Evidence map›Paper›PMID 21811255›Full record

ArticleBritish journal of cancer2011

A two-phase case-control study for colorectal cancer genetic susceptibility: candidate genes from chromosomal regions 9q22 and 3q22.

A Abulí, C Fernández-Rozadilla, M D Giráldez, J Muñoz, V Gonzalo, X Bessa, L Bujanda, J M Reñé, A Lanas, A M García and 18 more

Open access · hybridAbstract readMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

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  18. Debate about TGFBR1 and the susceptibility to colorectal cancer.World journal of gastrointestinal oncology · 2012
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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

28 authors at 19 institutions in 3 countries.

A AbulíDepartment of Gastroenterology, Hospital Clínic, CIBERehd, IDIBAPS, University of Barcelona, Villarroel 170, 08036, Barcelona, Catalonia, Spain.
C Fernández-Rozadilla
M D Giráldez
J Muñoz
V Gonzalo
X Bessa
L Bujanda
J M Reñé
A Lanas
A M García
J Saló
L Argüello
A Vilella
R Carreño
R Jover
R M Xicola
X Llor
L Carvajal-Carmona
I P M Tomlinson
D J Kerr
R S Houlston
J M Piqué
A Carracedo
A Castells
M Andreu
C Ruiz-Ponte
S Castellví-Bel
Gastrointestinal Oncology Group of the Spanish Gastroenterological Association
Universitat de Barcelona · ESCentre for Human Genetics · GBConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESFundación Pública Galega de Medicina Xenómica · ESPompeu Fabra University · ESUniversity of Illinois Chicago · USBiogipuzkoa Health Research Institute · ESCentre for Biomedical Network Research on Rare Diseases · ESCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas · ESFundación para la Formación e Investigación Sanitarias de la Región de Murcia · ESHospital Clínico Universitario Lozano Blesa · ESHospital Son Llatzer · ESHospital Universitari Arnau de Vilanova · ESHospital Universitari de Vic · ESHospital Universitari i Politècnic La Fe · ESHospital Universitari Sant Joan D'Alacant · ESInstitute of Cancer Research · GBParc de Salut · ESUniversity of Oxford · GB

Funding

Wellcome Trust 090532
6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) is the second cause of cancer-related death in the Western world. Much of the CRC genetic risk remains unidentified and may be attributable to a large number of common, low-penetrance genetic variants. Genetic linkage studies in CRC families have reported additional association with regions 9q22-31, 3q21-24, 7q31, 11q, 14q and 22q. There are several plausible candidate genes for CRC susceptibility within the aforementioned linkage regions including PTCH1, XPA and TGFBR1 in 9q22-31, and EPHB1 and MRAS in 3q21-q24.

methodsCRC cases and matched controls were from EPICOLON, a prospective, multicentre, nationwide Spanish initiative, composed of two independent phases. Phase 1 corresponded to 515 CRC cases and 515 controls, whereas phase 2 consisted of 901 CRC cases and 909 controls. Genotyping was performed for 172 single-nucleotide polymorphisms (SNPs) in 84 genes located within regions 9q22-31 and 3q21-q24.

resultsNone of the 172 SNPs analysed in our study could be formally associated with CRC risk. However, rs1444601 (TOPBP1) and rs13088006 (CDV3) in region 3q22 showed interesting results and may have an effect on CRC risk.

conclusionsTOPBP1 and CDV3 genetic variants on region 3q22 may modulate CRC risk. Further validation and meta-analysis should be undertaken in larger CRC cohorts.

Indexed as

Chromosomes, Human, Pair 3Chromosomes, Human, Pair 9Genetic Predisposition to DiseaseAgedAntigens, CDCarrier ProteinsCase-Control StudiesColorectal NeoplasmsDNA-Binding ProteinsGenetic Association StudiesGPI-Linked ProteinsHumansMaleNuclear ProteinsPolymorphism, Single NucleotideSemaphorinsAntigens, CDCarrier ProteinsDNA-Binding ProteinsGPI-Linked ProteinsNuclear ProteinsSEMA7A protein, humanSemaphorinsTOPBP1 protein, human

Identifiers

PMID21811255
PMCPMC3171011
OpenAlexW1965913932

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.