Evidence map›Paper›PMID 18500355›Full record

ReviewBritish journal of pharmacology2008

Pharmacological targeting of the KIT growth factor receptor: a therapeutic consideration for mast cell disorders.

B M Jensen, C Akin, A M Gilfillan

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Genome-wide association and meta-analysis of bipolar disorder in individuals of European ancestry.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Pooled it
  2. Trial
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  6. Review
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  11. Review
  12. Targeting KIT by frameshifting mRNA transcripts as a therapeutic strategy for aggressive mast cell neoplasms.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
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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 1 country.

B M JensenRefLab, National University Hospital, Copenhagen N, Denmark.
C Akin
A M Gilfillan
National Institutes of Health · USUniversity of Michigan–Ann Arbor · US

Funding

Critical signaling nodes regulating mast cell releasibility phenotypesZIAAI000967 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI METCALFE, DEAN D · 2009 to 2012
$1.4M
Activation of Mast Cells in Disease States: Pharmacological ModificationZ01AI000967 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI METCALFE, DEAN D · 2006 to 2008
$772k
Intramural NIH HHS
6 · The paper itself

Abstract

KIT is a member of the tyrosine kinase family of growth factor receptors which is expressed on a variety of haematopoietic cells including mast cells. Stem cell factor (SCF)-dependent activation of KIT is critical for mast cell homeostasis and function. However, when KIT is inappropriately activated, accumulation of mast cells in tissues results in mastocytosis. Such dysregulated KIT activation is a manifestation of specific activating point mutations within KIT, with the human D816V mutation considered as a hallmark of human systemic mastocytosis. A number of other activating mutations in KIT have recently been identified and these mutations may also contribute to aberrant mast cell growth. In addition to its role in mast cell growth, differentiation and survival, localized concentration gradients of SCF may control the targeting of mast cells to specific tissues and, once resident within these tissues, mast cell activation by antigen may also be amplified by SCF. Thus, KIT inhibitors may have potential application in multiple conditions linked to mast cells including systemic mastocytosis, anaphylaxis, and asthma. In this review, we discuss the role of KIT in the context of mast cells in these disease states and how recent advances in the development of inhibitors of KIT activity and function may offer novel therapies for the treatment of these disorders.

Indexed as

Drug Delivery SystemsAnaphylaxisAnimalsAsthmaHumansMastocytosisProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene Proteins c-kitStem Cell FactorProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene Proteins c-kitStem Cell Factor

Identifiers

PMID18500355
PMCPMC2518463
OpenAlexW1581912975

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.