High cerebral blood volume in human gliomas predicts deletion of chromosome 1p: Preliminary results of molecular studies in gliomas with elevated perfusion
✍ Scribed by Meng Law; Jennie E. Brodsky; James Babb; Marc Rosenblum; Douglas C. Miller; David Zagzag; Michael L. Gruber; Glyn Johnson
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 454 KB
- Volume
- 25
- Category
- Article
- ISSN
- 1053-1807
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✦ Synopsis
Abstract
Purpose
To determine if increased perfusion using dynamic susceptibility contrast perfusion MRI (DSC MRI) in gliomas may be predictive of 1p19q deletions. Loss of heterozygosity of chromosomes 1p and 19q confers responsiveness to chemotherapy improving survival in gliomas.
Materials and Methods
We retrospectively reviewed 16 patients who had DSC MRI and molecular studies of their excised gliomas for 1p19q deletions. Allelic status was assessed by loss of heterozygosity using polymerase chain reaction (PCR). DNA was extracted from paraffin curls of brain tumor sections and nail clippings. Relative cerebral blood volume (rCBV) measurements were then statistically compared with the presence of 1p and 19q deletions.
Results
Patients with 1p19q deletions (N = 7) demonstrated rCBV values of 10.54 ± 2.93. Patients without 1p deletions (N = 9) had rCBV values of 4.84 ± 2.4 (P = 0.012). Logistic regression demonstrated that rCBV was able to predict the presence of a 1p deletion to significance levels of 0.038 and 0.044, adjusted and not adjusted for age and sex, respectively. The kappa coefficient for the agreement between predicted deletion status using rCBV and the truedeletion status was 0.746 (P = 0.0028). Deletions of 19q alone, or together with 1p deletions, were not associated with high rCBV.
Conclusion
Histopathologic, molecular, and imaging evidence supports increased neovascularity in gliomas with 1p deletions in this preliminary study. We propose a diagnostic algorithm to obtain molecular studies in gliomas demonstrating high rCBV. J. Magn. Reson. Imaging 2007;25:1113–1119. © 2007 Wiley‐Liss, Inc.