Patient-specific prostate tumour growth simulation: a first step towards the digital twin

Front Physiol. 2024 Oct 30:15:1421591. doi: 10.3389/fphys.2024.1421591. eCollection 2024.

Abstract

Prostate cancer (PCa) is a major world-wide health concern. Current diagnostic methods involve Prostate-Specific Antigen (PSA) blood tests, biopsies, and Magnetic Resonance Imaging (MRI) to assess cancer aggressiveness and guide treatment decisions. MRI aligns with in silico medicine, as patient-specific image biomarkers can be obtained, contributing towards the development of digital twins for clinical practice. This work presents a novel framework to create a personalized PCa model by integrating clinical MRI data, such as the prostate and tumour geometry, the initial distribution of cells and the vasculature, so a full representation of the whole prostate is obtained. On top of the personalized model construction, our approach simulates and predicts temporal tumour growth in the prostate through the Finite Element Method, coupling the dynamics of tumour growth and the transport of oxygen, and incorporating cellular processes such as proliferation, differentiation, and apoptosis. In addition, our approach includes the simulation of the PSA dynamics, which allows to evaluate tumour growth through the PSA patient's levels. To obtain the model parameters, a multi-objective optimization process is performed to adjust the best parameters for two patients simultaneously. This framework is validated by means of data from four patients with several MRI follow-ups. The diagnosis MRI allows the model creation and initialization, while subsequent MRI-based data provide additional information to validate computational predictions. The model predicts prostate and tumour volumes growth, along with serum PSA levels. This work represents a preliminary step towards the creation of digital twins for PCa patients, providing personalized insights into tumour growth.

Keywords: computational oncology; finite element method (FEM); imaging biomarkers; in-silico model; patient-specific; prostate cancer.

Grants and funding

The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. We would like to express our gratitude to our collaborators from HULAFE, and Quibim S.L. for their essential contribution in retrieving and processing the patient specific clinical data required for the development of this work. This research was funded by Next-Generation EU (ProCanAid Grant No. PLEC 2021-007709). The authors also acknowledge the support of the Aragon Government through Group T50 23R.