Evidence map›Paper›PMID 22926736›Full record

ArticleFamilial cancer2012

Low penetrance alleles as risk modifiers in familial and sporadic breast cancer.

Eva Esteban Cardeñosa, Inmaculada de Juan Jiménez, Sarai Palanca Suela, Isabel Chirivella González, Angel Segura Huerta, Ana Santaballa Beltran, María Casals El Busto, Eva Barragán González, Oscar Fuster Lluch, José Bermúdez Edo and 1 more

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Familial cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.2field-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

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

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. 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

11 authors at 5 institutions in 1 country.

Eva Esteban CardeñosaLaboratory of Molecular Biology, Service of Clinical Analysis, Escuela de Enfermería 7ª, Hospital Universitario La Fe, Avenida Campanar 21, Valencia, Spain.
Inmaculada de Juan Jiménez
Sarai Palanca Suela
Isabel Chirivella González
Angel Segura Huerta
Ana Santaballa Beltran
María Casals El Busto
Eva Barragán González
Oscar Fuster Lluch
José Bermúdez Edo
Pascual Bolufer Gilabert
Hospital Universitari i Politècnic La Fe · ESInstituto de Investigación Sanitaria La Fe · ESHospital Clínico Universitario de Valencia · ESLeitat Technological Center · ESUniversitat de València · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the study is to investigate the relevance of rs1056663 and rs2708861 HUS1 polymorphisms, and rs104548, rs2981582 and rs2910164 polymorphisms of CASP8, FGFR2 and micro RNA 146A genes, respectively, as risk modifiers in hereditary breast or ovarian cancer (BC/OC) and risk factors in sporadic BC. We performed a case-control study in 189 healthy controls (CG) and 538 BC/OC cases, 340 with familial history of BC/OC (130 carriers of BRCA1/2 mutations and 210 non-carriers) and 198 sporadic BC/OC. The polymorphisms were assessed by real-time PCR using primers and fluorescent-labelled hybridization probes. We found statistically significant differences between familial BC/OC and CG for rs1056663 and rs2708861 HSU1 polymorphisms and rs2981582 FGFR2 polymorphism, particularly in non-carriers of BRCA1/2 mutations. In this group we found statistical differences for rs1056663 HSU1 and rs2981582 FGFR2 polymorphisms (p-trend < 0.006). The logistic regression confirmed that rs2981582 FGFR2 polymorphism (OR = 2.09; 95 % CI 1.35, 3.20) and the interaction between rs1056663 and rs2708861 HUS1 polymorphisms increased the risk of cancer (OR = 1.87; 95 % CI 1.19, 2.92). Furthermore, we found that the presence of rs1056663 and rs2708861 HUS1 polymorphisms is associated with early age of presentation of BC (p = 0.015) in the group of non-carriers of BRCA1/2 mutations. In addition, no association of the polymorphisms studied in sporadic BC was observed. In conclusion, the HUS1 and FGFR2 polymorphisms act as risk BC modifiers in familial BC/OC, particularly in the group of non-carriers of BRCA1/2 mutations.

Indexed as

Genetic Predisposition to DiseaseAdultAgedAged, 80 and overBRCA1 ProteinBRCA2 ProteinBreast NeoplasmsCase-Control StudiesCaspase 8Cell Cycle ProteinsDNAFemaleGene FrequencyGenes, ModifierGenetic TestingGerm-Line MutationBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanCASP8 protein, humanCaspase 8Cell Cycle ProteinsDNAFGFR2 protein, humanHUS1 protein, humanMicroRNAsMIRN146 microRNA, humanReceptor, Fibroblast Growth Factor, Type 2

Identifiers

PMID22926736
OpenAlexW2046953775

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.