Adult cerebellar glioblastoma cases have different characteristics from supratentorial glioblastoma

Utsuki, Satoshi; Oka, Hiroyuki; Miyajima, Yoshiteru; Kijima, Chihiro; Yasui, Yoshie; Fujii, Kiyotaka

doi:10.1007/s10014-011-0070-0

Cited by 38 publications

(46 citation statements)

References 19 publications

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“…The wild-type of the IDH1 gene was detected in all five cases. In addition, Utsuki et al (27) detected wild-type IDH1 in all four cerebellar GBMs they examined by immunostaining. These results contradict the hypothesis that cerebellar GBMs are of the secondary type.…”

Section: Discussionmentioning

confidence: 98%

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Clinical characteristics and pathogenesis of cerebellar glioblastoma

Takahashi

Makino

Nakamura

et al. 2014

Molecular Medicine Reports

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Abstract. Cerebellar glioblastomas (GBMs) are rare, with neither their pathogenesis nor prognosis being completely understood. The present study aimed to clarify the clinical characteristics of cerebellar GBMs by comparison with supratentorial GBMs, focusing particularly on the pathogenesis. The clinical factors between cerebellar (n=10) and supratentorial (n=216) GBMs were compared. Additionally, p53 and epidermal growth factor receptor (EGFR) levels were investigated in six patients by immunostaining as well as the isocitrate dehydrogenase 1 (IDH1) status of five patients by direct sequencing. Eight males and two females participated in the present study, the mean age at diagnosis was 56.6 years and the range 37-75 years. Four patients presented with hydrocephalus and one with brainstem involvement, and two patients were diagnosed with neurofibromatosis type 1. Two patients had previously received radiotherapy, eight patients received postoperative radiotherapy and seven chemotherapy. The mean Karnofsky performance status (KPS) score was lower in patients with cerebellar GBMs compared to those with supratentorial GBM; however, the survival times did not differ between the two groups. All of the cases of six cerebellar GBMs were p53-positive and EGFR-negative, as detected by immunostaining, consistent with secondary GBM. However, no IDH1 mutations were detected in any of the five cases of cerebellar GBMs analyzed, indicating that these tumors were not of the secondary type. The KPS score with cerebellar GBMs may be lower due to hydrocephalus, which was ameliorated by surgery but may have impacted the survival rate. It was confirmed that cerebellar GBMs were identical to supratentorial GBMs with respect to its clinical features, with the possible exception of the KPS score. The present study's genetic analyses indicated that cerebellar GBMs may develop via a pathway different from that of either primary or secondary GBM.

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Section: Discussionmentioning

confidence: 98%

“…Returning to the original topic of cerebellar GBM, Utsuki et al (27) reported that all four cerebellar GBMs they encountered were p53-positive and EGFR-negative by immunostaining. Saito et al (28) identified that all of the seven cerebellar GBMs they examined were EGFR-negative, and six out of the seven were p53-positive.…”

Section: Discussionmentioning

confidence: 99%

Clinical characteristics and pathogenesis of cerebellar glioblastoma

Takahashi

Makino

Nakamura

et al. 2014

Molecular Medicine Reports

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“…Our current investigation has the limitations of a solitary GBM used for analysis and therefore these same studies should be applied to great number of glial neoplasms from a variety of locations [36,37]. However, lectins can be used as recognition tools for these glycan markers that are located on the surface of cells, allowing easy access for cell sorting, culturing, and harvesting of a specific cell population.…”

Section: Discussionmentioning

confidence: 99%

Lectins Identify Glycan Biomarkers on Glioblastoma-Derived Cancer Stem Cells

Tucker-Burden

Chappa

Krishnamoorthy³

et al. 2012

Stem Cells and Development

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Glioblastoma (GBM) is a highly aggressive primary brain tumor with a poor prognosis. Despite aggressive therapy with surgery, radiotherapy, and chemotherapy, nearly all patients succumb to disease within 2 years. Several studies have supported the presence of stem-like cells in brain tumor cultures that are CD133-positive, are capable of self-renewal, and give rise to all cell types found within the tumor, potentially perpetuating growth. CD133 is a widely accepted marker for glioma-derived cancer stem cells; however, its reliability has been questioned, creating a need for other identifiers of this biologically important subpopulation. We used a panel of 20 lectins to identify differences in glycan expression found in the glycocalyx of undifferentiated gliomaderived stem cells and differentiated cells that arise from them. Fluorescently labeled lectins that specifically recognize a-N-acetylgalactosamine (GalNAc) and a-N-acetylglucosamine (GlcNAc) differentially bound to the cell surface based on the state of cellular differentiation. GalNAc and GlcNAc were highly expressed on the surface of undifferentiated cells and showed markedly reduced expression over a 12-day duration of differentiation. Additionally, the GalNAc-recognizing lectin Dolichos biflorus agglutinin was capable of specifically selecting and sorting glioma-derived stem cell populations from an unsorted tumor stock and this subpopulation had proliferative properties similar to CD133+ cells in vitro and also had tumor-forming capability in vivo. Our preliminary results on a single cerebellar GBM suggest that GalNAc and GlcNAc are novel biomarkers for identifying glioma-derived stem cells and can be used to isolate cancer stem cells from unsorted cell populations, thereby creating new cell lines for research or clinical testing.

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“…They may occur in the spinal cord but arise more frequently in the brain (Ostrom et al, 2014b). Their topology can be either supratentorial (thus above the tentorium cerebelli) or infratentorial (Utsuki et al, 2012). According to the predominant cell type, gliomas can be classified into four main categories: astrocytomas arose from astrocytes, oligodendrogliomas arose from oligodendrocytes, ependymomas developed from ependymal cells, and mixed gliomas such as oligoastrocytomas (Louis et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Overview of Transforming Growth Factor β Superfamily Involvement in Glioblastoma Initiation and Progression

Nana¹,

Yang²,

Lin³

2015

Asian Pacific Journal of Cancer Prevention

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Glioblastoma, also known as glioblastoma multiforme (GBM), is the most aggressive of human brain tumors and has a stunning progression with a mean survival of one year from the date of diagnosis. High cell proliferation, angiogenesis and/or necrosis are histopathological features of this cancer, which has no efficient curative therapy. This aggressiveness is associated with particular heterogeneity of the tumor featuring multiple genetic and epigenetic alterations, but also with implications of aberrant signaling driven by growth factors. The transforming growth factor β (TGFβ) superfamily is a large group of structurally related proteins including TGFβ subfamily members Nodal, Activin, Lefty, bone morphogenetic proteins (BMPs) and growth and differentiation factor (GDF). It is involved in important biological functions including morphogenesis, embryonic development, adult stem cell differentiation, immune regulation, wound healing and inflammation. This superfamily is also considered to impact on cancer biology including that of GBM, with various effects depending on the member. The TGFβ subfamily, in particular, is overexpressed in some GBM types which exhibit aggressive phenotypes. This subfamily impairs anti-cancer immune responses in several ways, including immune cells inhibition and major histocompatibility (MHC) class I and II abolishment. It promotes GBM angiogenesis by inducing angiogenic factors such as vascular endothelial growth factor (VEGF), plasminogen activator inhibitor (PAI-I) and insulinlike growth factor-binding protein 7 (IGFBP7), contributes to GBM progression by inducing metalloproteinases (MMPs), "pro-neoplastic" integrins (αvβ3, α5β1) and GBM initiating cells (GICs) as well as inducing a GBMmesenchymal phenotype. Equally, Nodal promotes GICs, induces cancer metabolic switch and supports GBM cell proliferation, but is negatively regulated by Lefty. Activin promotes GBM cell proliferation while GDF yields immune-escape function. On the other hand, BMPs target GICS and induce differentiation and sensitivity to chemotherapy. This multifaceted involvement of this superfamily in GBM necessitates different strategies in anti-cancer therapy. While suppressing the TGFβ subfamily yields advantageous results, enhancing BMPs production is also beneficial.

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Adult cerebellar glioblastoma cases have different characteristics from supratentorial glioblastoma

Cited by 38 publications

References 19 publications

Clinical characteristics and pathogenesis of cerebellar glioblastoma

Clinical characteristics and pathogenesis of cerebellar glioblastoma

Lectins Identify Glycan Biomarkers on Glioblastoma-Derived Cancer Stem Cells

Overview of Transforming Growth Factor β Superfamily Involvement in Glioblastoma Initiation and Progression

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