Evidence map›Paper›PMID 24466111›Full record

ArticlePloS one2014

Fibroblast growth factor receptor 3 interacts with and activates TGFβ-activated kinase 1 tyrosine phosphorylation and NFκB signaling in multiple myeloma and bladder cancer.

Lisa Salazar, Tamara Kashiwada, Pavel Krejci, April N Meyer, Malcolm Casale, Matthew Hallowell, William R Wilcox, Daniel J Donoghue, Leslie Michels Thompson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Associations ofCancers · 2024
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Cancer Occurrence as the Upcoming Complications of COVID-19.Frontiers in molecular biosciences · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. LncRNAEpigenomics · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Role of the NFκB-signaling pathway in cancer.OncoTargets and therapy · 2018
    Review
  20. SilencingOncology letters · 2017
    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

9 authors at 4 institutions in 2 countries.

Lisa SalazarDepartment of Psychiatry and Human Behavior, University of California Irvine, Irvine, California, United States of America.
Tamara KashiwadaDepartment of Biological Chemistry, University of California Irvine, Irvine, California, United States of America.
Pavel KrejciMedical Genetics Institute, Cedars-Sinai Medical Center, Los Angeles, California, United States of America ; Institute of Experimental Biology, Masaryk University and Department of Cytokinetics, Institute of Biophysics AS CR, v.v.i., Brno, Czech Republic ; Department of Pediatrics, UCLA School of Medicine, Los Angeles, California, United States of America.
April N MeyerDepartment of Chemistry and Biochemistry, University of California San Diego, La Jolla, California, United States of America.
Malcolm CasaleDepartment of Neurobiology and Behavior, University of California Irvine, Irvine, California, United States of America.
Matthew HallowellDepartment of Psychiatry and Human Behavior, University of California Irvine, Irvine, California, United States of America.
William R WilcoxMedical Genetics Institute, Cedars-Sinai Medical Center, Los Angeles, California, United States of America ; Department of Pediatrics, UCLA School of Medicine, Los Angeles, California, United States of America.
Daniel J DonoghueDepartment of Chemistry and Biochemistry, University of California San Diego, La Jolla, California, United States of America ; Moores Cancer Center, University of California San Diego, La Jolla, California, United States of America.
Leslie Michels ThompsonDepartment of Psychiatry and Human Behavior, University of California Irvine, Irvine, California, United States of America ; Department of Biological Chemistry, University of California Irvine, Irvine, California, United States of America ; Department of Neurobiology and Behavior, University of California Irvine, Irvine, California, United States of America ; Chao Family Comprehensive Cancer Center, University of California Irvine, Irvine, California, United States of America.
University of California, Irvine · USUniversity of California, San Diego · USCedars-Sinai Medical Center · USUniversity of California, Los Angeles · US

Funding

Univ.of Calif., Irvine Cancer Center Support GrantP30CA062203 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Christine Hui · 1994 to 2026
$57.9M
NCI NIH HHS P30 CA062203
6 · The paper itself

Abstract

Cancer is a major public health problem worldwide. In the United States alone, 1 in 4 deaths is due to cancer and for 2013 a total of 1,660,290 new cancer cases and 580,350 cancer-related deaths are projected. Comprehensive profiling of multiple cancer genomes has revealed a highly complex genetic landscape in which a large number of altered genes, varying from tumor to tumor, impact core biological pathways and processes. This has implications for therapeutic targeting of signaling networks in the development of treatments for specific cancers. The NFκB transcription factor is constitutively active in a number of hematologic and solid tumors, and many signaling pathways implicated in cancer are likely connected to NFκB activation. A critical mediator of NFκB activity is TGFβ-activated kinase 1 (TAK1). Here, we identify TAK1 as a novel interacting protein and target of fibroblast growth factor receptor 3 (FGFR3) tyrosine kinase activity. We further demonstrate that activating mutations in FGFR3 associated with both multiple myeloma and bladder cancer can modulate expression of genes that regulate NFκB signaling, and promote both NFκB transcriptional activity and cell adhesion in a manner dependent on TAK1 expression in both cancer cell types. Our findings suggest TAK1 as a potential therapeutic target for FGFR3-associated cancers, and other malignancies in which TAK1 contributes to constitutive NFκB activation.

Indexed as

ApoptosisBiomarkers, TumorBlotting, WesternCell AdhesionCell ProliferationGene Expression ProfilingHumansImmunoprecipitationMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMultiple MyelomaNF-kappa BOligonucleotide Array Sequence AnalysisPeptide FragmentsPhosphorylationReal-Time Polymerase Chain ReactionBiomarkers, TumorFGFR3 protein, humanMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesNF-kappa BPeptide FragmentsReceptor, Fibroblast Growth Factor, Type 3RNA, MessengerTransforming Growth Factor betaTyrosine

Identifiers

PMID24466111
PMCPMC3900522
OpenAlexW2090103734

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.