Brain slice invasion model reveals genes differentially regulated in glioma invasion

Holtkamp, Nikola; Afanasieva, Anastasia; Elstner, Anja; Landeghem, Frank K.H. van; Könneker, Matthias; Kuhn, Susanne; Kettenmann, Helmut; Deimling, Andreas von

doi:10.1016/j.bbrc.2005.08.253

Cited by 26 publications

(21 citation statements)

References 32 publications

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“…In particular, a myelinated substrate that consists of living neurites and oligodendrocyte-derived myelin constituents can be used to investigate what triggers glioma cells to contact myelinated fibers and migrate within the normal brain. In contrast with various in vitro and in vivo models, such as glioma spheroids, intracranial implantation (Bruce et al, 2000;Goplen et al, 2006), and brain-slice culture techniques (Auer et al, 1981;Holtkamp et al, 2005;Izumoto et al, 1996;Laerum et al, 2001), the present model mimics white matter. The disappearance of myelinated fibers in cell cultures makes chick tissue a useful model for addressing questions concerning glioma migration.…”

Section: Discussionmentioning

confidence: 89%

“…Assessments of glioma migration have employed various in vitro and in vivo models, such as glioma spheroids (Valster et al, 2005 for review), intracranial implantation (Bruce et al, 2000;Farin et al, 2006;Goplen et al, 2006), and brain-slice culture techniques (Auer et al, 1981;Holtkamp et al, 2005;Laerum et al, 2001;Valster et al, 2005 for review), and time-lapse migration assays (Demuth et al, 2000). Assays that block migration have been implemented in cell cultures (Giese et al, 1998;Grobben et al, 2002, for review) and in the Boyden chamber model (Boyden, 1962;Schichor et al, 2005).…”

Section: Introductionmentioning

confidence: 98%

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Rocks are expressed in brain tumors and are required for glioma‐cell migration on myelinated axons

Oellers

Schröer

Senner

et al. 2008

Glia

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The interactions between migrating glioma cells and myelinated fiber tracts are poorly understood. We identified that C6 glioma cells can migrate along myelinated chicken retinal axons in a novel coculture, thereby expressing small GTPases of the Rho family and serine/threonine Rho-associated kinases (ROCKs). We found that the ROCK1 isoform is also highly expressed in native human high-grade gliomas. Glioma cells migrated faster in vitro along myelinated axons than on laminin-1, with the former but not the latter being specifically and reversibly blocked by the ROCK inhibitor Y27632. These data suggest that the mechanisms underlying the migration of glioma cells on myelinated axons differ from those underlying the migration on extracellular matrix molecules such as laminin-1.

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Section: Discussionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 98%

Rocks are expressed in brain tumors and are required for glioma‐cell migration on myelinated axons

Oellers

Schröer

Senner

et al. 2008

Glia

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“…Since this initial study, there have been several more that have used these methods to evaluate rodent-based brain tissue models (Cavaliere et al 2006;Holopainen 2005;Holtkamp et al 2005;Tanaka et al 1994;Valster et al 2005). Humanbased brain tissue models have been primarily limited to fetal tissue (Jakovcevski and Zecevic 2005;Lyman et al 1992;Tenenbaum et al 2004) and cadaveric tissue (Bsibsi et al 2006;Verwer et al 2002).…”

Section: Establishment Of An Ex Vivo Human Model To Study Human Diseasementioning

confidence: 99%

“…The preparation of organotypic cultures has primarily been limited to rodent-based research (Cavaliere et al 2006;Holopainen 2005;Holtkamp et al 2005;Stoppini et al 1991;Tanaka et al 1994;Valster et al 2005). Preparation of adult human brain cultures has only been reported twice in the literature (Jung et al 1999;Jung et al 2002).…”

Section: Introductionmentioning

confidence: 99%

Preservation of glial cytoarchitecture from ex vivo human tumor and non-tumor cerebral cortical explants: A human model to study neurological diseases

Chaichana

Capilla-González

González-Pérez

et al. 2007

Journal of Neuroscience Methods

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For the human brain, in vitro models that accurately represent what occurs in vivo are lacking. Organotypic models may be the closest parallel to human brain tissue outside of a live patient. However, this model has been limited primarily to rodent-derived tissue. We present an organotypic model to maintain intraoperatively collected human tumor and non-tumor explants ex vivo for a prolonged period of time (∼ 11 days) without any significant changes to the tissue cytoarchitecture as evidenced through immunohistochemistry and electron microscopy analyses. The ability to establish and reliably predict the cytoarchitectural changes that occur with time in an organotypic model of tumor and non-tumor human brain tissue has several potential applications including the study of cell migration on actual tissue matrix, drug toxicity on neural tissue, and pharmacological treatment for brain cancers, among others.

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“…Disease Cyclin B1 is a gene identified to be increased in glioma cells invading brain slice cultures (Holtkamp et al, 2005). Human glioma tissue microarrays indicate a positive expression rate of CDK1/cyclin B1 with a positive correlation with pathologic grades .…”

Section: Gliomamentioning

confidence: 99%

CCNB1 (cyclin B1)

Perez‐Stable¹

2011

Atlas of Genetics and Cytogenetics in Oncology and Haematology

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IdentityOther names: CCNB HGNC (Hugo): CCNB1 Location: 5q13.2 DNA/RNA Description 9 exons; 2,087 bp; 433 residues CCNB1 transcript 1. 8 exons; 1,833 bp; 397 residues CCNB1 transcript 2. TranscriptionTwo alternative transcripts resulting from distinct transcription initiation sites. One is constitutively expressed and the other is G2/M cell cycle-regulated. PseudogeneNo verified pseudogenes. Protein DescriptionCyclin B1 (48.337 kDa) is a member of the cyclin family of proteins whose levels vary during the cell cycle in order to activate specific cyclin-dependent kinases (CDKs) required for the proper progression through the cell cycle. Cyclin B1 protein begins to increase during G2, peaks in mitosis, and is rapidly degraded before the cell cycle is completed. Cyclin B1 interacts with CDK1 to form a complex known as the maturation-promoting factor (MPF), which is essential for cell cycle progression through mitosis. When chromosomes are properly aligned during anaphase, rapid degradation of cyclin B1 by anaphase-promoting complex/cyclosome (APC/C) is required for mitotic exit and completion of the cell cycle. ExpressionCyclin B1 is overexpressed in a variety of cancers compared to normal cells and tissues. In normal tissues, low levels of cyclin B1 is detected in testis, thymus, bone marrow, and smooth muscle (CCNB1 expression). In most primary tumors, the expression of cyclin B1 is "unscheduled" (unrestricted to particular phases of the cycle), whereas in normal lymphocytes, the expression of cyclin B1 is restricted to very late S and G2 + M phases of the cell cycle (Gorczyca et al., 1997). LocalisationDuring interphase, cyclin B1 is concentrated in the cytoplasm but can shuttle to the nucleus (Pines and Hunter, 1991).Diagram of sequence domains for cyclin B1. The destruction box (DB) is required for degradation of cyclin B1 at the metaphase-toanaphase transition. The cytoplasmic retention sequence (CRS) and the nuclear export signal (NES) are critical determinants of cyclin B1 localization during mitosis. The cyclin box is required for interaction with CDK1.

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Brain slice invasion model reveals genes differentially regulated in glioma invasion

Cited by 26 publications

References 32 publications

Rocks are expressed in brain tumors and are required for glioma‐cell migration on myelinated axons

Rocks are expressed in brain tumors and are required for glioma‐cell migration on myelinated axons

Preservation of glial cytoarchitecture from ex vivo human tumor and non-tumor cerebral cortical explants: A human model to study neurological diseases

CCNB1 (cyclin B1)

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