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Open AccessJournal ArticleDOI

A Review of Mathematical Models for Tumor Dynamics and Treatment Resistance Evolution of Solid Tumors

TLDR
The opportunities of a model‐based approach as discussed in this review can be of great benefit for future optimizing and personalizing anticancer treatment.
Abstract
Increasing knowledge of intertumor heterogeneity, intratumor heterogeneity, and cancer evolution has improved the understanding of anticancer treatment resistance. A better characterization of cancer evolution and subsequent use of this knowledge for personalized treatment would increase the chance to overcome cancer treatment resistance. Model-based approaches may help achieve this goal. In this review, we comprehensively summarized mathematical models of tumor dynamics for solid tumors and of drug resistance evolution. Models displayed by ordinary differential equations, algebraic equations, and partial differential equations for characterizing tumor burden dynamics are introduced and discussed. As for tumor resistance evolution, stochastic and deterministic models are introduced and discussed. The results may facilitate a novel model-based analysis on anticancer treatment response and the occurrence of resistance, which incorporates both tumor dynamics and resistance evolution. The opportunities of a model-based approach as discussed in this review can be of great benefit for future optimizing and personalizing anticancer treatment.

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Citations
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Journal ArticleDOI

On tumoural growth and treatment under cellular dedifferentiation

TL;DR: In this paper , a mathematical model of cancer stem cell (CSC) driven tumour growth was extended to also include dedifferentiation, which increased the likelihood of tumorigenesis and the speed of tumoural growth, both modulated by the proliferative potential of non-stem cancer cells.
Journal ArticleDOI

Computational analysis of 5-fluorouracil anti-tumor activity in colon cancer using a mechanistic pharmacokinetic/pharmacodynamic model

TL;DR: In this article , an integrated mechanistic pharmacokinetics/pharmacodynamics (PK/PD) model was developed to examine the influence of 5-Fluorouracil (5-FU) as an S-phase specific doublestrand break (DSB)-inducing agent on tumor proliferation.

Optimizing Cancer Drug Treatment Models Using Process Dynamics

TL;DR: An overarching model that can be highly tuned to a patient’s individual physiology and cancer type is developed, derived from basic pharmacokinetic principles and mass transfer and tied together using process dynamics to relate a treatment input to a cancer reduction output.
Proceedings ArticleDOI

Efficient numerical solution of the brain glioblastomas proliferation-invasion model

TL;DR: This work numerically solve the Partial Differential Equation modelling the proliferation-invasion of brain glioblastomas and suggests that solution times may be reduced by exploiting the underlying structure of the derived system of algebraic equations.
Proceedings ArticleDOI

Indirect supervised fine-tuning of a tumor model parameter estimator neural network

TL;DR: In this paper , another supervised neural network was used to solve the applied differential equations faster with fewer algebraic steps than the traditionally used ODE solvers, which can be used in further research as an unconstrained optimization technique for parameter fitting.
References
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BookDOI

The Case Study

TL;DR: On May 25, 1977, IEEE member, Virginia Edgerton, a senior information scientist employed by the City of New York, telephoned the chairman of CSIT's Working Group on Ethics and Employment Practices, having been referred to the committee by IEEE Headquarters.
Journal ArticleDOI

Liquid biopsies come of age: towards implementation of circulating tumour DNA

TL;DR: The field is now in an exciting transitional period in which ctDNA analysis is beginning to be applied clinically, although there is still much to learn about the biology of cell-free DNA.
Journal ArticleDOI

Chemoresistance Evolution in Triple-Negative Breast Cancer Delineated by Single-Cell Sequencing

TL;DR: The data showed that resistant genotypes were pre-existing and adaptively selected by NAC, while transcriptional profiles were acquired by reprogramming in response to chemotherapy in TNBC patients.
Book ChapterDOI

The Mathematical Model

TL;DR: The death rate per tumor cell due to immunological response is proportional to the total number of antigen-producing (tumor) cells; thus, the total death rate is quadratic.
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