Evidence map›Paper›PMID 22147894›Full record

ArticleBlood2012

Global gene expression profiling in mouse plasma cell tumor precursor and bystander cells reveals potential intervention targets for plasma cell neoplasia.

Jason LeGrand, Eun Sung Park, Hongyang Wang, Shalu Gupta, James D Owens, Patrick J Nelson, Wendy DuBois, Thomas Bair, Siegfried Janz, J Frederic Mushinski

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2012. 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
0.3field-weighted citation impact, top 41% 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, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Transgenic mouse model of IgMBlood cancer journal · 2016
    Article
  4. Article
  5. 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

10 authors at 5 institutions in 1 country.

Jason LeGrandMolecular Genetics Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, MD 20892, USA.
Eun Sung Park
Hongyang Wang
Shalu Gupta
James D Owens
Patrick J Nelson
Wendy DuBois
Thomas Bair
Siegfried Janz
J Frederic Mushinski
National Cancer Institute · USNational Institutes of Health · USCenter for Cancer Research · USUniversity of Iowa · USUniversity of Iowa Holden Comprehensive Cancer Center

Funding

Animal Model and Genotyping Core Support FacilityZICBC011047 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DU BOIS DE VROYLANDE, WENDY · 2009 to 2025
$23.1M
Defining genetic pathways of plasma-cell neoplasiaR01CA151354 · NCI · UNIVERSITY OF IOWA · PI JANZ, SIEGFRIED · 2010 to 2022
$3.9M
Intramural NIH HHSNCI NIH HHS R01 CA151354NCI NIH HHS R01CA151354
6 · The paper itself

Abstract

Tumor progression usually proceeds through several sequential stages, any of which could be targets for interrupting the progression process if one understood these steps at the molecular level. We extracted nascent plasma cell tumor (PCT) cells from within inflammatory oil granulomas (OG) isolated from IP pristane-injected BALB/c.iMyc(Eμ) mice at 5 different time points during tumor progression. We used laser capture microdissection to collect incipient PCT cells and analyzed their global gene expression on Affymetrix Mouse Genome 430A microarrays. Two independent studies were performed with different sets of mice. Analysis of the expression data used ANOVA and Bayesian estimation of temporal regulation. Genetic pathway analysis was performed using MetaCore (GeneGo) and IPA (Ingenuity). The gene expression profiles of PCT samples and those of undissected OG samples from adjacent sections showed that different genes and pathways were mobilized in the tumor cells during tumor progression, compared with their stroma. Our analysis implicated several genetic pathways in PCT progression, including biphasic (up- and then down-regulation) of the Spp1/osteopontin-dependent network and up-regulation of mRNA translation/protein synthesis. The latter led to a biologic validation study that showed that the AMPK-activating diabetes drug, metformin, was a potent specific PCT inhibitor in vitro.

Indexed as

AnimalsAntineoplastic AgentsCell Line, TumorCell ProliferationGene Expression ProfilingGene Expression Regulation, NeoplasticGranuloma, Plasma CellMetforminMiceMice, Inbred BALB CMice, TransgenicMolecular Targeted TherapyNeoplasms, Plasma CellOligonucleotide Array Sequence AnalysisOsteopontinProto-Oncogene Proteins c-mycAntineoplastic AgentsMetforminMyc protein, mouseOsteopontinProto-Oncogene Proteins c-mycRNA, MessengerSpp1 protein, mouse

Identifiers

PMID22147894
PMCPMC3271714
OpenAlexW2068887872

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.