Evidence map›Paper›PMID 21996731›Full record

ReviewOncogene2012

Breast cancer genome-wide association studies: there is strength in numbers.

D Fanale, V Amodeo, L R Corsini, S Rizzo, V Bazan, A Russo

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 4 pooled it
7.8field-weighted citation impact, top 2% 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

57 citing papers in PubMed, 4 syntheses or guidelines pooled it, 112 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Review
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  8. Ropivacaine as a novel AKT1 specific inhibitor regulates the stemness of breast cancer.Journal of experimental & clinical cancer research : CR · 2024
    Article
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  13. Correlation betweenReports of biochemistry & molecular biology · 2020
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  17. Associations betweenBioscience reports · 2019
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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

6 authors at 2 institutions in 2 countries.

D FanaleDepartment of Surgical and Oncological Sciences, Section of Medical Oncology, University of Palermo, Palermo, Italy.
V Amodeo
L R Corsini
S Rizzo
V Bazan
A Russo
University of Palermo · ITTemple University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer (BC) is a heterogeneous disease that exhibits familial aggregation. Family linkage studies have identified high-penetrance genes, BRCA1, BRCA2, PTEN and TP53, that are responsible for inherited BC syndromes. Moreover, a combination of family-based and population-based approaches indicated that genes involved in DNA repair, such as CHEK2, ATM, BRIP and PALB2, are associated with moderate risk. Therefore, all of these known genes account for only 25% of the familial aggregation cases. Recently, genome wide association studies (GWAS) in BC revealed single nucleotide polymorphisms (SNPs) in five novel genes associated to susceptibility: TNRC9, FGFR2, MAP3K1, H19 and lymphocyte-specific protein 1 (LSP1). The most strongly associated SNP was in intron 2 of the FGFR2 gene that is amplified and overexpressed in 5-10% of BC. rs3803662 of TNRC9 gene has been shown to be the SNP with the strongest association with BC, in particular, this polymorphism seems to be correlated with bone metastases and estrogen receptor positivity. Relevant data indicate that SNP rs889312 in MAP3K1 is correlated with BC susceptibility only in BRCA2 mutation carriers, but is not associated with an increased risk in BRCA1 carriers. Finally, different SNPs in LSP1 and H19 and in minor genes probably were associated with BC risk. New susceptibility allelic variants associated with BC risk were recently discovered including potential causative genes involved in regulation of cell cycle, apoptosis, metabolism and mitochondrial functions. In conclusion, the identification of disease susceptibility loci may lead to a better understanding of the biological mechanism for BC to improve prevention, early detection and treatment.

Indexed as

Genome-Wide Association StudyMultifactorial InheritanceApoptosis Regulatory ProteinsBreast NeoplasmsFemaleGenetic Predisposition to DiseaseHigh Mobility Group ProteinsHumansMAP Kinase Kinase Kinase 1Microfilament ProteinsPolymorphism, Single NucleotideReceptor, Fibroblast Growth Factor, Type 2Receptors, ProgesteroneTrans-ActivatorsApoptosis Regulatory ProteinsFGFR2 protein, humanHigh Mobility Group ProteinsLSP1 protein, humanMAP3K1 protein, humanMAP Kinase Kinase Kinase 1Microfilament ProteinsReceptor, Fibroblast Growth Factor, Type 2Receptors, ProgesteroneTOX3 protein, humanTrans-Activators

Identifiers

PMID21996731
OpenAlexW2082402899

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.