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Survival Related Genes on Chromosomes 6 and 17 in Medulloblastoma
Version 1
: Received: 13 May 2024 / Approved: 13 May 2024 / Online: 13 May 2024 (10:43:37 CEST)
A peer-reviewed article of this Preprint also exists.
Vriend, J.; Liu, X.-Q. Survival-Related Genes on Chromosomes 6 and 17 in Medulloblastoma. Int. J. Mol. Sci. 2024, 25, 7506. Vriend, J.; Liu, X.-Q. Survival-Related Genes on Chromosomes 6 and 17 in Medulloblastoma. Int. J. Mol. Sci. 2024, 25, 7506.
Abstract
Survival of Medulloblastoma (MB) depends on various factors, including the gene expression profiles of MB tumor tissues. In this study, we identified 967 MB survival related genes (SRBs) using the gene expression dataset of Cavalli et al. (2017) and the Cox proportional hazards regression model. Notably, the SRGs were over-represented on chromosomes 6 and 17, known for the abnormalities monosomy 6 and isochromosome 17 in MB. The most significant SRG was HMGA1 (high mobility group AT-hook 1), which is a known oncogene and a histone H1 competitor. High expression of HMGA1 was associated with worse survival, primarily in the Group 3γ subtype. The high expression of HMGA1 was unrelated to any known somatic copy number alteration. Most SRGs on chromosome 17p were associated with low expression in Group 4β, the MB subtype with 93% deletion of 17p and 98% copy gain of 17q. Pathway analysis showed that both chromosomes 6 and 17 included SRGs related to telomere maintenance and provide a rationale for testing telomerase inhibitors in Group 3 MBs. We conclude that HMGA1, along with other SRGs on chromosome 6 and 17 warrant further investigation as potential therapeutic targets in selected subgroups or subtypes of MB.
Keywords
medulloblastoma; gene expression; survival related genes; hazard ratios; chromosome 6; chromosome 17; HMGA1
Subject
Biology and Life Sciences, Biochemistry and Molecular Biology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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