Takashi Sakamoto

ORCID: 0000-0003-0811-3926
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About
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Research Areas
  • Acute Myeloid Leukemia Research
  • Histone Deacetylase Inhibitors Research
  • Cancer therapeutics and mechanisms
  • T-cell and Retrovirus Studies
  • Protein Degradation and Inhibitors
  • Vector-Borne Animal Diseases
  • Genetic diversity and population structure
  • Aquaculture Nutrition and Growth
  • Lung Cancer Diagnosis and Treatment
  • Epigenetics and DNA Methylation
  • RNA and protein synthesis mechanisms
  • Synthetic Organic Chemistry Methods
  • Identification and Quantification in Food
  • Advanced Radiotherapy Techniques
  • Ubiquitin and proteasome pathways
  • CRISPR and Genetic Engineering
  • Virus-based gene therapy research
  • Metastasis and carcinoma case studies
  • Physiological and biochemical adaptations
  • Genetic and phenotypic traits in livestock
  • Genetic Mapping and Diversity in Plants and Animals
  • Effects of Radiation Exposure
  • Radiomics and Machine Learning in Medical Imaging
  • Dermatologic Treatments and Research
  • Immune cells in cancer

Kyoto Katsura Hospital
2025

Kyoto College of Medical Science
2024

Kyoto University
2004-2023

Princess Margaret Cancer Centre
2019-2023

University Health Network
2019-2023

Tokyo University of Marine Science and Technology
1994-2017

Hunan Agricultural University
2015

The Cancer Institute Hospital
1993-1994

Nara Medical University
1993

Angioimmunoblastic T cell lymphoma (AITL) is a peripheral that originates from follicular helper (Tfh) cells and exhibits prominent tumor microenvironment (TME). IDH2 TET2 mutations co-occur frequently in AITL, but their contribution to tumorigenesis poorly understood. We developed an AITL mouse model driven by Idh2 Tet2 mutations. Malignant Tfh display aberrant transcriptomic epigenetic programs impair TCR signaling. Neoplastic bearing combined show altered cross-talk with germinal center B...

10.1016/j.ccell.2023.01.003 article EN cc-by-nc-nd Cancer Cell 2023-02-01

Human APOBEC3 proteins play pivotal roles in intracellular defense against viral infection by catalyzing deamination of cytidine residues, leading to base substitutions DNA. Activation-induced deaminase (AID), another member the APOBEC family, is capable editing immunoglobulin (Ig) and non-Ig genes, aberrant expression AID leads tumorigenesis. However, it remains unclear whether (A3) affect stability human genome. Here we demonstrate that both A3A A3B can induce into genome as can. highly...

10.1038/srep00806 article EN cc-by-nc-sa Scientific Reports 2012-11-13

Abstract Acute myeloid leukemia (AML) pathogenesis often involves a mutation in the NPM1 nucleolar chaperone, but bases for its transforming properties and overall association with favorable therapeutic responses remain incompletely understood. Here we demonstrate that an oncogenic mutant form of (NPM1c) impairs mitochondrial function. NPM1c also hampers formation promyelocytic (PML) nuclear bodies (NB), which are regulators fitness key senescence effectors. Actinomycin D (ActD), antibiotic...

10.1158/2159-8290.cd-21-0177 article EN cc-by-nc-nd Cancer Discovery 2021-07-23

Mutations in IDH1,IDH2, and TET2 are recurrently observed myeloid neoplasms. IDH1 IDH2 encode isocitrate dehydrogenase isoforms, which normally catalyze the conversion of to α-ketoglutarate (α-KG). Oncogenic IDH1/2 mutations confer neomorphic activity, leading production D-2-hydroxyglutarate (D-2-HG), a potent inhibitor α-KG-dependent enzymes include TET methylcytosine dioxygenases. Given their mutual exclusivity neoplasms, IDH1, IDH2, may converge on common oncogenic mechanism. Contrary...

10.1073/pnas.2208176120 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2023-01-18

PURPOSE This multi-institutional prospective cohort trial aimed to demonstrate the changes in physician-evaluated dysphagia and patient-reported outcomes (PROs) after palliative external beam radiotherapy (EBRT) patients with incurable esophageal cancer presenting dysphagia. MATERIALS AND METHODS We evaluated rates of freedom from progression improvement along longitudinal PROs (European Organization for Research Treatment Cancer [EORTC] Quality Life-Core 30 Questionnaire [QLQ-C30] OES-18)...

10.1200/op.24.00429 article EN JCO Oncology Practice 2025-03-13

Adult T cell leukemia (ATL) is an aggressive malignancy caused by human virus type 1 (HTLV-1) and has a poor prognosis. We analyzed the cytotoxic effects of various nucleoside analog reverse transcriptase inhibitors (NRTIs) for HIV-1 on ATL cells found that abacavir potently selectively kills cells. Although NRTIs have minimal genotoxicities host cells, therapeutic concentration induced numerous DNA double-strand breaks (DSBs) in chromosomal DSBs persisted over time but not other lines,...

10.1126/sciadv.1400203 article EN cc-by-nc Science Advances 2015-04-03

The prognosis of aggressive adult T-cell leukemia/lymphoma (ATL) is poor, and allogeneic hematopoietic stem cell transplantation (allo-HSCT) a curative treatment. In order to identify favorable prognostic patients after intensive chemotherapy, who therefore might not require upfront allo-HSCT, we aimed improve risk stratification ATL aged <70 years. clinical factors genetic mutations were incorporated into modeling for overall survival (OS). We generated the m7-ATLPI, clinicogenetic model...

10.3324/haematol.2022.281510 article EN cc-by-nc Haematologica 2023-02-16

Adult T‐cell leukemia ( ATL ) has a poor prognosis as result of severe immunosuppression and rapid tumor progression with resistance to conventional chemotherapy. Recent integrated‐genome analysis revealed mutations in many genes involved the signaling pathway, suggesting that aberration this pathway is an important factor pathogenesis ‐cell proliferation. We screened si RNA library examine signaling‐pathway functionality found PI 3K/Akt/ mTOR critical therefore investigated effect mammalian...

10.1111/cas.13431 article EN cc-by-nc Cancer Science 2017-10-27

The transcription factor NF-κB plays a key regulatory role in lymphocyte activation and generation of immune response. Stimulation T cell receptor (TCR) induces phosphorylation CARMA1 by PKCθ, resulting formation CARMA1-Bcl10-MALT1 (CBM) complex at lipid rafts subsequently leading to activation. While many molecular events have been reported, it is less understood how this negatively regulated. We performed cell-based screening for negative regulators TCR-mediated activation, using...

10.1371/journal.pone.0085762 article EN cc-by PLoS ONE 2014-01-17

Herpesviral hematopoietic necrosis caused by goldfish virus (now identified as cyprinid herpesvirus 2, CyHV-2) has contributed to economic losses in Carassius auratus culture and is becoming a major obstacle Prussian carp C. gibelio aquaculture China. Several reports have described difficulties culturing the virus, with total loss of infectivity within several passages cell culture. We succeeded propagating CyHV-2 high infectious titer RyuF-2 line newly derived from fin Ryukin variety using...

10.3354/dao02885 article EN Diseases of Aquatic Organisms 2015-05-22

Dinucleotide–repeat DNA polymorphisms for rainbow trout, Oncorhynchus mykiss, are described. The potential applications of these markers in fisheries science discussed.

10.1006/jfbi.1994.1100 article EN Journal of Fish Biology 1994-06-01

The large yellow croaker (Larimichthys crocea) is one of the largest marine net-cage cultured species in oceans around China.In present study, we isolated and characterized 13 polymorphic microsatellite markers from genomic libraries L. crocea.Loci were screened for 10 wild specimens 2 sites southeast China.All loci polymorphic.The number alleles per locus ranged to 21.The expected heterozygosity 0.233 0.838 observed 0.527 0.935.Eleven highly informative (polymorphic information content...

10.4238/2015.august.14.7 article EN Genetics and Molecular Research 2015-01-01

<div>Abstract<p>Acute myeloid leukemia (AML) pathogenesis often involves a mutation in the NPM1 nucleolar chaperone, but bases for its transforming properties and overall association with favorable therapeutic responses remain incompletely understood. Here we demonstrate that an oncogenic mutant form of (NPM1c) impairs mitochondrial function. NPM1c also hampers formation promyelocytic (PML) nuclear bodies (NB), which are regulators fitness key senescence effectors. Actinomycin D...

10.1158/2159-8290.c.6549472.v1 preprint EN 2023-04-03
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