Mathematical Model of the Disruption of the Glucose Homeostasis in Cancer Patients
Mentor 1
Gabriella Pinter
Mentor 2
Peter Hinow
Start Date
16-4-2021 12:00 AM
Description
Abstract Cancer is associated with risk factors and co-morbidities that can affect a patient’s treatment as well as decrease the success rate of therapy. One of these factors is impaired glucose/ insulin homeostasis that manifests itself in insulin resistance. It is known that cancer cells multiply copiously using a large amount of amino acids and energy, primarily in the form of glucose which is obtained by reprogramming their host organism’s metabolism. Mathematical models can help understand the interplay between different cell populations competing for glucose in healthy subjects and people with cancer. In this work, a model is constructed for cancer-free individuals and is calibrated by parameter optimization based on literature research and results from published studies. Moving forward, the model for healthy subjects will be used as a basis in parametrizing and optimizing the model when cancer is present. Additionally, insulin levels and insulin receptors in a cancer patient will be considered and examined as hyperinsulinemia occurs frequently. The understanding of glucose homeostasis and its disruption by cancer cells can shed light on the potential use of antidiabetic drugs in cancer therapy. One of these medications, Metformin, has shown promises of higher survival rates in colorectal cancer, whereas insulin is associated with lower rates of survival.
Mathematical Model of the Disruption of the Glucose Homeostasis in Cancer Patients
Abstract Cancer is associated with risk factors and co-morbidities that can affect a patient’s treatment as well as decrease the success rate of therapy. One of these factors is impaired glucose/ insulin homeostasis that manifests itself in insulin resistance. It is known that cancer cells multiply copiously using a large amount of amino acids and energy, primarily in the form of glucose which is obtained by reprogramming their host organism’s metabolism. Mathematical models can help understand the interplay between different cell populations competing for glucose in healthy subjects and people with cancer. In this work, a model is constructed for cancer-free individuals and is calibrated by parameter optimization based on literature research and results from published studies. Moving forward, the model for healthy subjects will be used as a basis in parametrizing and optimizing the model when cancer is present. Additionally, insulin levels and insulin receptors in a cancer patient will be considered and examined as hyperinsulinemia occurs frequently. The understanding of glucose homeostasis and its disruption by cancer cells can shed light on the potential use of antidiabetic drugs in cancer therapy. One of these medications, Metformin, has shown promises of higher survival rates in colorectal cancer, whereas insulin is associated with lower rates of survival.
