Evidence map›Paper›PMID 25527450›Full record

ArticleCancer letters2015

Nintedanib, a triple angiokinase inhibitor, enhances cytotoxic therapy response in pancreatic cancer.

Niranjan Awasthi, Stefan Hinz, Rolf A Brekken, Margaret A Schwarz, Roderich E Schwarz

Open access · greenAbstract read
In one paragraph

Article in Cancer letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 15% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
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  7. Proteomics in pancreatic cancer.Biomarker research · 2025
    Review
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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

5 authors at 3 institutions in 1 country.

Niranjan AwasthiDepartment of Surgery, Indiana University School of Medicine, South Bend, IN 46617; Division of Surgical Oncology, Department of Surgery, The University of Texas Southwestern Medical Center, Dallas, TX 75390. Electronic address: nawasthi@iupui.edu.
Stefan HinzDivision of Surgical Oncology, Department of Surgery, The University of Texas Southwestern Medical Center, Dallas, TX 75390.
Rolf A BrekkenDivision of Surgical Oncology, Department of Surgery, The University of Texas Southwestern Medical Center, Dallas, TX 75390.
Margaret A SchwarzDepartment of Pediatrics, Indiana University School of Medicine, South Bend, IN 46617.
Roderich E SchwarzDepartment of Surgery, Indiana University School of Medicine, South Bend, IN 46617; Division of Surgical Oncology, Department of Surgery, The University of Texas Southwestern Medical Center, Dallas, TX 75390; Indiana University Health Goshen Center for Cancer Care, Indiana University School of Medicine, South Bend, IN 46617.
The University of Texas Southwestern Medical Center · USIndiana University · USIndiana University School of Medicine

Funding

EMAP II: Pulmonary Vascular MediatorR01HL114977 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI SCHWARZ, MARGARET A · 2012 to 2015
$1.8M
NHLBI NIH HHS R01 HL114977
6 · The paper itself

Abstract

Angiogenesis remains a sensible target for pancreatic ductal adenocarcinoma (PDAC) therapy. VEGF, PDGF, FGF and their receptors are expressed at high levels and correlate with poor prognosis in human PDAC. Nintedanib is a triple angiokinase inhibitor that targets VEGFR1/2/3, FGFR1/2/3 and PDGFRα/β signaling. We investigated the antitumor activity of nintedanib alone or in combination with the cytotoxic agent gemcitabine in experimental PDAC. Nintedanib inhibited proliferation of cells from multiple lineages found in PDAC, with gemcitabine enhancing inhibitory effects. Nintedanib blocked PI3K/MAPK activity and induced apoptosis in vitro and in vivo. In a heterotopic model, net local tumor growth compared to controls (100%) was 60.8 ± 10.5% in the gemcitabine group, -2.1 ± 9.9% after nintedanib therapy and -12.4 ± 16% after gemcitabine plus nintedanib therapy. Effects of therapy on intratumoral proliferation, microvessel density and apoptosis corresponded with tumor growth inhibition data. In a PDAC survival model, median animal survival after gemcitabine, nintedanib and gemcitabine plus nintedanib was 25, 31 and 38 days, respectively, compared to 16 days in controls. The strong antitumor activity of nintedanib in experimental PDAC supports the potential of nintedanib-controlled mechanisms as targets for improved clinical PDAC therapy.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisCarcinoma, Pancreatic DuctalCell Line, TumorCell ProliferationDeoxycytidineGemcitabineHumansIndolesNeoplasms, ExperimentalNeovascularization, PathologicPancreatic NeoplasmsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsReceptors, Fibroblast Growth FactorDeoxycytidineGemcitabineIndolesnintedanibPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsReceptors, Fibroblast Growth FactorReceptors, Platelet-Derived Growth FactorReceptors, Vascular Endothelial Growth FactorAngiogenesisChemotherapyCombination therapyNintedanibPancreatic cancer

Identifiers

PMID25527450
PMCPMC4450873
OpenAlexW2134657639

What OpenQuestion holds

Textmetadata
LicenceTDM
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.