Download Abstract - Cancer Imaging Archive Wiki

Presentation Abstract
Title:
O-289 - Associations between Genomic Features and Quantitative Histogram
Analysis of Diffusion and Diffusion Tensor Imaging of Glioblastomas: A TCGA
Glioma Phenotype Research Group Project
Keywords: Glioblastoma; diffusion; brain tumor
Authors:
Hwang, S. N.1·Holder, C. A.1·Desai, H.1·Clifford, R.2·Huang, E.2·Hammoud,
D.3·Wintermark, M.4·Colen, R. R.5·Jain, R.6·Freymann, J.7·Flanders, A.8·TCGA
Glioma Phenotype Research Group
1
Emory University School of Medicine, Atlanta, GA, 2National Cancer Institute,
Bethesda, MD, 3National Institute of Health, Bethesda, MD, 4University of
Virginia, Charlotteville, VA, 5Brigham and Womens Hospital, Boston, MA, 6Henry
Ford Health System, Detroit, MI, 7SAIC-Frederick, Inc., Frederick, VA, 8Thomas
Jefferson University Hospital, Philadelphia, PA.
Abstract
Body:
Purpose
Investigate associations between genomic features and quantitative parameters
derived by histogram analysis of diffusion and diffusion tensor imaging of
glioblastomas.
Materials & Methods
As part of The Cancer Genome Atlas (TCGA) MRI characterization project of the
National Cancer Institute, the multiinstitutional TCGA Glioma Phenotype Research
Group has been investigating MRI, including diffusion imaging and diffusion
tensor imaging, as a means of predicting the genomic features of glioblastomas. For
the current work, quantitative histogram analysis was performed on apparent
diffusion coefficient (ADC) and fractional anisotropy (FA) maps for correlation
with genomic features. Small, noninclusive regions of interest (ROI) were selected
manually within cerebrospinal fluid (CSF), normal-appearing corpus callosum
(usually splenium but placed in the genu if tumor involved the splenium), and
normal-appearing white matter (centrum semiovale) to obtain characteristic values
for these sites. Voxel ADC and FA values were normalized by the characteristic
values measured in the ROIs. The volume of tumor was defined on the basis of the
b = 0 diffusion image by application of an Otsu thresholding method using the NIH
ImageJ software. Mean, median, standard deviation, skew, and kurtosis of the
normalized ADC and FA histograms were computed from voxels within tumor.
Tumor volume also was computed. The diffusion histogram analysis has been
performed on 39 of the TCGA glioblastomas at the time current time. Eighteen of
these data sets also included DTI. Genomic features of the tumors were obtained
from TCGA’s publicly available information (TCGA, Nature 455:1061, 2008),
including mutation status (presence versus absence of a gene mutation) for the
TP53, PTEN, EGFR, NF1, and IDH1 genes. On the basis of copy number data,
subgroups were identified, including tumors with high-level EGFR gene
amplification, high-level PDGFRA amplification, homozygous deletions of
CDKN2A, and deletions of NF1.
Student’s t-test was applied for statistical analysis.
Results
Tumors with a TP53 mutation were found to have lower ADC normalized by CSF
(p = 0.037, mean 34 versus 40). Tumors with high EGFR amplification
demonstrated histograms with a narrowed distribution of FA normalized by the
corpus callosum as demonstrated by decreased standard deviation (p = 0.027).
Tumors with PDGRFA amplification demonstrated significant broadening of the
ADC histogram normalized by CSF as demonstrated by increased standard
deviation (p = 0.03). Tumors with PDGRFA amplification also demonstrated
decreased FA normalized by white matter (p = 0.037, mean 36 versus 48; p = 0.03,
median 32 versus 44). Tumors with CDKN2A homozygous deletion demonstrated
a small but statistically significant increase in ADC normalized by the corpus
callosum compared to tumors without the deletion (p = 0.05, median 38.5 versus
37.0).
Conclusion
Quantitative histogram analysis of ADC and FA maps may provide a noninvasive
means of predicting genomic features of tumors. This information may be helpful in
predicting outcomes and tailoring treatment.
American Society of Neuroradiology
2210 Midwest Road, Suite 207
Oak Brook, IL 60523-8205
Phone: (630) 574-0220
Fax: (630) 574-1740