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. 2022 Jan 21;11(3):362. doi: 10.3390/cells11030362

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Figure A8 — Comparison of the aging transcriptome of healthy brain and that of lower-grade glioma (LGG). (a) The pairwise correlation heatmap between the samples indicates correlation between different LGG-methylation and aging groups (red), e.g., between E1, E2 and E6 and the newborn brain. (b) The river plot visualizes distribution of LGG tumor methylomes of the different E-groups among the age groups. The SOM portraits of the LGG were obtained using exSOM method applied to the aging data. (c) Distribution of samples of the E-groups among the age groups (part above) and vice versa, of the age groups among the LGG-groups (part below). (d) Characteristics of the E(xpression) subtypes regarding IDH mutation status, chromosomal aberrations (7+/10−gains at chromosome 7 and losses at chromosome 10, 1p/19q cod codeletion at chromosomes 1p and 19q). Comparison of the aging methylomes of healthy brain and that of lower-grade glioma (LGG). The pairwise correlation heatmap between the samples indicates strong correlation between different LGG-methylation and aging groups (red), e.g., between M1 (IDH-wt group) and the prenatal brain. The LGG methylation data were trained together with the healthy brain methylomes using exSOM transfer learning [32]. The river plot visualizes distribution of LGG tumor methylomes of the different M-groups among the age groups. The SOM portraits of the LGG were obtained using exSOM method applied to the aging data. Distribution of samples of the M-groups among the age groups (part above) and vice versa, of the age groups among the LGG-groups (part below). Characteristics of the M(ethylation) subtypes regarding IDH mutation status, chromosomal aberrations (7+/10−gains at chromosome 7 and losses at chromosome 10, 1p/19q cod codeletion at chromosomes 1p and 19q), GCIMP type and characteristics (GBM glioblastoma, MES mesenchymal, PA pilocytic astrocytoma, IDH-A IDH mutated astrocytoma, IDH-O IDH mutated oligodendroglioma). Aging profiles of DNA-methylation of genes hypermethylated in the GCIMP [81] and CIMP colon cancer [91], of PRC2 targets and cycling genes [92] and of the integral expression of genes at chromosomes 7, 10 and 19.