Contribution of modelling chemotherapy-induced hematological toxicity for clinical practice.

Anticancer chemotherapies are responsible for numerous adverse events. Among these, hematological toxicity is one of the main causes for ending treatment. These toxicities decrease production of red blood cells (anemia), production of white blood cells (neutropenia or granulocytopenia), and production of platelets (thrombocytopenia), which may be life-threatening to the patient. Preventing such discontinuation would be valuable for treating patients more effectively. In order to achieve this goal, numerous mathematical and physiological or semiphysiological models have been developed. The complexity of models has increased over the years, from empiric E(max) models to mechanistic models including physiological mechanisms such as feedback control. This review discusses several approaches of modelling hematological toxicities illustrated with some examples: pharmacodynamic models for the hematological toxicity of 5-fluorouracil, epirubicin, melphalan, paclitaxel, topotecan, and indisulam.