<p>Simulated model profiles with changes in: A) Apoptosis duration, <i>T<sub>A</sub></i>, B) Maximum drug efficacy, <i>E<sub>max</sub></i>, and C) Drug potency, <i>EC<sub>50</sub></i>. D) Signature profile of cycle-specific drug mechanism model with dose escalation. Simulation were carried with parameters values of <i>T</i> = 1 day, <i>T<sub>A</sub></i> = 4 days, <i>p<sub>0</sub></i> = 2, <i>k<sub>in0</sub></i> = 0.05 g/day, <i>w<sub>th</sub></i> = 10 g, <i>E<sub>max</sub></i> = 1 and <i>EC<sub>50</sub></i> = 0.01 concentration, unless otherwise indicated. Arrows indicate dose administration at days 10, 20 and 30.</p
The main two pitfalls of therapeutics in clinical oncology, that limit increasing drug doses, are un...
BACKGROUND: In vitro generated dose-response curves of human cancer cell lines are widely used to de...
<p>Here we consider a baseline mutation rate per cell division of 10<sup>−8</sup> and the effect of ...
<p>Sensitivity coefficient of the (A) uninfected cells, (B) infected cells, and (C) the viral load w...
<p>Cell cycle and apoptosis data were quantified for the indicated fold-changes relative to vehicle ...
The cell cycle is implicated in diseases that are the leading cause of mortality and morbidity in th...
Objectives: A major challenge in drug discovery and development is the prediction, in a strictly qua...
This dissertation presents a collection of mathematical models for cellular response to the most com...
International audienceCell response heterogeneity upon drug treatment is a leading cause of reduced ...
This work studies three differential equation models of the leukemia cell cycle: a population balanc...
Cancer chemotherapy agents are assessed for their therapeutic utility primarily by their ability to ...
Objectives: This presentation aims at describing how modeling framework incorporating biomarker data...
<p>Time course simulations were run for up to 48 hours from steady states belonging to different par...
<p>Breakdown, by mechanism of action, of top 24 most effective simulated drugs (those scoring 0.9 or...
(A) Control with low transition rates and no drug exposure. (B) Drug-sensitive cells with drug intro...
The main two pitfalls of therapeutics in clinical oncology, that limit increasing drug doses, are un...
BACKGROUND: In vitro generated dose-response curves of human cancer cell lines are widely used to de...
<p>Here we consider a baseline mutation rate per cell division of 10<sup>−8</sup> and the effect of ...
<p>Sensitivity coefficient of the (A) uninfected cells, (B) infected cells, and (C) the viral load w...
<p>Cell cycle and apoptosis data were quantified for the indicated fold-changes relative to vehicle ...
The cell cycle is implicated in diseases that are the leading cause of mortality and morbidity in th...
Objectives: A major challenge in drug discovery and development is the prediction, in a strictly qua...
This dissertation presents a collection of mathematical models for cellular response to the most com...
International audienceCell response heterogeneity upon drug treatment is a leading cause of reduced ...
This work studies three differential equation models of the leukemia cell cycle: a population balanc...
Cancer chemotherapy agents are assessed for their therapeutic utility primarily by their ability to ...
Objectives: This presentation aims at describing how modeling framework incorporating biomarker data...
<p>Time course simulations were run for up to 48 hours from steady states belonging to different par...
<p>Breakdown, by mechanism of action, of top 24 most effective simulated drugs (those scoring 0.9 or...
(A) Control with low transition rates and no drug exposure. (B) Drug-sensitive cells with drug intro...
The main two pitfalls of therapeutics in clinical oncology, that limit increasing drug doses, are un...
BACKGROUND: In vitro generated dose-response curves of human cancer cell lines are widely used to de...
<p>Here we consider a baseline mutation rate per cell division of 10<sup>−8</sup> and the effect of ...