Modeling dynamics of cancer radiovirotherapy.

Advances in genetic engineering have paved the way for a new therapy for cancer, which is called virotherapy. This treatment uses genetically engineered viruses which selectively infect, replicate in, and destroy cancer cells without damaging normal cells. Furthermore, current research and clinical trials have indicated that these viruses can be delivered as single agents or in combination with other therapies.

Modeling the Spatiotemporal Dynamics of Oncolytic Viruses and Radiotherapy as a Treatment for Cancer.

Virotherapy is a novel treatment for cancer, which may be delivered as a single agent or in combination with other therapies. Research studies indicated that the combination of viral therapy and radiation therapy has synergistic antitumor effects in and . In this paper, we proposed two models in the form of partial differential equations to investigate the spatiotemporal dynamics of tumor cells under virotherapy and radiovirotherapy.

Mechanistic Model for Cancer Growth and Response to Chemotherapy.

Cancer treatment has developed over the years; however not all patients respond to this treatment, and therefore further research is needed. In this paper, we employ mathematical modeling to understand the behavior of cancer and its interaction with therapy. We study a drug delivery and drug-cell interaction model along with cell proliferation.

A hybrid agent-based model of the developing mammary terminal end bud.

Mammary gland ductal elongation is spearheaded by terminal end buds (TEBs), where populations of highly proliferative cells are maintained throughout post-pubertal organogenesis in virgin mice until the mammary fat pad is filled by a mature ductal tree. We have developed a hybrid multiscale agent-based model to study how cellular differentiation pathways, cellular proliferation capacity, and endocrine and paracrine signaling play a role during development of the mammary gland. A simplified cellular phenotypic hierarchy that includes stem, progenitor, and fully differentiated cells within the TEB was implemented.

Theory and Experimental Validation of a Spatio-temporal Model of Chemotherapy Transport to Enhance Tumor Cell Kill.

Cancer treatment efficacy can be significantly enhanced through the elution of drug from nano-carriers that can temporarily stay in the tumor vasculature. Here we present a relatively simple yet powerful mathematical model that accounts for both spatial and temporal heterogeneities of drug dosing to help explain, examine, and prove this concept. We find that the delivery of systemic chemotherapy through a certain form of nano-carriers would have enhanced tumor kill by a factor of 2 to 4 over the standard therapy that the patients actually received.

Predictive Modeling of Drug Response in Non-Hodgkin's Lymphoma.

We combine mathematical modeling with experiments in living mice to quantify the relative roles of intrinsic cellular vs. tissue-scale physiological contributors to chemotherapy drug resistance, which are difficult to understand solely through experimentation. Experiments in cell culture and in mice with drug-sensitive (Eµ-myc/Arf-/-) and drug-resistant (Eµ-myc/p53-/-) lymphoma cell lines were conducted to calibrate and validate a mechanistic mathematical model.

Nikolaevskiy equation with dispersion.

The Nikolaevskiy equation was originally proposed as a model for seismic waves and is also a model for a wide variety of systems incorporating a neutral "Goldstone" mode, including electroconvection and reaction-diffusion systems. It is known to exhibit chaotic dynamics at the onset of pattern formation, at least when the dispersive terms in the equation are suppressed, as is commonly the practice in previous analyses. In this paper, the effects of reinstating the dispersive terms are examined.