Evidence map›Paper›PMID 28822081›Full record

ArticleCancer microenvironment : official journal of the International Cancer Microenvironment Society2017

Expression Profiling of the MAP Kinase Phosphatase Family Reveals a Role for DUSP1 in the Glioblastoma Stem Cell Niche.

Bradley N Mills, George P Albert, Marc W Halterman

Open access · bronzeAbstract read
In one paragraph

Article in Cancer microenvironment : official journal of the International Cancer Microenvironment Society, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  12. Cancers · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Dual-Specificity Phosphatase Regulation in Neurons and Glial Cells.International journal of molecular sciences · 2019
    Review
  18. Article
  19. 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

3 authors at 1 institution in 1 country.

Bradley N MillsDepartment of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, 14642, USA.
George P AlbertCenter for Neurotherapeutics Discovery, University of Rochester Medical Center, 601 Elmwood Avenue, Box 645, Rochester, NY, 14642, USA.
Marc W HaltermanCenter for Neurotherapeutics Discovery, University of Rochester Medical Center, 601 Elmwood Avenue, Box 645, Rochester, NY, 14642, USA. Marc_Halterman@urmc.rochester.edu.ORCID http://orcid.org/0000-0002-1022-8565
University of Rochester Medical Center · US

Funding

Targeting phosphatase regulated cleavage of HIF-1-alpha in ischemic brain injuryR01NS076617 · NINDS · UNIVERSITY OF ROCHESTER · PI HALTERMAN, MARC W · 2011 to 2015
$1.6M
MKP-1 Effects on HIF-1alpha and Glycolytic Metabolism in Glioblastoma multiformeF31CA180358 · NCI · UNIVERSITY OF ROCHESTER · PI MILLS, BRADLEY N. · 2013 to 2016
$172k
National Cancer Institute CA180358National Institute of Neurological Disorders and Stroke NS076617NCI NIH HHS F31 CA180358NINDS NIH HHS R01 NS076617
6 · The paper itself

Abstract

The dual specificity phosphatases (DUSPs) constitute a family of stress-induced enzymes that provide feedback inhibition on mitogen-activated protein kinases (MAPKs) critical in key aspects of oncogenic signaling. While described in other tumor types, the landscape of DUSP mRNA expression in glioblastoma (GB) remains largely unexplored. Interrogation of the REpository for Molecular BRAin Neoplasia DaTa (REMBRANDT) revealed induction (DUSP4, DUSP6), repression (DUSP2, DUSP7-9), or mixed (DUSP1, DUSP5, DUSP10, DUSP15) DUSP transcription of select DUSPs in bulk tumor specimens. To resolve features specific to the tumor microenvironment, we searched the Ivy Glioblastoma Atlas Project (Ivy GAP) repository, which highlight DUSP1, DUSP5, and DUSP6 as the predominant family members induced within pseudopalisading and perinecrotic regions. The inducibility of DUSP1 in response to hypoxia, dexamethasone, or the chemotherapeutic agent camptothecin was confirmed in GB cell lines and tumor-derived stem cells (TSCs). Moreover, we show that loss of DUSP1 expression is a characteristic of TSCs and correlates with expression of tumor stem cell markers in situ (ABCG2, PROM1, L1CAM, NANOG, SOX2). This work reveals a dynamic pattern of DUSP expression within the tumor microenvironment that reflects the cumulative effects of factors including regional ischemia, chemotherapeutic exposure among others. Moreover, our observation regarding DUSP1 dysregulation within the stem cell niche argue for its importance in the survival and proliferation of this therapeutically resistant population.

Indexed as

CamptothecinDexamethasoneDUSP1Glioblastoma multiformeHypoxiaMitogen-activated protein kinasesTemozolomideTumor stem cell

Identifiers

PMID28822081
PMCPMC5750201
OpenAlexW2748516402

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.