Evidence map›Paper›PMID 28153789›Full record

ReviewCancer letters2017

Oncogenic signaling of MEK5-ERK5.

Van T Hoang, Thomas J Yan, Jane E Cavanaugh, Patrick T Flaherty, Barbara S Beckman, Matthew E Burow

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

61 citing papers in PubMed, 99 citations in OpenAlex.

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  7. A CpG Epigenetic Switch Reverts PFAS ToxicityAn In Vitro Study.Environment & health (Washington, D.C.) · 2025
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  16. Investigation ofIn silico pharmacology · 2025
    Article
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  19. Review
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1 more citing papers are in PubMed but not listed here.

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

6 authors at 4 institutions in 1 country.

Van T HoangDepartment of Medicine-Section of Hematology and Medical Oncology, Tulane University, New Orleans, LA, USA.
Thomas J YanDepartment of Medicine-Section of Hematology and Medical Oncology, Tulane University, New Orleans, LA, USA.
Jane E CavanaughDepartment of Pharmacological Sciences, Division of Medicinal Chemistry, Mylan School of Pharmacy, Duquesne University, Pittsburgh, PA, USA.
Patrick T FlahertyDepartment of Pharmacological Sciences, Division of Medicinal Chemistry, Mylan School of Pharmacy, Duquesne University, Pittsburgh, PA, USA.
Barbara S BeckmanDepartment of Pharmacology, Tulane University, New Orleans, LA, USA.
Matthew E BurowDepartment of Medicine-Section of Hematology and Medical Oncology, Tulane University, New Orleans, LA, USA; Department of Pharmacology, Tulane University, New Orleans, LA, USA; Tulane Cancer Center, Tulane University, New Orleans, LA, USA. Electronic address: mburow@tulane.edu.
Tulane University · USDuquesne University · USMylan (United States) · USTulane Medical Center · US

Funding

Kinase mediated suppression of metastasis in breast cancerR01CA174785 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI COLLINS-BUROW, BRIDGETTE MICHELLE · 2016 to 2020
$1.8M
MEK5-Erk5 in breast cancer resistanceR01CA125806 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI BUROW, MATTHEW E. · 2010 to 2014
$1.5M
Novel small molecule inhibitors of MEK5_ERK5 for the treatment of breast cancerR15CA176496 · NCI · DUQUESNE UNIVERSITY · PI CAVANAUGH, JANE E · 2014 to 2014
$394k
NCI NIH HHS R01 CA125806NCI NIH HHS R01 CA174785NCI NIH HHS R15 CA176496
6 · The paper itself

Abstract

Mitogen-activated protein kinases (MAPKs) regulate diverse cellular processes including proliferation, cell survival, differentiation, and apoptosis. While conventional MAPK constituents have well-defined roles in oncogenesis, the MEK5 pathway has only recently emerged in cancer research. In this review, we consider the MEK5 signaling cascade, focusing specifically on its involvement in drug resistance and regulation of aggressive cancer phenotypes. Moreover, we explore the role of MEK5/ERK5 in tumorigenesis and metastatic progression, discussing the discrepancies in preclinical studies and assessing its viability as a therapeutic target for anti-cancer agents.

Indexed as

Signal TransductionAnimalsAntineoplastic AgentsApoptosisCell DifferentiationCell ProliferationDrug Resistance, NeoplasmHumansMAP Kinase Kinase 5Mitogen-Activated Protein Kinase 7Molecular Targeted TherapyMutationNeoplasmsProtein Kinase InhibitorsProto-Oncogene ProteinsAntineoplastic AgentsMAP2K5 protein, humanMAPK7 protein, humanMAP Kinase Kinase 5Mitogen-Activated Protein Kinase 7Protein Kinase InhibitorsProto-Oncogene ProteinsCellular signalingKinase inhibitorsMEK5-ERK5Mitogen-activated protein kinaseTargeted therapies

Identifiers

PMID28153789
PMCPMC5901897
OpenAlexW2582457346

What OpenQuestion holds

Textmetadata
LicenceTDM
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.