  Known as one of the hallmarks of cancer [30], cancer cell invasion of human
body tissue is a complicated spatio-temporal multiscale process which enables a
localised solid tumour to transform into a systemic, metastatic and fatal
disease. This process explores and takes advantage of the reciprocal relation
that solid tumours establish with the extracellular matrix (ECM) components and
other multiple distinct cell types from the surrounding microenvironment.
Through the secretion of various proteolytic enzymes such as matrix
metalloproteinases (MMP) or the urokinase plasminogen activator (uPA), the
cancer cell population alters the configuration of the surrounding ECM
composition and overcomes the physical barriers to ultimately achieve local
cancer spread into the surrounding tissue. The active interplay between the
tissue-scale tumour dynamics and the molecular mechanics of the involved
proteolytic enzymes at the cell-scale underlines the biologically multiscale
character of invasion, and raises the challenge of modelling this process with
an appropriate multiscale approach. In this paper, we present a new two-scale
moving boundary model of cancer invasion that explores the tissue scale tumour
dynamics in conjunction with the molecular dynamics of the urokinase
plasminogen activation system. Building on the multiscale moving boundary
method proposed in [58], the modelling that we propose here allows us to study
the changes in tissue scale tumour morphology caused by the cell-scale uPA
micro-dynamics occurring along the invasive edge of the tumour. Our
computational simulation results demonstrate a range of heterogeneous dynamics
which are qualitatively similar to the invasive growth patterns observed in a
number of different types of cancer, such as the tumour infiltrative growth
patterns discussed in [33].
