Role of epigenetic regulation by nuclear tyrosine kinases in hematologic malignancies

2015 Fiscal Year Final Research Report

• Project/Area Number: 26893036
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Hematology
• Research Institution: Chiba University
• Principal Investigator: Aoyama Kazumasa 千葉大学, 医学(系)研究科(研究院), 特任研究員 (50734266)
• Project Period (FY): 2014-08-29 – 2016-03-31
• Keywords: エピジェネティックス / 癌 / チロシンキナーゼ

Outline of Final Research Achievements

A constitutively active mutant of Abl tyrosine kinase causes chronic myelogenous leukemia (CML). In this study, we showed that Abl-mediated tyrosine phosphorylation leads to stabilization of histone deacetylase 1 accompanied by global histone deacetylations. Furthermore, we demonstrated that JAK2V617F, which is a constitutively active mutant of JAK2 tyrosine kinase and is found in patients with myeloproliferative neoplasms (MPN), cooperates with polycomb repressive complex2 in regulation of histone H3 lysine27 trimethylation. These results suggest that tyrosine kinases-regulated histone modifications plays an important role in CML and MPN.

Free Research Field

分子生物学