Evidence map›Paper›PMID 29606348›Full record

ArticleCancer cell2018

GKAP Acts as a Genetic Modulator of NMDAR Signaling to Govern Invasive Tumor Growth.

Leanne Li, Qiqun Zeng, Arjun Bhutkar, José A Galván, Eva Karamitopoulou, Daan Noordermeer, Mei-Wen Peng, Alessandra Piersigilli, Aurel Perren, Inti Zlobec and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

57 citing papers in PubMed, 83 citations in OpenAlex.

  1. Review
  2. Distinct Malignant Cell States and Myeloid Glutamate Signaling Associated with Aggressive Pancreatic Neuroendocrine Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
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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

13 authors at 5 institutions in 3 countries.

Leanne LiSwiss Institute of Cancer Research, School of Life Sciences, Swiss Federal Institute of Technology Lausanne (EPFL), 1015 Lausanne, Switzerland.
Qiqun ZengSwiss Institute of Cancer Research, School of Life Sciences, Swiss Federal Institute of Technology Lausanne (EPFL), 1015 Lausanne, Switzerland.
Arjun BhutkarDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
José A GalvánInstitute of Pathology, University of Bern, Murtenstrasse 31, 3008 Bern, Switzerland.
Eva KaramitopoulouInstitute of Pathology, University of Bern, Murtenstrasse 31, 3008 Bern, Switzerland.
Daan NoordermeerSwiss Institute of Cancer Research, School of Life Sciences, Swiss Federal Institute of Technology Lausanne (EPFL), 1015 Lausanne, Switzerland.
Mei-Wen PengSwiss Institute of Cancer Research, School of Life Sciences, Swiss Federal Institute of Technology Lausanne (EPFL), 1015 Lausanne, Switzerland.
Alessandra PiersigilliInstitute of Pathology, University of Bern, Murtenstrasse 31, 3008 Bern, Switzerland; School of Life Science, Swiss Federal Institute of Technology Lausanne (EPFL), 1015 Lausanne, Switzerland.
Aurel PerrenInstitute of Pathology, University of Bern, Murtenstrasse 31, 3008 Bern, Switzerland.
Inti ZlobecInstitute of Pathology, University of Bern, Murtenstrasse 31, 3008 Bern, Switzerland.
Hugh RobinsonDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK.
M Luisa Iruela-ArispeDepartment of Molecular, Cell and Developmental Biology, Jonsson Comprehensive Cancer Center and Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA.
Douglas HanahanSwiss Institute of Cancer Research, School of Life Sciences, Swiss Federal Institute of Technology Lausanne (EPFL), 1015 Lausanne, Switzerland. Electronic address: douglas.hanahan@epfl.ch.
École Polytechnique Fédérale de Lausanne · CHUniversity of Bern · CHMassachusetts Institute of Technology · USUniversity of California, Los Angeles · USUniversity of Cambridge · GB

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
NCI NIH HHS P30 CA016042
6 · The paper itself

Abstract

Genetic linkage analysis previously suggested that GKAP, a scaffold protein of the N-methyl-D-aspartate receptor (NMDAR), was a potential modifier of invasion in a mouse model of pancreatic neuroendocrine tumor (PanNET). Here, we establish that GKAP governs invasive growth and treatment response to NMDAR inhibitors of PanNET via its pivotal role in regulating NMDAR pathway activity. Combining genetic knockdown of GKAP and pharmacological inhibition of NMDAR, we implicate as downstream effectors FMRP and HSF1, which along with GKAP demonstrably support invasiveness of PanNET and pancreatic ductal adenocarcinoma cancer cells. Furthermore, we distilled genome-wide expression profiles orchestrated by the NMDAR-GKAP signaling axis, identifying transcriptome signatures in tumors with low/inhibited NMDAR activity that significantly associate with favorable patient prognosis in several cancer types.

Indexed as

Signal TransductionAnimalsAntineoplastic AgentsCarcinoma, NeuroendocrineCarcinoma, Pancreatic DuctalCell Line, TumorFragile X Messenger Ribonucleoprotein 1Gene Expression ProfilingGene Expression Regulation, NeoplasticHeat Shock Transcription FactorsHumansMiceNeoplasm InvasivenessNeoplasm TransplantationPancreatic NeoplasmsPrognosisAntineoplastic AgentsDLGAP1 protein, humanFMR1 protein, humanFragile X Messenger Ribonucleoprotein 1Heat Shock Transcription FactorsHSF1 protein, humanReceptors, N-Methyl-D-AspartateSAP90-PSD95 Associated Proteinscancer modifierFMRPGKAP/Dlgap1GluN2b/NR2b/Grin2bglutamate receptorHSF1memantineMK801NMDARpancreatic ductal adenocarcinoma (PDAC)RIP1Tag2

Identifiers

PMID29606348
PMCPMC5896248
OpenAlexW2794818891

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.