This work presents a thorough analysis of reconstruction of global wave fields (governed by the inhomogeneous wave equation and the Maxwell vector wave equation) from sensor time series data of the wave field. Three major problems are considered. First, an analysis of circumstances under which wave fields can be fully reconstructed from a network of fixed-location sensors is presented. It is proven that, in many cases, wave fields can be fully reconstructed from a single sensor, but that such reconstructions can be sensitive to small perturbations in sensor placement. Generally, multiple sensors are necessary. The next problem considered is how to obtain a global approximation of an electromagnetic wave field in the presence of an amplifying noisy current density from sensor time series data. This type of noise, described in terms of a cylindrical Wiener process, creates a nonequilibrium system, derived from Maxwell’s equations, where variance increases with time. In this noisy system, longer observation times do not generally provide more accurate estimates of the field coefficients. The mean squared error of the estimates can be decomposed into a sum of the squared bias and the variance. As the observation time $\tau$ increases, the bias decreases as $\mathcal{O}(1/\tau)$ but the variance increases as $\mathcal{O}(\tau)$. The contrasting time scales imply the existence of an ``optimal'' observing time (the bias-variance tradeoff). An iterative algorithm is developed to construct global approximations of the electric field using the optimal observing times. Lastly, the effect of sensor acceleration is considered. When the sensor location is fixed, measurements of wave fields composed of plane waves are almost periodic and so can be written in terms of a standard Fourier basis. When the sensor is accelerating, the resulting time series is no longer almost periodic. This phenomenon is related to the Doppler effect, where a time transformation must be performed to obtain the frequency and amplitude information from the time series data. To obtain frequency and amplitude information from accelerating sensor time series data in a general inhomogeneous medium, a randomized algorithm is presented. The algorithm is analyzed and example wave fields are reconstructed.

The representation of a patient’s characteristics as the parameters of a model is a key component in many studies of personalized medicine, where the underlying mathematical models are used to describe, explain, and forecast the course of treatment. In this context, clinical observations form the bridge between the mathematical frameworks and applications. However, the formulation and theoretical studies of the models and the clinical studies are often not completely compatible, which is one of the main obstacles in the application of mathematical models in practice. The goal of my study is to extend a mathematical framework to model prostate cancer based mainly on the concept of cell-quota within an evolutionary framework and to study the relevant aspects for the model to gain useful insights in practice. Specifically, the first aim is to construct a mathematical model that can explain and predict the observed clinical data under various treatment combinations. The second aim is to find a fundamental model structure that can capture the dynamics of cancer progression within a realistic set of data. Finally, relevant clinical aspects such as how the patient's parameters change over the course of treatment and how to incorporate treatment optimization within a framework of uncertainty quantification, will be examined to construct a useful framework in practice.

Cancer is a major health problem in the world today and is expected to become an even larger one in the future. Although cancer therapy has improved for many cancers in the last several decades, there is much room for further improvement. Mathematical modeling has the advantage of being able to test many theoretical therapies without having to perform clinical trials and experiments. Mathematical oncology will continue to be an important tool in the future regarding cancer therapies and management.

This dissertation is structured as a growing tumor. Chapters 2 and 3 consider spheroid models. These models are adept at describing 'early-time' tumors, before the tumor needs to co-opt blood vessels to continue sustained growth. I consider two partial differential equation (PDE) models for spheroid growth of glioblastoma. I compare these models to in vitro experimental data for glioblastoma tumor cell lines and other proposed models. Further, I investigate the conditions under which traveling wave solutions exist and confirm numerically.

As a tumor grows, it can no longer be approximated by a spheroid, and it becomes necessary to use in vivo data and more sophisticated modeling to model the growth and diffusion. In Chapter 4, I explore experimental data and computational models for describing growth and diffusion of glioblastoma in murine brains. I discuss not only how the data was obtained, but how the 3D brain geometry is created from Magnetic Resonance (MR) images. A 3D finite-difference code is used to model tumor growth using a basic reaction-diffusion equation. I formulate and test hypotheses as to why there are large differences between the final tumor sizes between the mice.

Once a tumor has reached a detectable size, it is diagnosed, and treatment begins. Chapter 5 considers modeling the treatment of prostate cancer. I consider a joint model with hormonal therapy as well as immunotherapy. I consider a timing study to determine whether changing the vaccine timing has any effect on the outcome of the patient. In addition, I perform basic analysis on the six-dimensional ordinary differential equation (ODE). I also consider the limiting case, and perform a full global analysis.