Evidence map›Paper›PMID 27863175›Full record

ArticleCPT: pharmacometrics & systems pharmacology2016

Modeling Longitudinal Preclinical Tumor Size Data to Identify Transient Dynamics in Tumor Response to Antiangiogenic Drugs.

L G Hutchinson, H-J Mueller, E A Gaffney, P K Maini, J Wagg, A Phipps, C Boetsch, H M Byrne, B Ribba

Open access · goldAbstract read
In one paragraph

Article in CPT: pharmacometrics & systems pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Pharmacodynamic Drug-Drug Interactions.Clinical pharmacology and therapeutics · 2019
    Review
  7. Article
  8. Article
  9. LiposomalTheranostics · 2017
    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

9 authors at 5 institutions in 4 countries.

L G HutchinsonWolfson Centre for Mathematical Biology, Mathematical Institute, University of Oxford, Oxford, UK.
H-J MuellerPharma Research and Early Development, Roche Innovation Centre Munich, Munich, Germany.
E A GaffneyWolfson Centre for Mathematical Biology, Mathematical Institute, University of Oxford, Oxford, UK.
P K MainiWolfson Centre for Mathematical Biology, Mathematical Institute, University of Oxford, Oxford, UK.
J WaggRoche Pharmaceutical Research & Early Development, Roche Innovation Center, Basel, Switzerland.
A PhippsPharma Research and Early Development, Roche Innovation, Welwyn Garden City, UK.
C BoetschRoche Pharmaceutical Research & Early Development, Roche Innovation Center, Basel, Switzerland.
H M ByrneWolfson Centre for Mathematical Biology, Mathematical Institute, University of Oxford, Oxford, UK.
B RibbaPharma Research and Early Development, Roche Innovation Centre Munich, Munich, Germany.
Roche (Switzerland) · CHUniversity of Oxford · GBMathematical Institute of the Slovak Academy of Sciences · SKRoche Pharma AG (Germany) · DERoche (United Kingdom) · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Experimental evidence suggests that antiangiogenic therapy gives rise to a transient window of vessel normalization, within which the efficacy of radiotherapy and chemotherapy may be enhanced. Preclinical experiments that measure components of vessel normalization are invasive and expensive. We have developed a mathematical model of vascular tumor growth from preclinical time-course data in a breast cancer xenograft model. We used a mixed-effects approach for model parameterization, leveraging tumor size data to identify a period of enhanced tumor growth that could potentially correspond to the transient window of vessel normalization. We estimated the characteristics of the window for mice treated with an anti-VEGF antibody (bevacizumab) or with a bispecific anti-VEGF/anti-angiopoietin-2 antibody (vanucizumab). We show how the mathematical model could theoretically be used to predict how to coordinate antiangiogenic therapy with radiotherapy or chemotherapy to maximize therapeutic effect, reducing the need for preclinical experiments that directly measure vessel normalization parameters.

Indexed as

Models, BiologicalAngiogenesis InhibitorsAnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedBevacizumabBreast NeoplasmsCell Line, TumorCombined Modality TherapyFemaleHumansLongitudinal StudiesMiceMice, SCIDModels, StatisticalNeovascularization, PathologicAngiogenesis InhibitorsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedBevacizumabvanucizumab

Identifiers

PMID27863175
PMCPMC5192995
OpenAlexW2552006856

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.