Vascular networks due to dynamically arrested crystalline ordering of elongated cells

Palm, Margriet; Merks, Roeland

doi:10.1103/physreve.87.012725

Cited by 25 publications

(36 citation statements)

References 44 publications

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“…Cell division can be triggered when certain conditions are met, such as the cell reaches a certain size (Jiang et al, 2005), or volume-to-surface ratio (Stott et al, 1999), or can depend on the time since last division (Sottoriva et al, 2011), and so on. Further extensions make it possible to model, e.g., the effect of cell shape (Merks et al, 2006; Starruß et al, 2007; Palm and Merks, 2013), anisotropic differential adhesion (Zajac et al, 2003), persistent cell motion (Szabó et al, 2010; Kabla, 2012). These behaviors can be made specific for the cell types τ(σ) included in the model, e.g., tumor, stromal, necrotic tumor cell, and cancer stem cells.…”

Section: A Multi-particle Cell-based Methods On the Lattice: The Cellmentioning

confidence: 99%

“…In this section we will review a cellular Potts model studying the growth dynamics of vascular tumors. Models focusing on the mechanisms of angiogenesis (for example: Manoussaki et al, 1996; Gamba et al, 2003; Merks et al, 2006, 2008; Szabo et al, 2007, 2008; Bauer et al, 2009; Daub and Merks, 2013; Palm and Merks, 2013) are reviewed elsewhere (for example, Chaplain et al, 2006; Jiang et al, 2012; Peirce et al, 2012; Bentley et al, 2013). …”

Section: Vascular Tumor Growthmentioning

confidence: 99%

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Cellular Potts Modeling of Tumor Growth, Tumor Invasion, and Tumor Evolution

Szabó¹,

Merks²

2013

Front. Oncol.

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172

130

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Despite a growing wealth of available molecular data, the growth of tumors, invasion of tumors into healthy tissue, and response of tumors to therapies are still poorly understood. Although genetic mutations are in general the first step in the development of a cancer, for the mutated cell to persist in a tissue, it must compete against the other, healthy or diseased cells, for example by becoming more motile, adhesive, or multiplying faster. Thus, the cellular phenotype determines the success of a cancer cell in competition with its neighbors, irrespective of the genetic mutations or physiological alterations that gave rise to the altered phenotype. What phenotypes can make a cell “successful” in an environment of healthy and cancerous cells, and how? A widely used tool for getting more insight into that question is cell-based modeling. Cell-based models constitute a class of computational, agent-based models that mimic biophysical and molecular interactions between cells. One of the most widely used cell-based modeling formalisms is the cellular Potts model (CPM), a lattice-based, multi particle cell-based modeling approach. The CPM has become a popular and accessible method for modeling mechanisms of multicellular processes including cell sorting, gastrulation, or angiogenesis. The CPM accounts for biophysical cellular properties, including cell proliferation, cell motility, and cell adhesion, which play a key role in cancer. Multiscale models are constructed by extending the agents with intracellular processes including metabolism, growth, and signaling. Here we review the use of the CPM for modeling tumor growth, tumor invasion, and tumor progression. We argue that the accessibility and flexibility of the CPM, and its accurate, yet coarse-grained and computationally efficient representation of cell and tissue biophysics, make the CPM the method of choice for modeling cellular processes in tumor development.

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Section: A Multi-particle Cell-based Methods On the Lattice: The Cellmentioning

confidence: 99%

Section: Vascular Tumor Growthmentioning

confidence: 99%

Cellular Potts Modeling of Tumor Growth, Tumor Invasion, and Tumor Evolution

Szabó¹,

Merks²

2013

Front. Oncol.

Self Cite

172

130

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“…a patchy nutrient environment) and 'followers' that are not [46], since in our case the stromal cells do not follow a global directional cue. On a biological level, the dynamic construction of leadership we use in the cancer-stromal model reflects the experimental observation that leadership in collective cancer cell migration can be defined not by genotype but by the spatial rsfs.royalsocietypublishing.org Interface Focus 3: 20130017 structure of the cell population itself and differential access to microenvironmental factors [13,47].…”

Section: Discussionmentioning

confidence: 99%

“…It is an emergent phenomenon and a universality class, in which the largescale properties of the collective result from the activities of individuals, but are to some extent independent of the specific behaviour of individuals [10,11]. Similarly, in cell biology, collective migration of groups of closely interacting cells has been implicated in such behaviours as organ morphogenesis during embryonic development or vascularization [4,[12][13][14][15] and, the main motivation for our study, cell invasion during cancer progression [13,16].…”

Section: Introductionmentioning

confidence: 99%

Tumour–stromal interactions generate emergent persistence in collective cancer cell migration

2013

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One contribution of 11 to a Theme Issue 'Integrated cancer biology models'. Cancer cell collective migration is a complex behaviour leading to the invasion of cancer cells into surrounding tissue, often with the aid of stromal cells in the microenvironment, such as macrophages or fibroblasts. Although tumour-tumour and tumour-stromal intercellular signalling have been shown to contribute to cancer cell migration, we lack a fundamental theoretical understanding of how aggressive invasion emerges from the synergy between these mechanisms. We use a computational self-propelled particle model to simulate intercellular interactions between co-migrating tumour and stromal cells and study the emergence of collective movement. We find that tumour-stromal interaction increases the cohesion and persistence of migrating mixed tumour-stromal cell clusters in a noisy and unbounded environment, leading to increased cell cluster size and distance migrated by cancer cells. Although environmental constraints, such as vasculature or extracellular matrix, influence cancer migration in vivo, our model shows that cell-cell interactions are sufficient to generate cohesive and persistent movement. From our results, we conclude that inhibition of tumour-stromal intercellular signalling may present a viable therapeutic target for disrupting collective cancer cell migration.

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“…Different from the CA models discussed before, the CPM explicitly represents the cell shape which has made the CPM a popular tool to model morphogenic processes such as cell sorting [53,103], cancer and tumor growth [104][105][106][107][108][109][110], and angiogenesis [25,[111][112][113][114][115][116][117].…”

Section: Cellular Automaton With Many Lattice Sites Per Cell (Type C;mentioning

confidence: 99%

Simulating tissue mechanics with agent-based models: concepts, perspectives and some novel results

et al. 2015

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In this paper we present an overview of agentbased models that are used to simulate mechanical and physiological phenomena in cells and tissues, and we discuss underlying concepts, limitations, and future perspectives of these models. As the interest in cell and tissue mechanics increase, agent-based models are becoming more common the modeling community. We overview the physical aspects, complexity, shortcomings, and capabilities of the major agent-based model categories: lattice-based models (cellular automata, lattice gas cellular automata, cellular Potts models), off-lattice models (center-based models, deformable cell models, vertex models), and hybrid discrete-continuum models. In this way, we hope to assist future researchers in choosing a model for the phenomenon they want to model and understand. The article also contains some novel results.

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Vascular networks due to dynamically arrested crystalline ordering of elongated cells

Cited by 25 publications

References 44 publications

Cellular Potts Modeling of Tumor Growth, Tumor Invasion, and Tumor Evolution

Cellular Potts Modeling of Tumor Growth, Tumor Invasion, and Tumor Evolution

Tumour–stromal interactions generate emergent persistence in collective cancer cell migration

Simulating tissue mechanics with agent-based models: concepts, perspectives and some novel results

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