Evidence map›Paper›PMID 20584561›Full record

ReviewJournal of the American Academy of Dermatology2011

Tyrosine kinases in inflammatory dermatologic disease.

Ricardo T Paniagua, David F Fiorentino, Lorinda Chung, William H Robinson

Registry-linked trialAbstract readReview
In one paragraph

Review in Journal of the American Academy of Dermatology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03694067 (Assessment of the Role of the JAK-STAT Pathway in the Pathogenesis of Male Androgenetic Alopecia), which is not on this map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 43% 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.

NCT03694067 completednot on this mapstarted 2018, after this paper: background citation

Assessment of the Role of the JAK-STAT Pathway in the Pathogenesis of Male Androgenetic Alopecia

TypeobservationalSponsorCairo UniversityRan2018 to 2019Enrolled25ConditionsAndrogenetic AlopeciaArmsPunch skin biopsy
3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. 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

4 authors at 2 institutions in 1 country.

Ricardo T PaniaguaDivision of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, California; Geriatric Research Education and Clinical Center, Palo Alto Department of Veterans Affairs Health Care System, Palo Alto, California.
David F FiorentinoDepartment of Dermatology, Stanford University School of Medicine, Stanford, California.
Lorinda ChungDivision of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, California; Geriatric Research Education and Clinical Center, Palo Alto Department of Veterans Affairs Health Care System, Palo Alto, California.
William H RobinsonDivision of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, California; Geriatric Research Education and Clinical Center, Palo Alto Department of Veterans Affairs Health Care System, Palo Alto, California. Electronic address: wrobins@stanford.edu.
Geriatric Research Education and Clinical Center · USStanford University · US

Funding

Tyrosine Kinase Pathways in Rheumatoid ArthritisR01AR054822 · NIAMS · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI ROBINSON, WILLIAM H · 2007 to 2011
$1.5M
Proteomic Identification of Actionable Biomarkers in Rheumatoid ArthritisRC1AR058713 · NIAMS · STANFORD UNIVERSITY · PI ROBINSON, WILLIAM H · 2009 to 2010
$1.0M
Anti-Fibrinogen Autoimmunity in Rheumatoid ArthritisR21AI069160 · NIAID · STANFORD UNIVERSITY · PI ROBINSON, WILLIAM H · 2007 to 2008
$454k
NIAID NIH HHS R21 AI069160NIAMS NIH HHS R01 AR054822NIAMS NIH HHS R01-AR-054822NIAMS NIH HHS RC1 AR058713
6 · The paper itself

Abstract

Tyrosine kinases (TKs) are enzymes that catalyze the phosphorylation of tyrosine residues on protein substrates. They are key components of signaling pathways that drive an array of cellular responses including proliferation, differentiation, migration, and survival. Specific TKs have recently been identified as critical to the pathogenesis of several autoimmune and inflammatory diseases. Small-molecule inhibitors of TKs are emerging as a novel class of therapy that may provide benefit in certain patient subsets. In this review, we highlight TK signaling implicated in inflammatory dermatologic diseases, evaluate strategies aimed at inhibiting these aberrant signaling pathways, and discuss prospects for future drug development.

Indexed as

BiomarkersDermatitisDermatomyositisDrug Delivery SystemsFemaleFollow-Up StudiesHumansMalePhosphorylationProtein Kinase InhibitorsProtein-Tyrosine KinasesRisk AssessmentScleroderma, SystemicSignal TransductionTreatment OutcomeBiomarkersProtein Kinase InhibitorsProtein-Tyrosine Kinases

Identifiers

PMID20584561
PMCPMC2948077
OpenAlexW1996416446

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.