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Gunes Orman, Matthias W. Wagner, Daniel Seeburg, Carlos A. Zamora, Alexander Oshmyansky, Aylin Tekes, Andrea Poretti, George I. Jallo, Thierry A. G. M. Huisman, and Thangamadhan Bosemani

OBJECT

The authors compared the efficacy of combining 2D+3D CT reconstructions with standard 2D CT images in the diagnosis of linear skull fractures in children with head trauma.

METHODS

This was a retrospective evaluation of consecutive head CT studies of children presenting with head trauma. Two experienced pediatric neuroradiologists in consensus created the standard of reference. Three readers independently evaluated the 2D CT images alone and then in combination with the 3D reconstructions for the diagnosis of linear skull fractures. Sensitivity and specificity in the diagnosis of linear skull fractures utilizing 2D and 2D+3D CT in combination were measured for children less than 2 years of age and for all children for analysis by the 3 readers.

RESULTS

Included in the study were 250 consecutive CT studies of 250 patients (167 boys and 83 girls). The mean age of the children was 7.82 years (range 4 days to 17.4 years). 2D+3D CT combined had a higher sensitivity and specificity (83.9% and 97.1%, respectively) compared with 2D alone (78.2% and 92.8%, respectively) with statistical significance for specificity (p < 0.05) in children less than 2 years of age. 2D+3D CT combined had a higher sensitivity and specificity (81.3% and 90.5%, respectively) compared with 2D alone (74.5% and 89.1%, respectively) with statistical significance for sensitivity (p < 0.05) in all children.

CONCLUSIONS

In this study, 2D+3D CT in combination showed increased sensitivity in the diagnosis of linear skull fractures in all children and increased specificity in children less than 2 years of age. In children less than 2 years of age, added confidence in the interpretation of fractures by distinguishing them from sutures may have a significant implication in the setting of nonaccidental trauma. Furthermore, 3D CT is available at no added cost, scan time, or radiation exposure, providing trainees and clinicians with limited experience an additional valuable tool for routine imaging of pediatric head trauma.

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Louise Stögbauer, Christian Thomas, Andrea Wagner, Nils Warneke, Eva Christine Bunk, Oliver Grauer, Julian Canisius, Werner Paulus, Walter Stummer, Volker Senner, and Benjamin Brokinkel

OBJECTIVE

Chemotherapeutic options for meningiomas refractory to surgery or irradiation are largely unknown. Human telomerase reverse transcriptase (hTERT) promoter methylation with subsequent TERT expression and telomerase activity, key features in oncogenesis, are found in most high-grade meningiomas. Therefore, the authors investigated the impact of the demethylating agent decitabine (5-aza-2′-deoxycytidine) on survival and DNA methylation in meningioma cells.

METHODS

hTERT promoter methylation, telomerase activity, TERT expression, and cell viability and proliferation were investigated prior to and after incubation with decitabine in two benign (HBL-52 and Ben-Men 1) and one malignant (IOMM-Lee) meningioma cell line. The global effects of decitabine on DNA methylation were additionally explored with DNA methylation profiling.

RESULTS

High levels of TERT expression, telomerase activity, and hTERT promoter methylation were found in IOMM-Lee and Ben-Men 1 but not in HBL-52 cells. Decitabine induced a dose-dependent significant decrease of proliferation and viability after incubation with doses from 1 to 10 μM in IOMM-Lee but not in HBL-52 or Ben-Men 1 cells. However, effects in IOMM-Lee cells were not related to TERT expression, telomerase activity, or hTERT promoter methylation. Genome-wide methylation analyses revealed distinct demethylation of 14 DNA regions after drug administration in the decitabine-sensitive IOMM-Lee but not in the decitabine-resistant HBL-52 cells. Differentially methylated regions covered promoter regions of 11 genes, including several oncogenes and tumor suppressor genes that to the authors' knowledge have not yet been described in meningiomas.

CONCLUSIONS

Decitabine decreases proliferation and viability in high-grade but not in benign meningioma cell lines. The effects of decitabine are TERT independent but related to DNA methylation changes of promoters of distinct tumor suppressor genes and oncogenes.