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1.
Anticancer Res ; 44(6): 2425-2436, 2024 Jun.
Article in English | MEDLINE | ID: mdl-38821607

ABSTRACT

BACKGROUND/AIM: Despite the advances in oncology and cancer treatment over the past decades, cancer remains one of the deadliest diseases. This study focuses on further understanding the complex nature of cancer by using mathematical tumor modeling to understand, capture as best as possible, and describe its complex dynamics under chemotherapy treatment. MATERIALS AND METHODS: Focusing on autoregressive with exogenous inputs, i.e., ARX, and adaptive neuro-fuzzy inference system, i.e., ANFIS, models, this work investigates tumor growth dynamics under both single and combination anticancer agent chemotherapy treatments using chemotherapy treatment data on xenografted mice. RESULTS: Four ARX and ANFIS models for tumor growth inhibition were developed, estimated, and evaluated, demonstrating a strong correlation with tumor weight data, with ANFIS models showing superior performance in handling the multi-agent tumor growth complexities. These findings suggest potential clinical applications of the ANFIS models through further testing. Both types of models were also tested for their prediction capabilities across different chemotherapy schedules, with accurate forecasting of tumor growth up to five days in advance. The use of adaptive prediction and sliding (moving) data window techniques allowed for continuous model updating, ensuring more robust predictive capabilities. However, long-term forecasting remains a challenge, with accuracy declining over longer prediction horizons. CONCLUSION: While ANFIS models showed greater reliability in predictions, the simplicity and rapid deployment of ARX models offer advantages in situations requiring immediate approximations. Future research with larger, more diverse datasets and by exploring varying model complexities is recommended to improve the models' reliability and applicability in clinical decision-making, thereby aiding the development of personalized chemotherapy regimens.


Subject(s)
Neoplasms , Animals , Mice , Humans , Neoplasms/drug therapy , Neoplasms/pathology , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Antineoplastic Combined Chemotherapy Protocols/pharmacology , Xenograft Model Antitumor Assays , Fuzzy Logic , Antineoplastic Agents/therapeutic use , Antineoplastic Agents/pharmacology , Tumor Burden/drug effects
2.
Anticancer Res ; 40(9): 5181-5189, 2020 Sep.
Article in English | MEDLINE | ID: mdl-32878806

ABSTRACT

BACKGROUND/AIM: Mathematical models have long been considered as important tools in cancer biology and therapy. Herein, we present an advanced non-linear mathematical model that can predict accurately the effect of an anticancer agent on the growth of a solid tumor. MATERIALS AND METHODS: Advanced non-linear mathematical optimization techniques and human-to-mouse experimental data were used to develop a tumor growth inhibition (TGI) estimation model. RESULTS: Using this mathematical model, we could accurately predict the tumor mass in a human-to-mouse pancreatic ductal adenocarcinoma (PDAC) xenograft under gemcitabine treatment up to five time periods (points) ahead of the last treatment. CONCLUSION: The ability of the identified TGI dynamic model to perform satisfactory short-term predictions of the tumor growth for up to five time periods ahead was investigated, evaluated and validated for the first time. Such a prediction model could not only assist the pre-clinical testing of putative anticancer agents, but also the early modification of a chemotherapy schedule towards increased efficacy.


Subject(s)
Antineoplastic Agents/pharmacology , Models, Theoretical , Nonlinear Dynamics , Xenograft Model Antitumor Assays , Algorithms , Animals , Antineoplastic Agents/administration & dosage , Antineoplastic Agents/pharmacokinetics , Carcinoma, Pancreatic Ductal/drug therapy , Carcinoma, Pancreatic Ductal/pathology , Cell Proliferation/drug effects , Disease Models, Animal , Humans , Mice , Pancreatic Neoplasms/drug therapy , Pancreatic Neoplasms/pathology
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