Experimental control of neoplastic progression in cell populations: Foulds' rules revisited.

Rubin, Harry

doi:10.1073/pnas.91.14.6619

Cited by 29 publications

(12 citation statements)

References 24 publications

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“…It is important to mention that, according to this concept, systemic tumoral growth increases both intrinsic and extrinsic stress and therefore leads to a higher selection pressure and mutational probability. Since this may advance tumor progression, it clearly argues against Foulds' rule III (that tumor growth and progression are independent) (Foulds, 1954;Rubin, 1994). In the next iteration of the model, we will simulate the conditions which create regional genetic instability and study the e!ect of speci"c mutations in tumor cells on the macroscopic growth of tumors.…”

Section: Discussionmentioning

confidence: 98%

Simulated Brain Tumor Growth Dynamics Using a Three-Dimensional Cellular Automaton

Kansal

Torquato

Harsh

et al. 2000

Journal of Theoretical Biology

379

282

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We have developed a novel and versatile three-dimensional cellular automaton model of brain tumor growth. We show that macroscopic tumor behavior can be realistically modeled using microscopic parameters. Using only four parameters, this model simulates Gompertzian growth for a tumor growing over nearly three orders of magnitude in radius. It also predicts the composition and dynamics of the tumor at selected time points in agreement with medical literature. We also demonstrate the flexibility of the model by showing the emergence, and eventual dominance, of a second tumor clone with a different genotype. The model incorporates several important and novel features, both in the rules governing the model and in the underlying structure of the model. Among these are a new definition of how to model proliferative and non-proliferative cells, an isotropic lattice, and an adaptive grid lattice.

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Section: Discussionmentioning

confidence: 98%

Simulated Brain Tumor Growth Dynamics Using a Three-Dimensional Cellular Automaton

Kansal

Torquato

Harsh

et al. 2000

Journal of Theoretical Biology

379

282

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“…Clonal outgrowth of each subpopulation is proposed to precede the next mutagenic event (Nowell 1976) and specific mutations are proposed to occur in a stereotyped sequence (Vogelstein and Kinzler 1993). Heritable change and clonal outgrowth can occur with, or without, changing DNA sequence and, in principle, either type of inheritance could fulfill a step of cancerous transformation (Rubin 1994). Phenocopies might occur first with their eventual replacement by more stable or dramatic sequence-based modes of inheritance.…”

Section: Differing Lineage Qualitiesmentioning

confidence: 99%

Hereditary stability and variation in evolution and development

Thaler

1999

Evolution and Development

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SUMMARY Evolution and development are both lineage processes but are often conceptualized as occurring by different and mutually exclusive mechanisms. It is conventionally asserted that evolution occurs via the random generation of diversity and the subsequent survival of those that pass selection. On the other hand, development is too often presented as proceeding via the unfolding of a deterministic program encoded in the DNA sequence. In biology, universal generalizations are rare and dogmas are often wrong for particular cases. Deterministic mechanisms contribute some of the new DNA sequences that subsequently become substrates for natural selection. Conversely, stochastic and selective mechanisms are intrinsic to development, and also to maintenance of the immune, and possibly, nervous systems. Cancer appears to be another process that straddles distinctions between evolutionary and developmental modes of hereditary change and stabilization. DNA sequence changes are an essential feature of many cancers, but there are also aspects of the disease similar to developmental lineage gone awry. The literature suggests that the cellular changes that give rise to cancer occur by mechanisms commonly associated with both evolutionary and developmental lineage pathways.

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“…Lest we think that deletions occurring at just a few specific loci are the carcinogenic culprits, we find that the type of transformed focus produced in cell culture by each independent transforming event is unique [25]. And if that uniqueness is not readily apparent from visual inspection, when we combine it with the heterogeneity of the reduced growth rate [26], we can say that any of an enormous number of deletions can contribute to progressive transformation if we are dealing with an already susceptible cell which can be defined as preneoplastic.…”

Section: Significance For Cliniciansmentioning

confidence: 97%

Cancer and complexity: Correlations and complementarity

Rubin

1998

J. Surg. Oncol.

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Experimental control of neoplastic progression in cell populations: Foulds' rules revisited.

Abstract: Foulds introduced six rules of tumor progression based on his observations of spontcancer in mice and generalized them to all forms of neoplasa

Cited by 29 publications

References 24 publications

Simulated Brain Tumor Growth Dynamics Using a Three-Dimensional Cellular Automaton

Simulated Brain Tumor Growth Dynamics Using a Three-Dimensional Cellular Automaton

Hereditary stability and variation in evolution and development

Cancer and complexity: Correlations and complementarity

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