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Background: The pan-immune-inflammation value (PIV) has been associated with survival outcomes across various cancer types. This study investigates the association between PIV and overall and progression-free survival in endometrial cancer patients receiving adjuvant chemotherapy.
Materials And Methods: A retrospective analysis was conducted on 138 endometrial cancer patients treated at our center between January 2014 and January 2024. Eligible patients received adjuvant chemotherapy following surgery and had preoperative blood tests available for PIV calculation. PIV was calculated as neutrophil count × platelet count × monocyte count/lymphocyte count. Survival outcomes were analyzed using Kaplan-Meier and Cox regression methods.
Results: The median PIV was 352 [interquartile range (IQR): 199-600], with higher scores significantly associated with advanced International Federation of Gynecology and Obstetrics (FIGO) stage (p = 0.007) and extensive lymphovascular invasion (LVI) (p = 0.03). Multivariate analysis identified PIV [hazard ratio (HR): 1.001, p = 0.015], FIGO stage III-IV (HR: 5.957, p < 0.001), adjuvant radiotherapy (HR: 0.288, p = 0.002), and extensive LVI (HR: 2.295, p = 0.014) as independent prognostic factors for overall survival (OS). A PIV greater than 350 was linked to a 3.2-fold increase in mortality risk (p < 0.001). Additionally, radiotherapy in conjunction with adjuvant chemotherapy significantly improved OS in patients with a high PIV (> 350), but not in those with a low PIV (≤ 350).
Conclusion: The PIV score is a significant prognostic marker for survival in endometrial cancer patients receiving adjuvant chemotherapy. Patients with a high PIV score may benefit from the addition of radiotherapy to their treatment regimen. Further studies are needed to validate the PIV score as a predictive marker for adjuvant radiotherapy in this population.
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http://dx.doi.org/10.5603/rpor.105859 | DOI Listing |
Proteomics Clin Appl
September 2025
AIBioMed Research Group, Taipei Medical University, Taipei, Taiwan.
Background: Endometrial carcinoma (EC) represents a significant clinical challenge due to its pronounced molecular heterogeneity, directly influencing prognosis and therapeutic responses. Accurate classification of molecular subtypes (CNV-high, CNV-low, MSI-H, POLE) and precise tumor mutational burden (TMB) assessment is crucial for guiding personalized therapeutic interventions. Integrating proteomics data with advanced machine learning (ML) techniques offers a promising strategy for achieving precise, clinically actionable classification and biomarker discovery in EC.
View Article and Find Full Text PDFInt J Gynecol Cancer
August 2025
Radiation Department, A.O. S. Croce e Carle Teaching Hospital, Cuneo CN, Italy.
Int Immunol
September 2025
Department of Immunology, Graduate School of Medicine, Kyoto University.
B cells play a critical role in tumor immunity, with their presence associated with improved prognosis in various cancers, including endometrial cancer (EC). However, the nature of the B cell response within the tumor microenvironment (TME) remains incompletely understood. In this study, we conducted single-cell analyses of B cells and CD4+ T cells in the TME of EC.
View Article and Find Full Text PDFEur J Surg Oncol
September 2025
Barzilai University Medical Center, Ashkelon, Israel; Faculty of Health Sciences, Ben-Gurion University of Negev, Beer-Sheva, Israel.
Objective: To compare the survival of women with high grade endometrial cancer between asymptomatic and women presenting bleeding symptoms.
Design: An Israel Gynecologic Oncology Group multi-center retrospective cohort study.
Methods: The study included women who underwent surgery for high-grade endometrial cancer.
Transl Oncol
September 2025
The University of New Mexico, Albuquerque, NM, USA. Electronic address:
Ovarian and endometrial cancers frequently harbor a mutation in the tumor suppressor gene TP53, which occurs in over 90 % of ovarian cancers and in the most aggressive endometrial cancers. The normal tumor suppressive functions of p53 are disrupted, resulting in unregulated cell growth and therapeutic resistance to standard treatments including chemotherapy and PARP inhibitors. Hence, a novel therapeutic strategy is urgently needed for p53 mutant gynecologic cancers, and we propose that converting mutant p53 to a wild type conformation and restoring its tumor suppressive functions has the potential to greatly improve treatment.
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