Journal
PLOS COMPUTATIONAL BIOLOGY
Volume 13, Issue 1, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pcbi.1005259
Keywords
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Funding
- Marie Curie Intra European Fellowship [FP7-PEOPLE-2013IEF, 627025]
- European FP7 [FP7-ICT-2011-9, 601040]
- Engineering & Physical Sciences Research Council-UK [EP/K020439/1]
- European Research Council [336839]
- EPSRC [EP/K020439/1, EP/H046410/1, EP/M020533/1] Funding Source: UKRI
- Engineering and Physical Sciences Research Council [EP/K020439/1, EP/H046410/1, EP/M020533/1] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0509-10143] Funding Source: researchfish
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Vascularisation is a key feature of cancer growth, invasion and metastasis. To better understand the governing biophysical processes and their relative importance, it is instructive to develop physiologically representative mathematical models with which to compare to experimental data. Previous studies have successfully applied this approach to test the effect of various biochemical factors on tumour growth and angiogenesis. However, these models do not account for the experimentally observed dependency of angiogenic network evolution on growth-induced solid stresses. This work introduces two novel features: the effects of hapto- and mechanotaxis on vessel sprouting, and mechano-sensitive dynamic vascular remodelling. The proposed three-dimensional, multiscale, in-silico model of dynamically coupled angiogenic tumour growth is specified to in-vivo and in-vitro data, chosen, where possible, to provide a physiologically consistent description. The model is then validated against in-vivo data from murine mammary carcinomas, with particular focus placed on identifying the influence of mechanical factors. Crucially, we find that it is necessary to include hapto- and mechanotaxis to recapitulate observed time-varying spatial distributions of angiogenic vasculature.
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