Evidence map›Paper›PMID 17001308›Full record

ArticleOncogene2007

Transforming function of the LSM1 oncogene in human breast cancers with the 8p11-12 amplicon.

K L Streicher, Z Q Yang, S Draghici, S P Ethier

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

37 citing papers in PubMed, 57 citations in OpenAlex.

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  13. Clinical Significance and Potential Role ofFrontiers in genetics · 2021
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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

4 authors at 2 institutions in 1 country.

K L StreicherBreast Cancer Program, Karmanos Cancer Institute, Detroit, MI 48201, USA. streiche@karmanos.org
Z Q Yang
S Draghici
S P Ethier
The Barbara Ann Karmanos Cancer Institute · USWayne State University · US

Funding

Tumor Biology and Microenvironment (Program 1)P30CA022453 · NCI · WAYNE STATE UNIVERSITY · PI PAUL M STEMMER · 1985 to 2026
$68.4M
Breast cancer oncogenes on the 8p11 amplicon.R01CA100724 · NCI · WAYNE STATE UNIVERSITY · PI ETHIER, STEPHEN P. · 2003 to 2014
$3.5M
Activity-Dependent Gene Expression in Human EpilepsyR01NS045207 · NINDS · WAYNE STATE UNIVERSITY · PI LOEB, JEFFREY A · 2003 to 2010
$2.1M
Novel Algorithms &Organisms for Onto-ToolsR01HG003491 · NHGRI · WAYNE STATE UNIVERSITY · PI DRAGHICI, SORIN · 2005 to 2007
$877k
Software tools for pediatric neuroimagingR21EB000990 · NIBIB · WAYNE STATE UNIVERSITY · PI MUZIK, OTTO · 2002 to 2004
$442k
Infrastructure equipment for gene expression analysisS10RR017857 · NCRR · WAYNE STATE UNIVERSITY · PI DRAGHICI, SORIN · 2003 to 2003
$188k
Markers for the Early Detection of Ovarian CancerR21CA100740 · NCI · WAYNE STATE UNIVERSITY · PI TAINSKY, MICHAEL A · 2003 to 2003
$151k
NCI NIH HHS P30 CA022453NCI NIH HHS R01 CA100724NCI NIH HHS R21 CA100740NCI NIH HHS R21 CA10074001NCRR NIH HHS 1S10 RR01785701NCRR NIH HHS S10 RR017857NHGRI NIH HHS R01 HG003491NIBIB NIH HHS 1R21 EB0099001NIBIB NIH HHS R21 EB000990NINDS NIH HHS 1R01NS04520701NINDS NIH HHS R01 NS045207
6 · The paper itself

Abstract

Amplification of the 8p11-12 region occurs in 15-20% of breast cancers, but the driving oncogene at this locus has yet to be definitively identified. We mapped the 8p11-12 amplicon in breast cancer cell lines and primary human breast cancers and identified the candidate oncogene human Sm-like protein (hLsm1, LSM1) based on increases in copy number and expression level relative to human mammary epithelial cells. To examine the oncogenic role of LSM1, we overexpressed this gene in MCF10A mammary epithelial cells and inhibited its production in the SUM44 breast cancer cell line, which has a natural amplification and overexpression of LSM1. Our data confirmed that LSM1 is an oncogene from the 8p11-12 amplicon by showing that hLsm1 overexpression induced growth factor-independent proliferation and soft agar colony formation in MCF10A cells, and hLsm1 inhibition in SUM44 cells dramatically reduced soft agar growth. Little is known about hLsm1 function other than its involvement in mRNA degradation; therefore, we used expression microarray analysis to investigate how hLsm1 affects cell transformation in MCF10A and SUM44 cells. We identified numerous genes altered following hLsm1 overexpression common to SUM44 breast cancer cells that play important roles in cell cycle regulation, cell proliferation and other cancer-promoting processes. Future work will continue to characterize these important changes to achieve a more complete understanding of the mechanism of hLsm1's effect on cancer progression.

Indexed as

Gene AmplificationOncogenesBreast NeoplasmsCell Line, TumorCell ProliferationCell Transformation, NeoplasticChromosomes, Human, Pair 8Culture Media, ConditionedFemaleGene DosageGene Expression ProfilingHumansInsulin-Like Growth Factor IProto-Oncogene ProteinsRNA-Binding ProteinsRNA, Small InterferingCulture Media, ConditionedInsulin-Like Growth Factor ILSM1 protein, humanProto-Oncogene ProteinsRNA-Binding ProteinsRNA, Small Interfering

Identifiers

PMID17001308
PMCPMC2435249
OpenAlexW2168107793

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.