Differential diagnosis of small cell glioblastoma and anaplastic oligodendroglioma: a case report of an elderly man

Takahashi, Keiichi; Tsuda, Masumi; Kanno, Hiromi; Murata, Junko; Mahabir, Roshan; Ishida, Yusuke; Kimura, Taichi; Tanino, Mishie; Nishihara, Hiroshi; Nagashima, Kazuo; Tanaka, Shinya

doi:10.1007/s10014-013-0158-9

Cited by 5 publications

(4 citation statements)

References 13 publications

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“…Suppression of PTEN and activation of the PI3K/AKT/mTOR pathway is an established oncogenic driver (438). Deletion of PTEN induces many types of cancers, including human liver cancer (79), bladder cancer (93), prostate cancer (34,89,635), glioblastoma (152,539), gastric and colorectal cancer (86,441), urothelial carcinoma (454), pleural mesothelioma (5), thyroid cancer (567), cholangiocarcinoma (624), and endometrial cancer (337). Indeed, PTEN mutations are among the most frequently found genetic changes associated with cancer (471).…”

Section: Genetic Manipulation Of Regenerationmentioning

confidence: 99%

Spinal Cord Regeneration

Young

2014

Cell Transplant

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Three theories of regeneration dominate neuroscience today, all purporting to explain why the adult central nervous system (CNS) cannot regenerate. One theory proposes that Nogo, a molecule expressed by myelin, prevents axonal growth. The second theory emphasizes the role of glial scars. The third theory proposes that chondroitin sulfate proteoglycans (CSPGs) prevent axon growth. Blockade of Nogo, CSPG, and their receptors indeed can stop axon growth in vitro and improve functional recovery in animal spinal cord injury (SCI) models. These therapies also increase sprouting of surviving axons and plasticity. However, many investigators have reported regenerating spinal tracts without eliminating Nogo, glial scar, or CSPG. For example, many motor and sensory axons grow spontaneously in contused spinal cords, crossing gliotic tissue and white matter surrounding the injury site. Sensory axons grow long distances in injured dorsal columns after peripheral nerve lesions. Cell transplants and treatments that increase cAMP and neurotrophins stimulate motor and sensory axons to cross glial scars and to grow long distances in white matter. Genetic studies deleting all members of the Nogo family and even the Nogo receptor do not always improve regeneration in mice. A recent study reported that suppressing the phosphatase and tensin homolog (PTEN) gene promotes prolific corticospinal tract regeneration. These findings cannot be explained by the current theories proposing that Nogo and glial scars prevent regeneration. Spinal axons clearly can and will grow through glial scars and Nogo-expressing tissue under some circumstances. The observation that deleting PTEN allows corticospinal tract regeneration indicates that the PTEN/AKT/mTOR pathway regulates axonal growth. Finally, many other factors stimulate spinal axonal growth, including conditioning lesions, cAMP, glycogen synthetase kinase inhibition, and neurotrophins. To explain these disparate regenerative phenomena, I propose that the spinal cord has evolved regenerative mechanisms that are normally suppressed by multiple extrinsic and intrinsic factors but can be activated by injury, mediated by the PTEN/ AKT/mTOR, cAMP, and GSK3b pathways, to stimulate neural growth and proliferation.

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Section: Genetic Manipulation Of Regenerationmentioning

confidence: 99%

Spinal Cord Regeneration

Young

2014

Cell Transplant

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“…Clinically, in the early stage, glioblastoma is difficult to diagnose, due to its non-specific clinical features and its rapidly worsening symptoms [ 13 ]. One of the most significant diagnoses on glioblastoma is the recognition and distinction of primary glioblastoma from the secondary ones, due to their distinct pathological characteristics [ 14 ]. However, distinguishing the two pathological groups using only traditional clinical testing methods, including Magnetic Resonance Imaging (MRI), is challenging [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

“…One of the most significant diagnoses on glioblastoma is the recognition and distinction of primary glioblastoma from the secondary ones, due to their distinct pathological characteristics [ 14 ]. However, distinguishing the two pathological groups using only traditional clinical testing methods, including Magnetic Resonance Imaging (MRI), is challenging [ 14 ]. Under such circumstances, the genetic background of such subgroup of glioblastomas has been introduced to perform differential diagnosis.…”

Section: Introductionmentioning

confidence: 99%

Identification of the Gene Expression Rules That Define the Subtypes in Glioma

Cai

Zhang

et al. 2018

JCM

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As a common brain cancer derived from glial cells, gliomas have three subtypes: glioblastoma, diffuse astrocytoma, and anaplastic astrocytoma. The subtypes have distinctive clinical features but are closely related to each other. A glioblastoma can be derived from the early stage of diffuse astrocytoma, which can be transformed into anaplastic astrocytoma. Due to the complexity of these dynamic processes, single-cell gene expression profiles are extremely helpful to understand what defines these subtypes. We analyzed the single-cell gene expression profiles of 5057 cells of anaplastic astrocytoma tissues, 261 cells of diffuse astrocytoma tissues, and 1023 cells of glioblastoma tissues with advanced machine learning methods. In detail, a powerful feature selection method, Monte Carlo feature selection (MCFS) method, was adopted to analyze the gene expression profiles of cells, resulting in a feature list. Then, the incremental feature selection (IFS) method was applied to the obtained feature list, with the help of support vector machine (SVM), to extract key features (genes) and construct an optimal SVM classifier. Several key biomarker genes, such as IGFBP2, IGF2BP3, PRDX1, NOV, NEFL, HOXA10, GNG12, SPRY4, and BCL11A, were identified. In addition, the underlying rules of classifying the three subtypes were produced by Johnson reducer algorithm. We found that in diffuse astrocytoma, PRDX1 is highly expressed, and in glioblastoma, the expression level of PRDX1 is low. These rules revealed the difference among the three subtypes, and how they are formed and transformed. These genes are not only biomarkers for glioma subtypes, but also drug targets that may switch the clinical features or even reverse the tumor progression.

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“…In this study, we also focused on the prognostic research for small cell astrocytoma/GBM for the reason that it shares some similar features with embryonal tumors. The cytogenetical investigations for IDH1/2 mutation, 1p/19q loss, and PTEN alteration are strongly supportive methods for the differential diagnosis of small cell GBM [8]. PTEN also represents a putative tumor suppressor gene in MB because loss of PTEN function would contribute to an over-activation of the PI3K/AKT signaling pathway, which is activated in MB [9].…”

Section: Introductionmentioning

confidence: 99%

A prognostic analysis of pediatrics central nervous system small cell tumors: evaluation of EGFR family gene amplification and overexpression

Liu

Zhang

et al. 2014

Diagn Pathol

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BackgroundCentral nervous system (CNS) tumors are the most common solid tumors that occur in children, however there were few big-data follow-up analysis published in China. Overexpression of epidermal growth factor receptor (EGFR) family members was reported on glioblastoma (GBM) and medulloblastoma (MB) before. However, the correlation between EGFR family members expression with prognosis of MB, supratentorial primitive neuroectodermal tumor (PNET) and small cell GBM is unclear in Chinese children.MethodsA retrospective and survival analysis was performed on children (age ≤ 16 years) diagnosed as CNS primary small cell tumors in the Affiliated Provincial Hospital, Shandong University from 2000 to 2012, including MB (n = 44), PNET (n = 8) and small cell GBM (n = 19). The expression of EGFR, ERBB-2, ERBB-3 and ERBB-4 were detected by immunohistochemistry (IHC). The fluorescence in situ hybridization (FISH) was used to observe the amplification of EGFR and ERBB-2 gene.ResultsMedian survival times of MBs, small GBMs and PNETs were 23 ± 6.7 months, 8 ± 4.7 months and 10 ± 1.4 months. Expression and amplification of ERBB-2, ERBB-3 and ERBB-4 were not observed in all tumor samples. The multiply Cox regression suggested the overexpression and amplification of EGFR were negative prognostic factors for MB. Radiotherapy had the positive function for all pediatric patients.ConclusionOverexpression of EGFR predicts poor outcomes of MBs, small cell GBMs and PNETs, suggesting those three CNS tumor subtypes can be considered as one group for the potential common mechanism. The current individual treatment and big data analysis of pediatric CNS embryonal tumors and GBM continues to be very challenging in China.Virtual SlidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/7649640001237474

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Differential diagnosis of small cell glioblastoma and anaplastic oligodendroglioma: a case report of an elderly man

Cited by 5 publications

References 13 publications

Spinal Cord Regeneration

Spinal Cord Regeneration

Identification of the Gene Expression Rules That Define the Subtypes in Glioma

A prognostic analysis of pediatrics central nervous system small cell tumors: evaluation of EGFR family gene amplification and overexpression

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