Evidence map›Paper›PMID 20567916›Full record

ArticleFamilial cancer2010

Screening for large genomic rearrangements of the BRIP1 and CHK1 genes in Finnish breast cancer families.

Szilvia Solyom, Katri Pylkäs, Robert Winqvist

Abstract read
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In one paragraph

Article in Familial cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. CD138Aging · 2020
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Roles of Chk1 in cell biology and cancer therapy.International journal of cancer · 2014
    Review
  9. Article
  10. 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

3 authors at 2 institutions in 1 country.

Szilvia SolyomLaboratory of Cancer Genetics, Department of Clinical Genetics and Biocenter Oulu, Oulu University Hospital, University of Oulu, PO Box 5000, 90014 Oulu, Finland.
Katri Pylkäs
Robert Winqvist
Oulu University Hospital · FIUniversity of Oulu · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In search for susceptibility genes that could explain an additional portion of familial breast cancer clustering in Finland, we set out to evaluate the presence of large genomic rearrangements in two candidate genes, BRIP1 and CHK1. BRIP1 is a BRCA1 associated protein that is mutated in a fraction of familial breast cancer and Fanconi anemia cases. To date, the role of large BRIP1 deletions in breast cancer susceptibility is not well-characterized. CHK1 is a critical maintainer of cell cycle checkpoints and genomic stability, and is also involved in the BRCA1 and FA protein signalling pathways. Although CHK1 is a very important protein for cell cycle and DNA integrity maintenance control, no mutations in this gene has yet been associated with predisposition to cancer. For the present study, blood DNA from affected index persons of 111 Northern Finnish breast cancer families was assessed for possible constitutional exonic deletions or amplifications in the BRIP1 and CHK1 genes by using the multiplex ligation-dependent probe amplification method. Our results showed that exonic deletions or amplifications affecting the BRIP1 and CHK1 genes seem not to contribute to hereditary breast cancer susceptibility in the Finnish population. To our knowledge, this is the first attempt to determine the existence of large CHK1 deletions in familial breast cancer or in any disease with a hereditary background.

Indexed as

Gene RearrangementGenetic Predisposition to DiseaseAdultBreast NeoplasmsCheckpoint Kinase 1DNA-Binding ProteinsDNA Mutational AnalysisDNA, NeoplasmFamilyFanconi Anemia Complementation Group ProteinsFemaleFinlandGenotypeHumansMaleMass ScreeningBRIP1 protein, humanCheckpoint Kinase 1CHEK1 protein, humanDNA-Binding ProteinsDNA, NeoplasmFanconi Anemia Complementation Group ProteinsProtein KinasesRNA Helicases

Identifiers

PMID20567916
OpenAlexW2051222731

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.