Multiscale modeling of tumor growth and angiogenesis: Evaluation of tumor-targeted therapy.

The dynamics of tumor growth and associated events cover multiple time and spatial scales, generally including extracellular, cellular and intracellular modifications. The main goal of this study is to model the biological and physical behavior of tumor evolution in presence of normal healthy tissue...

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Autores principales: Sahar Jafari Nivlouei, M Soltani, João Carvalho, Rui Travasso, Mohammad Reza Salimpour, Ebrahim Shirani
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Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2021
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Acceso en línea:https://doaj.org/article/6670e6ade52a4997bed2b65e6f3fa671
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spelling oai:doaj.org-article:6670e6ade52a4997bed2b65e6f3fa6712021-11-25T05:40:35ZMultiscale modeling of tumor growth and angiogenesis: Evaluation of tumor-targeted therapy.1553-734X1553-735810.1371/journal.pcbi.1009081https://doaj.org/article/6670e6ade52a4997bed2b65e6f3fa6712021-06-01T00:00:00Zhttps://doi.org/10.1371/journal.pcbi.1009081https://doaj.org/toc/1553-734Xhttps://doaj.org/toc/1553-7358The dynamics of tumor growth and associated events cover multiple time and spatial scales, generally including extracellular, cellular and intracellular modifications. The main goal of this study is to model the biological and physical behavior of tumor evolution in presence of normal healthy tissue, considering a variety of events involved in the process. These include hyper and hypoactivation of signaling pathways during tumor growth, vessels' growth, intratumoral vascularization and competition of cancer cells with healthy host tissue. The work addresses two distinctive phases in tumor development-the avascular and vascular phases-and in each stage two cases are considered-with and without normal healthy cells. The tumor growth rate increases considerably as closed vessel loops (anastomoses) form around the tumor cells resulting from tumor induced vascularization. When taking into account the host tissue around the tumor, the results show that competition between normal cells and cancer cells leads to the formation of a hypoxic tumor core within a relatively short period of time. Moreover, a dense intratumoral vascular network is formed throughout the entire lesion as a sign of a high malignancy grade, which is consistent with reported experimental data for several types of solid carcinomas. In comparison with other mathematical models of tumor development, in this work we introduce a multiscale simulation that models the cellular interactions and cell behavior as a consequence of the activation of oncogenes and deactivation of gene signaling pathways within each cell. Simulating a therapy that blocks relevant signaling pathways results in the prevention of further tumor growth and leads to an expressive decrease in its size (82% in the simulation).Sahar Jafari NivloueiM SoltaniJoão CarvalhoRui TravassoMohammad Reza SalimpourEbrahim ShiraniPublic Library of Science (PLoS)articleBiology (General)QH301-705.5ENPLoS Computational Biology, Vol 17, Iss 6, p e1009081 (2021)
institution DOAJ
collection DOAJ
language EN
topic Biology (General)
QH301-705.5
spellingShingle Biology (General)
QH301-705.5
Sahar Jafari Nivlouei
M Soltani
João Carvalho
Rui Travasso
Mohammad Reza Salimpour
Ebrahim Shirani
Multiscale modeling of tumor growth and angiogenesis: Evaluation of tumor-targeted therapy.
description The dynamics of tumor growth and associated events cover multiple time and spatial scales, generally including extracellular, cellular and intracellular modifications. The main goal of this study is to model the biological and physical behavior of tumor evolution in presence of normal healthy tissue, considering a variety of events involved in the process. These include hyper and hypoactivation of signaling pathways during tumor growth, vessels' growth, intratumoral vascularization and competition of cancer cells with healthy host tissue. The work addresses two distinctive phases in tumor development-the avascular and vascular phases-and in each stage two cases are considered-with and without normal healthy cells. The tumor growth rate increases considerably as closed vessel loops (anastomoses) form around the tumor cells resulting from tumor induced vascularization. When taking into account the host tissue around the tumor, the results show that competition between normal cells and cancer cells leads to the formation of a hypoxic tumor core within a relatively short period of time. Moreover, a dense intratumoral vascular network is formed throughout the entire lesion as a sign of a high malignancy grade, which is consistent with reported experimental data for several types of solid carcinomas. In comparison with other mathematical models of tumor development, in this work we introduce a multiscale simulation that models the cellular interactions and cell behavior as a consequence of the activation of oncogenes and deactivation of gene signaling pathways within each cell. Simulating a therapy that blocks relevant signaling pathways results in the prevention of further tumor growth and leads to an expressive decrease in its size (82% in the simulation).
format article
author Sahar Jafari Nivlouei
M Soltani
João Carvalho
Rui Travasso
Mohammad Reza Salimpour
Ebrahim Shirani
author_facet Sahar Jafari Nivlouei
M Soltani
João Carvalho
Rui Travasso
Mohammad Reza Salimpour
Ebrahim Shirani
author_sort Sahar Jafari Nivlouei
title Multiscale modeling of tumor growth and angiogenesis: Evaluation of tumor-targeted therapy.
title_short Multiscale modeling of tumor growth and angiogenesis: Evaluation of tumor-targeted therapy.
title_full Multiscale modeling of tumor growth and angiogenesis: Evaluation of tumor-targeted therapy.
title_fullStr Multiscale modeling of tumor growth and angiogenesis: Evaluation of tumor-targeted therapy.
title_full_unstemmed Multiscale modeling of tumor growth and angiogenesis: Evaluation of tumor-targeted therapy.
title_sort multiscale modeling of tumor growth and angiogenesis: evaluation of tumor-targeted therapy.
publisher Public Library of Science (PLoS)
publishDate 2021
url https://doaj.org/article/6670e6ade52a4997bed2b65e6f3fa671
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