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ePoster Display

19P - Evaluation of different pharmacokinetic-pharmacodynamic models for tumor growth delay prediction after chemotherapy


16 Sep 2021


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Cytotoxic Therapy;  Basic Science

Tumour Site


Ivan Terterov


Annals of Oncology (2021) 32 (suppl_5): S361-S375. 10.1016/annonc/annonc684


I.N. Terterov1, V. Chubenko1, N.A. Knyazev1, V. Klimenko1, A.A. Bogdanov1, V.M. Moiseyenko2, A.A. Bogdanov1

Author affiliations

  • 1 Scientific Department, St. Petersburg Clinical Research and Practical Center of Specialized Types of Medical Care (Oncologic), 197758 - Saint-Petersburg/RU
  • 2 Administration, St. Petersburg Clinical Research and Practical Center of Specialized Types of Medical Care (Oncologic), 197758 - Saint-Petersburg/RU


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Abstract 19P


In preclinical studies to rank anticancer agents for their efficacy the delay in tumor growth after impermanent drug exposure is often used. For a more detailed description of the anticancer drug action, mathematical pharmacokinetics/pharmacodynamics (PK/PD) models were developed. Such models allow predicting tumor growth time evolution and particularly the delay for various drug dosages. Each PK/PD model is based on the mathematical formulation of the biological processes underlying the antitumor drug action. However, the parameterization and the choice of the dominant effect in the model may be ambiguous. Thus choosing the proper PK/PD model for the numerical description of the tumor growth remains a not straightforward task. In this work, we tested the performance of different PK/PD models to describe tumor volume delay.


We compared a popular TGI model (Simeoni et.al.) which is based on cytotoxic effect, and the Minimal model (MM, recently proposed by us) that incorporates both anti-angiogenic and cytotoxic effects in separate terms. All calculations were done using the SciPy package. For tests we obtained tumor growth data from different gemcitabine regimens in SHR mice with s.c. injected Ehrlich carcinoma cells.


Both models well capture tumor volume delay when fitted to mean volumes in a group treated with single dose gemcitabine (i.p. 25 mg/kg) with slight difference in simulated tumor growth curves during the short period after injection. With parameters obtained above, predictions of the MM model for metronomic gemcitabine treatment group (i.p. 0.5 mg/kg, each day) were close to experimental values, while the predicted tumor growth curve by the TGI model significantly differed.


Our results emphasize the need of caution in the choice of the proper PK/PD model in preclinical studies, even when the model satisfactorily fits tumor growth delay. To have a predictive power the model should contain terms that adequately describe the biological mechanism of anticancer drug action.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.


Has not received any funding.


All authors have declared no conflicts of interest.

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