Integration of Ki67 and Pan-Immune Inflammation Value (PIV) into a Predictive Nomogram for Pathologic Complete Response in Triple-Negative Breast Cancer - research article

Q: What biomarkers were integrated to predict pathologic complete response (pCR) in TNBC?

The study evaluated Ki67 proliferation index and the pan-immune-inflammation value (PIV, neutrophil × monocyte × platelet / lymphocyte) and combined them for biomarker-defined stratification.

Q: How was the study cohort designed and what treatments were included?

A multicenter retrospective cohort included 137 TNBC patients treated with anthracycline–taxane-based neoadjuvant therapy between 2015 and 2023, with or without carboplatin.

Q: Which Ki67–PIV subgroup showed the highest pCR rate and what factors independently associated with pCR?

The High Ki67–Low PIV subgroup had the highest pCR proportion (84%). In multivariable analysis, the High Ki67–Low PIV phenotype and carboplatin-containing NAT were independently associated with higher pCR likelihood.

Sep 23, 2026

Uploaded by Đào

Triple-negative breast cancer (TNBC) exhibits marked heterogeneity in response to neoadjuvant therapy, creating a need for simple, reproducible biomarkers predicting pathologic complete response (pCR). A multicenter retrospective cohort of 137 TNBC patients received anthracycline–taxane-based NAT (2015–2023) with or without carboplatin. Ki67 and pan-immune-inflammation value (PIV, neutrophil × monocyte × platelet / lymphocyte) were analyzed for pCR association and used to stratify Ki67–PIV subgroups. A nomogram integrating clinical factors, regimen, and Ki67–PIV subgroup showed good discrimination and calibration; the High Ki67–Low PIV phenotype and carboplatin-containing NAT were independently linked to higher pCR likelihood.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages12

Reading Time30 min

AccessFree to download

Abstract

Background

Methods

Results

Conclusion

Introduction

Guclu-Kantar etal. BMC Cancer (2026) 26:505 BMC Cancer [https://doi.org/10.1186/s12885-026-15842-5](https://doi.org/10.1186/s12885-026-15842-5) RESEARCH Open Access Integration of Ki67 and Pan-Immune- Inflammation Value (PIV) into a predictive nomogram for pathologic complete response in triple-negative breast cancer (Ki67 and inflammation in triple-negative breast cancer) Taliha Guclu-Kantar1, Ozgur Tanriverdi2*, Ismail Bayrakci3, Bilgin Demir4, Gokhan Colak4, Sait Kitaplı2, Ali Alkan2, Gamze Gokoz-Doğu1, Sernaz Topaloglu3 and Sabri Barutca4 Abstract Background Triple-negative breast cancer (TNBC) shows substantial heterogeneity in response to neoadjuvant therapy (NAT) . Simple, reproducible biomarkers that help identify patients more likely to achieve pathologic complete response (pCR) are needed. Methods This multicenter retrospective cohort included 137 patients with TNBC treated with anthracycline–taxane– based NAT between 2015 and 2023, with or without carboplatin. The Ki67 proliferation index and pan-immuneinflammation value (PIV = neutrophil × monocyte × platelet / lymphocyte) were evaluated for their association with pCR Receiver operating characteristic (ROC) analyses identified optimal cut-offs (Ki67: 27 . 5%; PIV: 292) . Patients were categorized into four Ki67–PIV subgroups. Multivariable logistic regression was used to examine associations with pCR, and a nomogram was developed incorporating tumor size, clinical nodal status, chemotherapy regimen, and Ki67–PIV subgroup. Discrimination, calibration, and internal validation were assessed using ROC AUC, calibration plots, and bootstrap resampling (B = 1000) . Results The overall pCR rate was 41%(56/137) . pCR rates differed across Ki67–PIV subgroups (p < 0. 001), with the High Ki67–Low PIV subgroup showing the highest pCR proportion (84%; 31/37) and the lowest proportions observed in Low Ki67–High PIV (12%; 4/34) and Low Ki67–Low PIV (11%; 1/9) subgroups. In multivariable analysis, the High Ki67–Low PIV phenotype was independently associated with pCR (OR 1. 88, 95% CI 1.34–2. 97; p < 0. 001), and carboplatin-containing NAT was also independently associated with higher pCR likelihood (OR 1. 75, 95% CI 1.12–2. 64; p < 0. 001) . The nomogram demonstrated strong discrimination (AUC = 0 . 86), with a bootstrap-corrected AUC of 0.84 and good calibration. Conclusion In this retrospective multicenter cohort, integrating Ki67 and PIV enabled biomarker-defined stratification of pCR after NAT inTNBC. A nomogram incorporating clinical variables, regimen, and the Ki67–PIV *Correspondence: Ozgur Tanriverdi[dr.ozgur.tanriverdi@gmail.com](dr.ozgur.tanriverdi@gmail.com) Full list of author information is available at the end of the article © The Author(s) 2026. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit [http://creati](http://creati)[vecommons.org/licenses/by-nc-nd/4.0/](vecommons.org/licenses/by-nc-nd/4.0/.)[.](vecommons.org/licenses/by-nc-nd/4.0/.) Guclu-Kantar et al. BMC Cancer (2026) 26:505 Page 2 of 12 phenotype may provide a pragmatic

FAQs

What biomarkers were integrated to predict pathologic complete response (pCR) in TNBC?

The study evaluated Ki67 proliferation index and the pan-immune-inflammation value (PIV, neutrophil × monocyte × platelet / lymphocyte) and combined them for biomarker-defined stratification.

How was the study cohort designed and what treatments were included?

A multicenter retrospective cohort included 137 TNBC patients treated with anthracycline–taxane-based neoadjuvant therapy between 2015 and 2023, with or without carboplatin.

Which Ki67–PIV subgroup showed the highest pCR rate and what factors independently associated with pCR?

The High Ki67–Low PIV subgroup had the highest pCR proportion (84%). In multivariable analysis, the High Ki67–Low PIV phenotype and carboplatin-containing NAT were independently associated with higher pCR likelihood.

Sep 23, 2026

Uploaded by Đào