東京大学 · 免疫学・微生物学
山岸真琴教授の研究室は、成人T細胞白血病・リンパ腫（ATL）をはじめとするT細胞腫瘍の発症機構を、エピジェネティクスとエピトランスクリプトミクスの視点から解明しています。特に、H3K27メチル化やm⁶A修飾といったエピジェネティックな修飾が、がんの発現異常や治療抵抗性に与える影響を、ゲノム・エピジェノム・トランスクリプトームの統合的解析によって解明しています。臨床応用に結びつく新規標的の同定や、がん治療の新たな戦略の構築を目指しています。
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
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