Evidence map›Paper›PMID 21082043›Full record

ArticleNeoplasia (New York, N.Y.)2010

Integrative functional genomics analysis of sustained polyploidy phenotypes in breast cancer cells identifies an oncogenic profile for GINS2.

Juha K Rantala, Henrik Edgren, Laura Lehtinen, Maija Wolf, Kristine Kleivi, Hans Kristian Moen Vollan, Anna-Riina Aaltola, Petra Laasola, Sami Kilpinen, Petri Saviranta and 2 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 57 citations in OpenAlex.

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  15. The dualistic origin of human tumors.Seminars in cancer biology · 2018
    Review
  16. Article
  17. Article
  18. Article
  19. Vitamin D receptor and RXR in the post-genomic era.Journal of cellular physiology · 2015
    Review
  20. Cell line modeling for systems medicine in cancers (review).International journal of oncology · 2014
    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

12 authors at 5 institutions in 2 countries.

Juha K RantalaMedical Biotechnology, VTT Technical Research Centre of Finland, Turku, Finland.
Henrik Edgren
Laura Lehtinen
Maija Wolf
Kristine Kleivi
Hans Kristian Moen Vollan
Anna-Riina Aaltola
Petra Laasola
Sami Kilpinen
Petri Saviranta
Kristiina Iljin
Olli Kallioniemi
VTT Technical Research Centre of Finland · FIUniversity of Helsinki · FIInstitute for Molecular Medicine Finland · FIUniversity of Oslo · NOUniversity of Turku · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aneuploidy is among the most obvious differences between normal and cancer cells. However, mechanisms contributing to development and maintenance of aneuploid cell growth are diverse and incompletely understood. Functional genomics analyses have shown that aneuploidy in cancer cells is correlated with diffuse gene expression signatures and aneuploidy can arise by a variety of mechanisms, including cytokinesis failures, DNA endoreplication, and possibly through polyploid intermediate states. To identify molecular processes contributing to development of aneuploidy, we used a cell spot microarray technique to identify genes inducing polyploidy and/or allowing maintenance of polyploid cell growth in breast cancer cells. Of 5760 human genes screened, 177 were found to induce severe DNA content alterations on prolonged transient silencing. Association with response to DNA damage stimulus and DNA repair was found to be the most enriched cellular processes among the candidate genes. Functional validation analysis of these genes highlighted GINS2 as the highest ranking candidate inducing polyploidy, accumulation of endogenous DNA damage, and impairing cell proliferation on inhibition. The cell growth inhibition and induction of polyploidy by suppression of GINS2 was verified in a panel of breast cancer cell lines. Bioinformatic analysis of published gene expression and DNA copy number studies of clinical breast tumors suggested GINS2 to be associated with the aggressive characteristics of a subgroup of breast cancers in vivo. In addition, nuclear GINS2 protein levels distinguished actively proliferating cancer cells suggesting potential use of GINS2 staining as a biomarker of cell proliferation as well as a potential therapeutic target.

Indexed as

Gene Expression ProfilingGene Expression Regulation, NeoplasticPolyploidyBreast NeoplasmsCell LineCell Line, TumorChromosomal Proteins, Non-HistoneCluster AnalysisFemaleGenomicsHumansMicroscopy, ConfocalOligonucleotide Array Sequence AnalysisProto-Oncogene ProteinsReverse Transcriptase Polymerase Chain ReactionRNA InterferenceChromosomal Proteins, Non-HistoneGINS2 protein, humanProto-Oncogene Proteins

Identifiers

PMID21082043
PMCPMC2981730
OpenAlexW1559357300

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.