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Dataset holding methylation, expression level and clinical data related to NDRG4 promoter hypermethylation: a mechanistic biomarker associated with metastatic progression in breast cancer patients

dataset
posted on 2019-04-09, 13:51 authored by Elisa Jandrey, Ricardo Moura, Luciana N. S. Andrade, Camila Maria Longo Machado, Luiz Felipe Campesato, Katia Ramos Moreira Leite, Lilian Tiemi Inoue, Paula Fontes Asprino, Ana Paula Medeiros da Silva, Alfredo Carlos Simões Dornellas de Barros, André Carvalho, Vladmir Cordeiro de Lima, Dirce Maria Carraro, Helena Brentani, Isabela Werneck Cunha, Fernando Augusto Soares, Raphael Bessa Parmigiani, Roger Chammas, Anamaria Aranha Camargo, Erico Tosoni Costa
The dataset contains data supporting the related publication: NDRG4 promoter hypermethylation: a mechanistic biomarker associated with metastatic progression in breast cancer patients. The data consist of four .xlsx MS Excel data files, which are also supplementary information files in the related publication.

Background:

N-Myc downstream-regulated gene 4 (NDRG4) is an intracellular protein that is predominantly expressed in the normal brain and heart. The related study investigates the role of NDRG4 expression in normal breast tissue and the relevant impact of DNA promoter hypermethylation in breast primary tumors and tumor cell lines, along with the potential of NDRG4 promoter hypermethylation as a mechanistic biomarker of breast cancer metastasis.

This approach represents a method for assessing risk of developing metastatic disease alternative to e.g. simple number of positive axillary lymph nodes in combination with clinicopathological factors. The molecular approach presented, using a multigene expression panel, involves analysis of a set of cancer-related genes.

Study design summary and sample sizes:

To explore the relationship between NDRG4 promoter methylation and expression levels and patient clinicopathological parameters and outcome, survival analysis for the NDRG4 promoter methylation was conducted in 782 patients dichotomized in higher and lower methylation groups by MethSurv. The correlation between the presence of NDRG4 methylation and well-established prognostic factors was also explored in an existing cohort of 61 patients with invasive breast ductal carcinoma from AC Camargo Cancer Center (ACC).

The methods includes microarray analysis of 64 genes - 11 of which were interrogated via MsigDB, and in silico expression and methylation analysis using paired normal and primary breast tumors obtained from The Cancer Genome Atlas (TCGA) through the MethHC database.


Format and content of data files:
The figure and table numbers referenced are those of the related research article.

1) Data supporting figure S2 raw.xlsx:
Methylation data (β-values) for entire NDRG4 gene in breast cancer patients (Island, N and S Shelf and N shore) obtained from MethSurv online (https://biit.cs.ut.ee/methsurv/)

2) Supplementary Table S1 processed.xlsx:
4457 Open Reading frame ESTs (ORESTES) expression levels supporting this study and annotation data, like chr. position, quality (based on BLAT alignment), HGNC symbol, Ensembl gene ID, coverage and others.

3) Supplementary Table S2 raw.xlsx: A cDNA microarray and quantitative PCR expression data and enrichment analysis of top 16 genes induced by 5-aza-dC treatments in MDA-MB231 breast cancer cell line. Enrichment analysis were obtained from http://software.broadinstitute.org/gsea/index.jsp

4) Supplementary Table S3.xlsx: Clinical data of A.C.Camargo Cancer Center's 61 patients with breast invasive ductal carcinoma analyzed in this study, specifically presence of NDRG4-SPR methylation andw well-established prognostic factors, including grouped age, Scarff-Bloom-Richardson grade and tumour size.

Ethical approval:

Study was approved by the Brazilian National and by ACC Ethics Committees (728/2000, 1357/10).

Funding

This work was supported by grants from: FAPESP – 652 São Paulo Research Foundation (2009/53819-1) and LICR.

History

Research Data Support

Research data support provided by Springer Nature.