Promoter methylation of TRIM9 as a marker for detection of circulating tumor DNA in breast cancer patients

Mishima, Chieko; Kagara, Naofumi; Matsui, Saki; Tanei, Tomonori; Naoi, Yasuto; Shimoda, Masafumi; Shimomura, Atsushi; Shimazu, Kenzo; Kim, Seung Jin; Noguchi, Shinzaburo

doi:10.1186/s40064-015-1423-7

Cited by 24 publications

(19 citation statements)

References 34 publications

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“…Strategies used in DNA methylation analysis can be classified into two groups: site-specific and genome-wide methylation detections. Currently, detection of site-specific methylations of DNA has been conduced more often [14] , [153] , [154] , [155] . Many methods originally used for site-specific detection of genomic DNA methylations are suitable for site-specific detection of ctDNA methylations as well.…”

Section: Methods For Detecting Ctdnasmentioning

confidence: 99%

Circulating Tumor DNA as Biomarkers for Cancer Detection

Han

Wang

Sun

2017

Genomics, Proteomics &Amp; Bioinformatics

200

163

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Detection of circulating tumor DNAs (ctDNAs) in cancer patients is an important component of cancer precision medicine ctDNAs. Compared to the traditional physical and biochemical methods, blood-based ctDNA detection offers a non-invasive and easily accessible way for cancer diagnosis, prognostic determination, and guidance for treatment. While studies on this topic are currently underway, clinical translation of ctDNA detection in various types of cancers has been attracting much attention, due to the great potential of ctDNA as blood-based biomarkers for early diagnosis and treatment of cancers. ctDNAs are detected and tracked primarily based on tumor-related genetic and epigenetic alterations. In this article, we reviewed the available studies on ctDNA detection and described the representative methods. We also discussed the current understanding of ctDNAs in cancer patients and their availability as potential biomarkers for clinical purposes. Considering the progress made and challenges involved in accurate detection of specific cell-free nucleic acids, ctDNAs hold promise to serve as biomarkers for cancer patients, and further validation is needed prior to their broad clinical use.

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Section: Methods For Detecting Ctdnasmentioning

confidence: 99%

Circulating Tumor DNA as Biomarkers for Cancer Detection

Han

Wang

Sun

2017

Genomics, Proteomics &Amp; Bioinformatics

200

163

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“…Recently, an analysis of the number of driver and passenger mutations in cancers revealed a generally greater number of aberrations in DNA methylation compared to the number of somatic mutations (several hundreds to 1,000 vs. up to 80, respectively, per tumor) . Furthermore, reports have indicated that DNA methylation patterns are effective tumor markers , and DNA methylation‐based biomarkers might facilitate the detection of cancer at very early stages of tumorigenesis . In fact, our data suggested that DNA methylation was strongly associated with tumorigenesis in hiPSC‐NS/PCs, even those that had been passaged relatively few times (Fig.…”

Section: Discussionmentioning

confidence: 57%

Whole-Genome DNA Methylation Analyses Revealed Epigenetic Instability in Tumorigenic Human iPS Cell-Derived Neural Stem/Progenitor Cells

et al. 2017

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Although human induced pluripotent stem cell (hiPSC) derivatives are considered promising cellular resources for regenerative medicine, their tumorigenicity potentially limits their clinical application in hiPSC technologies. We previously demonstrated that oncogenic hiPSC-derived neural stem/progenitor cells (hiPSC-NS/PCs) produced tumor-like tissues that were distinct from teratomas. To gain insight into the mechanisms underlying the regulation of tumorigenicity in hiPSC-NS/PCs, we performed an integrated analysis using the Infinium HumanMethylation450 BeadChip array and the HumanHT-12 v4.0 Expression BeadChip array to compare the comprehensive DNA methylation and gene expression profiles of tumorigenic hiPSC-NS/PCs (253G1-NS/PCs) and non-tumorigenic cells (201B7-NS/PCs). Although the DNA methylation profiles of 253G1-hiPSCs and 201B7-hiPSCs were similar regardless of passage number, the methylation status of the global DNA methylation profiles of 253G1-NS/PCs and 201B7-NS/PCs differed; the genomic regions surrounding the transcriptional start site of the CAT and PSMD5 genes were hypermethylated in 253G1-NS/PCs but not in 201B7-NS/PCs. Interestingly, the aberrant DNA methylation profile was more pronounced in 253G1-NS/PCs that had been passaged more than 15 times. In addition, we identified aberrations in DNA methylation at the RBP1 gene locus; the DNA methylation frequency in RBP1 changed as 253G1-NS/PCs were sequentially passaged. These results indicate that different NS/PC clones have different DNA methylomes and that DNA methylation patterns are unstable as cells are passaged. Therefore, DNA methylation profiles should be included in the criteria used to evaluate the tumorigenicity of hiPSC-NS/PCs in the clinical setting. Stem Cells 2017;35:1316-1327.

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“…Methylation profiling of cfDNA has been investigated in cancer diagnostics and assessment of therapeutic outcomes [18][19][20][21][22][23][24]. Guo et al have shown that identifying methylation patterns from cfDNA can be used to map tissue-of-origin in lung and colorectal cancer patients [25].…”

Section: Discussionmentioning

confidence: 99%