Evidence map›Paper›PMID 24572700›Full record

ArticleClinical and translational gastroenterology2014

Significant evidence of linkage for a gene predisposing to colorectal cancer and multiple primary cancers on 22q11.

Craig Teerlink, Quentin Nelson, Randall Burt, Lisa Cannon-Albright

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 44% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Craig TeerlinkDivision of Genetic Epidemiology, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA.
Quentin NelsonDivision of Genetic Epidemiology, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA.
Randall Burt1] Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah, USA [2] Division of Gastroenterology, Department of Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA.
Lisa Cannon-Albright1] Division of Genetic Epidemiology, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA [2] George E. Wahlen Department of Veterans Affairs Medical Center, Salt Lake City, Utah, USA.
University of Utah · USHuntsman Cancer Institute · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
NCI NIH HHS P30 CA042014
6 · The paper itself

Abstract

objectivesThe genetic basis of colorectal cancer (CRC) is not completely specified. Part of the difficulty in mapping predisposition genes for CRC may be because of phenotypic heterogeneity. Using data from a population genealogy of Utah record linked to a statewide cancer registry, we identified a subset of CRC cases that exhibited familial clustering in excess of that expected for all CRC cases in general, which may represent a genetically homogeneous subset of CRC.

methodsUsing a new familial aggregation method referred to as the subset genealogic index of familiality (subsetGIF), combined with detailed information from a statewide tumor registry, we identified a subset of CRC cases that exhibited excess familial clustering above that expected for CRC: CRC cases who had at least one other primary tumor at a different site. A genome-wide linkage analysis was performed on a set of high-risk CRC pedigrees that included multiple CRC cases with additional primaries to identify evidence for predisposition loci.

resultsA total of 13 high-risk CRC pedigrees with multiple CRC cases with other primary cancers were identified. Linkage analysis identified one pedigree with a significant linkage signal at 22q11 (LOD (logarithm (base 10) of odds)=3.39).

conclusionsA predisposition gene or variant for CRC that also predisposes to other primary cancers likely resides on chromosome 22q11. The ability to use statewide population genealogy and tumor registry data was critical to identify an informative subset of CRC cases that is possibly more genetically homogeneous than CRC in general, and may have improved statistical power for predisposition locus identification in this study.

Identifiers

PMID24572700
PMCPMC3940837
OpenAlexW1999058429

What OpenQuestion holds

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Registered trials

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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.