Evidence map›Paper›PMID 32058294›Full record

ReviewOral oncology2020

The p38/MKP-1 signaling axis in oral cancer: Impact of tumor-associated macrophages.

Zhenning Li, Fa-Yu Liu, Keith L Kirkwood

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Oral oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 62 citations in OpenAlex.

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  17. AberrantBiomedicines · 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

3 authors at 2 institutions in 2 countries.

Zhenning LiDepartment of Oromaxillofacial-Head and Neck Surgery, School and Hospital of Stomatology, China Medical University, Liaoning Province Key Laboratory of Oral Disease, Shenyang, China; Department of Medical Genetics, China Medical University, Shenyang, China; Department of Oral Biology, School of Dental Medicine, University at Buffalo, Buffalo, NY, USA.
Fa-Yu LiuDepartment of Oromaxillofacial-Head and Neck Surgery, School and Hospital of Stomatology, China Medical University, Liaoning Province Key Laboratory of Oral Disease, Shenyang, China; Department of Oral Biology, School of Dental Medicine, University at Buffalo, Buffalo, NY, USA.
Keith L KirkwoodDepartment of Oral Biology, School of Dental Medicine, University at Buffalo, Buffalo, NY, USA; Department of Head and Neck/Plastic and Reconstructive Surgery, Roswell Park Comprehensive Cancer Center, Buffalo, NY, USA. Electronic address: klkirk@buffalo.edu.
University at Buffalo, State University of New York · USRoswell Park Comprehensive Cancer Center · US

Funding

Post-Transcriptional Control of Aging-Associated Inflammation and Bone Homeostasis (Administrative Supplement)R01DE028258 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI KIRKWOOD, KEITH L · 2018 to 2022
$2.1M
DUSP1 and Sexual Dimorphism in PeriodontitisR21DE027017 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI KIRKWOOD, KEITH L · 2018 to 2019
$439k
Bioinformatic Approaches for Understanding Macrophage Plasticity and Microbiome in Oral DiseasesK18DE029526 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI KIRKWOOD, KEITH L · 2020 to 2020
$94k
NIDCR NIH HHS K18 DE029526NIDCR NIH HHS R01 DE028258NIDCR NIH HHS R21 DE027017
6 · The paper itself

Abstract

Oral squamous cell carcinomas (OSCC) constitute over 95% of all head and neck malignancies. As a key component of the tumor microenvironment (TME), chronic inflammation contributes towards the development, progression, and regional metastasis of OSCC. Tumor associated macrophages (TAMs) associated with OSSC promote tumorigenesis through the production of cytokines and pro-inflammatory factors that are critical role in the various steps of malignant transformation, including tumor growth, survival, invasion, angiogenesis, and metastasis. The mitogen-activated protein kinases (MAPKs) can regulate inflammation along with a wide range of cellular processes including cell metabolism, proliferation, motility, apoptosis, survival, differentiation and play a crucial role in cell growth and survival in physiological and pathological processes including innate and adaptive immune responses. Dual specificity MAPK phosphatases (MKPs) deactivates MAPKs. MKPs are considered as an important feedback control mechanism that limits MAPK signaling and subsequent target gene expression. This review outlines the role of MKP-1, the founding member of the MKP family, in OSCC and the TME. Herein, we summarize recent progress in understanding the regulation of p38 MAPK/MKP-1 signaling pathways via TAM-related immune responses in OSCC development, progression and treatment outcomes.

Indexed as

FemaleHumansMaleMitogen-Activated Protein KinasesMouth Neoplasmsp38 Mitogen-Activated Protein KinasesTumor-Associated MacrophagesTumor MicroenvironmentMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesMKP-1Oral cancerp38 mitogen activating kinasesTumor-associated macrophagesTumor microenvironment

Identifiers

PMID32058294
PMCPMC7136140
OpenAlexW3006330194

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.