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Quantifying the role of angiogenesis in malignant progression of gliomas

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Quantifying the role of angiogenesis in malignant progression of gliomas : In Silico modeling integrates imaging and histology. / Swanson, K.R.; Rockne, Russell C.; Alvord Jr., E.C.; Claridge, Jonathan; Chaplain, Mark A.; Anderson, Alexander R.A.

In: Cancer Research, Vol. 71, No. 24, 2011, p. 7366-7375.

Research output: Contribution to journalArticle

Harvard

Swanson, KR, Rockne, RC, Alvord Jr., EC, Claridge, J, Chaplain, MA & Anderson, ARA 2011, 'Quantifying the role of angiogenesis in malignant progression of gliomas: In Silico modeling integrates imaging and histology' Cancer Research, vol 71, no. 24, pp. 7366-7375., 10.1158/0008-5472.CAN-11-1399

APA

Swanson, K. R., Rockne, R. C., Alvord Jr., E. C., Claridge, . J., Chaplain, M. A., & Anderson, A. R. A. (2011). Quantifying the role of angiogenesis in malignant progression of gliomas: In Silico modeling integrates imaging and histology. Cancer Research, 71(24), 7366-7375. 10.1158/0008-5472.CAN-11-1399

Vancouver

Swanson KR, Rockne RC, Alvord Jr. EC, Claridge J, Chaplain MA, Anderson ARA. Quantifying the role of angiogenesis in malignant progression of gliomas: In Silico modeling integrates imaging and histology. Cancer Research. 2011;71(24):7366-7375. Available from: 10.1158/0008-5472.CAN-11-1399

Author

Swanson, K.R.; Rockne, Russell C.; Alvord Jr., E.C.; Claridge, Jonathan; Chaplain, Mark A.; Anderson, Alexander R.A. / Quantifying the role of angiogenesis in malignant progression of gliomas : In Silico modeling integrates imaging and histology.

In: Cancer Research, Vol. 71, No. 24, 2011, p. 7366-7375.

Research output: Contribution to journalArticle

Bibtex - Download

@article{a27ec59716dc4932bbad342274a36327,
title = "Quantifying the role of angiogenesis in malignant progression of gliomas: In Silico modeling integrates imaging and histology",
author = "K.R. Swanson and Rockne, {Russell C.} and {Alvord Jr.}, E.C. and Jonathan Claridge and Chaplain, {Mark A.} and Anderson, {Alexander R.A.}",
year = "2011",
doi = "10.1158/0008-5472.CAN-11-1399",
volume = "71",
number = "24",
pages = "7366--7375",
journal = "Cancer Research",
issn = "0008-5472",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - Quantifying the role of angiogenesis in malignant progression of gliomas

T2 - In Silico modeling integrates imaging and histology

A1 - Swanson,K.R.

A1 - Rockne,Russell C.

A1 - Alvord Jr.,E.C.

A1 - Claridge, Jonathan

A1 - Chaplain,Mark A.

A1 - Anderson,Alexander R.A.

AU - Swanson,K.R.

AU - Rockne,Russell C.

AU - Alvord Jr.,E.C.

AU - Claridge, Jonathan

AU - Chaplain,Mark A.

AU - Anderson,Alexander R.A.

PY - 2011

Y1 - 2011

N2 - Gliomas are uniformly fatal forms of primary brain neoplasms that vary from low- to high-grade (glioblastoma). Whereas low-grade gliomas are weakly angiogenic, glioblastomas are among the most angiogenic tumors. Thus, interactions between glioma cells and their tissue microenvironment may play an important role in aggressive tumor formation and progression. To quantitatively explore how tumor cells interact with their tissue microenvironment, we incorporated the interactions of normoxic glioma cells, hypoxic glioma cells, vascular endothelial cells, diffusible angiogenic factors, and necrosis formation into a first-generation, biologically based mathematical model for glioma growth and invasion. Model simulations quantitatively described the spectrum of in vivo dynamics of gliomas visualized with medical imaging. Furthermore, we investigated how proliferation and dispersal of glioma cells combine to induce increasing degrees of cellularity, mitoses, hypoxia-induced neoangiogenesis and necrosis, features that characterize increasing degrees of "malignancy," and we found that changes in the net rates of proliferation (?) and invasion (D) are not always necessary for malignant progression. Thus, although other factors, including the accumulation of genetic mutations, can change cellular phenotype (e.g., proliferation and invasion rates), this study suggests that these are not required for malignant progression. Simulated results are placed in the context of the current clinical World Health Organization grading scheme for studying specific patient examples. This study suggests that through the application of the proposed model for tumor-microenvironment interactions, predictable patterns of dynamic changes in glioma histology distinct from changes in cellular phenotype (e.g., proliferation and invasion rates) may be identified, thus providing a powerful clinical tool. ©2011 AACR.

AB - Gliomas are uniformly fatal forms of primary brain neoplasms that vary from low- to high-grade (glioblastoma). Whereas low-grade gliomas are weakly angiogenic, glioblastomas are among the most angiogenic tumors. Thus, interactions between glioma cells and their tissue microenvironment may play an important role in aggressive tumor formation and progression. To quantitatively explore how tumor cells interact with their tissue microenvironment, we incorporated the interactions of normoxic glioma cells, hypoxic glioma cells, vascular endothelial cells, diffusible angiogenic factors, and necrosis formation into a first-generation, biologically based mathematical model for glioma growth and invasion. Model simulations quantitatively described the spectrum of in vivo dynamics of gliomas visualized with medical imaging. Furthermore, we investigated how proliferation and dispersal of glioma cells combine to induce increasing degrees of cellularity, mitoses, hypoxia-induced neoangiogenesis and necrosis, features that characterize increasing degrees of "malignancy," and we found that changes in the net rates of proliferation (?) and invasion (D) are not always necessary for malignant progression. Thus, although other factors, including the accumulation of genetic mutations, can change cellular phenotype (e.g., proliferation and invasion rates), this study suggests that these are not required for malignant progression. Simulated results are placed in the context of the current clinical World Health Organization grading scheme for studying specific patient examples. This study suggests that through the application of the proposed model for tumor-microenvironment interactions, predictable patterns of dynamic changes in glioma histology distinct from changes in cellular phenotype (e.g., proliferation and invasion rates) may be identified, thus providing a powerful clinical tool. ©2011 AACR.

UR - http://www.scopus.com/inward/record.url?scp=84255170467&partnerID=8YFLogxK

U2 - 10.1158/0008-5472.CAN-11-1399

DO - 10.1158/0008-5472.CAN-11-1399

M1 - Article

JO - Cancer Research

JF - Cancer Research

SN - 0008-5472

IS - 24

VL - 71

SP - 7366

EP - 7375

ER -

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