ArticlePloS one2019
Mathematical models for cytarabine-derived myelosuppression in acute myeloid leukaemia.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- Exploring innovative G-CSF schedules in AML cytarabine-based consolidation through a digital twin study of white blood cell recovery.PloS one · 2026Article
- Digital twin models for predicting venetoclax and azacitidine-induced neutropenia in patients with acute myeloid leukemia.NPJ digital medicine · 2025Article
- Modelling post-chemotherapy stem cell dynamics in the bone marrow niche of AML patients.Scientific reports · 2024Article
- AML consolidation therapy: timing matters.Journal of cancer research and clinical oncology · 2023Article
- Pharmacokinetic-pharmacodynamic modeling of maintenance therapy for childhood acute lymphoblastic leukemia.Scientific reports · 2023Article
- An integrative systems biology approach to overcome venetoclax resistance in acute myeloid leukemia.PLoS computational biology · 2022Article
- Model-Based Simulation of Maintenance Therapy of Childhood Acute Lymphoblastic Leukemia.Frontiers in physiology · 2020Article
- Prediction of leukocyte counts during paediatric acute lymphoblastic leukaemia maintenance therapy.Scientific reports · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigate the personalisation and prediction accuracy of mathematical models for white blood cell (WBC) count dynamics during consolidation treatment using intermediate or high-dose cytarabine (Ara-C) in acute myeloid leukaemia (AML). Ara-C is the clinically most relevant cytotoxic agent for AML treatment. We extend a mathematical model of myelosuppression and a pharmacokinetic model of Ara-C with different hypotheses of Ara-C's pharmacodynamic effects. We cross-validate the 12 model variations using dense WBC count measurements from 23 AML patients. Surprisingly, the prediction accuracy remains satisfactory in each of the models despite different modelling hypotheses. Therefore, we compare average clinical and calculated WBC recovery times for different Ara-C schedules as a successful methodology for model discrimination. As a result, a new hypothesis of a secondary pharmacodynamic effect on the proliferation rate seems plausible. Furthermore, we demonstrate the impact of treatment timing on subsequent nadir values based on personalised predictions as a possibility for influencing/controlling myelosuppression.
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