Evidence map›Paper›PMID 29970903›Full record

ArticleOncogene2018

Synergistic anti-angiogenic treatment effects by dual FGFR1 and VEGFR1 inhibition in FGFR1-amplified breast cancer.

Kristina Golfmann, Lydia Meder, Mirjam Koker, Caroline Volz, Sven Borchmann, Lars Tharun, Felix Dietlein, Florian Malchers, Alexandra Florin, Reinhard Büttner and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

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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

14 authors at 4 institutions in 2 countries.

Kristina GolfmannDepartment I of Internal Medicine, University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany.
Lydia MederDepartment I of Internal Medicine, University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany.
Mirjam KokerDepartment I of Internal Medicine, University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany.
Caroline VolzDepartment I of Internal Medicine, University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany.
Sven BorchmannDepartment I of Internal Medicine, University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany.
Lars TharunInstitute for Pathology, University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany.
Felix DietleinElse Kröner Forschungskolleg Clonal Evolution in Cancer, University Hospital Cologne, 50931, Cologne, Germany.
Florian MalchersDepartment of Translational Genomics, University Hospital Cologne, Weyertal 115b, 50931, Cologne, Germany.
Alexandra FlorinInstitute for Pathology, University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany.
Reinhard BüttnerCenter for Molecular Medicine Cologne, University of Cologne, Robert-Koch Straße 21, 50931, Cologne, Germany.
Neal RosenProgram in Molecular Pharmacology, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Vanessa Rodrik-OutmezguineProgram in Molecular Pharmacology, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Michael HallekDepartment I of Internal Medicine, University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany.
Roland T UllrichDepartment I of Internal Medicine, University Hospital Cologne, Kerpener Straße 62, 50937, Cologne, Germany. roland.ullrich@uk-koeln.de.
University Hospital Cologne · DEUniversity of Cologne · DEMemorial Sloan Kettering Cancer Center · USBroad Institute · US

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) UL379/1-1Fritz Thyssen Stiftung (Fritz Thyssen Foundation) 10.16.1.028MN
6 · The paper itself

Abstract

FGFR1 amplification has been found in 15% of patients with breast cancer and has been postulated as a promising marker to predict response against FGFR inhibitors. However, early phase clinical trials of selective FGFR inhibitors demonstrated only limited efficacy in FGFR1-amplified breast cancer patients. We found that BGJ398, an FGFR inhibitor, effectively inhibited phosphorylation of FGFR1 and MEK/ERK signaling in FGFR1-amplified breast cancer without affecting tumor cell proliferation. However, FGFR1 knockout inhibited tumor angiogenesis in vivo. We unraveled that FGFR1 regulates the secretion of the proangiogenic vascular endothelial growth factor (VEGF) in a MAPK-dependent manner. We further found that FGF-FGFR1 signaling induces an autocrine activation of VEGF-VEGFR1 pathway that again amplifies VEGF secretion via VEGF-VEGFR1-AKT signaling. Targeting both VEGFR1 and FGFR1 resulted in synergistic anti-angiogenic treatment effects in vivo. We thus postulate synergistic treatment effects in FGFR1/VEGFR1-positive breast cancer patients by dual targeting of FGFR and VEGFR.

Indexed as

Angiogenesis InhibitorsAnimalsAntineoplastic Combined Chemotherapy ProtocolsBreast NeoplasmsCell Line, TumorDrug SynergismFemaleHeterograftsHumansMiceMice, Inbred NODNaphthalenesNeovascularization, PathologicPhenylurea CompoundsPiperidinesPyrimidinesAngiogenesis InhibitorsE-3810FGFR1 protein, humaninfigratinibNaphthalenesPhenylurea CompoundsPiperidinesPyrimidinesQuinazolinesQuinolinesReceptor, Fibroblast Growth Factor, Type 1vandetanibVascular Endothelial Growth Factor Receptor-1

Identifiers

PMID29970903
OpenAlexW2810008403

What OpenQuestion holds

Textmetadata
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.