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Berger. J Transl Genet Genom 2023;7:183-5 Journal of Translational
DOI: 10.20517/jtgg.2023.23
Genetics and Genomics
Editorial Open Access
Obesity associated cancers, genetics, epigenetics
and elephants
Nathan A. Berger
Case Comprehensive Cancer Center, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.
Correspondence to: Prof. Nathan A. Berger, MD, Case Comprehensive Cancer Center, School of Medicine, Case Western
Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106, USA. E-mail: nab@case.edu
How to cite this article: Berger NA. Obesity associated cancers, genetics, epigenetics and elephants. J Transl Genet Genom
2023;7:183-5. https://dx.doi.org/10.20517/jtgg.2023.23
Received: 31 Jul 2023 Accepted: 22 Aug 2023 Published: 24 Aug 2023
Academic Editor: Andrea L. Gropman Copy Editor: Fangyuan Liu Production Editor: Fangyuan Liu
Obesity is estimated to affect more than 110 million children and 640 million adults and is associated with
significant co-morbidities, including cardiovascular diseases, Type II diabetes mellitus, and thirteen types of
cancer . JTGG recently published a special edition focused on Genetics and Epigenetics of Obesity
[1]
Associated Cancers to help better understand factors driving the obesity - cancer linkage.
Qu et al. reported that, compared to low-fat diet, when subjecting the C57Bl6J APC and C57Bl6J APC Min/+
+/+
mice to high-fat diet for only 3 days, there was a noticeable shift in the acetylation of Lysine 27 in
Histone H3 (H3K27ac), an epigenetic determinant of transcriptionally active chromatin, favoring fatty acid
metabolism in support of accelerated growth while simultaneously suppressing immunologic mechanisms
[2]
that could potentially contribute to the control of tumor growth . Not all transcriptional changes were
associated with H3K27 acetylation, suggesting the potential involvement of other epigenetic mechanisms.
Interestingly, at the early time point of 3 days on high-fat diet, there were epigenetic signs indicating
activation of Wnt signaling, but no signs by RNA Seq that this pathway was upregulated .
[2]
Using similar techniques to measure H3K27ac, Li et al. showed that 15-20 weeks of high-fat diet feeding to
C57Bl6 mice reproduced the chromatin gene enhancer landscape to resemble that in colorectal cancer .
[3]
They showed that genes dysregulated by high-fat diet were connected to inflammation, cancer, cellular
movement, and tissue development. When similar studies were conducted in NAG-1 transgenic mice,
© The Author(s) 2023. Open Access This article is licensed under a Creative Commons Attribution 4.0
International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing,
adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as
long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and
indicate if changes were made.
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