Abstract

[This corrects the article DOI: 10.18632/oncotarget.20659.].

Highlights

  • Hodgkin lymphoma (HL) is a well-established malignancy and accounts for about 8~13% of all lymphomas [1, 2] with the classical type being the commonest

  • Chidamide inhibits the proliferation of Hodgkin lymphoma cell lines through apoptosis pathway

  • We demonstrated chidamide inhibits the proliferation of Hodgkin lymphoma cell lines through apoptosis pathway and arresting cell cycle in G0/G1 phase

Read more

Summary

Introduction

Hodgkin lymphoma (HL) is a well-established malignancy and accounts for about 8~13% of all lymphomas [1, 2] with the classical type being the commonest. Excessive activation of histone deacetylase (HDAC) and hyper-methylation of promoter region of tumor suppressor gene are two most studied aspects of epigenetic abnormalities in cancer. The selective class I HDAC inhibitor, has been approved for the treatment of peripheral T-cell lymphoma in China, but its activity on HL has not been tested yet. In vitro studies showed that Decitabine could inhibit the function of MYC gene by upregulating the expression of ID2 [16] and synergistically suppressing the proliferation of diffuse large B cell lymphoma cell lines with HDAC inhibitor Panobinostat [17]. The purpose of this study is to investigate the antitumor activity of chidamide and synergistic inhibition effects when combined with decitabine in HL cell lines

Objectives
Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call