scholarly journals Global DNA Methylation, Measured by the Luminometric Methylation Assay (LUMA), Associates with Postmenopausal Breast Cancer in Non-Obese and Physically Active Women

2015 ◽  
Vol 6 (6) ◽  
pp. 548-554 ◽  
Author(s):  
Lauren E. McCullough ◽  
Jia Chen ◽  
Alexandra J. White ◽  
Xinran Xu ◽  
Yoon Hee Cho ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Postmenopausal Breast Cancer ◽  
Global Dna Methylation ◽  
Physically Active ◽  
Methylation Assay ◽  
Luminometric Methylation Assay

scholarly journals Artificial Light at Night of Different Spectral Compositions Differentially Affects Tumor Growth in Mice: Interaction With Melatonin and Epigenetic Pathways

2018 ◽  
Vol 25 (1) ◽  
pp. 107327481881290 ◽  
Author(s):  
A. E. Zubidat ◽  
B. Fares ◽  
F. Fares ◽  
A. Haim
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Tumor Growth ◽  
Short Wavelength ◽  
Global Dna Methylation ◽  
Artificial Light ◽  
Dna Hypomethylation ◽  
Light At Night ◽  
Cancer Burden ◽  
Melatonin Suppression

Lighting technology is rapidly advancing toward shorter wavelength illuminations that offer energy-efficient properties. Along with this advantage, the increased use of such illuminations also poses some health challenges, particularly breast cancer progression. Here, we evaluated the effects of artificial light at night (ALAN) of 4 different spectral compositions (500-595 nm) at 350 Lux on melatonin suppression by measuring its urine metabolite 6-sulfatoxymelatonin, global DNA methylation, tumor growth, metastases formation, and urinary corticosterone levels in 4T1 breast cancer cell-inoculated female BALB/c mice. The results revealed an inverse dose-dependent relationship between wavelength and melatonin suppression. Short wavelength increased tumor growth, promoted lung metastases formation, and advanced DNA hypomethylation, while long wavelength lessened these effects. Melatonin treatment counteracted these effects and resulted in reduced cancer burden. The wavelength suppression threshold for melatonin-induced tumor growth was 500 nm. These results suggest that short wavelength increases cancer burden by inducing aberrant DNA methylation mediated by the suppression of melatonin. Additionally, melatonin suppression and global DNA methylation are suggested as promising biomarkers for early diagnosis and therapy of breast cancer. Finally, ALAN may manifest other physiological responses such as stress responses that may challenge the survival fitness of the animal under natural environments.

Abstract 5615: Global DNA methylation by LUMA predicts breast cancer risk in a population-based study

2011 ◽  
Author(s):  
Xinran Xu ◽  
Marilie D. Gammon ◽  
James G. Wetmur ◽  
Susan L. Teiltelbaum ◽  
Patrick T. Bradshaw ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Population Based ◽  
Global Dna Methylation ◽  
Population Based Study

scholarly journals Epigenome-wide DNA methylation and risk of breast cancer: a systematic review

BMC Cancer ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Kaoutar Ennour-Idrissi ◽  
Dzevka Dragic ◽  
Francine Durocher ◽  
Caroline Diorio
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Risk Of Bias ◽  
Global Dna Methylation ◽  
Dna Hypomethylation ◽  
Epigenetic Age ◽  
Potential Biomarker

Abstract Background DNA methylation is a potential biomarker for early detection of breast cancer. However, robust evidence of a prospective relationship between DNA methylation patterns and breast cancer risk is still lacking. The objective of this study is to provide a systematic analysis of the findings of epigenome-wide DNA methylation studies on breast cancer risk, in light of their methodological strengths and weaknesses. Methods We searched major databases (MEDLINE, EMBASE, Web of Science, CENTRAL) from inception up to 30th June 2019, for observational or intervention studies investigating the association between epigenome-wide DNA methylation (using the HM450k or EPIC BeadChip), measured in any type of human sample, and breast cancer risk. A pre-established protocol was drawn up following the Cochrane Reviews rigorous methodology. Study selection, data abstraction, and risk of bias assessment were performed by at least two investigators. A qualitative synthesis and systematic comparison of the strengths and weaknesses of studies was performed. Results Overall, 20 studies using the HM450k BeadChip were included, 17 of which had measured blood-derived DNA methylation. There was a consistent trend toward an association of global blood-derived DNA hypomethylation and higher epigenetic age with higher risk of breast cancer. The strength of associations was modest for global hypomethylation and relatively weak for most of epigenetic age algorithms. Differences in length of follow-up periods may have influenced the ability to detect associations, as studies reporting follow-up periods shorter than 10 years were more likely to observe an association with global DNA methylation. Probe-wise differential methylation analyses identified between one and 806 differentially methylated CpGs positions in 10 studies. None of the identified differentially methylated sites overlapped between studies. Three studies used breast tissue DNA and suffered major methodological issues that precludes any conclusion. Overall risk of bias was critical mainly because of incomplete control of confounding. Important issues relative to data preprocessing could have limited the consistency of results. Conclusions Global DNA methylation may be a short-term predictor of breast cancer risk. Further studies with rigorous methodology are needed to determine spatial distribution of DNA hypomethylation and identify differentially methylated sites associated with risk of breast cancer. Prospero registration number CRD42020147244

scholarly journals Global DNA methylation levels in girls with and without a family history of breast cancer

Epigenetics ◽  
2011 ◽  
Vol 6 (1) ◽  
pp. 29-33 ◽  
Author(s):  
Hui-Chen Wu ◽  
Esther M. John ◽  
Jennifer S. Ferris ◽  
Theresa H. Keegan ◽  
Wendy K. Chung ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Family History ◽  
Global Dna Methylation ◽  
History Of

scholarly journals Relationships between Global DNA Methylation in Circulating White Blood Cells and Breast Cancer Risk Factors

2017 ◽  
Vol 2017 ◽  
pp. 1-25 ◽  
Author(s):  
Nayha Chopra-Tandon ◽  
Haotian Wu ◽  
Kathleen F. Arcaro ◽  
Susan R. Sturgeon
Keyword(s):  
Breast Cancer ◽  
Risk Factors ◽  
Dna Methylation ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
The Other ◽  
Global Dna Methylation ◽  
Cancer Risk Factors ◽  
Wide Range ◽  
Breast Cancer Risk Factors

It is not yet clear whether white blood cell DNA global methylation is associated with breast cancer risk. In this review we examine the relationships between multiple breast cancer risk factors and three markers of global DNA methylation:LINE-1, 5-mdC, andAlu. A literature search was conducted using Pubmed up to April 1, 2016, using combinations of relevant outcomes such as “WBC methylation,” “blood methylation,” “bloodLINE-1methylation,” and a comprehensive list of known and suspected breast cancer risk factors. Overall, the vast majority of reports in the literature have focused onLINE-1. There was reasonably consistent evidence across the studies examined that males have higher levels ofLINE-1methylation in WBC DNA than females. None of the other demographic, lifestyle, dietary, or health condition risk factors were consistently associated withLINE-1DNA methylation across studies. With the possible exception of sex, there was also little evidence that the wide range of breast cancer risk factors we examined were associated with either of the other two global DNA methylation markers: 5-mdC andAlu. One possible implication of the observed lack of association between global WBC DNA methylation and known breast cancer risk factors is that the association between global WBC DNA methylation and breast cancer, if it exists, is due to a disease effect.

LUMA (LUminometric Methylation Assay)—A high throughput method to the analysis of genomic DNA methylation

2006 ◽  
Vol 312 (11) ◽  
pp. 1989-1995 ◽  
Author(s):  
Mohsen Karimi ◽  
Sofia Johansson ◽  
Dirk Stach ◽  
Martin Corcoran ◽  
Dan Grandér ◽  
...  
Keyword(s):  
Dna Methylation ◽  
High Throughput ◽  
Genomic Dna ◽  
Methylation Assay ◽  
High Throughput Method ◽  
Luminometric Methylation Assay
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