Evidence map›Paper›PMID 24400068›Full record

ArticlePloS one2014

Exploiting the synergy between carboplatin and ABT-737 in the treatment of ovarian carcinomas.

Harsh Vardhan Jain, Alan Richardson, Michael Meyer-Hermann, Helen M Byrne

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Bcl-2/Bcl-xOncology letters · 2017
    Article
  5. Mathematical models of breast and ovarian cancers.Wiley interdisciplinary reviews. Systems biology and medicine · 2016
    Review
  6. Article
  7. Article
  8. Article
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

4 authors at 4 institutions in 3 countries.

Harsh Vardhan JainDepartment of Mathematics, Florida State University, Tallahassee, Florida,United States of America.
Alan RichardsonInstitute for Science and Technology in Medicine, Keele University, Stoke-on-Trent, United Kingdom.
Michael Meyer-HermannDepartment of Systems Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany ; Bio Centre for Life Science, Braunschweig University of Technology, Braunschweig, Germany.
Helen M ByrneOxford Centre for Collaborative and Applied Mathematics, Mathematical Institute, University of Oxford, Oxford, United Kingdom ; Department of Computer Science, University of Oxford, Oxford, United Kingdom.
Florida State University · USHelmholtz Centre for Infection Research · DEKeele University · GBUniversity of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Platinum drug-resistance in ovarian cancers mediated by anti-apoptotic proteins such as Bcl-xL is a major factor contributing to the chemotherapeutic resistance of recurrent disease. Consequently, concurrent inhibition of Bcl-xL in combination with chemotherapy may improve treatment outcomes for patients. Here, we develop a mathematical model to investigate the potential of combination therapy with ABT-737, a small molecule inhibitor of Bcl-xL, and carboplatin, a platinum-based drug, on a simulated tumor xenograft. The model is calibrated against in vivo experimental data, wherein xenografts established in mice were treated with ABT-737 and/or carboplatin on a fixed periodic schedule. The validated model is used to predict the minimum drug load that will achieve a predetermined level of tumor growth inhibition, thereby maximizing the synergy between the two drugs. Our simulations suggest that the infusion-duration of each carboplatin dose is a critical parameter, with an 8-hour infusion of carboplatin given weekly combined with a daily bolus dose of ABT-737 predicted to minimize residual disease. The potential of combination therapy to prevent or delay the onset of carboplatin-resistance is also investigated. When resistance is acquired as a result of aberrant DNA-damage repair in cells treated with carboplatin, drug delivery schedules that induce tumor remission with even low doses of combination therapy can be identified. Intrinsic resistance due to pre-existing cohorts of resistant cells precludes tumor regression, but dosing strategies that extend disease-free survival periods can still be identified. These results highlight the potential of our model to accelerate the development of novel therapeutics such as BH3 mimetics.

Indexed as

Models, BiologicalAlgorithmsAnimalsBiphenyl CompoundsCarboplatinCell Line, TumorComputer SimulationDisease Models, AnimalDrug Resistance, NeoplasmDrug SynergismFemaleHumansMiceNitrophenolsOvarian NeoplasmsPiperazinesABT-737Biphenyl CompoundsCarboplatinNitrophenolsPiperazinesSulfonamides

Identifiers

PMID24400068
PMCPMC3882219
OpenAlexW1965119671

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.