Evidence map›Paper›PMID 17891399›Full record

ArticleCancer chemotherapy and pharmacology2008

Pharmacodynamic model for chemotherapy-induced anemia in rats.

Sukyung Woo, Wojciech Krzyzanski, William J Jusko

Open access · greenAbstract read
In one paragraph

Article in Cancer chemotherapy and pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 43 citations in OpenAlex.

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  4. Review
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  10. Feedback control indirect response models.Journal of pharmacokinetics and pharmacodynamics · 2016
    Article
  11. Pharmacodynamic model for chemoradiotherapy-induced thrombocytopenia in mice.Journal of pharmacokinetics and pharmacodynamics · 2015
    Article
  12. Article
  13. Article
  14. Lifespan based indirect response models.Journal of pharmacokinetics and pharmacodynamics · 2012
    Review
  15. Mechanism-based pharmacodynamic modeling.Methods in molecular biology (Clifton, N.J.) · 2012
    Article
  16. Article
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Sukyung WooDepartment of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, State University of New York at Buffalo, 565 Hochstetter Hall, Buffalo, NY 14260, USA.
Wojciech Krzyzanski
William J Jusko
University at Buffalo, State University of New York · US

Funding

MATHEMATICAL MODELS IN PHARMACODYNAMICSR01GM057980 · NIGMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI JUSKO, WILLIAM J., KRZYZANSKI, WOJCIECH · 1998 to 2013
$3.4M
NIGMS NIH HHS R01 GM057980
6 · The paper itself

Abstract

Anticancer agents often cause bone marrow toxicity resulting in progressive anemia which may influence the therapeutic effects of erythropoietic-stimulating agents. The objective of this study was to develop a pharmacodynamic (PD) model to describe chemotherapy-induced anemia in rats. Anemia was induced in male Wistar rats with a single intravenous (i.v.) injection of 60 mg/kg carboplatin. Hematological responses including reticulocytes, red blood cells (RBC), hemoglobin, and endogenous rat erythropoietin (EPO) were measured for up to 4 weeks. A catenary, lifespan-based, indirect response model served as a basic PD model to represent erythroid cellular populations in the bone marrow and blood involved in erythropoiesis. The model assumed that actively proliferating progenitor cells in the bone marrow are sensitive to anti-cancer agents and subject to an irreversible removal process. The removal rate of the target cells is proportional to drug activity concentrations and the cell numbers. An additional RBC loss from the circulation resulting from thrombocytopenia was described by a first-order process. The turnover process of rat EPO and EPO-mediated feedback inhibition mechanism regulated by hemoglobin changes were incorporated. Reticulocyte counts decreased rapidly and reached a nadir by day 3 after administration of carboplatin and returned to the baseline by day 13. This was followed by a gradual increase and the rebound peak occurred at about day 15. The hemoglobin nadir was approximately 9 g/dl observed at about 11-13 days compared to its normal value of 13 g/dl and hemoglobin returned to the baseline by day 30. The increase in endogenous rat EPO mirrored inversely hemoglobin changes and the maximum increase was observed soon after the hemoglobin nadir. The carboplatin-treated rats exhibited progressive anemia. The proposed model adequately described the time course of hematological changes after carboplatin in rats and can be a useful tool to explore potential strategies for the management of anemia caused by chemotherapy.

Indexed as

AlgorithmsAnemiaAnimalsAntineoplastic AgentsBlood Cell CountCarboplatinCell CountComputer SimulationDisease Models, AnimalDisease ProgressionEnzyme-Linked Immunosorbent AssayErythropoietinHematopoiesisHemoglobinsLeukocyte CountMaleAntineoplastic AgentsCarboplatinErythropoietinHemoglobins

Identifiers

PMID17891399
PMCPMC2671004
OpenAlexW2004226158

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.