Eiso Hiyama

Prof. Dr. Eiso Hiyama

Hiroshima University, Hiroshima, Japan
orcid

Research Focus & Metrics

Academic Career Length

37Years (1990-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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13 March 2007 in British Journal of Cancer
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Journal Article
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EHEiso Hiyama
Eiso Hiyama
KHK Hiyama
K Hiyama
Telomeres, guanine-rich tandem DNA repeats of the chromosomal end, provide chromosomal stability, and cellular replication causes their loss. In somatic cells, the activity of telomerase, a reverse transcriptase that can elongate telomeric repeats, is usually diminished after birth so that the telomere length is gradually shortened with cell divisions, and triggers cellular senescence. In embryonic stem cells, telomerase is activated and maintains telomere length and cellular immortality; however, the level of telomerase activity is low or absent in the majority of stem cells regardless of their proliferative capacity. Thus, even in stem cells, except for embryonal stem cells and cancer stem cells, telomere shortening occurs during replicative ageing, possibly at a slower rate than that in normal somatic cells. Recently, the importance of telomere maintenance in human stem cells has been highlighted by studies on dyskeratosis congenital, which is a genetic disorder in the human telomerase component. The regulation of telomere length and telomerase activity is a complex and dynamic process that is tightly linked to cell cycle regulation in human stem cells. Here we review the role of telomeres and telomerase in the function and capacity of the human stem cells.

1 May 2003 in Cancer Letters
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Journal Article
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EHEiso Hiyama
Eiso Hiyama
KHKeiko Hiyama
Keiko Hiyama

21 January 2002 in Oncogene
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EHEiso Hiyama
Eiso Hiyama
KHKeiko Hiyama
Keiko Hiyama

20 September 2021 in Nature Communications
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GNGenta Nagae
Genta Nagae
SYShogo Yamamoto
Shogo Yamamoto
MFMasashi Fujita
Masashi Fujita
TFTakanori Fujita
Takanori Fujita
ANAya Nonaka
Aya Nonaka
EHEiso Hiyama
Eiso Hiyama
Hepatoblastoma (HB) is the most common pediatric liver malignancy; however, hereditary predisposition and acquired molecular aberrations related to HB clinicopathological diversity are not well understood. Here, we perform an integrative genomic profiling of 163 pediatric liver tumors (154 HBs and nine hepatocellular carcinomas) based on the data acquired from a cohort study (JPLT-2). The total number of somatic mutations is precious low (0.52/Mb on exonic regions) but correlated with age at diagnosis. Telomerase reverse transcriptase (TERT)promoter mutations are prevalent in the tween HBs, selective in the transitional liver cell tumor (TLCT, > 8 years old). DNA methylation profiling reveals that classical HBs are characterized by the specific hypomethylated enhancers, which are enriched with binding sites for ASCL2, a regulatory transcription factor for definitive endoderm in Wnt-pathway. Prolonged upregulation of ASCL2, as well as fetal-liver-like methylation patterns ofIGF2promoters, suggests their “cell of origin” derived from the premature hepatoblast, similar to intestinal epithelial cells, which are highly proliferative. Systematic molecular profiling of HB is a promising approach for understanding the epigenetic drivers of hepatoblast carcinogenesis and deriving clues for risk stratification.

1 April 2008 in The Lancet
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EHEiso Hiyama
Eiso Hiyama
TITomoko Iehara
Tomoko Iehara
TSTohru Sugimoto
Tohru Sugimoto
MFMasahiro Fukuzawa
Masahiro Fukuzawa
YHYutaka Hayashi
Yutaka Hayashi
MOMegu Ohtaki
Megu Ohtaki

1 October 2014
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Journal Article
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EHEiso Hiyama
Eiso Hiyama
Pediatric hepatoblastoma: diagnosis and treatment