Cell proliferation in explant cultures of malignant gliomas

Haynes, Laurence W.; Davis, B. E.; Mitchell, J. A.; Weller, Roy O.

doi:10.1007/bf00690972

Cited by 11 publications

(2 citation statements)

References 16 publications

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“…[22][23][24][25] Studies of glioma cell explants have shown that the regions of highest mitotic activity extend along the advancing edge of solid tumor tissue, ie, at the interface of solid explant and culture medium. 26,27 Selection of a block of "representative" tumor for immunostaining does not necessarily guarantee that the most proliferative area of the neoplasm is present in that block. 20 Maruno and colleagues 28 found that the distribution of Ki-67-positive nuclei was variable in different sections of solid GBM tissue.…”

Section: Discussionmentioning

confidence: 99%

Comparison of Proliferation Indices in Glioblastoma Multiforme by Whole Tissue Section vs Tissue Microarray

2003

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Tissue microarrays (TMAs) reduce the amount of tissue analyzed with the assumption that protein and gene expression patterns are homogeneous throughout tumors. Many tumor types, including glioblastoma multiforme (GBM), are heterogeneous in many regards, including cell proliferation. We retrospectively compared Ki-67 labeling indices (LIs) determined by whole tissue section (WTS) vs TMA in a series of 50 GBMs from 45 patients. A paired t test indicated that the difference between average LIs obtained from a TMA vs a WTS was not significant (P = .51). There was no correlation between TMA and WTS (r = 0.042; P = .77), indicating that the methods yielded very different results in individual tumors. The Ki-67 LI did not always correlate with the tissue section in an individual tumor; however, when evaluating a large number of tumors on a TMA, the LI range and mean LI were roughly comparable with the LI range and mean LI determined from the WTS.

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Section: Discussionmentioning

confidence: 99%

Comparison of Proliferation Indices in Glioblastoma Multiforme by Whole Tissue Section vs Tissue Microarray

2003

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“…While the possibility of cellular overgrowth producing changes in glioma phenotype has been previously proposed on the basis of descriptive evidence [15,22,49,50] there have been minimal quantitative data to support this proposal. Many glioma cells in culture contain fibronectin, reticulin, type IV collagen, and laminin [16,28,29,51,52].…”

Section: Discussionmentioning

confidence: 99%

Products of cells from gliomas: IX. Evidence that two fundamentally different mechanisms change extracellular matrix expression by gliomas

et al. 1995

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Four human astrocytic gliomas of high grade of malignancy were each evaluated in tissue and in vitro for percentages of cells expressing glial fibrillary acidic protein (GFAP), collagen type IV, laminin and fibronectin assessed by immunofluorescence with counterstaining of nuclear DNA. Percentages of cells with reticulin and cells binding fluorescein-labeled Ulex europaeus agglutinin were also assessed. In tissue, each extracellular matrix (ECM) component was associated with cells in the walls of abnormal proliferations of glioma vessels, and all four tumors had the same staining pattern. Two strikingly different patterns of conversion of gene product expression emerged during in vitro cultivation. (1). In the most common pattern, percentages of all six markers consistently shifted toward the exact phenotype of mesenchymal cells in abnormal vascular proliferations: increased reticulin, collagen type IV, laminin and fibronectin; markedly decreased glial marker GFAP and absent endothelial marker Ulex europaeus agglutinin. The simplest explanation of this constellation of changes coordinated toward expression of vascular ECM markers is that primary glioma cell cultures are overgrown by mesenchymal cells from the abnormal vascular proliferations of the original glioma. These cell cultures were tested for in situ hybridization (ISH) signals of chromosomes 7 and 10. Cells from one glioma had diploid signals. Cells from the other glioma had aneuploid signals indicating they were neoplastic; however, their signals reflected different numerical chromosomal aberrations than those common to neoplastic glia. (2). The second pattern was different. Cells with ISH chromosomal signals of neoplastic glia retained GFAP, and gained collagen type IV. Their laminin and fibronectin diminished, but persisted among a lower percentage of cells. Cloning and double immunofluorescence confirmed the presence of individual cells with glial and mesenchymal markers. A cell expressing GFAP in addition to either fibronectin, reticulin or collagen type IV is not a known constituent of glioblastoma tissue. This provides evidence of a second mechanism of conversion of gene expression in gliomas.

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Tissue Culture in the Diagnosis of Brain Tumors

Escalona-Zapata¹

1990

Diagnostic Neuropathology

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Cell proliferation in explant cultures of malignant gliomas

Cited by 11 publications

References 16 publications

Comparison of Proliferation Indices in Glioblastoma Multiforme by Whole Tissue Section vs Tissue Microarray

Comparison of Proliferation Indices in Glioblastoma Multiforme by Whole Tissue Section vs Tissue Microarray

Products of cells from gliomas: IX. Evidence that two fundamentally different mechanisms change extracellular matrix expression by gliomas

Tissue Culture in the Diagnosis of Brain Tumors

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