Evidence map›Paper›PMID 24056967›Full record

ArticleOncogene2014

Identification of LMX1B as a novel oncogene in human ovarian cancer.

L He, L Guo, V Vathipadiekal, P A Sergent, W B Growdon, D A Engler, B R Rueda, M J Birrer, S Orsulic, G Mohapatra

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

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  13. Analysis of the lipidome of xenografts using MALDI-IMS and UHPLC-ESI-QTOF.Journal of the American Society for Mass Spectrometry · 2014
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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

10 authors at 5 institutions in 1 country.

L He1] Department of Pathology, Massachusetts General Hospital, Boston, MA, USA [2] Harvard Medical School, Boston, MA, USA.
L GuoVincent Center for Reproductive Biology, Department of Vincent Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA, USA.
V Vathipadiekal1] Harvard Medical School, Boston, MA, USA [2] Division of Hematology-Oncology and Center for Cancer Research, Massachusetts General Hospital, Boston, MA, USA.
P A SergentVincent Center for Reproductive Biology, Department of Vincent Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA, USA.
W B Growdon1] Harvard Medical School, Boston, MA, USA [2] Vincent Center for Reproductive Biology, Department of Vincent Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA, USA.
D A EnglerDepartment of Statistics, Brigham Young University, Provo, UT, USA.
B R Rueda1] Harvard Medical School, Boston, MA, USA [2] Vincent Center for Reproductive Biology, Department of Vincent Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA, USA.
M J Birrer1] Harvard Medical School, Boston, MA, USA [2] Division of Hematology-Oncology and Center for Cancer Research, Massachusetts General Hospital, Boston, MA, USA.
S OrsulicWomen's Cancer Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
G Mohapatra1] Department of Pathology, Massachusetts General Hospital, Boston, MA, USA [2] Harvard Medical School, Boston, MA, USA.
Harvard University · USSaint Vincent Hospital · USBrigham Young University · USCancer Research Institute · USMassachusetts General Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancers are thought to result from the accumulation of multiple genetic aberrations that transform ovarian and/or fallopian tube surface epithelial cells, allowing for their abnormal growth, proliferation and metastasis. In the report presented here, we carried out genome-wide copy-number analysis using comparative genomic hybridization on a panel of mouse ovarian cancer (OVCA) cell lines previously established in our laboratory. We identified a recurrent focal amplification on mouse chromosomal region 2qB, which contains the LIM-homeodomain-containing transcription factor 1B (Lmx1b) gene. LMX1B is not expressed in normal human ovary, but is expressed in many human OVCA cell lines and primary tumors. High expression of LMX1B correlates with poor outcome. To clarify the role of LMX1B in ovarian carcinogenesis, we transduced LMX1B into a panel of mouse and human OVCA cell lines and demonstrated that LMX1B strongly promotes migration of cancer cells in culture and promotes xenograft growth in nude mice. Conversely, knockdown of LMX1B in a human cell line with endogenous high expression of LMX1B inhibits cell migration in vitro and tumor growth in vivo. Microarray analysis of cells overexpressing LMX1B identified the nuclear factor (NF)-κB pathway as a potential mediator of tumor progression and subsequent treatment of NFκB inhibitor decreased the migratory capacity of these cells. Thus, our data demonstrate that LMX1B is a novel oncogene in OVCA pathogenesis.

Indexed as

OncogenesAnimalsCarcinogenesisCell Line, TumorFemaleGene AmplificationHumansLIM-Homeodomain ProteinsMiceMice, Inbred NODMice, SCIDNeoplasm TransplantationNF-kappa BOligonucleotide Array Sequence AnalysisOvarian NeoplasmsSignal TransductionLIM homeobox transcription factor 1 betaLIM-Homeodomain ProteinsNF-kappa BTranscription Factors

Identifiers

PMID24056967
OpenAlexW2013101563

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.