Evidence map›Paper›PMID 27356891›Full record

ArticleFamilial cancer2016

Undefined familial colorectal cancer and the role of pleiotropism in cancer susceptibility genes.

Sara E Dobbins, Peter Broderick, Daniel Chubb, Ben Kinnersley, Amy L Sherborne, Richard S Houlston

Open access · hybridAbstract read
In one paragraph

Article in Familial cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Frontiers in oncology · 2021
    Article
  5. Review
  6. Review
  7. Article
  8. 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

6 authors at 1 institution in 1 country.

Sara E DobbinsDivision of Genetics and Epidemiology, The Institute of Cancer Research, London, UK. sara.dobbins@icr.ac.uk.
Peter BroderickDivision of Genetics and Epidemiology, The Institute of Cancer Research, London, UK.
Daniel ChubbDivision of Genetics and Epidemiology, The Institute of Cancer Research, London, UK.
Ben KinnersleyDivision of Genetics and Epidemiology, The Institute of Cancer Research, London, UK.
Amy L SherborneDivision of Pathology, The Institute of Cancer Research, London, UK.
Richard S HoulstonDivision of Genetics and Epidemiology, The Institute of Cancer Research, London, UK.
Institute of Cancer Research · GB

Funding

Cancer Research UK 15116Cancer Research UK C1298/A8362Medical Research Council G1001799Medical Research Council MR/N01104X/1Wellcome TrustWellcome Trust WT095219MA
6 · The paper itself

Abstract

Although family history is a major risk factor for colorectal cancer (CRC) a genetic diagnosis cannot be obtained in over 50 % of familial cases when screened for known CRC cancer susceptibility genes. The genetics of undefined-familial CRC is complex and recent studies have implied additional clinically actionable mutations for CRC in susceptibility genes for other cancers. To clarify the contribution of non-CRC susceptibility genes to undefined-familial CRC we conducted a mutational screen of 114 cancer susceptibility genes in 847 patients with early-onset undefined-familial CRC and 1609 controls by analysing high-coverage exome sequencing data. We implemented American College of Medical Genetics and Genomics standards and guidelines for assigning pathogenicity to variants. Globally across all 114 cancer susceptibility genes no statistically significant enrichment of likely pathogenic variants was shown (6.7 % cases 57/847, 5.3 % controls 85/1609; P = 0.15). Moreover there was no significant enrichment of mutations in genes such as TP53 or BRCA2 which have been proposed for clinical testing in CRC. In conclusion, while we identified genes that may be considered interesting candidates as determinants of CRC risk warranting further research, there is currently scant evidence to support a role for genes other than those responsible for established CRC syndromes in the clinical management of familial CRC.

Indexed as

Genetic PleiotropyGenetic Predisposition to DiseaseBRCA1 ProteinBRCA2 ProteinCase-Control StudiesColorectal NeoplasmsHeterozygoteHumansMutationProto-Oncogene ProteinsRecQ HelicasesTumor Suppressor ProteinsBloom syndrome proteinBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanFLCN protein, humanProto-Oncogene ProteinsRecQ HelicasesTumor Suppressor ProteinsCancer susceptibilityColorectalExome sequencingFamilial colorectal cancerGermlinePleiotropism

Identifiers

PMID27356891
PMCPMC5010824
OpenAlexW2461906200

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.