Senchukova MA, Zubareva EY, Saidler NV, Krivolapova LV. Lack of cytoplasmic expression of a new marker programmed cell death ligand-1 in tumor cells is significant. World J Exp Med 2025; 15(4): 110890 [DOI: 10.5493/wjem.v15.i4.110890]
Corresponding Author of This Article
Marina A Senchukova, Scientific and Clinical Center No. 3, Petrovsky National Research Centre of Surgery, Oktyabrsky Prospekt, 3, Moscow 108840, Troitsk, Russia. masenchukova@yandex.com
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Oncology
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Prospective Study
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Dec 20, 2025 (publication date) through Dec 19, 2025
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World Journal of Experimental Medicine
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2220-315x
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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
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Senchukova MA, Zubareva EY, Saidler NV, Krivolapova LV. Lack of cytoplasmic expression of a new marker programmed cell death ligand-1 in tumor cells is significant. World J Exp Med 2025; 15(4): 110890 [DOI: 10.5493/wjem.v15.i4.110890]
World J Exp Med. Dec 20, 2025; 15(4): 110890 Published online Dec 20, 2025. doi: 10.5493/wjem.v15.i4.110890
Lack of cytoplasmic expression of a new marker programmed cell death ligand-1 in tumor cells is significant
Marina A Senchukova, Evgeniya Yu Zubareva, Natalia V Saidler, Lyubov V Krivolapova
Marina A Senchukova, Scientific and Clinical Center No. 3, Petrovsky National Research Centre of Surgery, Moscow 108840, Troitsk, Russia
Evgeniya Yu Zubareva, Department of Oncology, Orenburg State Medical University, Orenburg 460021, Orenburgskaya Oblast’, Russia
Natalia V Saidler, Department of Pathology, Orenburg Regional Cancer Clinic, Orenburg 460021, Orenburgskaya Oblast’, Russia
Lyubov V Krivolapova, Scientific and Clinical Center No. 2, Petrovsky National Research Centre of Surgery, Moscow 117953, Moskva, Russia
Author contributions: Senchukova MA formulated the idea and aims of the study, wrote the first version of the manuscript and performed the analysis of the results and statistical processing of the results; Saidler NV made a significant contribution to the development of the study methodology, participated in the discussion of the obtained results, and revised and approved the final version; Zubareva EY collected and analyzed the data and made a significant contribution to the concept and design of the study, participated in the preparation of tables and figures; Krivolapova LV made a significant contribution to the selection and analysis of data and their discussion, as well as to the interpretation of the obtained results; All the authors wrote and approved the final version of the manuscript.
Supported by the Russian Science Foundation, No. 23-25-00183.
Institutional review board statement: This study was reviewed and approved by the Ethics Committee of Orenburg State Medical University (Russia, Orenburg; protocol No. 311 dated January 13, 2023).
Clinical trial registration statement: This study does not require registration as it does not meet the definition of a clinical trial.
Informed consent statement: All patients signed informed consent to participate in the clinical study.
Conflict-of-interest statement: All authors have no conflicts of interest to declare.
CONSORT 2010 statement: The authors have read the CONSORT 2010 statement—checklist of items, and the manuscript was prepared and revised according to the CONSORT 2010 statement—checklist of items.
Data sharing statement: Data from patients included in the study in Statistica10 table or Excel table formats can be provided upon request to the corresponding author at masenchukova@yandex.com.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Marina A Senchukova, Scientific and Clinical Center No. 3, Petrovsky National Research Centre of Surgery, Oktyabrsky Prospekt, 3, Moscow 108840, Troitsk, Russia. masenchukova@yandex.com
Received: June 18, 2025 Revised: July 13, 2025 Accepted: October 20, 2025 Published online: December 20, 2025 Processing time: 184 Days and 20.9 Hours
Abstract
BACKGROUND
Recent studies have indicated that an antibody against programmed cell death protein 1-ligand 1 (PDCD1-LG1), a new marker of programmed cell death-ligand 1 expression, is promising for studying the mechanisms of breast cancer (BC) progression and resistance to chemotherapy.
AIM
To compare the features of PDCD1-LG1 expression in chemoresistant luminal A BC and BC with high Ki67 indices.
METHODS
This prospective single-center observational cohort study included 148 patients with newly diagnosed primary resectable BC. The tumor sections were stained with antibodies against PDCD1-LG1. The statistical calculations were performed using Statistica software version 12.0. P < 0.05 was considered statistically significant.
RESULTS
Cytoplasmic PDCD1-LG1 (cPDCD1-LG1) expression was detected in the nonneoplastic epithelium, tumor cells (TCs) and immune cells (ICs). A lack of cPDCD1-LG1 expression in ≥ 20% of TCs and a PDCD1-LG1+ IC score ≥ 10% were associated with aggressive BC characteristics, including tumor G3, estrogen receptor-negative status, overexpression of human epidermal growth factor receptor 2 (HER2+), luminal B HER2+ BC, nonluminal HER2+ BC and triple-negative BC. The lack of cPDCD1-LG1 expression in < 20% of the TCs, in combination with a PDCD1-LG1+ IC score < 10% and G1, was characteristic of chemoresistant luminal A BC, whereas the lack of cPDCD1-LG1 expression in ≥ 20% of the TCs, combined with a PDCD1-LG1+ IC score ≥ 10%, was a predictor of high BC sensitivity to chemotherapy.
CONCLUSION
These results indicate that both the lack of cPDCD1 LG1 in TCs and the PDCD1 LG1 IC score and their combination may be important for assessing BC prognosis and sensitivity to chemotherapy.
Core Tip: We immunohistochemically studied the expression of programmed cell death protein 1 Ligand 1 (PDCD1 LG1) in tumor cells (TCs) and immune cells (ICs) in patients with breast cancer (BC). We revealed that a lack of cytoplasmic PDCD1 LG1 (cPDCD1 LG1) expression in ≥ 20% of TCs is characteristic of more aggressive BC subtypes, namely, G3 tumors, estrogen receptor-negative status and human epidermal growth factor receptor-2 overexpression. In addition, we established that the combined assessment of the lack of cPDCD1 LG1 expression in TCs and the PDCD1 LG1 score in ICs is one of the most significant predictors associated with BC chemotherapy sensitivity.
