Presentation
Known glioblastoma, biopsied via a burr hole with tumor progression despite Stupp protocol.
Patient Data
Known glioblastoma, biopsied via burr hole, located in the white matter of the posterior left frontal and left parietal lobes. It demonstrates marked increase in the degree of related intra-axial enhancement compared to the previous study (not shown).
Patchy enhancement extends from the medial margin of the lesion into the splenium of the corpus callosum where it is associated with fairly low in ADC values, tumoral trace on spectroscopy and markedly increased relative cerebral blood volume.
The mass is surrounded by extensive vasogenic edema extending into the left frontal and left parietal white matter as well as the insula and posterior limb left internal capsule.
Conclusion: Progression of high-grade tumor.
The enhancing component of the left parietal tumor has reduced in size. The punctate foci of subependymal enhancement and the expansile T2 hyperintensity along the splenium of the corpus callosum are unchanged. The previously seen vasogenic edema surrounding the tumor has markedly improved.
The tumor again demonstrates a rim of low ADC values, with persistently elevated cerebral blood volume. MR spectroscopy again demonstrates markedly elevated choline within the enhancing tumor and moderately elevated choline in the non-enhancing T2 hyperintense region. Of note, there is also elevated choline in the regions that are no longer T2 hyperintense.
Small areas of blood product (intrinsic high T1 signal).
Conclusion: The reduction of vasogenic edema and enhancement is likely due to bevacizumab-mediated change in blood-brain barrier permeability. The actual size of the viable tumor (based on the diffusion imaging, perfusion characteristics, and spectroscopy finding) has only modestly reduced. Overall, appearances are dominated by pseudoresponse.
Case Discussion
Histology
This histology is from the original biopsy (prior to the first study shown).
Sections show pieces of a moderately cellular diffusely infiltrating tumor. The tumor cells are enlarged and pleomorphic, with angulated nuclei, relatively fine chromatin and a central nucleolus. In some areas there appears to be some perinuclear clearing, while in other areas the tumor has a microcystic appearance. There are plentiful calcifications. Mitoses are not seen. There is no necrosis or microvascular proliferation.
Immunohistochemistry
GFAP: positive
OLIG2: positive
IDH1 R132H: negative (not mutated)
ATRX: positive (not mutated)
p53: mosaic (probably not mutated)
p16: positive
Ki67: 1-2%
BRAF V600E: negative
Synaptophysin: negative
NFP: negative
NeuN: negative I
Next-genereation sequencing
1p/19q codeletion: Not detected
EGFRamplification: Not detected
IDH1codon 132: No pathogenic variant detected
IDH2codon 172: No pathogenic variant detected
BRAFcodon 600: No pathogenic variant detected
H3F3Acodons 27 and 34: No pathogenic variant detected
TERTpromoter Chr5:1295228 (C228T) and chr5:1295250 (C250T): PATHOGENIC VARIANT DETECTED
Final diagnosis
Glioblastoma (IDH-wildtype).
Discussion
This case demonstrates the profound blood-brain-barrier reconstitution effects of bevacizumab that can result in a dramatic reduction in edema and enhancement without necessarily having an actual treatment effect on the tumor. This is best appreciated on rCBV and ADC.
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