Evidence map›Paper›PMID 28254151›Full record

ArticleNeoplasia (New York, N.Y.)2017

Role of Cyclooxygenase-2 Pathway in Creating an Immunosuppressive Microenvironment and in Initiation and Progression of Wilms' Tumor.

Paramahamsa Maturu, Devin Jones, E Cristy Ruteshouser, Qianghua Hu, Joseph M Reynolds, John Hicks, Nagireddy Putluri, Suhendan Ekmekcioglu, Elizabeth A Grimm, Chen Dong and 1 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  9. Artesunate targets cellular metabolism to regulate the Th17/Treg cell balance.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
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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

11 authors at 3 institutions in 1 country.

Paramahamsa MaturuDepartment of Genetics, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Unit 1010, Houston, TX 77030, USA; Department of Pediatrics, Section of Neonatology, Texas Children's Hospital, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: maturu@bcm.edu.
Devin JonesDepartment of Genetics, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Unit 1010, Houston, TX 77030, USA.
E Cristy RuteshouserDepartment of Genetics, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Unit 1010, Houston, TX 77030, USA.
Qianghua HuDepartment of Genetics, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Unit 1010, Houston, TX 77030, USA.
Joseph M ReynoldsDepartment of Immunology and Center for Inflammation and Cancer, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
John HicksDepartment of Pathology, Texas Children's Hospital, 6621 Fannin, Houston, TX, USA.
Nagireddy PutluriDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
Suhendan EkmekciogluDepartment of Pediatrics, Section of Neonatology, Texas Children's Hospital, Baylor College of Medicine, Houston, TX 77030, USA; Department of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Unit 0904, Houston, TX, USA.
Elizabeth A GrimmDepartment of Pediatrics, Section of Neonatology, Texas Children's Hospital, Baylor College of Medicine, Houston, TX 77030, USA; Department of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Unit 0904, Houston, TX, USA.
Chen DongDepartment of Immunology and Center for Inflammation and Cancer, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Willem W OverwijkDepartment of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Unit 0904, Houston, TX, USA.
The University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · USTexas Children's Hospital · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
TRANSCRIPTIONAL REGULATION OF WT-1P01CA034936 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI STRONG, LOUISE C · 1985 to 2010
$26.4M
Mouse Model Glomerulosclerosis Early Onset Renal FailureR01DK069599 · NIDDK · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUFF, VICKI · 2006 to 2010
$1.6M
NCI NIH HHS P01 CA034936NCI NIH HHS P30 CA016672NIDDK NIH HHS R01 DK069599
6 · The paper itself

Abstract

Wilms' tumors (WT), which accountfor 6% of all childhood cancers, arise from dysregulated differentiation of nephrogenic progenitor cells from embryonic kidneys. Though there is an improvement in the prognosis of WT, still 10% of patients with WT die due to recurrence. Thus more effective treatment approaches are necessary. We previously characterized the inflammatory microenvironment in human WT and observed the robust expression of COX-2. The aim of this study was to extend our studies to analyze the role of COX-2 pathway components in WT progression using a mouse model of WT. Herein, COX-2 pathway components such as COX-2, HIF1-α, p-ERK1/2, and p-STAT3 were upregulated in mouse and human tumor tissues. In our RPPA analysis, COX-2 was up-regulated in M15 cells after Wt1 gene was knocked down. Flow cytometry analysis showed the increased infiltration of immune suppressive inflammatory cells such as pDC's and Treg cells in tumors. The chemotactic chemokines responsible for the infiltration of these cells were also induced in CCR5 and CXCR4 dependent manner respectively. The immunosuppressive cytokines IL-10, TGF-β, and TNF-α were also up-regulated. Furthermore, more pronounced Th2 and Treg induced cytokine response was observed than Th1 response in tumors. Basing on all these evidences it is speculated that COX-2 pathway may be a beneficial target for the treatment of WT. It may be most effective as an adjuvant therapy together with other inhibitors. Thus, our current study provides a good rationale for initiating animal studies to confirm the efficacy of COX-2 inhibitors in decreasing tumor cell growth in vivo.

Indexed as

Immune ToleranceSignal TransductionAnimalsCell Line, TumorCell Transformation, NeoplasticCluster AnalysisCyclooxygenase 2CytokinesDisease Models, AnimalDisease ProgressionGene Expression ProfilingHumansInflammation MediatorsInsulin-Like Growth Factor IIMiceMice, KnockoutCyclooxygenase 2CytokinesInflammation MediatorsInsulin-Like Growth Factor IIWT1 Proteins

Identifiers

PMID28254151
PMCPMC6197604
OpenAlexW2592215614

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.