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).
코호트
1/5 보강
PICO 자동 추출 (휴리스틱, conf 2/4)
유사 논문P · Population 대상 환자/모집단
137 patients with TNBC treated with anthracycline–taxane–based NAT between 2015 and 2023, with or without carboplatin.
I · Intervention 중재 / 시술
추출되지 않음
C · Comparison 대조 / 비교
추출되지 않음
O · Outcome 결과 / 결론
A nomogram incorporating clinical variables, regimen, and the Ki67–PIV phenotype may provide a pragmatic approach for risk stratification, although external validation is required before broader clinical application. [SUPPLEMENTARY INFORMATION] The online version contains supplementary material available at 10.1186/s12885-026-15842-5.
[BACKGROUND] Triple-negative breast cancer (TNBC) shows substantial heterogeneity in response to neoadjuvant therapy (NAT).
- 95% CI 1.34–2.97
APA
Guclu-Kantar T, Tanriverdi O, et al. (2026). 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).. BMC cancer, 26(1). https://doi.org/10.1186/s12885-026-15842-5
MLA
Guclu-Kantar T, et al.. "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).." BMC cancer, vol. 26, no. 1, 2026.
PMID
41814226
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-immune-inflammation 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 ( < 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; < 0.001), and carboplatin-containing NAT was also independently associated with higher pCR likelihood (OR 1.75, 95% CI 1.12–2.64; < 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 in TNBC. A nomogram incorporating clinical variables, regimen, and the Ki67–PIV phenotype may provide a pragmatic approach for risk stratification, although external validation is required before broader clinical application.
[SUPPLEMENTARY INFORMATION] The online version contains supplementary material available at 10.1186/s12885-026-15842-5.
[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-immune-inflammation 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 ( < 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; < 0.001), and carboplatin-containing NAT was also independently associated with higher pCR likelihood (OR 1.75, 95% CI 1.12–2.64; < 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 in TNBC. A nomogram incorporating clinical variables, regimen, and the Ki67–PIV phenotype may provide a pragmatic approach for risk stratification, although external validation is required before broader clinical application.
[SUPPLEMENTARY INFORMATION] The online version contains supplementary material available at 10.1186/s12885-026-15842-5.