Evidence map›Paper›PMID 25083818›Full record

ArticleBlood cancer journal2014

Role of Bruton's tyrosine kinase (BTK) in growth and metastasis of INA6 myeloma cells.

R Bam, S U Venkateshaiah, S Khan, W Ling, S S Randal, X Li, Q Zhang, F van Rhee, B Barlogie, J Epstein and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Blood cancer journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Review
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 1 institution in 1 country.

R BamMyeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
S U VenkateshaiahMyeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
S KhanMyeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
W LingMyeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
S S RandalMyeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
X LiMyeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Q ZhangMyeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
F van RheeMyeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
B BarlogieMyeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
J EpsteinMyeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
S YaccobyMyeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
University of Arkansas for Medical Sciences · US

Funding

Tumor Cell-Microenvironment Interactions in the Molecular Pathogenesis of MultiplP01CA055819 · NCI · UNIV OF ARKANSAS FOR MED SCIS · PI BELLAMY, WILLIAM T · 1993 to 2013
$49.7M
Myeloma-Microenvironment Interaction DynamicsR01CA093897 · NCI · UNIV OF ARKANSAS FOR MED SCIS · PI YACCOBY, SHMUEL · 2002 to 2012
$2.5M
NCI NIH HHS CA093897NCI NIH HHS CA55819NCI NIH HHS P01 CA055819NCI NIH HHS R01 CA093897
6 · The paper itself

Abstract

Bruton's tyrosine kinase (BTK) and the chemokine receptor CXCR4 are linked in various hematologic malignancies. The aim of the study was to understand the role of BTK in myeloma cell growth and metastasis using the stably BTK knockdown luciferase-expressing INA6 myeloma line. BTK knockdown had reduced adhesion to stroma and migration of myeloma cells toward stromal cell-derived factor-1. BTK knockdown had no effect on short-term in vitro growth of myeloma cells, although clonogenicity was inhibited and myeloma cell growth was promoted in coculture with osteoclasts. In severe combined immunodeficient-rab mice with contralaterally implanted pieces of bones, BTK knockdown in myeloma cells promoted their proliferation and growth in the primary bone but suppressed metastasis to the contralateral bone. BTK knockdown myeloma cells had altered the expression of genes associated with adhesion and proliferation and increased mammalian target of rapamycin signaling. In 176 paired clinical samples, BTK and CXCR4 expression was lower in myeloma cells purified from a focal lesion than from a random site. BTK expression in random-site samples was correlated with proportions of myeloma cells expressing cell surface CXCR4. Our findings highlight intratumoral heterogeneity of myeloma cells in the bone marrow microenvironment and suggest that BTK is involved in determining proliferative, quiescent or metastatic phenotypes of myeloma cells.

Indexed as

Gene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticAgammaglobulinaemia Tyrosine KinaseAnimalsBone NeoplasmsCell AdhesionCell Line, TumorCell MovementGene Knockdown TechniquesHeterograftsHumansMiceMice, SCIDMultiple MyelomaNeoplasm MetastasisNeoplasm TransplantationAgammaglobulinaemia Tyrosine KinaseBTK protein, humanBtk protein, mouseCXCR4 protein, humanProtein-Tyrosine KinasesReceptors, CXCR4

Identifiers

PMID25083818
PMCPMC4219470
OpenAlexW1998217665

What OpenQuestion holds

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Registered trials

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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.