Evidence map›Paper›PMID 12519307›Full record

ArticleImmunology2003

Functional and phenotypic studies of two variants of a human mast cell line with a distinct set of mutations in the c-kit proto-oncogene.

Magnus Sundström, Harissios Vliagoftis, Peter Karlberg, Joseph H Butterfield, Kenneth Nilsson, Dean D Metcalfe, Gunnar Nilsson

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.

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  20. International journal of molecular sciences · 2022
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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

7 authors at 4 institutions in 2 countries.

Magnus SundströmLaboratory of Tumor Biology, Department of Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Harissios Vliagoftis
Peter Karlberg
Joseph H Butterfield
Kenneth Nilsson
Dean D Metcalfe
Gunnar Nilsson
Uppsala University · SEMayo Clinic in Florida · USNational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Molecular Biology Of Mast Cell Growth &DifferentiationZ01AI000513 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI METCALFE, DEAN D · 1988 to 2008
$2.0M
Molecular Biology Of Mast Cell Growth And DifferentiationZIAAI000513 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI METCALFE, DEAN D · 2009 to 2012
$1.3M
6 · The paper itself

Abstract

The human mast cell line (HMC)-1 cell line is growth-factor independent because of a constitutive activity of the receptor tyrosine kinase Kit. Such deregulated Kit activity has also been suggested causative in gastrointestinal stromal tumours (GISTs) and mastocytosis. HMC-1 is the only established continuously growing human mast cell line and has therefore been widely employed for in vitro studies of human mast cell biology. In this paper we describe two sublines of HMC-1, named HMC-1(560 ) and HMC-1(560,816 ), with different phenotypes and designated by the locations of specific mutations in the c-kit proto-oncogene. Activating mutations in the Kit receptor were characterized using the pyrosequencing trade mark method. Both sublines have a heterozygous T to G mutation at codon 560 in the juxtamembrane region of the c-kit gene causing an amino acid substitution of Gly-560 for Val. In contrast, only HMC-1(560,816) cells have the c-kitV816 mutation found in mast cell neoplasms causing an Asp-->Val substitution in the intracellular kinase domain. Kit was constitutively phosphorylated on tyrosine residues and associated with phosphatidylinositol 3'-kinase (PI 3-kinase) in both variants of HMC-1, but this did not lead to a constitutive phosphorylation of Akt or extracellular regulated protein kinase (ERK), which are signalling molecules normally activated by the interaction of stem cell factor (SCF) with Kit. The documentation and characterization of two sublines of HMC-1 cells provides both information on the biological consequences of mutations in Kit and recognition of the availability of what in reality are two distinct cultured human mast cell lines.

Indexed as

MutationCell Culture TechniquesCell CycleCell DivisionCell LineHumansImmunophenotypingKaryotypingMast CellsPhosphorylationProto-Oncogene MasProto-Oncogene Proteins c-kitSignal TransductionStem Cell FactorTyrosineMAS1 protein, humanProto-Oncogene MasProto-Oncogene Proteins c-kitStem Cell FactorTyrosine

Identifiers

PMID12519307
PMCPMC1782858
OpenAlexW2007742656

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.