The Forms of Growth in Gliomas and Their Practical Significance

Scherer, Hans-Joachim

doi:10.1093/brain/63.1.1

Cited by 349 publications

(155 citation statements)

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“…Histological analysis revealed that the tumors are highly infiltrative with human nuclear antigen-expressing cells widely disseminated from the tumor injection site ( Figure 4A, white arrow), primarily along white matter tracts, but also infiltrating the cortex and striatum. These are the same pathways of infiltration that are seen in our PDGF model, as well as in human patients with glioblastoma (Sherer, 1940). As in the PDGF-driven tumors, myosin IIA is markedly up-regulated in tumor compared with brain ( Figure 4, B and BЈ), whereas myosin IIB is expressed at similar levels (Figures 4, C and CЈ).…”

Section: Myosin II Isoform Expression In Gliomassupporting

confidence: 72%

“…Part of the reason for this state of affairs is that although gliomas rarely metastasize outside the CNS, they are capable of spreading long distances within the brain (Sherer, 1940;Burger and Kleihues, 1989;Hoelzinger et al, 2007). This invasive behavior limits the effectiveness of local therapies and contributes to the high mortality rate seen in these tumors (Lim et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

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The Role of Myosin II in Glioma Invasion of the Brain

Beadle

Assanah

Monzo

et al. 2008

MBoC

292

334

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The ability of gliomas to invade the brain limits the efficacy of standard therapies. In this study, we have examined glioma migration in living brain tissue by using two novel in vivo model systems. Within the brain, glioma cells migrate like nontransformed, neural progenitor cells-extending a prominent leading cytoplasmic process followed by a burst of forward movement by the cell body that requires myosin II. In contrast, on a two-dimensional surface, glioma cells migrate more like fibroblasts, and they do not require myosin II to move. To explain this phenomenon, we studied glioma migration through a series of synthetic membranes with defined pore sizes. Our results demonstrate that the A and B isoforms of myosin II are specifically required when a glioma cell has to squeeze through pores smaller than its nuclear diameter. They support a model in which the neural progenitor-like mode of glioma invasion and the requirement for myosin II represent an adaptation needed to move within the brain, which has a submicrometer effective pore size. Furthermore, the absolute requirement for myosin II in brain invasion underscores the importance of this molecular motor as a potential target for new anti-invasive therapies to treat malignant brain tumors. INTRODUCTIONMalignant gliomas are a group of primary brain tumors that have remained resistant to therapy and that have a dismal prognosis (Buckner et al., 2007;Stupp et al., 2007). Part of the reason for this state of affairs is that although gliomas rarely metastasize outside the CNS, they are capable of spreading long distances within the brain (Sherer, 1940;Burger and Kleihues, 1989;Hoelzinger et al., 2007). This invasive behavior limits the effectiveness of local therapies and contributes to the high mortality rate seen in these tumors (Lim et al., 2007). Preventing glioma invasion therefore has the potential to convert this highly malignant tumor into a focal disease, which could then be effectively treated with focal therapies, such as radiation and surgery. Realizing this outcome, however, will require a detailed understanding how gliomas invade normal brain.Gliomas typically invade the brain by migrating long distances through white matter tracts and by infiltrating cortex and subcortical gray matter structures. Brain parenchyma (neuropil) is composed of tightly packed neuronal and glial processes, and it is characterized by extracellular spaces that are in the submicrometer range (Thorne and Nicholson, 2006). This environment therefore represents a particular mechanical challenge to motile cells, such as gliomas, that need to insinuate themselves through a highly constraining brain matrix to migrate. Unfortunately, there is very little information about how glioma cells accomplish this process in vivo. Some insight is provided by studies of embryonic and early postnatal brain, where neural progenitor cells migrate along radial glial cells, and to some extent through the white matter and cortex before stopping and differentiating into mature neurons and glia. Ti...

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Section: Myosin II Isoform Expression In Gliomassupporting

confidence: 72%

Section: Introductionmentioning

confidence: 99%

The Role of Myosin II in Glioma Invasion of the Brain

Beadle

Assanah

Monzo

et al. 2008

MBoC

292

334

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“…We categorized no or trace enhancement as nonenhancement (NEAA), and conspicuously enhancing tumors as EAA. In our attempt to define tumor margins, we adapted glioma growth pattern classifications originally set forth as anatomic descriptions (7,8) to typical appearances we noted on MRI scans. All patients were injected with Magnevist at a standard dose of 0.1 mmol/kg, and all patients were scanned in 1.5 T magnets.…”

Section: Pre-and Postoperative Mri Extent Of Resectionmentioning

confidence: 99%

“…Scherer (7), and later Daumas-Duport (8), described forms of tumor growth, and discussed how these tumors vary in how they interact with surrounding parenchyma. Some tumors are expansive, primarily pushing the surrounding neuropil aside, while the more infiltrative and invasive tumors, on the other hand, show a wide margin of microscopic invasion into the surrounding parenchyma.…”

mentioning

confidence: 99%

Revisiting anaplastic astrocytomas I: An expansive growth pattern is associated with a better prognosis

Moulding

Friedman

Curtis

et al. 2008

Magnetic Resonance Imaging

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Purpose:To study whether anaplastic astrocytomas that are nonenhancing and/or well-circumscribed (expansive) are associated with a better prognosis. Results: Kaplan-Meier curves showed improved survival in NEAA, expansive tumors, and RPA 1 class patients. Within RPA class I patients, expansive growth pattern remained a significant advantage in survival time. Examining extent of resection also showed that patients with gross total resections (GTR) had a better prognosis. A multivariate (Cox proportional hazards) analysis showed that patient age and expansive tumor phenotype affected outcome, whereas RPA class, enhancement, and GTR did not. Materials and Methods Conclusion:Circumscribed growth in histologically proven anaplastic astrocytoma, which has not been emphasized in past studies, has a considerable survival advantage.

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“…Glioblastoma predominantly originates and diffusely spreads in the subcortical white matter. 12) The typical growth pattern originates from the margin between the cortex and subcortex, with deep growth into the white matter. However, our two cases showed different growth patterns of superficial origin.…”

Section: Discussionmentioning

confidence: 99%

Early Neuroimaging Findings of Glioblastoma Mimicking Non-neoplastic Cerebral Lesion -Two Case Reports-

Jung

2007

Neurol. Med. Chir.(Tokyo)

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A 54-year-old man and a 63-year-old woman presented with glioblastoma manifesting as seizure and headache, respectively. Magnetic resonance imaging of the two patients revealed hypointense area on T 1 -weighted imaging, and hyperintense area on T 2 -weighted and diffusion-weighted imaging, with no enhancement after gadolinium administration. Both patients underwent conservative therapy under diagnoses of non-neoplastic cerebral lesion. Six months later, they suffered aggravated symptoms and new neurological deficits. Follow-up magnetic resonance imaging revealed hypointense area on diffusion-weighted imaging and ring enhancement on T 1 -weighted imaging with gadolinium at the site of the previously detected lesions. The tumors showed growth pattern of superficial origin. The large enhanced masses were totally removed through craniotomy under neuronavigator guidance. The histological diagnoses were glioblastoma. Glioblastoma may mimic non-neoplastic conditions on neuroimaging in the early stages. Close follow up of such patients is essential.

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The Forms of Growth in Gliomas and Their Practical Significance

Cited by 349 publications

References 0 publications

The Role of Myosin II in Glioma Invasion of the Brain

The Role of Myosin II in Glioma Invasion of the Brain

Revisiting anaplastic astrocytomas I: An expansive growth pattern is associated with a better prognosis

Early Neuroimaging Findings of Glioblastoma Mimicking Non-neoplastic Cerebral Lesion -Two Case Reports-

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