PMC9168299_01
Gadolinium-enhanced T1-weighted magnetic resonance imaging (GdT1WI) of Cases 1 and 2. Case 1: Preoperative GdT1WI reveals an enhanced cystic tumor on the right side of the midbrain tegmentum (a). Postoperative magnetic resonance imaging indicates partial resection of the tumor (b). GdT1WI obtained 15 months after the initial surgery reveals tumor regression (c). After 30 months, follow-up GdT1WI reveals regrowth of the enhanced tumor (d). GdT1WI obtained immediately after the second surgery indicates gross total tumor resection (e). GdT1WI obtained 3 years after the second surgery reveals no recurrence (f). Case 2: Preoperative GdT1WI reveals an enhanced cystic tumor on the left side of the midbrain tegmentum (g). Postoperative GdT1WI indicates subtotal resection of the tumor (h). GdT1WI obtained 2 years after the second surgery reveals no recurrence (i).
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F1
GdT1WI MRI revealed a cystic tumor with thin-wall enhancement on the left side of the midbrain tegmentum [Figure 1g]. The patient underwent subtotal tumor resection through an occipital transtentorial approach [Figure 1h]. Follow-up MRI 3 years postsurgery revealed no tumor recurrence [Figure 1i].
PMC9168299_02
Gadolinium-enhanced T1-weighted magnetic resonance imaging (GdT1WI) of Cases 1 and 2. Case 1: Preoperative GdT1WI reveals an enhanced cystic tumor on the right side of the midbrain tegmentum (a). Postoperative magnetic resonance imaging indicates partial resection of the tumor (b). GdT1WI obtained 15 months after the initial surgery reveals tumor regression (c). After 30 months, follow-up GdT1WI reveals regrowth of the enhanced tumor (d). GdT1WI obtained immediately after the second surgery indicates gross total tumor resection (e). GdT1WI obtained 3 years after the second surgery reveals no recurrence (f). Case 2: Preoperative GdT1WI reveals an enhanced cystic tumor on the left side of the midbrain tegmentum (g). Postoperative GdT1WI indicates subtotal resection of the tumor (h). GdT1WI obtained 2 years after the second surgery reveals no recurrence (i).
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F1
GdT1WI MRI revealed a cystic tumor with thin-wall enhancement on the left side of the midbrain tegmentum [Figure 1g]. The patient underwent subtotal tumor resection through an occipital transtentorial approach [Figure 1h]. Follow-up MRI 3 years postsurgery revealed no tumor recurrence [Figure 1i].
Histological findings of Case 1. Hematoxylin and Eosin (HE) staining demonstrate coexistence of glial and neurocytic components (a). Higher magnification reveals the glial component (b) and neurocytic component (c). The glial component is GFAP positive (d) and the neurocytic component is synaptophysin positive (e). HE staining of the recurrent tissue does not reveal malignant changes (f). The black bar indicates 100 um.
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F2
Cases 1 [Figure 2a-f] and 2 [Figure 3a-e] revealed similar histological findings. Hematoxylin and Eosin (HE) staining demonstrated a biphasic pattern of glial and neurocytic architecture [Figures 2a-c and 3a-c]. The former component, comprising an astrocyte-like structure, was positive for GFAP [Figure 2d and 3d], and the latter component, comprising neurocytic rosettes and perivascular pseudorosettes, was positive for synaptophysin [Figure 2e and 3e]. [Figure 2f] shows the HE staining of the recurrent tissue in Case 1 without malignant changes.
Histological findings of Case 2. Hematoxylin and Eosin staining (a-c) demonstrates glial (b) and neurocytic (c) components, confirmed by GFAP (d) and synaptophysin (e) staining, respectively. The black bar indicates 100 um.
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F3
Cases 1 [Figure 2a-f] and 2 [Figure 3a-e] revealed similar histological findings. Hematoxylin and Eosin (HE) staining demonstrated a biphasic pattern of glial and neurocytic architecture [Figures 2a-c and 3a-c]. The former component, comprising an astrocyte-like structure, was positive for GFAP [Figure 2d and 3d], and the latter component, comprising neurocytic rosettes and perivascular pseudorosettes, was positive for synaptophysin [Figure 2e and 3e]. [Figure 2f] shows the HE staining of the recurrent tissue in Case 1 without malignant changes.
Molecular analysis of Case 1 (a and b) and Case 2 (c and d). Sanger sequencing reveals FGFR1 K656E mutation (c.1966A>G, arrow) in the recurrent specimen (a), and the DNA methylation-based classification reveals flattened copy-number alterations corresponding to those of RGNT (b). Pyrosequencing reveals a mutation at the C228T of TERT promoter (c, red arrow) and the DNA methylation-based classification reveals flattened copy-number alterations corresponding to those of RGNT (d).
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F4
Molecular analysis of fresh frozen tissue from the recurrent tumor specimen revealed FGFR1 K656E mutation [Figure 4a], but no other mutations in IDH1, IDH2, BRAF, H3F3A, H3F3A, HIST1H3B, TERTp, or KIAA1549-BRAF fusion [Table 1]. The analysis of copy-number variations calculated from the DNA methylation array showed a balanced profile [Figure 4b]. Molecular analyses using the initial FFPE specimen revealed no FGFR1 mutations but revealed TERTp C228T mutation [Table 1 and Figure 4c]. The analysis of copy-number variations calculated from the DNA methylation array revealed a balanced profile [Figure 4d].