Cell Cycle: Regulation by Cyclins

Kitazono, Ana A.; Gerald, Jonathan N. Fitz; Kron, Stephen J.

doi:10.1038/npg.els.0001364

Cited by 1 publication

(3 citation statements)

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“…In general, changes in (e.g., down to the values not less than ) depend on various genotoxic biological signals (e.g., Massagué, 2004;Kitazono et al, 1999).…”

Section: The Hyperplastic-tumor/nonquiescent-cell Asymptotementioning

confidence: 99%

“…Serum is known as a medium containing various mitogenic cytokines. Another group of the above mechanisms is inherently associated with the D-type cyclins (e.g., Kitazono, et al, 1999). Overexpression of these cyclins (e.g., Sherr, 1995, p. 187;Kitazono, et al, 1999, the section "D cyclins"; Hatzimanikatis et al, 1999, p. 635) shortens (in particular, by reduction of in (6.3)) and weakens the -stage effect thereby switching the cells to the (almost-)NQ behavior.…”

Section: Valuementioning

confidence: 99%

“…This gives them a special role as cell division initiators." (Kitazono, et al, 1999, the section "D cyclins"). "The fundamental role of D-type cyclins is to integrate extracellular signals" such as automitogens (AMGs), autocrine mitogenic cytokines, "with the cell cycle machinery."…”

Section: Valuementioning

confidence: 99%

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The Minimal, Phase-Transition Model for the Cell-Number Maintenance by the Hyperplasia-Extended Homeorhesis

2006

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Oncogenic hyperplasia is the first and inevitable stage of formation of a (solid) tumor. This stage is also the core of many other proliferative diseases. The present work proposes the first minimal model that combines homeorhesis with oncogenic hyperplasia where the latter is regarded as a genotoxically activated homeorhetic dysfunction. This dysfunction is specified as the transitions of the fluid of cells from a fluid, homeorhetic state to a solid, hyperplastic-tumor state, and back. The key part of the model is a nonlinear reaction-diffusion equation (RDE) where the biochemical-reaction rate is generalized to the one in the wellknown Schlögl physical theory of the non-equilibrium phase transitions. A rigorous analysis of the stability and qualitative aspects of the model, where possible, are presented in detail. This is related to the spatially homogeneous case, i.e. when the above RDE is reduced to a nonlinear ordinary differential equation. The mentioned genotoxic activation is treated as a prevention of the quiescent G0-stage of the cell cycle implemented with the threshold mechanism that employs the critical concentration of the cellular fluid and the nonquiescentcell-duplication time. The continuous tumor morphogeny is described as a time-space-dependent cellular-fluid concentration. There are no sharp boundaries (i.e. no concentration jumps exist) between the domains of the homeorhesis-and tumor-cell populations. No presumption on the shape of a tumor is used. To estimate a tumor in specific quantities, the model provides the time-dependent tumor locus, volume, and boundary that also points out the tumor shape and size. The above features are indispensable in the quantitative development of antiproliferative drugs or therapies and strategies to prevent oncogenic hyperplasia in cancer and other proliferative diseases. The work proposes an analytical-numerical method for solving the aforementioned RDE. A few topics for future research are suggested.

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“…In general, changes in (e.g., down to the values not less than ) depend on various genotoxic biological signals (e.g., Massagué, 2004;Kitazono et al, 1999).…”

Section: The Hyperplastic-tumor/nonquiescent-cell Asymptotementioning

confidence: 99%

Section: Valuementioning

confidence: 99%