Purpose <p>To systematically evaluate the role of <sup>18</sup>F-Fluorodeoxyglucose Positron Emission Tomography/Computed Tomography (<sup>18</sup>F-FDG PET/CT) metabolic parameters in assessing the degree of MYCN amplification status, chromosome aberrations at 1p36 and 11q23, and predicting event-free survival (EFS) in neuroblastoma patients.</p> Materials and methods <p>This retrospective cohort study included 200 pathologically confirmed neuroblastoma cases. Patients were categorized based on MYCN status (normal, gain, amplified) and chromosomal deletion patterns at 1p36 and 11q23 (normal, imbalance, deletions). Quantitative PET/CT parameters, including maximum standardized uptake value (SUVmax), mean standardized uptake value (SUVmean), metabolic tumor volume (MTV), and total lesion glycolysis (TLG) and the maximum diameter of the tumor (LEGmax) were analyzed. Diagnostic accuracy was assessed using receiver operating characteristic (ROC) curve analysis, while survival outcomes were evaluated via Kaplan–Meier (K-M) estimates and Cox proportional hazards modeling.</p> Results <p>Progressive increases in adverse prognostic biomarkers were significantly associated with higher MYCN copy number and greater severity of 1p36 and 11q23 deletions. Significant differences were observed across MYCN status categories in clinical characteristics, pathological indicators, PET/CT imaging features, and metabolic parameters. However, no significant differences were noted between the 1p36 or 11q23 imbalance and deletion groups. The MTV demonstrated superior discriminative ability for MYCN amplification and gain (AUC = 0.62, 95%CI 0.50–0.74). The K-M survival&#xa0;analysis indicated that patients with higher values of LEGmax, TLG, MTV, and bone marrow involvement (BMI) positivity exhibited significantly lower EFS compared to those with lower values. In contrast, SUVmax and SUVmean showed no significant associations with EFS. Univariate analysis identified pretreatment MTV (HR = 1.002, <i>p</i> = 0.012), TLG (HR = 1.001, <i>p</i> = 0.013), LEGmax (HR = 1.228, <i>p</i> &lt; 0.001), and bone marrow involvement (HR = 8.657, <i>p</i> = 0.003) as predictors of reduced EFS. The LEGmax parameter emerged as the independent prognostic biomarker (HR = 1.184, <i>p</i> = 0.010) for EFS.</p> Conclusion <p>Significant differences were observed in clinical features, pathological indicators, PET/CT imaging features, and metabolic parameters among the MYCN normal, MYCN gain, and MYCN amplified groups. Pre-treatment MTV effectively differentiated various degrees of MYCN amplification. Pre-treatment <sup>18</sup>F-FDG PET/CT may provide more precise risk stratification and predict prognosis in neuroblastoma.</p>

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Predictive value of 18F-FDG PET metabolic parameters for MYCN amplification, 1p36 and 11q23 chromosomal aberration, and prognosis in neuroblastoma: a nuclear medicine imaging study

  • Yu Wang,
  • Chao Wang,
  • Siqi Li,
  • Mingyu Zhang,
  • Ying Kan,
  • Wei Wang,
  • Jigang Yang

摘要

Purpose

To systematically evaluate the role of 18F-Fluorodeoxyglucose Positron Emission Tomography/Computed Tomography (18F-FDG PET/CT) metabolic parameters in assessing the degree of MYCN amplification status, chromosome aberrations at 1p36 and 11q23, and predicting event-free survival (EFS) in neuroblastoma patients.

Materials and methods

This retrospective cohort study included 200 pathologically confirmed neuroblastoma cases. Patients were categorized based on MYCN status (normal, gain, amplified) and chromosomal deletion patterns at 1p36 and 11q23 (normal, imbalance, deletions). Quantitative PET/CT parameters, including maximum standardized uptake value (SUVmax), mean standardized uptake value (SUVmean), metabolic tumor volume (MTV), and total lesion glycolysis (TLG) and the maximum diameter of the tumor (LEGmax) were analyzed. Diagnostic accuracy was assessed using receiver operating characteristic (ROC) curve analysis, while survival outcomes were evaluated via Kaplan–Meier (K-M) estimates and Cox proportional hazards modeling.

Results

Progressive increases in adverse prognostic biomarkers were significantly associated with higher MYCN copy number and greater severity of 1p36 and 11q23 deletions. Significant differences were observed across MYCN status categories in clinical characteristics, pathological indicators, PET/CT imaging features, and metabolic parameters. However, no significant differences were noted between the 1p36 or 11q23 imbalance and deletion groups. The MTV demonstrated superior discriminative ability for MYCN amplification and gain (AUC = 0.62, 95%CI 0.50–0.74). The K-M survival analysis indicated that patients with higher values of LEGmax, TLG, MTV, and bone marrow involvement (BMI) positivity exhibited significantly lower EFS compared to those with lower values. In contrast, SUVmax and SUVmean showed no significant associations with EFS. Univariate analysis identified pretreatment MTV (HR = 1.002, p = 0.012), TLG (HR = 1.001, p = 0.013), LEGmax (HR = 1.228, p < 0.001), and bone marrow involvement (HR = 8.657, p = 0.003) as predictors of reduced EFS. The LEGmax parameter emerged as the independent prognostic biomarker (HR = 1.184, p = 0.010) for EFS.

Conclusion

Significant differences were observed in clinical features, pathological indicators, PET/CT imaging features, and metabolic parameters among the MYCN normal, MYCN gain, and MYCN amplified groups. Pre-treatment MTV effectively differentiated various degrees of MYCN amplification. Pre-treatment 18F-FDG PET/CT may provide more precise risk stratification and predict prognosis in neuroblastoma.