From: Epigenetic instability of imprinted genes in human cancers

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From: Epigenetic instability of imprinted genes in human cancers Figure 4. DNA methylation analysis of GNAS-ICR. A set of human DNA derived from two normal (brain and liver) and six cancer tissues (breast, lung, kidney, colon, ovary and liver) were treated with the bisulfite conversion protocol, which were then analyzed with COBRA (A) and individual sequencing (C). For COBRA analyses, the PCR products from GNAS-ICR were digested with TaqI, displaying the unmethylated and methylated portion of each PCR product. The amounts of these two fragments from three independent trials were quantified based on their band density using ImageJ software, and mean methylation with 95% confidence intervals were plotted (B). As predicted, two normal tissues displayed 50% methylation levels on GNAS-ICR. On the other hand, three cancer tissues showed hypermethylation and one tissue displayed hypomethylation. All of these PCR products were also sequenced using a NGS platform, and the bisulfite sequence reads were analyzed with BiQ Analyzer HT Tool (C). Two representative graphic illustrations are shown: red and blue boxes indicate methylated and unmethylated CpG sites, respectively. The names of some of tissues start with either N- or C- to differentiate the origin of samples, normal and cancer tissues. From: Epigenetic instability of imprinted genes in human cancers Nucleic Acids Res. 2015;43(22):10689-10699. doi:10.1093/nar/gkv867 Nucleic Acids Res | © The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

From: Epigenetic instability of imprinted genes in human cancers Figure 5. Summary of DNA methylation level changes. A series of DNA methylation analyses on imprinted genes were conducted using a set of normal and cancer samples. The results were subsequently summarized with a table showing the average DNA methylation level and corresponding 95% confidence interval per each sample in a given tissue (bottom). Statistically significant changes relative to those observed from two normal tissues determined by t-test were also summarized in a separate table (top). In this table, red, green and gray boxes indicate hyper, hypomethylation and no change, respectively. It is important to note that some of ICRs and DMRs did not show 50% DNA methylation levels in normal tissues due to the technical issues that are mainly caused by inefficient restriction enzyme digestion. From: Epigenetic instability of imprinted genes in human cancers Nucleic Acids Res. 2015;43(22):10689-10699. doi:10.1093/nar/gkv867 Nucleic Acids Res | © The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

From: Epigenetic instability of imprinted genes in human cancers Figure 7. Frequency of DNA methylation changes among the normal and cancer samples. The DNA methylation changes observed in three genomic regions (GNAS-ICR, USP29-Pro, ECR18) were further analyzed in terms of their frequency using a set of breast DNA, which is made of 8 normal and 40 cancer samples. A subset of COBRA results from three regions is presented (A), and the entire set of results is also summarized as a table (B). From: Epigenetic instability of imprinted genes in human cancers Nucleic Acids Res. 2015;43(22):10689-10699. doi:10.1093/nar/gkv867 Nucleic Acids Res | © The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

From: Epigenetic instability of imprinted genes in human cancers Figure 6. DNA methylation level changes of the PEG3 and H19/IGF2 domains. A set of human DNA derived from two normal (brain and liver) and six cancer tissues (breast, lung, kidney, colon, ovary and liver) were used to survey the DNA methylation levels of the PEG3 domain (A) and the H19/IGF2 domain (B). Three genomic regions for each domain were targeted and analyzed with COBRA as shown in the upper panel. The bottom panel shows the genomic structures of two imprinted domains along with their DNA methylation changes observed in cancers. From: Epigenetic instability of imprinted genes in human cancers Nucleic Acids Res. 2015;43(22):10689-10699. doi:10.1093/nar/gkv867 Nucleic Acids Res | © The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

From: Epigenetic instability of imprinted genes in human cancers Figure 3. Expression and DNA methylation level changes of cancer genes. Expression levels (A) and DNA methylation levels (B) of cancer genes (represented by columns) were compared between the primary tumor and normal solid tissue cells of various cancers (represented by rows) using TCGA database (The Cancer Genome Atlas). Statistically significant down- and upregulations were indicated by green and red boxes, respectively, while no significant change with gray boxes. The actual tables used for these images are available as Supplementary Data 3–4. (C) This graph summarizes in how many cancer types the DNA methylation levels of each gene are different between the tumor and normal cells. From: Epigenetic instability of imprinted genes in human cancers Nucleic Acids Res. 2015;43(22):10689-10699. doi:10.1093/nar/gkv867 Nucleic Acids Res | © The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

From: Epigenetic instability of imprinted genes in human cancers Figure 2. DNA methylation level changes of imprinted genes in human cancers. (A) DNA methylation levels of imprinted genes (represented by columns) were compared between the primary tumor and normal solid tissue cells of various cancers (represented by rows) using TCGA database (The Cancer Genome Atlas). Statistically significant down- and upregulations were indicated by green and red boxes, respectively, while no significant change with gray boxes. The actual table used for this image is available as Supplementary Data 2. (B) This graph summarizes in how many cancer types the DNA methylation levels of each imprinted gene differ between the tumor and normal cells. From: Epigenetic instability of imprinted genes in human cancers Nucleic Acids Res. 2015;43(22):10689-10699. doi:10.1093/nar/gkv867 Nucleic Acids Res | © The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

From: Epigenetic instability of imprinted genes in human cancers Figure 1. Expression level changes of imprinted genes in human cancers. (A) Expression levels of imprinted genes (represented by columns) were compared between the primary tumor and normal solid tissue cells of various cancers (represented by rows) using TCGA database (The Cancer Genome Atlas). Statistically significant down- and upregulations were indicated by green and red boxes, respectively, while no significant change with gray boxes. XIST has been included in this series of analyses due to its 50% DNA methylation levels in females although it is not an imprinted gene. The actual table used for this image is available as Supplementary Data 1. (B) This graph summarizes how many imprinted genes show down and upregulations for each cancer type. (C) This graph summarizes in how many cancer types the expression levels of each imprinted gene are changed between the tumor and normal cells. Individual cancer types are represented with the following abbreviations: BRCA (breast invasive carcinoma), KICH (kidney chromophobe), LUAD (lung adenocarcinoma), LUNG (lung cancer), KIRC (kidney renal clear cell carcinoma), UCEC (uterine corpus endometrioid carcinoma), COADREAD (colon and rectum adenocarcinoma), COAD (colon adenocarcinoma), PRAD (prostate adenocarcinoma), LUSC (lung squamous cell carcinoma), THCA (thyroid carcinoma), KIRP (kidney renal papillary cell carcinoma), GBM (glioblastoma multiforme), STAD (stomach adenocarcinoma), BLCA (bladder urothelial carcinoma), READ (rectum adenocarcinoma), LAML (acute myeloid leukemia), LIHC (liver hepatocellular carcinoma), ESCA (esophageal carcinoma), CESC (cervical squamous cell carcinoma and endocervical adenocarcinoma), PCPG (pheochromocytoma and paraganglioma), SARC (sarcoma) and PAAD (pancreatic adenocarcinoma). From: Epigenetic instability of imprinted genes in human cancers Nucleic Acids Res. 2015;43(22):10689-10699. doi:10.1093/nar/gkv867 Nucleic Acids Res | © The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.