Evidence map›Paper›PMID 27056048›Full record

ArticleDisease models & mechanisms2016

Inhibition of fibroblast growth factor receptor 3-dependent lung adenocarcinoma with a human monoclonal antibody.

Yongjun Yin, Xiaodi Ren, Craig Smith, Qianxu Guo, Maria Malabunga, Ilhem Guernah, Yiwei Zhang, Juqun Shen, Haijun Sun, Nabil Chehab and 3 more

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  4. Review
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  11. Achondroplasia: Development, pathogenesis, and therapy.Developmental dynamics : an official publication of the American Association of Anatomists · 2017
    Review
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

13 authors at 3 institutions in 1 country.

Yongjun YinDepartment of Developmental Biology, Washington University School of Medicine, Saint Louis, MO 63110, USA.
Xiaodi RenDepartment of Quantitative Biology, Eli Lilly and Company, New York, NY 10016, USA.
Craig SmithDepartment of Developmental Biology, Washington University School of Medicine, Saint Louis, MO 63110, USA.
Qianxu GuoDepartment of Cancer Angiogenesis, Eli Lilly and Company, New York, NY 10016, USA.
Maria MalabungaDepartment of Immunology, Eli Lilly and Company, New York, NY 10016, USA.
Ilhem GuernahDepartment of Immunology, Eli Lilly and Company, New York, NY 10016, USA.
Yiwei ZhangDepartment of Antibody Technology, Eli Lilly and Company, New York, NY 10016, USA.
Juqun ShenDepartment of Antibody Technology, Eli Lilly and Company, New York, NY 10016, USA.
Haijun SunDepartment of Bioprocess Sciences, Eli Lilly and Company, New York, NY 10016, USA.
Nabil ChehabDepartment of Immunology, Eli Lilly and Company, New York, NY 10016, USA.
Nick LoizosDepartment of Immunology, Eli Lilly and Company, New York, NY 10016, USA.
Dale L LudwigDepartment of Bioprocess Sciences, Eli Lilly and Company, New York, NY 10016, USA.
David M OrnitzDepartment of Developmental Biology, Washington University School of Medicine, Saint Louis, MO 63110, USA dornitz@wustl.edu.
Eli Lilly (United States) · USWashington University in St. Louis · USAngiogenesis Foundation · US

Funding

REGULATION OF LUNG DEVELOPMENT BY FGF9 SIGNALING PATHWAYSR01HL111190 · NHLBI · WASHINGTON UNIVERSITY · PI ORNITZ, DAVID M · 2012 to 2020
$3.9M
NHLBI NIH HHS R01 HL111190
6 · The paper itself

Abstract

Activating mutations in fibroblast growth factor receptor 3 (FGFR3) have been identified in multiple types of human cancer and in congenital birth defects. In human lung cancer, fibroblast growth factor 9 (FGF9), a high-affinity ligand for FGFR3, is overexpressed in 10% of primary resected non-small cell lung cancer (NSCLC) specimens. Furthermore, in a mouse model where FGF9 can be induced in lung epithelial cells, epithelial proliferation and ensuing tumorigenesis is dependent on FGFR3. To develop new customized therapies for cancers that are dependent on FGFR3 activation, we have used this mouse model to evaluate a human monoclonal antibody (D11) with specificity for the extracellular ligand-binding domain of FGFR3, that recognizes both human and mouse forms of the receptor. Here, we show that D11 effectively inhibits signaling through FGFR3 in vitro, inhibits the growth of FGFR3-dependent FGF9-induced lung adenocarcinoma in mice, and reduces tumor-associated morbidity. Given the potency of FGF9 in this mouse model and the absolute requirement for signaling through FGFR3, this study validates the D11 antibody as a potentially useful and effective reagent for treating human cancers or other pathologies that are dependent on activation of FGFR3.

Indexed as

AdenocarcinomaAdenocarcinoma of LungAnimalsAntibodies, BlockingAntibodies, MonoclonalBronchiolesCell ProliferationFibroblast Growth Factor 9HumansLigandsLung NeoplasmsMacrophagesMicePulmonary AlveoliReceptor, Fibroblast Growth Factor, Type 3Antibodies, BlockingAntibodies, MonoclonalFGF9 protein, humanFGFR3 protein, humanFibroblast Growth Factor 9LigandsReceptor, Fibroblast Growth Factor, Type 3AdenocarcinomaFGFR3Fibroblast growth factor receptor 3Inhibitory monoclonal antibodyLung cancerNSCLC

Identifiers

PMID27056048
PMCPMC4892666
OpenAlexW2345591304

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.