Background/Objectives: Triple-negative breast cancer (TNBC) is a highly aggressive subtype with limited therapeutic options, and identifying reliable biomarkers for diagnosis and prognosis is crucial for improving patient outcomes. Mitochondrial DNA (mtDNA) copy number has been linked to an increased risk of developing various types of cancer, including breast cancer. However, there is a lack of understanding regarding how mtDNA copy number variations may influence the development and progression of TNBC. Methods: This study investigated mtDNA copy number in TNBC tumors and corresponding normal breast tissues from 23 TNBC patients who received neoadjuvant chemotherapy. The relative mtDNA copy number was estimated using quantitative PCR for the NADH dehydrogenase subunit 1 (ND1) and subunit 5 (ND5) regions. Results: The results showed a significant decrease in mtDNA copy number in TNBC tumor tissues compared to corresponding normal breast tissue. However, no significant correlation was found between mtDNA content and clinical parameters such as age, tumor size, or chemotherapy response. Conclusions: These results suggest that while mtDNA content decreases in TNBC tumors, it may not directly influence these clinical characteristics. Despite some inconsistencies in the literature regarding mtDNA dynamics in cancer, this study supports the potential of mtDNA as a biomarker for TNBC. Larger cohort studies are needed to further validate these results and explore the role of mtDNA in guiding personalized treatment strategies for TNBC patients.

Purpose: Vancomycin therapeutic drug monitoring is essential for optimizing efficacy and reducing the risk of vancomycin-associated acute kidney injury (VA-AKI). Although recent guidelines recommend the ratio of area under the curve over 24 h to minimum inhibitory concentration (AUC ₂₄ /MIC)–based monitoring over trough concentration-based monitoring, differences between AUC ₂₄ /MIC estimation methods (e.g., pharmacokinetic equations and Bayesian approaches) may influence therapeutic classification in clinical practice. In addition, pharmacogenetic factors contributing to interindividual variability in vancomycin exposure remain incompletely characterized. Methods: This prospective, single-center cohort study included adult patients who received intravenous vancomycin for at least 72 h between June 2024 and April 2025. Vancomycin trough and peak plasma concentrations were measured using an enzyme-linked immunosorbent assay. AUC ₂₄ /MIC values were calculated using pharmacokinetic equation and Bayesian method. Agreement in therapeutic classification between trough concentration–based and AUC ₂₄ /MIC-based monitoring was assessed. Associations between the rs2789047 genetic variant and relevant parameters were also evaluated. Results: Thirty-six patients were included, of whom 38.9% developed VA-AKI. Despite strong correlations between trough concentration and AUC ₂₄ /MIC values ( r = 0.84–0.87), substantial discordance in therapeutic classification was observed, with agreement rates of 63.9% for pharmacokinetic equation-based and 66.7% for Bayesian-based compared with trough concentration-based monitoring. In contrast, pharmacokinetic equation-based and Bayesian-based methods demonstrated strong concordance (86.1%). Higher trough concentrations and AUC ₂₄ /MIC values were significantly associated with VA-AKI ( p < 0.001). Carriers of rs2789047 A-allele exhibited higher trough concentrations and reduced elimination rates. Conclusion: Trough concentration-based monitoring frequently misclassified vancomycin exposure compared with AUC ₂₄ /MIC–based approaches. Pharmacogenetic variability may further influence vancomycin exposure.

Objective: Gastric cancer is the second leading cause of cancer-related death worldwide. 5-Fluorouracil (5-FU) is one of the most commonly used drugs to treat cancer, but 5-FU and its forms are characterized by wide inter-individual pharmacokinetic variability. ABCC5 and ABCC11 are members of the ABC transporter superfamily and play a role in the efflux of antineoplastic drugs like 5-FU. Methods: The influence of two SNPs in ABCC5 (rs562, T>C) and ABCC11 (rs17822931, G>A) was evaluated based on the pharmacokinetics and toxicity of 5-FU in HER2-negative advanced gastric cancer patients treated with cisplatin and 5-FU (n=18). The genetic variants and plasma 5-FU concentrations were detected by RT-PCR and HPLC, respectively. Results: There was no statistically significant difference between 5-FU AUC0-96 h values and ABCC5 (rs562; T>C), 21.04 ±3.46 vs 16.65 μg.h/mL, p=0,261) and ABCC11 (rs17822931; G>A), 17.04 ±4.39 vs 54 ±3.79 mg.h/L, p=0,564) variants. Similarly, there were no statistically significant differences between the variants and the most frequently observed side effects of diarrhea and mucositis. Conclusion: We recommend investigating the noted SNPs more precisely in a larger study population with more comprehensive evaluation.