bioRxiv Science⌕ Search

bioRxiv · 10.1101/428326

Mathematical Models for the Influence of Cytarabine on White Blood Cell Dynamics in Acute Myeloid Leukemia

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 leukemia (AML). Ara-C is the clinically most relevant cytotoxic agent for AML treatment.\n\nWe extend the gold-standard model of myelosuppression and a pharmacokinetic model of Ara-C with different hypotheses of Ara-Cs pharmacodynamic effects. We cross-validate 12 mathematical models using dense WBC count measurements from 23 AML patients. Surprisingly, the prediction accuracies are similarly good 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 how personalized predictions of the impact of treatment timing on subsequent nadir values could be used for clinical decision support.\n\nAuthor summaryThe major obstacle in accurately predicting the outcome of a medical therapy is the vast variation in individual response patterns. It concerns both the subjective experience of the patient and the objectively measurable achievement of a clinical remission with restoration of normal blood counts. Here, we address acute myeloid leukemia (AML)-chemotherapy using cytarabine (Ara-C) as this drug is this most important component of AML-treatment. In addition to the wide spectrum of genetic aberrations involved in pathogenesis leading to variations in patient response patterns, another facet of personalised medicine awaits exploration of its full potential: a systematic, mathematical approach to understand and manipulate the dynamics of relevant biomarkers. We use personalised mathematical models to describe and predict white blood cell (WBC) counts during AML consolidation treatment. We analyse why and to what extent low WBC counts, a serious adverse event during therapy, occur. In a comprehensive approach we investigate published models, compare them with our extended models and outline the impact of modelling assumptions and varying chemotherapy schedules on prediction accuracy and model discrimination. Our numerical results confirm the clinical finding that a newly proposed schedule is superior with respect to WBC recovery and shed new light on the reasons why.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Jost, F., Schalk, E., Rinke, K., Fischer, T., Sager, S.. 2018-09-27. Mathematical Models for the Influence of Cytarabine on White Blood Cell Dynamics in Acute Myeloid Leukemia. https://doi.org/10.1101/428326

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Gene regulatory architecture in antibiotic resistance is optimized for specific dynamic regimens

Cellular responses to antibiotics face a fundamental trade-off: resistance must be deployed quickly enough to prevent the accumulation of drug inside the cell, but expression of resistance genes is costly in the absence of the drug. Therefore, antibiotic responses are typically regulated, controlling not only whether resistance is expressed, but also when, how strongly, and for how long. These regulatory strategies are implemented through the strength and arrangement of promoters and operators. However, it is still not clear how the dynamics of drug exposure select for specific regulatory strategies. Here, we develop a dynamical model of a typical antibiotic response, where a transcriptional repressor senses the drug and regulates expression of a resistance protein, coupled to the effects of the drug on cell growth and gene expression. We define a cost function that weighs the different burdens imposed on the cell over the course of the response, and perform in silico optimization of the regulatory parameters under different selective pressures for three architectures of increasing complexity: constitutive expression of resistance, repression by a constitutively expressed repressor, and repression by a self-regulated repressor. We find that strong drug exposures favor constitutive expression of resistance, high costs of basal expression favor repression by a constitutive repressor, and self-regulation of the repressor is favored only when the response must provide protection while also restraining overexpression of resistance. Stochastic simulations further show that self-regulation of the repressor protects cells against fluctuations in repressor levels, which cause unnecessary induction of resistance before exposure and failed induction after exposure. This framework links the dynamics of the environment to the evolution of gene regulation, providing a basis to predict which regulatory strategies are expected to arise under specific selective pressures.

systems biology↗

Photographic age gap is associated with frailty and predicts survival in laboratory mice

Ageing studies in mice need biomarkers that are cheap, non-invasive and repeatable. We asked how much of a mouse's age can be read from an ordinary photograph, and whether the part that cannot be explained by age carries biological information. We assembled 2,846 photographs of 1,292 mice (four strains, 1 to 34 months old) from seven facilities and predicted age with a frozen self-supervised vision model (DINOv2) and a ridge regression, always tested on facilities the model had never seen. Absolute age transferred poorly between facilities (median absolute error 138 days), because each facility's photographs carried an offset. Relative age transferred well: among mice photographed in the same session, the older mouse was predicted older in 65% of pairs, rising above 95% for age differences over 500 days, and the later photograph of the same mouse was predicted older in 63% of repeat pairs. Sex, in comparison, was inferred more reliably (87%). Mice predicted older than their age were frailer (+0.12 SD per 100 days) and had shorter survival (hazard ratio 1.14 per 100 days), and fourth generation (G4) telomerase-deficient mice looked 151 days older than their wild-type controls. Routine photographs therefore carry a real biological age signal that can be read at no extra cost, best used to compare mice photographed together.

systems biology↗

Intestinal molecular siphoning by engineered bacterial spores for non-systemic treatment of nicotine addiction

Eradicating toxic small molecules from the body typically requires the administrations of therapeutic agents for systemic circulation and tissue distribution, resulting in inevitable adverse events from off-target effects. Here, we propose a intestinal molecular siphoning approach for treating diseases caused by toxic substances, in which enzymatic degradation of a toxic substance in the intestinal lumen serves as a driving force for the diffusion of the toxic substance from blood to gut, and continuous elimination of the toxic substance in the gut could effectively ease substance dependence. Using nicotine as a model substance, a live bacterial system was constructed by displaying a trypsin-resistant nicotine oxidase on the surface of Bacillus subtilis spores, and encapsulating in enteric-coated microspheres for gastric protection and targeted intestinal release. After oral treatments with the live bacterial system in mice, peak concentrations of nicotine in blood and brain were remarkably reduced compared to controls. Moreover, the live bacterial system could effectively attenuate nicotine addiction by suppressing dopamine reward surges to reverse withdrawal hyperalgesia, preventing the upregulation of nicotinic acetylcholine receptors, and alleviating anxiety-like behaviors. These findings show the potential of intestinal molecular siphoning as a target-independent therapeutic strategy for lowering circulating toxic substances through non-systemic enzyme reprogramming.

systems biology↗