Evidence map›Paper›PMID 18350249›Full record

ArticleJournal of human genetics2008

Analysis of GADD45A sequence variations in French Canadian families with high risk of breast cancer.

Sylvie Desjardins, Geneviève Ouellette, Yvan Labrie, Jacques Simard, INHERIT BRCAs, Francine Durocher

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PubMed Publisher
In one paragraph

Article in Journal of human genetics, 2008. 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
0.4field-weighted citation impact, top 31% 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, 8 citations in OpenAlex.

  1. Roles for GADD45 in Development and Cancer.Advances in experimental medicine and biology · 2022
    Review
  2. Review
  3. 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

6 authors at 2 institutions in 1 country.

Sylvie DesjardinsCancer Genomics Laboratory, Oncology and Molecular Endocrinology Research Centre, Centre Hospitalier Universitaire de Québec and Laval University, 2705 Laurier Boulevard, T2-53, G1V 4G2, Québec City, QC, Canada.
Geneviève OuelletteCancer Genomics Laboratory, Oncology and Molecular Endocrinology Research Centre, Centre Hospitalier Universitaire de Québec and Laval University, 2705 Laurier Boulevard, T2-53, G1V 4G2, Québec City, QC, Canada.
Yvan LabrieCancer Genomics Laboratory, Oncology and Molecular Endocrinology Research Centre, Centre Hospitalier Universitaire de Québec and Laval University, 2705 Laurier Boulevard, T2-53, G1V 4G2, Québec City, QC, Canada.
Jacques SimardCancer Genomics Laboratory, Oncology and Molecular Endocrinology Research Centre, Centre Hospitalier Universitaire de Québec and Laval University, 2705 Laurier Boulevard, T2-53, G1V 4G2, Québec City, QC, Canada.
INHERIT BRCAs
Francine DurocherCancer Genomics Laboratory, Oncology and Molecular Endocrinology Research Centre, Centre Hospitalier Universitaire de Québec and Laval University, 2705 Laurier Boulevard, T2-53, G1V 4G2, Québec City, QC, Canada. francine.durocher@crchul.ulaval.ca.
Centre hospitalier universitaire de Québec · CAUniversité Laval · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

GADD45A is an evolutionary conserved gene whose expression is regulated by two major tumor suppressor proteins involved in breast cancer etiology, namely, p53 and BRCA1, and which acts primarily in the control of the G2/M cell-cycle transition, apoptosis, and DNA repair. Following genotoxic stress, the p53 protein activates GADD45A transcription, whereas in absence of DNA damage, BRCA1 represses GADD45A expression through interaction with the zinc finger protein ZNF350. Moreover, BRCA1 can activate GADD45A gene expression through interactions with transcription factors binding to the gene promoter. On the basis of the intricate network of interactions between GADD45A, p53, and BRCA1, and the fact that both BRCA1 or TP53 mutations are involved in breast cancer tumorigenesis, we undertook the characterization of the entire coding sequence, intron/exon boundaries, and p53- and ZNF350-binding sequences of this potential breast cancer susceptibility candidate gene in a sample set of 96 women affected with breast cancer from non-BRCA1 and BRCA2 French Canadian families with a high risk of breast cancer and 95 healthy controls from the same population. Although none of the 12 identified sequence variations show a significant difference in frequency between both sample sets, haplotype phasing and frequency estimations identified a common haplotype displaying a higher frequency among the control group. As the variants present on this particular haplotype are noncoding variants in either intron 2 or 3, this finding will have to be further investigated in larger cohorts and other populations. In this regard, our study also identified tagging single nucleotide polymorphisms (tSNPs), providing useful data for other large-scale association studies.

Indexed as

Base SequenceBreast NeoplasmsCanadaCase-Control StudiesCell Cycle ProteinsDNA, NeoplasmFemaleFranceGADD45 ProteinsGenetic Predisposition to DiseaseGenetic VariationHaplotypesHumansLinkage DisequilibriumNuclear ProteinsPolymorphism, Single NucleotideCell Cycle ProteinsDNA, NeoplasmGADD45A protein, humanGADD45 ProteinsNuclear Proteins

Identifiers

PMID18350249
OpenAlexW2059031321

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.