Immunophenotypic differences between normal glia, astrocytomas and malignant gliomas: correlations with karyotype, natural history and survival

Jennings, Mark T.; Ebrahim, Salah A.D.; Thaler, Howard T.; Jennings, Vicki; Asadourian, Laura L.H.; Shapiro, Joan Rankin

doi:10.1016/0165-5728(89)90082-9

Cited by 27 publications

(10 citation statements)

References 40 publications

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“…The AAST demonstrated both anchorage-independent growth and nulnu xenograft formation, as well as a spectrum of cytogenetic and immunophenotypic changes from minimally to significantly aberrant. In contrast, the GBM were much easier to culture in vitro and exhibited greater karyotypic and antigenic divergence (Jennings et al, 1989(Jennings et al, , 1990Shapiro et al, 1984Shapiro et al, , 1985. We now show that the hyperdiploid GBM cultures differ in their growth-regulatory response to TGFP, as well.…”

Section: Discussionmentioning

confidence: 56%

“…The GBM cultures studied were SK-MG-3R, SK-MG-11, SK-MG-8, SK-DI, SK-MG-15, SK-MG-13, SK-MG-16, SK-GS-1R and SK-MG-2. These representative cultures and cell lines were chosen as considerable information was available regarding karyotype, experimental growth characteristics, immunophenotype and clinical history (Cairncross et al, 1982;Jennings et al, 1989Jennings et al, , 1990. In order to minimize in vitro artefact, the earliest available passages were studied.…”

Section: Derivation Of Cell Cultures and Cell Linesmentioning

confidence: 99%

“…Cultures of AST (V-AST-2, V-MG-18), and GBM (V-MG-8, V-MG-13, V-MG-20, V-MG-6) were newly established and studied within passages 1-4. Recurrent tumors were designated by R. Confirmation of the malignant nature of the tumor cultures was attempted through cytogenetic analysis and accepted experimental measures of malignancy such as anchorage-independent clonogenicity and xenograft tumorigenicity within non-irradiated Swiss nulnu mice, as previously reported (Jennings et al, 1989). Not all cultures yielded sufficient cell numbers for complete analysis.…”

Section: Derivation Of Cell Cultures and Cell Linesmentioning

confidence: 99%

“…In contrast, V-MG-6 was hyperdiploid (Table I). Cultures and cell lines were ranked in Table I on the basis of cytogenetic and immunophenotypic divergence (Jennings et al, 1989). Complete characterization V-MG-17 and V-MG-18 was not possible due to insufficient cell numbers.…”

Section: Newly-generated Glioma Culturesmentioning

confidence: 99%

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TGFβ₁ and TGFβ₂ are potential growth regulators for low‐grade and malignant gliomas in vitro: Evidence in support of an autocrine hypothesis

Jennings

Maciunas

Carver

et al. 1991

Intl Journal of Cancer

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104

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Low-grade astrocytomas, anaplastic astrocytomas and glioblastomas in vitro were found to ubiquitously produce the mRNA of transforming growth factor-beta (TGF beta). TGF beta 1 and TGF beta 2 mRNA were expressed to a lesser degree among the hyperdiploid malignant gliomas. By radioreceptor assay of conditioned medium, TGF beta was secreted predominantly in latent form, in both latent and active form, or only in active form within a panel of low-grade and malignant gliomas. The TGF beta receptor (types I, II, and III) was evident among the glioma lines. Many near-diploid gliomas were growth-inhibited by TGF beta 1 and TGF beta 2 in vitro. Most hyperdiploid glioblastomas showed a positive mitogenic response to exogenous TGF beta 1 and TGF beta 2. A synergistic or additive mitogenic interaction with epidermal growth factor and insulin was observed among some. Under serum-free conditions, anti-TGF beta antibody neutralized the expected growth-regulatory effect of endogenous TGF beta, thus establishing the specificity of the response in vitro. TGF beta 1 also enhanced the clonogenicity of certain gliomas which had been growth-stimulated in monolayer. Thus, basic elements in support of an autocrine hypothesis have been demonstrated: TGF beta mRNA was expressed among low-grade and malignant gliomas, TGF beta was secreted in latent and/or active form into conditioned media and appeared to serve as an endogenous regulator of glioma proliferation in vitro. The mitogenic response, either positive or negative, correlated with the degree of anaplasia and karyotypic divergence.

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Section: Discussionmentioning

confidence: 56%

Section: Derivation Of Cell Cultures and Cell Linesmentioning

confidence: 99%

Section: Derivation Of Cell Cultures and Cell Linesmentioning

confidence: 99%

Section: Newly-generated Glioma Culturesmentioning

confidence: 99%

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TGFβ₁ and TGFβ₂ are potential growth regulators for low‐grade and malignant gliomas in vitro: Evidence in support of an autocrine hypothesis

Jennings

Maciunas

Carver

et al. 1991

Intl Journal of Cancer

Self Cite

104

View full text Add to dashboard Cite

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“…More recently developed areas of active investigation include DNA analysis using flow cytometry (Coons et al, 1988) and cytophotometry (Davenport and McKeever, 1987), cytogenetics (Shapiro et al, 1981;Nistér et al, 1987;Griffin et al, 1988;James et al, 1988;Jenkins et al, 1989;Jennings et al, 1989;Bigner et al, 1990), and molecular genetics and molecu-106 Yates lar biology Wong et al, 1987;Bigner et al, 1988;Humphrey et al, 1988;McDonald and Dohrmann, 1988;Nistër et al, 1988;Cusimano, 1989;Matsumoto et al, 1990;Maxwell et al, 1990;Wasson et al, 1990). Considerable data have been generated about abnormal karyotypes, the production of growth factors and their receptors, and abnormal gene expression in neural tumors.…”

mentioning

confidence: 99%

An overview of principles for classifying brain tumors

Yates

1992

Molecular and Chemical Neuropathology

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The purpose of this review is to clarify for the nonneuropathologist some of the confusing issues concerning the classification of brain tumors. Following a short discussion of the commonly used methods to diagnose brain tumors clinically (frozen section, light and electron microscopy, immunohistochemistry), the general principles of classifying neural tumors are presented. Grading of tumors on the basis of histological anaplasia, and the concept that tumor cells can be related to specific cytological stages of normal cellular development (cytogenetic classification) are presented. The World Health Organization system of classifying neural tumors is an attempt to develop a standardized classification scheme with as few interpretative controversies as possible, but it has required revision as new information has been gained. The major clinical and biological features of the commonest tumor groups are then discussed. It is unlikely that improvements in the classification of brain tumors will be based solely on histological information. Definitions of tumor entities that will provide more accurate prognoses and bases for effective therapy will require considerably more information at the molecular level than is currently available.

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Expression pattern of galectin-3 in neural tumor cell lines

Kuklinski¹,

Pesheva

Heimann³

et al. 2000

J. Neurosci. Res.

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Galectin-3 is a member of the galectin family of beta-galactoside-specific animal lectins. Here we show that galectin-3 is constitutively expressed in 15 out of 16 glioma cell lines tested, but not by normal or reactive astrocytes, oligodendrocytes, glial O-2A progenitor cells and the oligodendrocyte precursor cell line Oli-neu. Galectin-3 is also expressed by one oligodendroglioma cell line, but not by primitive neuroectodermal tumor and 4 neuroblastoma cell lines tested so far. In all galectin-3 expressing cell lines, the lectin is predominantly, if not exclusively, localized intracellularly and carries an active carbohydrate recognition domain (shown for C6 rat glioma cells). Moreover, in contrast to primary astrocytes, glioma cells do not or only weakly adhere to substratum-bound galectin-3, probably reflecting an unusual glycosylation pattern. Our findings indicate that the expression of galectin-3 selectively correlates with glial cell transformation in the central nervous system and could thus serve as a marker for glial tumor cell lines and glial tumors.

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Immunophenotypic differences between normal glia, astrocytomas and malignant gliomas: correlations with karyotype, natural history and survival

Cited by 27 publications

References 40 publications

TGFβ₁ and TGFβ₂ are potential growth regulators for low‐grade and malignant gliomas in vitro: Evidence in support of an autocrine hypothesis

TGFβ₁ and TGFβ₂ are potential growth regulators for low‐grade and malignant gliomas in vitro: Evidence in support of an autocrine hypothesis

An overview of principles for classifying brain tumors

Expression pattern of galectin-3 in neural tumor cell lines

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Immunophenotypic differences between normal glia, astrocytomas and malignant gliomas: correlations with karyotype, natural history and survival

Cited by 27 publications

References 40 publications

TGFβ1 and TGFβ2 are potential growth regulators for low‐grade and malignant gliomas in vitro: Evidence in support of an autocrine hypothesis

TGFβ1 and TGFβ2 are potential growth regulators for low‐grade and malignant gliomas in vitro: Evidence in support of an autocrine hypothesis

An overview of principles for classifying brain tumors

Expression pattern of galectin-3 in neural tumor cell lines

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Product

Resources

About

TGFβ₁ and TGFβ₂ are potential growth regulators for low‐grade and malignant gliomas in vitro: Evidence in support of an autocrine hypothesis

TGFβ₁ and TGFβ₂ are potential growth regulators for low‐grade and malignant gliomas in vitro: Evidence in support of an autocrine hypothesis