Recent development in mathematical oncology in Asia and Australia

Wednesday, June 16 at 05:45pm (PDT)
Thursday, June 17 at 01:45am (BST)
Thursday, June 17 09:45am (KST)

SMB2021 SMB2021 Follow Tuesday (Wednesday) during the "MS15" time block.
Note: this minisymposia has multiple sessions. The second session is MS09-ONCO (click here).

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Yangjin Kim (Konkuk University, Korea, Republic of), Eunjung Kim (Korea Institute of Science and Technology, Korea)


Cancer is a nonlinear and multiscale system that involves complex interactions between molecules, cells, and tissue. Genetic mutations occurring at a subcellular molecule level could drive functional changes at the cellular level, leading to tissue-level changes. Tissue-level properties produce selection pressure that governs the distribution and growth of cancer cells. In particular, the tumor microenvironments such as extracellular matrix, vascular bed, stromal cells are known to modulate tumour progression. Therefore, a thorough understanding of tumor microenvironment would provide a foundation to generate new strategies in therapeutic drug development. To understand this complex dynamical system, many mathematical models have been developed at a sub-cellular, tissue, and multiscale level. The main aim of this session is to discuss current stages and challenges in cancer modeling in Asia. Specific goals of the session include: (i) to analyze both computational and analytical solutions to various mathematical models of tumor growth and progression, (ii) to discuss how mathematical models can be used to support better clinical decisions, (iii) to present models that have improved our biochemical/biomechanical understanding of the fundamental mechanism that drives tumor progression, (iv) to discuss new treatment strategies guided by mathematical models.

Dumitru Trucu

(Division of Mathematics, University of Dundee, DD1 4HN, Dundee, United Kingdom)
"Multiscale 3D Glioblastoma Modelling: Bulk and Leading Edge Dynamics within the Fibrous Brain Tissue"
Glioblastoma multiform is one of the most aggressive types of brain cancer, and the understanding of its progression remains one of the greatest challenges. In this talk we propose a multi-scale moving boundary approach for the glioblastoma cell population invasion within the brain fibrous environment. This will account on both the proteolytic dynamics at the tumour interface and on the interaction with brain fibres and the emerging collagen fibres at the site of the tumour. These interactions will be explored in their natural 3D setting by accounting on their genuinely multiscale character both in terms of the peritumoural proteolytic activity of the matrix degrading enzymes, and the cell-brain fibres interactions. Our 3D computational exportation suggests that although current imaging technologies provide valuable details of the brain’s underlying structure, in order to provide meaningful predictions for tumour growth and to test new hypotheses, we may need to use this information in a different, novel ways when we model glioblastoma mathematically.

Peter Kim

(University of Sydney, Australia)
"How do viruses move? Modelling diffusion of oncolytic virus in collagen-dense tumours"
Solid tumours develop much like a fortress, acquiring characteristics that protect them against invasion. A common trait observed in solid tumours is the synthesis of excess collagen which traps therapeutic agents, resulting in a lack of dispersion of treatment within the tumour mass. In most tumours this results in only a localised treatment. Often the tumour quickly recovers and continues to invade surrounding regions. Anti-tumour viral therapy, although consisting of nano-sized particles, is no exception to this rule. Experimental results show collagen density affects viral diffusion. More specifically, when injected, viruses will move to regions of low collagen concentration; therefore, accurately modelling viral diffusion is an important aspect of modelling virotherapy. To understand the underlying dynamics that impede viral diffusion in collagen, we derive, from first principles, a novel non-Fickian diffusion term and show that this diffusion term can accurately capture experimental observations. Then, using a system of partial differential equations we explore how treatment under this diffusion term differs from the standard Fickian diffusion, commonly used in virotherapy models. The disparity between results highlights a significant gap in our understanding of virotherapy modelling and could mean estimates based on Fickian diffusion need to be reassessed for their biological impact.

Da Zhou

(School of Mathematical Sciences, Xiamen University, China)
"Cancer suppression: ingredients utilized by cellular hierarchy"
Many fast renewing tissues are characterized by a hierarchical cellular architecture, with tissue specific stem cells at the root of the cellular hierarchy, differentiating into a whole range of specialized cells. Growing evidence shows that the hierarchical cellular architecture has a profound effect on cancer suppression. In this talk, we will show some cancer-suppression mechanisms possibly utilized by cellular hierarchy using mathematical models. Specifically, we are concerned about cell competition, different modes of cell division and their effects on cancer suppression.

Junho Lee

(Department of Mathematics, Konkuk University, Korea)
"Role of neutrophil extracellular traps in regulation of lung cancer invasion : a computational model"
Lung cancer is one of the leading causes of cancer-related deaths worldwide and is characterized by hijacking immune system for active growth and aggressive metastasis. Neutrophils, which require establishing immune activity against tumors as the first line of defense, are damaged by tumor cells, which in many ways promote tumor invasion. The mutual interaction between a tumor and neutrophils from bone marrow or in blood induces the critical transition of the naive form, called the N1 type, to the more aggressive phenotype, called the N2 tumor-associated neutrophils (TANs), which then promotes tumor invasion. In this study, we investigate the mutual interactions between the tumor cells and the neutrophils that facilitate tumor invasion by developing a mathematical model that involves taxis-reaction-diffusion equations for the critical components in the interaction. These include the densities of tumor and neutrophils, and the concentrations of signaling molecules (TGFbeta-CXCL8-MMP) and structure such as neutrophil extracellular traps (NETs). We apply the mathematical model to a Boyden invasion assay used in the experiments to demonstrate that the N2 TANs can enhance tumor cell invasion by secreting the neutrophil elastase. We show (i) that the model can reproduce the major experimental observation on NET-mediated cancer invasion, (ii) how stimulated neutrophils with different N1 and N2 landscapes shape the metastatic potential of the lung cancers and (iii) that the efficacy of anti-tumor and anti-invasion drugs depend on N1  N2 landscapes of stimulated neutrophils. The mathematical model tests several hypotheses to guide future experiments with the goal of the development of new anti-tumor strategies.

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Virtual conference of the Society for Mathematical Biology, 2021.