Continuous growth of mean tumor diameter in a subset of grade II gliomas

Mandonnet, Emmanuel; Delattre, Jean Yves; Tanguy, Marie Laure; Swanson, Kristin R.; Carpentier, Antoine F.; Duffau, Hugues; Cornu, Philippe; Effenterre, R. Van; Alvord, Ellsworth C.; Laurent, Césari

doi:10.1002/ana.10528

Cited by 442 publications

(301 citation statements)

References 11 publications

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“…The total mean diffusion was estimated based on two facts. First, Mandonnet et al (23), in a study of patients suffering from low-grade gliomas, reported that the diameter of the detectable part of the tumor expands about 4 mm per year. Second, one can show that the detectable diameter d obeys the asymptotic law (15) d͑t͒ ϳ 4 ͱD t, [12] for large time t, where D is the mean cell diffusion and the net proliferation constant for an exponential proliferation law.…”

Section: Choice Of Parametersmentioning

confidence: 99%

Simulation of anisotropic growth of low‐grade gliomas using diffusion tensor imaging

Jbabdi

Mandonnet

Duffau

et al. 2005

Magnetic Resonance in Med

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A recent computational model of brain tumor growth, developed to better describe how gliomas invade through the adjacent brain parenchyma, is based on two major elements: cell proliferation and isotropic cell diffusion. On the basis of this model, glioma growth has been simulated in a virtual brain, provided by a 3D segmented MRI atlas. However, it is commonly accepted that glial cells preferentially migrate along the direction of fiber tracts. Therefore, in this paper, the model has been improved by including anisotropic extension of gliomas. The method is based on a cell diffusion tensor derived from water diffusion tensor (as given by MRI diffusion tensor imaging). Results of simulations have been compared with two clinical examples demonstrating typical growth patterns of lowgrade gliomas centered around the insula. The shape and the kinetic evolution are better simulated with anisotropic rather than isotropic diffusion. The best fit is obtained when the anisotropy of the cell diffusion tensor is increased to greater anisotropy than the observed water diffusion tensor. The shape of the tumor is also influenced by the initial location of the tumor. Anisotropic brain tumor growth simulations provide a means to determine the initial location of a low-grade glioma as well as its cell diffusion tensor, both of which might reflect the biological characteristics of invasion. Key words: computational modeling; glioma; anisotropic growth; diffusion tensor; cell migration Low-grade (WHO grade II) gliomas are initially slowly evolving tumors, but can become rapidly fatal after anaplastic transformation. Because of their infiltrative characteristics, surgery alone fails to cure these tumors, even in their premalignant stage. Indeed, these tumors may not form a solid mass but may invade diffusely throughout the brain parenchyma as "gliomatosis cerebri."Recently, a biomathematical model (1) has been proposed to quantitatively describe the growth rates of gliomas visualized radiologically. This model takes into account the two major biological phenomena underlying the growth of gliomas at the cellular scale: proliferation and diffusion. The simplest choice for the proliferation term is a constant growth rate , leading to an exponentially growing total number of glioma cells. For the invasive properties of gliomas, cell migration is assumed to be a random walk, corresponding to a passive (Fickian) diffusion characterized by a single coefficient D. Simulations of this proliferation-diffusion equation are performed on a 3D T 1 MR structural image of the brain, with segmentation of CSF (which corresponds to the boundaries of the parenchyma), white matter, and gray matter images.In previous publications (2), the diffusion of cells in white matter is assumed to be 5 (to 100) times higher than in gray matter, consistent with observations that glioma cells migrate more quickly in white matter than in gray. Within white (or gray) matter, cell diffusion was considered an isotropic phenomenon. However, it is commonly accepted that gl...

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Section: Choice Of Parametersmentioning

confidence: 99%

Simulation of anisotropic growth of low‐grade gliomas using diffusion tensor imaging

Jbabdi

Mandonnet

Duffau

et al. 2005

Magnetic Resonance in Med

Self Cite

260

274

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“…Measurements of the radial growth rates of grade II astrocytomas AAs in patients who have not received adjuvant therapy demonstrate a modest annual increase of 2 mm/year. 4,5 Slow, persistent expansion characterizes these grade II-III astrocytomas.…”

Section: Accelerated Growth In Gbmmentioning

confidence: 99%

Vaso-occlusive and prothrombotic mechanisms associated with tumor hypoxia, necrosis, and accelerated growth in glioblastoma

Brat

Meir

2004

Laboratory Investigation

287

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Glioblastoma (GBM) has explosive biologic properties with rapid clinical progression leading to death. Its distinguishing pathologic features, necrosis with surrounding pseudopalisades and microvascular hyperplasia, are believed to be instrumental to its accelerated growth. Microvascular hyperplasia arises in response to the secretion of proangiogenic factors by hypoxic pseudopalisades and allows for peripheral neoplastic expansion. Mechanisms underlying necrosis and hypoxia remain obscure, but vaso-occlusive and prothrombotic contributions could be substantial. Recent investigations on the origin of pseudopalisades suggest that this morphologic phenomenon is created by a tumor cell population actively migrating away from a central hypoxic region and that, in at least a significant subset, hypoxia-induced migration appears due to vasoocclusion caused by intravascular thrombosis. Both vascular endothelial growth factor induced vascular permeability to plasma coagulation factors and the increased neoplastic expression of tissue factor likely contribute to a prothrombotic state favoring intravascular thrombosis. In addition to prothrombotic mechanisms, vaso-occlusion could also result from angiopoietin-2-mediated endothelial cell apoptosis and vascular regression, which follows neoplastic co-option of native vessels in animal models of gliomas. Vasoocclusive and prothrombotic mechanisms in GBM could readily explain the presence of pseudopalisades and coagulative necrosis in tissue sections, the emergence of central contrast enhancement and its rapid peripheral expansion on neuroimaging, and the dramatic shift to an accelerated rate of clinical progression. Since the hypoxic induction of angiogenesis appears to support further neoplastic growth, therapeutic targeting of the underlying vascular pathology and thrombosis could provide a new means to prolong time to progression.

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“…A mean tumor diameter increase of 4.1mm per year was reported in oligodendrogliomas or mixed gliomas on serial MR [17]. TMZ chemotherapy reversed this increase and led to an average tumor diameter decrease of 9.1 mm per year in one series [18].…”

Section: Discussionmentioning

confidence: 89%

Early metabolic responses in temozolomide treated low-grade glioma patients

et al. 2009

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(MR). A homogeneous population of 11 patients with progressive non-enhancing LGG was prospectively studied. Imaging was done at 6-months intervals starting six months, and in a second series starting three months after treatment initiation. F-18 fluoro-ethyl-l-tyrosine (FET) uptake was quantified with PET as metabolically active tumor volume, and was compared with the tumor volume on MR. Response was defined as ≥10% reduction of the initial tumor volume. Eight patients showed metabolic responses. Already 3 months after start of chemotherapy the active FET volumes decreased in 2 patients to a mean of 44% from baseline. First MR volume responses were noted at 6 months. Responders showed a volume reduction to 31 ± 23% (mean ± SD) from baseline for FET, and to 73 ± 26% for MR. The time to maximal volume reduction was 8.0 ± 4.4 months for FET, and 15.0 ± 3.0 months for MR. The initial metabolic response correlated with the best volume response on MR (Spearman Rank P = 0.011). Deactivation of amino acid transport represents an early indicator of chemotherapy response in LGG. Response assessment based on MR only has to be reconsidered. The time window obtained from PET may assist for individual treatment decisions in LGG patients. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 Wyss page 2 AbstractBackground: Amino acid transport and protein synthesis are important steps of tumor

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Continuous growth of mean tumor diameter in a subset of grade II gliomas

Cited by 442 publications

References 11 publications

Simulation of anisotropic growth of low‐grade gliomas using diffusion tensor imaging

Simulation of anisotropic growth of low‐grade gliomas using diffusion tensor imaging

Vaso-occlusive and prothrombotic mechanisms associated with tumor hypoxia, necrosis, and accelerated growth in glioblastoma

Early metabolic responses in temozolomide treated low-grade glioma patients

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