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Adult classical glioblastoma with a BRAF V600E mutation.

Takahashi Y, Akahane T, Sawada T, Ikeda H, Tempaku A, Yamauchi S, Nishihara H, Tanaka S, Nitta K, Ide W, Hashimoto I, Kamada H - World J Surg Oncol (2015)

Bottom Line: The B-Raf proto-oncogene serine/threonine kinase (B-Raf) is a member of the Raf kinase family.BRAF V600E mutation in these cases has been canonically detected using Sanger sequencing or immunohistochemistry but not with next-generation sequencing (NGS).We report here the detection of the BRAF V600E mutation in a patient with c-GBM and describe the patient's clinical course as well as the results of histopathological analysis.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Hokuto Hospital, 7-5, Inada, Obihiro, Hokkaido, 080-0039, Japan. yosinobu@hokuto7.or.jp.

ABSTRACT
The B-Raf proto-oncogene serine/threonine kinase (B-Raf) is a member of the Raf kinase family. The BRAF V600E mutation occurs frequently in certain brain tumors such as pleomorphic xanthoastrocytoma, ganglioglioma, and pilocytic astrocytoma, and less frequently in epithelioid and giant cell glioblastoma. BRAF V600E mutation in these cases has been canonically detected using Sanger sequencing or immunohistochemistry but not with next-generation sequencing (NGS). Moreover, to our knowledge, there is no detailed report of the BRAF V600E mutation in an adult glioblastoma with classical histologic features (c-GBM). Therefore, we performed NGS analysis to determine the mutational status of BRAF of 13 glioblastomas (GBMs) (11 primary and 2 secondary cases) and detected one tumor harboring the BRAF V600E mutation. We report here the detection of the BRAF V600E mutation in a patient with c-GBM and describe the patient's clinical course as well as the results of histopathological analysis.

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Related in: MedlinePlus

Histopathological features of theBRAFV600E-positive glioblastoma. (A-D) Hematoxylin and eosin (H & E) staining. (A, D) Multiple atypical spindle cells mixed with gemistocytes. (B) Microvascular proliferation, (C) pseudopalisading, (E) GFAP positive, (F) Ki67 (index was approximately 10%), (G) EMA positive, (H) pan-cytokeratin (AE1/AE3) negative, (I) EGFR negative, (J) P53 positive, (K) IDH1 negative, and (L)BRAF V600E positive.
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Fig2: Histopathological features of theBRAFV600E-positive glioblastoma. (A-D) Hematoxylin and eosin (H & E) staining. (A, D) Multiple atypical spindle cells mixed with gemistocytes. (B) Microvascular proliferation, (C) pseudopalisading, (E) GFAP positive, (F) Ki67 (index was approximately 10%), (G) EMA positive, (H) pan-cytokeratin (AE1/AE3) negative, (I) EGFR negative, (J) P53 positive, (K) IDH1 negative, and (L)BRAF V600E positive.

Mentions: Numerous atypical spindle cells were interspersed with gemistocytes (Figure 2A, D), and microvascular proliferation and pseudopalisading were present (Figure 2B, C). Tumor cells were highly positive for glial fibrillary acidic protein (GFAP; Figure 2E), and the Ki67 index was approximately 10% (Figure 2F). Expression of cytokeratins was undetectable in EMA+ tumor cells (Figure 2G, H). Findings of tumor cells negative for epidermal growth factor receptor (EGFR) but positive for P53 are typical of secondary GBM (Figure 2I, J). Expression of the IDH1 R132H mutant or the IDH1 R132H mutation was not detected using immunohistochemistry or NGS analysis, respectively (Figure 2K). In contrast, expression of the BRAF V600E mutant was detected using immunohistochemistry, and the BRAF V600E mutation was detected using NGS (Figure 2L).Figure 2


Adult classical glioblastoma with a BRAF V600E mutation.

Takahashi Y, Akahane T, Sawada T, Ikeda H, Tempaku A, Yamauchi S, Nishihara H, Tanaka S, Nitta K, Ide W, Hashimoto I, Kamada H - World J Surg Oncol (2015)

Histopathological features of theBRAFV600E-positive glioblastoma. (A-D) Hematoxylin and eosin (H & E) staining. (A, D) Multiple atypical spindle cells mixed with gemistocytes. (B) Microvascular proliferation, (C) pseudopalisading, (E) GFAP positive, (F) Ki67 (index was approximately 10%), (G) EMA positive, (H) pan-cytokeratin (AE1/AE3) negative, (I) EGFR negative, (J) P53 positive, (K) IDH1 negative, and (L)BRAF V600E positive.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4358908&req=5

Fig2: Histopathological features of theBRAFV600E-positive glioblastoma. (A-D) Hematoxylin and eosin (H & E) staining. (A, D) Multiple atypical spindle cells mixed with gemistocytes. (B) Microvascular proliferation, (C) pseudopalisading, (E) GFAP positive, (F) Ki67 (index was approximately 10%), (G) EMA positive, (H) pan-cytokeratin (AE1/AE3) negative, (I) EGFR negative, (J) P53 positive, (K) IDH1 negative, and (L)BRAF V600E positive.
Mentions: Numerous atypical spindle cells were interspersed with gemistocytes (Figure 2A, D), and microvascular proliferation and pseudopalisading were present (Figure 2B, C). Tumor cells were highly positive for glial fibrillary acidic protein (GFAP; Figure 2E), and the Ki67 index was approximately 10% (Figure 2F). Expression of cytokeratins was undetectable in EMA+ tumor cells (Figure 2G, H). Findings of tumor cells negative for epidermal growth factor receptor (EGFR) but positive for P53 are typical of secondary GBM (Figure 2I, J). Expression of the IDH1 R132H mutant or the IDH1 R132H mutation was not detected using immunohistochemistry or NGS analysis, respectively (Figure 2K). In contrast, expression of the BRAF V600E mutant was detected using immunohistochemistry, and the BRAF V600E mutation was detected using NGS (Figure 2L).Figure 2

Bottom Line: The B-Raf proto-oncogene serine/threonine kinase (B-Raf) is a member of the Raf kinase family.BRAF V600E mutation in these cases has been canonically detected using Sanger sequencing or immunohistochemistry but not with next-generation sequencing (NGS).We report here the detection of the BRAF V600E mutation in a patient with c-GBM and describe the patient's clinical course as well as the results of histopathological analysis.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Hokuto Hospital, 7-5, Inada, Obihiro, Hokkaido, 080-0039, Japan. yosinobu@hokuto7.or.jp.

ABSTRACT
The B-Raf proto-oncogene serine/threonine kinase (B-Raf) is a member of the Raf kinase family. The BRAF V600E mutation occurs frequently in certain brain tumors such as pleomorphic xanthoastrocytoma, ganglioglioma, and pilocytic astrocytoma, and less frequently in epithelioid and giant cell glioblastoma. BRAF V600E mutation in these cases has been canonically detected using Sanger sequencing or immunohistochemistry but not with next-generation sequencing (NGS). Moreover, to our knowledge, there is no detailed report of the BRAF V600E mutation in an adult glioblastoma with classical histologic features (c-GBM). Therefore, we performed NGS analysis to determine the mutational status of BRAF of 13 glioblastomas (GBMs) (11 primary and 2 secondary cases) and detected one tumor harboring the BRAF V600E mutation. We report here the detection of the BRAF V600E mutation in a patient with c-GBM and describe the patient's clinical course as well as the results of histopathological analysis.

Show MeSH
Related in: MedlinePlus