cisplatin powder (Randa / IA CALL)

Correction: Baicalin attenuates cisplatin-induced cochlear hair cell damage by modulating the ROS-p38 MAPK signaling pathway.

Zhang Qiongmin Q, Wang Yating Y, Zhang Chunhong C, Li Sisi S et al.

[This corrects the article DOI: 10.3389/fcell.2026.1742764.].

Response to the Letter to the Editor Entitled "Sodium-Glucose Cotransporter 2 Inhibitors for Cisplatin Nephrotoxicity: From Bench to Bedside, One Step at a Time".

Cintrón-García Juan J JJ, Mamlouk Omar O

Pathway Activity-Based Prognostic Risk Score Associated with Cisplatin Sensitivity in Small Cell Lung Cancer: Multi-Cohort Validation and Mechanistic Analysis.

Zhu Yaru Y, Dai Weiyuntian W, Lin Anqi A, Luo Peng P et al.

Small Cell Lung Cancer (SCLC), also referred to as small cell lung carcinoma, is a highly aggressive malignancy with a strong propensity for early metastasis. Platinum-based regimens are widely used as first-line chemotherapy; however, most patients relapse within one year, develop platinum resistance, and have poor outcomes. SCLC has few established clinically actionable driver alterations and currently lacks transcriptomic markers associated with cisplatin sensitivity that remain transportable across independent cohorts. We analyzed cisplatin drug-sensitivity data and matched transcriptomes from 39 SCLC cell lines in the Genomics of Drug Sensitivity in Cancer (GDSC2) database. Single-sample Gene Set Enrichment Analysis (ssGSEA) was used to score 236 Hallmark and Kyoto Encyclopedia of Genes and Genomes pathways. Correlation and differential analyses identified concordant pathways, yielding an eight-pathway set designated Overlap8. After prognostic validation in a local cohort (n = 45) using univariable and multivariable Cox regression, 144 model combinations were compared, and an equal-weight CoxBoost + plsRcox ensemble risk score was frozen. The unchanged model was applied to two independent external cohorts, GSE60052 and Tongji University (TU)-SCLC, followed by an external-only meta-analysis. Exploratory biological analyses used transcriptomic data from the cisplatin-resistant H446/H446DDP pair, the doxorubicin-induced non-platinum-resistant H69/H69AR control pair, and single-cell data from circulating tumor cell-derived xenografts and patient circulating tumor cells (GSE138267). All eight Overlap8 pathways were negatively correlated with the natural logarithm of the cisplatin half-maximal inhibitory concentration (ln(IC50)). In the local cohort, the univariable Hazard Ratios (HRs) for all eight pathways ranged from 0.54 to 0.65 and remained significant after adjustment for Tumor-Node-Metastasis (TNM) stage (adjusted HRs, 0.37- 0.48). The frozen risk score was independent of stage (adjusted HR = 2.61, P = 0.00067), and the bootstrap-corrected concordance index of the nomogram combining risk score and stage was 0.782, conditional on treating the previously derived risk score as fixed. Concordant prognostic associations were observed in GSE60052 (C-index = 0.694; HR per Standard Deviation (SD) = 2.13) and TU-SCLC (C-index = 0.640; HR per SD = 1.78). The meta-analysis of the two independent external cohorts yielded a pooled HR per SD of 1.87 (95% CI, 1.43-2.45), with concordant effect directions. MYC programs were downregulated in the cisplatin-resistant model but showed no concordant change in the non-platinum-resistant control. Single-cell analysis showed subtype-associated variation in MYC/proliferation activity; an exploratory samplelevel comparison of replicates from two resistant and two sensitive xenograft models yielded an unadjusted P-value of 0.72. The concordant effects across the two independent external cohorts support the prognostic relevance of coordinated MYC/proliferation-centered pathway activity beyond TNM stage. The cell-line and single-cell findings provide exploratory biological context for the coordinated MYC/proliferation signal. Because the external validation endpoint was overall survival rather than objective platinum response, predictive utility for treatment benefit cannot yet be inferred. Transcriptomic pathway activity centered on MYC/proliferation is associated with cisplatin sensitivity and overall survival in SCLC. The frozen ensemble score may support auxiliary prognostic stratification, but its ability to predict objective response or benefit from platinum-based therapy requires prospective validation in cohorts with treatment- response data.

Patient-derived organoid model for predicting chemotherapy response in patients with ampulla of Vater cancer: a prospective observational study.

Lee Hye Ji HJ, Park Sung Hee SH, Seo Hyung Il HI, Kim Dong Uk DU et al.

Ampulla of Vater cancer (AoVca) is a rare periampullary malignancy with a high recurrence rate after surgical resection and no established standard adjuvant chemotherapy. This study aimed to predict chemotherapy responses using patient-derived tumor organoids (PDTOs) from surgically resected tissues to identify an appropriate adjuvant chemotherapy regimen for AoVca patients. PDTOs were cultured from surgically resected AoVca tissues of 14 patients. Morphological and phenotypic consistency between PDTOs and primary tumors was verified using H&E and immunohistochemical staining for cytokeratin 7 and caudal-type homeobox 2. Drug sensitivity for 5-fluorouracil (5-FU), cisplatin, oxaliplatin, irinotecan, gemcitabine, and paclitaxel was assessed by comparing the IC50 values. PDTOs were successfully cultured from 11 of the 14 patients, with a phenotypic concordance rate of 82% (9 of 11). Ten PDTOs were successfully expanded for drug screening. These PDTOs showed universal resistance to cisplatin (n = 10), followed by irinotecan (n = 9) and paclitaxel (n = 8). Conversely, gemcitabine demonstrated the highest sensitivity, with resistance observed in only 1 PDTO, followed by 5-FU, which showed resistance in 4 cases. Gemcitabine was identified as the most responsive chemotherapeutic agent for AoVca based on PDTO drug screening. For combination therapy, oxaliplatin may be more appropriate than cisplatin. However, further clinical studies are required to validate these findings.