The University of Tokyo · Immunology and Microbiology
Professor Makoto Yamagishi's research lab focuses on the molecular and epigenomic mechanisms underlying T-cell malignancies, particularly adult T-cell leukemia-lymphoma (ATL) caused by human T-cell leukemia virus type 1 (HTLV-1). The lab investigates epigenetic regulation, including histone modifications (e.g., H3K27me3), chromatin remodeling, and epitranscriptomic modifications such as m⁶A on viral and host RNAs, to uncover novel therapeutic targets. By integrating multi-omics approaches—genomics, epigenomics, transcriptomics, and chromatin accessibility—researchers in the lab aim to decode disease pathogenesis and develop precision therapies for aggressive lymphomas.
Figures are computed from collected data and may differ slightly.
Epigenomes enable the rectification of disordered cancer gene expression, thereby providing new targets for pharmacological interventions. The clinical utility of targeting histone H3 lysine trimethylation (H3K27me3) as an epigenetic hallmark has been demonstrated<sup>1-7</sup>. However, in actual therapeutic settings, the mechanism by which H3K27me3-targeting therapies exert their effects and the response of tumour cells remain unclear. Here we show the potency and mechanisms of action and resi
Human T-cell leukemia virus type 1 (HTLV-1) broadly impacts host genes, affecting the infected cell population and inducing the development of a disease with a poor prognosis, adult T-cell leukemia-lymphoma (ATL). This study aimed to provide a comprehensive epigenomic characterization of the infected cell population and evaluated the transcriptome and chromatin structures of peripheral blood cells in HTLV-1-infected individuals using RNA sequencing (RNA-seq) and assay for transposase-accessible
Human T-cell Leukemia Virus Type 1 (HTLV-1) is a pathogenic human retrovirus that is responsible for intractable diseases such as adult T-cell leukemia-lymphoma (ATL), a malignancy with a poor patient prognosis. Although recent studies have delineated several genomic, epigenomic, and transcriptomic abnormalities associated with HTLV-1, to date the importance of epitranscriptomic modifications, particularly N<sup>6</sup>-methyladenosine (m<sup>6</sup>A), remains unclear. Here, we showed that the
T-cell lymphomas are clinically and biologically heterogeneous malignancies that comprise ~ 10% of non-Hodgkin lymphomas. Outcomes with first-line chemotherapy remain poor. Over the past decade, integrative genomic and epigenomic studies have defined recurrent abnormalities converging on proximal T-cell antigen receptor/costimulatory signaling to the NF-κB/NFAT, JAK/STAT, PI3K/AKT/mTOR, and NOTCH pathways, alongside pervasive alterations in chromatin modifiers and the DNA methylation machinery.
Adult T-cell leukemia/lymphoma (ATL) is an aggressive and refractory hematologic malignancy that is caused by human T-cell leukemia virus type-1 (HTLV-1) retrovirus. ATL results from a combination of viral latency and the accumulation of abnormalities throughout the genome, epigenome, transcriptome, and signaling pathways. Despite numerous studies, the data have been largely fragmentary, and a comprehensive understanding of this disease remains unclear. Recent comprehensive analyses have contrib
Open papers in the app to read, cite, and organize with AI.
