Differential prognostic impact of strong PD-L1 Expression and 18 F-FDG uptake in triple-negative breast cancer

Seo Hee Choi, Jee Suk Chang, Ja Seung Koo, Jong Won Park, Joo Hyuk Sohn, Ki Chang Keum, Chang Ok Suh, Yong Bae Kim

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)

Abstract

Objectives: Triple-negative breast cancers (TNBC) is an aggressive disease and often associated with early distant metastases, which negate the role of adjuvant radiotherapy. We studied the clinical utility of programmed death ligand-1 (PD-L1) and other available factors in predicting clinical outcome in TNBC. Methods: Of the 539 patients with newly diagnosed TNBC between 2004 and 2011, we analyzed 117 patients who had both tumor samples which PD-L1 protein expression could be evaluated using immunohistochemistry and initial staging 18 F-fluorodeoxyglucose (FDG) positron emission tomography (PET) data to find available immunologic or metabolic factors. Median follow-up duration was 53 months. Results: Strong PD-L1 expression was significantly associated with increased risk of recurrence along with tumor hypermetabolism. The systemic recurrence rate was significantly higher in the strong PD-L1 group than the weak PD-L1 group (35% vs. 11%; P=0.002); whereas there was no difference in locoregional failures (8% vs. 8%). Meanwhile, tumor hypermetabolism seemed to relate with an increase in overall recurrences (26% vs. 8%; P=0.019), not with specific type (locoregional, 9% vs. 3% [P=0.289]; systemic, 22% vs. 8% [P=0.051]). The relationship between PD-L1 expression and survival outcomes retained significance even after adjusting potential risk factors. Conclusions: PD-L1 and tumor metabolism might have role of predicting an increase in treatment failures. Especially, strong PD-L1 expression status was related to distant metastasis-dominant recurrence pattern which needs for intensive systemic therapy.

Original languageEnglish
Pages (from-to)1049-1057
Number of pages9
JournalAmerican Journal of Clinical Oncology: Cancer Clinical Trials
Volume41
Issue number11
DOIs
Publication statusPublished - 2018 Nov 1

Bibliographical note

Funding Information:
From the Departments of *Radiation Oncology; †Pathology; and ‡Internal Medicine, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, Republic of Korea. Supported by a faculty research grant from Yonsei University College of Medicine for 2015 (6-2015-0038). The authors declare no conflicts of interest. Reprints: Yong Bae Kim, MD, Department of Radiation Oncology, Yonsei Cancer Center, Yonsei University College of Medicine, 50 Yonsei-ro, Seodaemun-gu, Seoul 03722, Republic of Korea. E-mail: ybkim3@yuhs.ac. Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website, www. amjclinicaloncology.com. Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0277-3732/18/4111-1049 DOI: 10.1097/COC.0000000000000426

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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