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We began analyzing https://link.springer.com/article/10.1016/j.bulm.2003.10.001, but it redirected us to https://link.springer.com/article/10.1016/j.bulm.2003.10.001. The analysis below is for the second page.

Title[redir]:
Competition and natural selection in a mathematical model of cancer | Bulletin of Mathematical Biology
Description:
A malignant tumor is a dynamic amalgamation of various cell phenotypes, both cancerous (parenchyma) and healthy (stroma). These diverse cells compete over resources as well as cooperate to maintain tumor viability. Therefore, tumors are both an ecological community and an integrated tissue. An understanding of how natural selection operates in this unique ecological context should expose unappreciated vulnerabilities shared by all cancers. In this study I address natural selection’s role in tumor evolution by developing and exploring a mathematical model of a heterogenous primary neoplasm. The model is a system of nonlinear ordinary differential equations tracking the mass of up to two different parenchyma cell types, the mass of vascular endothelial cells from which new tumor blood vessels are built and the total length of tumor microvessels. Results predict the possibility of a hypertumor—a focus of aggressively reproducing parenchyma cells that invade and destroy part or all of the tumor, perhaps before it becomes a clinical entity. If this phenomenon occurs, then we should see examples of tumors that develop an aggressive histology but are paradoxically prone to extinction. Neuroblastoma, a common childhood cancer, may sometimes fit this pattern. In addition, this model suggests that parenchyma cell diversity can be maintained by a tissue-like integration of cells specialized to provide different services.

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  • Science
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🏙️ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 96,105,781 visitors per month in the current month.

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Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Doi.org could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

google, scholar, article, cancer, cell, tumor, growth, endothelial, selection, cells, vascular, biol, mathematical, model, tumors, nature, factor, privacy, cookies, content, biology, natural, parenchyma, angiogenesis, tumour, philadelphia, publish, search, nagy, stroma, access, bull, math, hypoxia, vegf, lung, eds, function, data, information, log, journal, research, blood, modeling, heterogeneity, discover, death, regression, cotran,

Topics {✒️}

vascular-specific growth factors month download article/chapter vascular endothelial cells high voltage electron-micrographs endothelial cell death natural selection operates address natural selection experimental tumour revealed endothelial cell survival endothelial adhesion molecules parenchyma cell types parenchyma cell diversity privacy choices/manage cookies natural selection arizona state university full article pdf mathematical biology aims tumour progression hypoxia-mediated selection cell growth androgen-dependent tumor kinetic heterogeneity prostate cancer progression european economic area heterogenous primary neoplasm check access invasive breast carcinoma diminished apoptotic potential small blood vessels ischemia-induced genes human normal livers instant access diverse cells compete human cells exposed vascular endothelium conditions privacy policy human lung cancer unique ecological context harvard university press blood vessel formation common childhood cancer maintain tumor viability tumor blood vessels tumor growth trends cell biol primary liver tumors accepting optional cookies related subjects increased ras expression immunoreactive matrix metalloproteinases

Questions {❓}

  • What might a stromal responsemean to prostate cancer progression?

Schema {🗺️}

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         headline:Competition and natural selection in a mathematical model of cancer
         description:A malignant tumor is a dynamic amalgamation of various cell phenotypes, both cancerous (parenchyma) and healthy (stroma). These diverse cells compete over resources as well as cooperate to maintain tumor viability. Therefore, tumors are both an ecological community and an integrated tissue. An understanding of how natural selection operates in this unique ecological context should expose unappreciated vulnerabilities shared by all cancers. In this study I address natural selection’s role in tumor evolution by developing and exploring a mathematical model of a heterogenous primary neoplasm. The model is a system of nonlinear ordinary differential equations tracking the mass of up to two different parenchyma cell types, the mass of vascular endothelial cells from which new tumor blood vessels are built and the total length of tumor microvessels. Results predict the possibility of a hypertumor—a focus of aggressively reproducing parenchyma cells that invade and destroy part or all of the tumor, perhaps before it becomes a clinical entity. If this phenomenon occurs, then we should see examples of tumors that develop an aggressive histology but are paradoxically prone to extinction. Neuroblastoma, a common childhood cancer, may sometimes fit this pattern. In addition, this model suggests that parenchyma cell diversity can be maintained by a tissue-like integration of cells specialized to provide different services.
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      description:A malignant tumor is a dynamic amalgamation of various cell phenotypes, both cancerous (parenchyma) and healthy (stroma). These diverse cells compete over resources as well as cooperate to maintain tumor viability. Therefore, tumors are both an ecological community and an integrated tissue. An understanding of how natural selection operates in this unique ecological context should expose unappreciated vulnerabilities shared by all cancers. In this study I address natural selection’s role in tumor evolution by developing and exploring a mathematical model of a heterogenous primary neoplasm. The model is a system of nonlinear ordinary differential equations tracking the mass of up to two different parenchyma cell types, the mass of vascular endothelial cells from which new tumor blood vessels are built and the total length of tumor microvessels. Results predict the possibility of a hypertumor—a focus of aggressively reproducing parenchyma cells that invade and destroy part or all of the tumor, perhaps before it becomes a clinical entity. If this phenomenon occurs, then we should see examples of tumors that develop an aggressive histology but are paradoxically prone to extinction. Neuroblastoma, a common childhood cancer, may sometimes fit this pattern. In addition, this model suggests that parenchyma cell diversity can be maintained by a tissue-like integration of cells specialized to provide different services.
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External Links {🔗}(100)

Analytics and Tracking {📊}

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