PMC10267364_01
(A, B) Non-contrast computed tomography imaging in April 2016 before the resection surgery. It demonstrates an expansive lesion on the right temporal lobe (A), associated with moderate oedema and compression of surrounding structures (B), including left deviation of the midline. (C-G) Histopathological analysis of tumor sample. Sections were stained with H&E (C) and display high cellularity. Scale bar: 100 mm. (D) Immunostaining for GFAP showing abundance of glial marker. Scale bar: 60 mm. (E) Sections were stained with H&E and arrowheads show examples of mitotic figures. Scale bar: 30 mm. (F) Using H&E staining, asterisk indicate the tumor necrotic center. Scale bar: 100 mm. (G) Using H&E staining, arrows point to abnormal microvascular proliferation. Scale bar: 40 mm. (H-K) MRI six months after the resection surgery in October 2016. Axial FLAIR (H), Axial T2-weighted (I), and axial post-contrast T1-weighted (J) images demonstrate surgical manipulation on the right temporal lobe. No enhancing or expansive lesions are seen. Axial r-CBV map (K) does not show areas of hyperperfusion. (L-N) MRI in May 2022. Axial FLAIR (L), and axial post-contrast T1-weighted images (M) demonstrate surgical manipulation on the right temporal lobe. No enhancing or expansive lesions are seen. Axial r-CBV map (N) does not show areas of hyperperfusion.
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F1
Imaging identified an expansive lesion associated with edema in the right temporal lobe, causing compression and midline deviation suggesting a brain tumor (Figures 1A, B). Histopathology confirmed the tumor as glioblastoma (Figures 1C-G). Six months after the surgery, the brain's magnetic resonance imaging (MRI) showed no evidence of tumor recurrence (Figures 1H-K). Two years and five months after the tumor resection, the patient was diagnosed with a brain aneurysm on the left hemisphere, contralateral to the previous glioblastoma lesion, and submitted to a microsurgical clipping (Supplementary Figures 1, 2). Since then, the patient has been followed up with MRI every 6 months without tumor recurrence (Figures 1L-N).
(A, B) Genetic alterations in Next Generation Sequencing. IDH1 and IDH2 genes had no Single Nucleotide Variation detected. (C) Positive neutralizing antibodies against ZIKV and DENV1. DENV (four serotypes) and ZIKV were tested with the patient's serum samples. Titers were calculated using the serum ability to reduce 90% of plaque number, compared to controls (using different virus). The cut-off used is 30. DENV1 and ZIKV presented similar neutralizing antibodies titers. Because of flavivirus classic cross-reaction, it is possible to conclude that the patient has flavivirus neutralizing antibodies. (D) Positive IgG antibodies against DENV detected by MAC-ELISA.
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F2
Throughput Sequencing identified that the tumor bears wild-type copies for IDH1 and IDH2 with mutations in oncogenes such as PIK3CA, clinically associated with patients who develop glioblastoma at a young age and poor survival prognosis (Figures 2A, B). The PRNT resulted in a cross-reaction between DENV and ZIKV antibodies (Figure 2C). In contrast, ELISA revealed that the patient is positive for DENV and negative for ZIKV and CHIKV IgG antibodies (Figure 2D). Two years and five months after the tumor resection, the patient was diagnosed with a brain aneurysm on the left hemisphere, contralateral to the previous glioblastoma lesion, and submitted to a microsurgical clipping (Supplementary Figures 1, 2).