nonendometrioid histology, and lymphovascular space invasion. We observed no significant associations between PD-L1 expression and EC-specific survival.

Conclusions PD-L1 is expressed in a significant proportion of EC and is associated with mismatch repair deficiency, potentially representing a mechanism of tumor immune evasion and a therapeutic target in EC.

  • PD-L1
  • Endometrial carcinoma
  • Mismatch repair protein
  • Lymph node metastasis

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Footnotes

  • The authors declare no conflicts of interest.

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