Evidence map›Paper›PMID 27300260›Full record

Trial reportCPT: pharmacometrics & systems pharmacology2016

Bridging Sunitinib Exposure to Time-to-Tumor Progression in Hepatocellular Carcinoma Patients With Mathematical Modeling of an Angiogenic Biomarker.

S Ait-Oudhia, D E Mager, V Pokuri, G Tomaszewski, A Groman, P Zagst, G Fetterly, R Iyer

Open access · goldAbstract readClinical Trial, Phase II
In one paragraph

Trial report 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 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Progress and Opportunities to Advance Clinical Cancer Therapeutics Using Tumor Dynamic Models.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Review
  6. 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

8 authors at 4 institutions in 1 country.

S Ait-OudhiaCenter for Pharmacometrics and Systems Pharmacology, Department of Pharmaceutics, College of Pharmacy, University of Florida, Orlando, Florida, USA.
D E MagerDepartment of Pharmaceutical Sciences, University at Buffalo, State University of New York, Buffalo, New York, USA.
V PokuriDepartment of Medical Oncology, Roswell Park Cancer Institute, Buffalo, New York, USA.
G TomaszewskiDepartment of Medical Oncology, Roswell Park Cancer Institute, Buffalo, New York, USA.
A GromanDepartment of Medical Oncology, Roswell Park Cancer Institute, Buffalo, New York, USA.
P ZagstDepartment of Medical Oncology, Roswell Park Cancer Institute, Buffalo, New York, USA.
G FetterlyClinical Pharmacology and Regulatory Affairs, Buffalo, New York, USA.
R IyerDepartment of Medical Oncology, Roswell Park Cancer Institute, Buffalo, New York, USA.
Roswell Park Comprehensive Cancer Center · USUnited States Nuclear Regulatory Commission · USUniversity at Buffalo, State University of New York · USUniversity of Florida · US

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MARK G FRATTINI · 1985 to 2026
$116.6M
NCI NIH HHS P30 CA016056
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is third in cancer-related causes of death worldwide and its treatment is a significant unmet medical need. Sunitinib is a selective tyrosine kinase inhibitor of the angiogenic biomarker: soluble vascular endothelial growth factor receptor-2 (sVEGFR2 ). Sunitinib failed its primary overall survival endpoint in patients with advanced HCC in a phase III trial compared to sorafenib. In the present study, pharmacokinetic-pharmacodynamic modeling was used to link drug-exposure to tumor-growth-inhibition (TGI) and time-to-tumor progression (TTP) through sVEGFR2 dynamics. The results suggest that 1) active drug concentration (i.e., sunitinib and its metabolite) inhibits the release of sVEGFR2 and that such inhibition is associated with TGI, and 2) daily sVEGFR2 exposure is likely a reliable predictor for the TTP in HCC patients. Moreover, the model quantitatively links the dynamics of an angiogenesis biomarker to TTP and accurately predicts observed literature-reported results of placebo treatment.

Indexed as

Angiogenesis InhibitorsAntineoplastic AgentsBiomarkers, TumorCarcinoma, HepatocellularDisease ProgressionHumansIndolesLiver NeoplasmsModels, TheoreticalNeovascularization, PathologicPilot ProjectsPyrrolesSunitinibSurvival RateTime FactorsVascular Endothelial Growth Factor Receptor-2Angiogenesis InhibitorsAntineoplastic AgentsBiomarkers, TumorIndolesPyrrolesSunitinibVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID27300260
PMCPMC5131886
OpenAlexW2436700741

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.