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Tomohito Yagi

Researcher at Kyoto Prefectural University of Medicine

Publications -  27
Citations -  936

Tomohito Yagi is an academic researcher from Kyoto Prefectural University of Medicine. The author has contributed to research in topics: Single-nucleotide polymorphism & Genotype. The author has an hindex of 13, co-authored 27 publications receiving 881 citations. Previous affiliations of Tomohito Yagi include SANTEN PHARMACEUTICAL CO., LTD..

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Identification of a gene expression signature associated with pediatric AML prognosis

TL;DR: The results indicate the existence of prognosis-associated genes that are independent of cell lineage and cytogenetic abnormalities, and they can provide therapeutic direction for individual risk-adapted therapy for pediatric AML patients.
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Three susceptible loci associated with primary open-angle glaucoma identified by genome-wide association study in a Japanese population

TL;DR: It turned out that 3 genetic loci probably associated with POAG have been identified, and these findings would provide the foundation for future studies to build on, such as for the metaanalysis, to reveal the molecular mechanism of the POAG pathogenesis.
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Characteristic perforin gene mutations of haemophagocytic lymphohistiocytosis patients in Japan.

TL;DR: Examination of the geographical origins of the ancestors in the perforin‐mutant HLH patients revealed that they mostly came from the Western part of Japan, suggesting that the present‐day cases may largely derive from a common ancestor.
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High frequency of Ikaros isoform 6 expression in acute myelomonocytic and monocytic leukemias: implications for up-regulation of the antiapoptotic protein Bcl-XL in leukemogenesis

TL;DR: The pathogenesis of myelomonocytic/monocytic AML may involve aberrant regulation of apoptosis due to unscheduled expression of the Ik6 isoform, which may inhibit the normal transcriptional regulation of hematopoietic cell development.
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Detection of clonotypic IGH and TCR rearrangements in the neonatal blood spots of infants and children with B-cell precursor acute lymphoblastic leukemia.

TL;DR: The findings strongly suggest a prenatal origin for some cases of B-cell precursor ALL lacking specific clonotypic abnormalities, which are supported by studies of identical infant twins with concordant leukemia and of nontwined patients with MLL gene rearrangements.