PMC8861510_01
MRI lesions in brain and spinal cord. [(A), 1-4] Head MRI shows lesions (marked with arrows) in the corpus callosum and left lateral periventricular area. T1 [(A) 1] shows a slightly low signal, while T2 [(A) 2] shows unevenly slightly high and low signals. Enhanced MRI [(A) 3-4] shows a high signal mass in the corpus callosum and left lateral periventricular area, with marked marginal enhancement and narrowing of the left lateral ventricle by compression. [(B) 1-2] Cervical spine MRI shows high-intensity signaling in the spinal cord at the C2-C7 vertebra levels and abnormal enhancement in the spinal cord at the C5-T4 vertebrae (marked with arrows).
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Brain 3T MRI [ Figure 1A  (1-4)] showed lesions in the corpus callosum and the left lateral periventricular area. Cervical-spine MRI [ Figure 1B  (1-2)] showed high-intensity signaling in the spinal cord at the C2-C7 vertebra levels and abnormal enhancement in the spinal cord at the C5-T4 vertebrae. The biopsy tissues were obtained from the corpus callosum, and the lesions are shown in brain MRI (in  Figure 1 , lesions marked with arrows).
Pulmonary artery embolisms. (A, B) Pulmonary computed tomography angiography shows multiple bilateral pulmonary artery embolisms (marked with arrows).
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A pulmonary computed tomography angiogram ( Figures 2A, B ) showed multiple bilateral pulmonary-artery embolisms.
Histopathology findings. Histopathological features of our case diagnosed as H3K27M mutant brain glioblastoma. The biopsy tissues were obtained from the corpus callosum and the lesions shown in brain MRI (in 
Figure 1A
, lesions marked with arrows). In 
Figure 3
, for x100 staining the scale bar = 5 microm and for x400 staining the scale bar = 20 microm. Hematoxylin and eosin (H&E). 
Figure 3
 [(A) 1 and 2] shows dense cell proliferation, with areas of a spindle-cell pattern and some pleomorphism, extensive mitosis, some atypical and karyomegaly, and nuclear irregularity. At approximately 40% [(A) 5: Ki67], the cell proliferation rate was high, showing positive glial fibrillary acid protein [(A) 3: GFAP]. This neoplastic lesion was positive for ATRX [(A) 4], H3K27M mutation [(B) 1-4], and H3K27me3(B5-8), while it was negative for IDH1R132H mutation [(A) 6]. Unfortunately, biopsy tissues of our patient are insufficient for further identification of H3K27me3(+) cells and for the squeezing of H3K27M and H3K27me3. Figure 3B-5 also showed positive H3k27me3 ICH staining of tonsil tissue for comparison.
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