Evidence map›Paper›PMID 26610810›Full record

ArticleBreast cancer research and treatment2016

Epigenetic regulation of ID4 in the determination of the BRCAness phenotype in breast cancer.

M T Branham, E Campoy, S Laurito, R Branham, G Urrutia, J Orozco, F Gago, R Urrutia, M Roqué

Open access · bronzeAbstract read
In one paragraph

Article in Breast cancer research and treatment, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  5. Cell-type-specific epigenomic variations associated withNAR genomics and bioinformatics · 2022
    Article
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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

9 authors at 2 institutions in 2 countries.

M T BranhamIHEM-CCT-CONICET Mendoza and National University of Cuyo, Mendoza, Argentina. mbranham@fcm.uncu.edu.ar.ORCID http://orcid.org/0000-0003-0362-0240
E CampoyIHEM-CCT-CONICET Mendoza and National University of Cuyo, Mendoza, Argentina.
S LauritoIHEM-CCT-CONICET Mendoza and National University of Cuyo, Mendoza, Argentina.
R BranhamIANIGLA-CCT-CONICET Mendoza, Mendoza, Argentina.
G UrrutiaIHEM-CCT-CONICET Mendoza and National University of Cuyo, Mendoza, Argentina.
J OrozcoGineco-Mamario Institute of Mendoza, Mendoza, Argentina.
F GagoGineco-Mamario Institute of Mendoza, Mendoza, Argentina.
R UrrutiaGI Research Unit, Division of Gastroenterology and Hepatology, Epigenomics Translational Program, Center for Individualized Medicine, Mayo Clinic, Rochester, USA.
M RoquéIHEM-CCT-CONICET Mendoza and National University of Cuyo, Mendoza, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARMayo Clinic · US

Funding

Tissue CoreP50CA102701 · NCI · MAYO CLINIC ROCHESTER · PI PETERSEN, GLORIA M. · 2004 to 2018
$32.7M
PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI GREGORY J. GORES · 2009 to 2026
$22.2M
ZINC FINGER GENES AND PANCREATIC CELL GROWTHR01DK052913 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI LOMBERK, GWEN, URRUTIA, RAUL A. · 1998 to 2023
$7.0M
The Role of Zinc Finger Genes in Pancreatic Cell GrowthR56DK052913 · NIDDK · MAYO CLINIC ROCHESTER · PI URRUTIA, RAUL A. · 2008 to 2008
$291k
NCI NIH HHS P50 CA102701NIDDK NIH HHS DK52913NIDDK NIH HHS P30 DK084567NIDDK NIH HHS P30DK084567NIDDK NIH HHS R01 DK052913
6 · The paper itself

Abstract

BRCAness breast tumors represent a group of sporadic tumors characterized by a reduction in BRCA1 gene expression. As BRCA1 is involved in double-strand breaks (DSBs) repair, dysfunctional BRCA pathway could make a tumor sensitive to DNA damaging drugs (e.g., platinum agents). Thus, accurately identifying BRCAness could contribute to therapeutic decision making in patients harboring these tumors. The purpose of this study was to identify if BRCAness tumors present a characteristic methylation profile and/or were related to specific clinico-pathological features. BRCAness was measured by MLPA in 63 breast tumors; methylation status of 98 CpG sites within 84 cancer-related genes was analyzed by MS-MLPA. Protein and mRNA expressions of the selected genes were measured by quantitative real-time PCR and Western Blot. BRCAness was associated with younger age, higher nuclear pleomorphism, and triple-negative (TN) status. Epigenetically, we found that the strongest predictors for BRCAness tumors were the methylations of MLH1 and PAX5 plus the unmethylations of CCND2 and ID4. We determined that ID4 unmethylation correlated with the expression levels of both its mRNA and protein. We observed an inverse relation between the expressions of ID4 and BRCA1. To the best of our knowledge, this is the first report suggesting an epigenetic regulation of ID4 in BRCAness tumors. Our findings give new information of BRCAness etiology and encourage future studies on potential drug targets for BRCAness breast tumors.

Indexed as

Epigenesis, GeneticGene Expression Regulation, NeoplasticGenes, BRCA1Genes, BRCA2PhenotypeAdultBiomarkers, TumorBreast NeoplasmsCarcinoma, Ductal, BreastCpG IslandsDNA MethylationDNA Modification MethylasesDNA Repair EnzymesEpigenomicsFemaleGene AmplificationBiomarkers, TumorDNA Modification MethylasesDNA Repair EnzymesID4 protein, humanInhibitor of Differentiation ProteinsMGMT protein, humanTumor Suppressor ProteinsAberrant DNA methylationBRCAnessBreast tumorsID4

Identifiers

PMID26610810
PMCPMC6036618
OpenAlexW2180334285

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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.