Evidence map›Paper›PMID 21829229›Full record

ArticleEuropean journal of human genetics : EJHG2012

Evidence of linkage to chromosomes 10p15.3-p15.1, 14q24.3-q31.1 and 9q33.3-q34.3 in non-syndromic colorectal cancer families.

Ian W Saunders, Jason Ross, Finlay Macrae, Graeme P Young, Ignacio Blanco, Jesper Brohede, Glenn Brown, Diana Brookes, Trevor Lockett, Peter L Molloy and 3 more

Open access · hybridAbstract read
In one paragraph

Article in European journal of human genetics : EJHG, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Whole-exome sequencing identifies rare pathogenic variants in new predisposition genes for familial colorectal cancer.Genetics in medicine : official journal of the American College of Medical Genetics · 2015
    Article
  6. Review
  7. Article
  8. Article
  9. Effects of Kruppel-like factor 6 on osteosarcoma cell biological behavior.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Article
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

13 authors at 6 institutions in 3 countries.

Ian W SaundersCSIRO Preventative Health Flagship, North Ryde, New South Wales, Australia.
Jason Ross
Finlay Macrae
Graeme P Young
Ignacio Blanco
Jesper Brohede
Glenn Brown
Diana Brookes
Trevor Lockett
Peter L Molloy
Victor Moreno
Gabriel Capella
Garry N Hannan
Commonwealth Scientific and Industrial Research Organisation · AUFlinders University · AUInstitut Català d'Oncologia · ESInstitut d'Investigació Biomédica de Bellvitge · ESThe Royal Melbourne Hospital · AUUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Up to 25% of colorectal cancer (CRC) may be caused by inherited genetic variants that have yet to be identified. Previous genome-wide linkage studies (GWLSs) have identified a new loci postulated to contain novel CRC risk genes amongst affected families carrying no identifiable mutations in any of the known susceptibility genes for familial CRC syndromes. To undertake a new GWLS, we recruited members from 54 non-syndromic families from Australia and Spain where at least two first-degree relatives were affected by CRC. We used single-nucleotide polymorphism arrays to genotype 98 concordant affected relative pairs that were informative for linkage analyses. We tested for genome-wide significance (GWS) for linkage to CRC using a quantile statistic method, and we found that GWS was achieved at the 5% level. Independently, using the PSEUDO gene-dropping algorithm, we also found that GWS for linkage to CRC was achieved (P=0.02). Merlin non-parametric linkage analysis revealed significant linkage to CRC for chromosomal region 10p15.3-p15.1 and suggestive linkage to CRC for regions on 14q and 9q. The 10p15.3-p15.1 has not been reported to be linked to hereditary CRC in previous linkage studies, but this region does harbour the Kruppel-like factor 6 (KLF6) gene that is known to be altered in common CRC. Further studies aimed at localising the responsible genes, and characterising their function will give insight into the factors responsible for susceptibility in such families, and perhaps shed further light on the mechanisms of CRC development.

Indexed as

Genetic LinkageAdenomaAdultAgedAlgorithmsAustraliaChromosomes, Human, Pair 10Chromosomes, Human, Pair 14Chromosomes, Human, Pair 9Colorectal NeoplasmsEthnicityFemaleGenes, NeoplasmGenetic Predisposition to DiseaseGenetic TestingGenome, HumanKLF6 protein, humanKruppel-Like Factor 6Kruppel-Like Transcription FactorsProto-Oncogene Proteins

Identifiers

PMID21829229
PMCPMC3234517
OpenAlexW2036450891

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.