Browsing by Subject "Oligodendroglioma"

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    DEC1 expression in 1p-aberrant oligodendroglial neoplasms
    (Murcia : F. Hernández, 2005) Preusser, Matthias; Birner, P.; Ambros, I.M.; Ambros, P.F.; Budka, H.; Harris, A.L.; Hainfellner, J.A.
    Background. Expression of hypoxia-related tissue factors in 1p-aberrant oligodendroglial neoplasms diminishes patient outcome. Differentiated embryochondrocyte expressed gene 1 (DEC1) has been described as novel hypoxia-related tissue factor. In our study, we assessed the expression of DEC1 in 1p aberrant oligodendroglial neoplasms and its association with necrosis and expression of hypoxia-inducible factor 1a (HIF-1a), carbonic anhydrase-9 (CA9), and vascular endothelial growth factor-mRNA (VEGF). Materials and methods. 44 primary and 16 recurrent oligodendroglial neoplasms with 1p-aberrations were investigated immunohistochemically for the expression of DEC1, HIF-1a, and CA9. Expression of VEGF was investigated using in situ hybridization. DEC1 expression was correlated with necrosis and with expression of HIF-1a, CA9, and VEGF. Results. DEC1 was expressed in tumor cell nuclei, and occasionally in nuclei of endothelial cells, and glial and neuronal cells of surrounding brain tissue. High expression (>10% of tumor cells immunolabeled) of DEC1 was found in 56 cases, low expression (<10% of tumor cells immunolabeled) was found in 3 cases. In 1 case no expression of DEC1 was evident. DEC1 expression showed no topographical association with necrosis or expression of HIF-1a, CA9, or VEGF. Conclusion. DEC1 expression is found in the majority of 1p-aberrant oligodendroglial neoplasms and does not correlate with necrosis or expression of HIF-1a, CA9, VEGF. Thus, immunohistochemical analysis of DEC1 expression is in our hands not suitable for detection of tissue hypoxia in this type of primary brain tumor.
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    Experimental neurocytomas
    (Murcia : F. Hernández, 1993) Vaquero, J.; Coca, S.; Zurita, M.; Oya, S.; Arias, A.; Morales, C.; Buján, J.; García, N .
    Four ethyl-nitrosourea (ENU)-induced oligodendroglioma-like tumors of the rat showing large rosettes on haematoxylin-eosin stain were studied by means of immunohistochemistry and electron microscopy, and their features compared with six human intraventricular neurocytomas. The similarities between the experimental and human tumors studied support the hypothesis that most of the so-called ENU-induced oligodendrogliomas in the rat are primitive neuroectodermal tumors with the tendency to differentiate toward a neuronal phenotype, and also suggest that the ENU-model of neurocarcinogenesis is useful for the induction of experimental neurocytomas.
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    Expression of neuronal and glial markers in so-called oligodendrogilial tumors induced by transplacental administration of ethyl-nitrosourea in the rat
    (Murcia : F. Hernández, 1992) Vaquero, J.; Coca, S.; Moreno M.; Oya, S.; Arias, A.; Zurita, M.; Morales, C.
    A series of 18 tumors with histological features of oligodendrogliomas, induced in the rat by means of transplacental ethyl-nitrosurea administration were studied for immunohistochemical demonstration of neuronal (synaptophysin and neurofilament protein) and glial (gliofibrillar acidic protein and vimentin) markers. Most of the tumors showed cells with strong positivity to synaptophysin and to a lesser degree, to neurofilament protein, suggesting the neuronal character of these neoplasms. In 10 tumors, cells with strong positivity to vimentin were found, and in three cases, tumoral cells expressed gliofibrillar acidic protein. The observation that ENU-induced oligodendroglial tumors express neuronal and, to a minor degree, glial markers, suggests their interpretation as prirnitive neuroectodermal tumors with clear neuronal differentiation.
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    Genetic analysis to complement histopathological diagnosis of brain tumors
    (Murcia : F. Hernández, 2007) Nakamura, M.; Shimada, K.; Ishida, E.; Nakase, H.; Konishi, N.
    Gliomas, the most frequent tumors originating in the human nervous system, are divided into various subtypes. Currently, microscopic examination alone is insufficient for classification and grading so that genetic profiles are increasingly being emphasized in recognition of the emerging role of molecular diagnostic approaches to glioma classification. Glioblastomas (WHO grade IV) may develop de novo (primary glioblastomas) or through progression from lower-grade astrocytomas (secondary glioblastomas), while both glioblastomas show similar histological features. In contrast, they do constitute distinct disease entities that evolve through different genetic pathways, and are likely to differ in prognosis and response to therapy. Oligodendrogliomas (WHO grade II) account for 2.7% of brain tumors and 5-18% of all gliomas. Since this tumor is recognized as a particular subtype of glioma that shows remarkable responses to chemotherapy, a correct diagnosis is of prime importance. The difficulty is that histological differentiation of oligodendrogliomas from diffuse astrocytomas is highly subjective in cases without typical morphological features and there is a lack of reliable immunohistochemical markers. While histological distinction of low-grade gliomas from reactive astrocytes is also often difficult, reactive astrocytes usually lack genetic alterations. More biological and molecular approaches to glioma classification thus appear warranted to provide improved means to achieve correct diagnoses.
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    IDH-mutant diffuse gliomas: tips and tricks in the era of genomic tumor classification
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2023) Ammendola, Serena; Broggi, Giuseppe; Barresi, Valeria
    According to the fifth edition of the World Health Organization (WHO) Classification, diffuse gliomas typically occurring in adults are classified as oligodendroglioma IDH-mutant and 1p/19q codeleted, astrocytoma IDH-mutant, and glioblastoma IDHwildtype. Among these, the former has the most favorable clinical course, whereas the latter has the worst prognosis. In IDH-mutant gliomas, the IDH1 p.R132H is the most frequent IDH mutation. Other mutations in IDH1 are rare and predominantly found in astrocytomas, whereas IDH2 mutations are mostly observed in oligodendrogliomas. Astrocytomas IDHmutant display frequent immunohistochemical loss of ATRX, which is mutually exclusive with 1p/19q codeletion. They are graded based on histopathological features and the presence of CDKN2A/B homozygous deletion, whereas the criteria for grading oligodendrogliomas are less defined. DNA methylation profiling has recently shown three additional distinct tumor types among diffuse IDHmutant gliomas: infratentorial astrocytoma IDH mutant; primary mismatch repair deficient IDH-mutant astrocytoma (PMRDIA); and oligosarcoma. Infratentorial astrocytoma IDH-mutant is enriched in IDH1 or IDH2 mutations that differ from the IDH1 p.R132H mutation and are detectable only by gene sequencing, displays less frequent ATRX loss and MGMT promoter methylation than supratentorial IDH-mutant astrocytomas, and may additionally harbor the H3 K27M mutation, which is typically found in H3 K27-altered diffuse midline glioma. PMRDIA occurs in the context of primary mismatch repair deficiency, is characterized by frequent MSH6 mutations, hypermutation, low frequency of MGMT promoter methylation, and poor clinical outcomes. Finally, oligosarcoma is a tumor featuring oligodendroglial and sarcomatous areas, and is characterized by worse outcome and frequent 1p/19q copy number loss of heterozygosity.