[Clinical Analysis on the Therapeutic Efficacy of Autologous Hematopoietic Stem Cell Transplantation in 56 Multiple Myeloma Patients].

Objective: To evaluate the therapeutic efficacy and prognosis of autologous stem Hematopoietic cell transplantation (auto-HSCT) in multiple myeloma (MM) patients.

Methods: A retrospective study was conducted for 56 patients diagnosed with MM and then received auto-HSCT in our hospital from December 2008 to September 2016.

Results: All the patients successfully underwent hematopoietic reconstruction without transplantation-related mortality (TRM).

High prevalence of hepatitis B virus infection in patients with aggressive B cell non-Hodgkin's lymphoma in China.

We retrospectively analyzed a large study to investigate the association of hepatitis B virus (HBV) with aggressive B cell non-Hodgkin's lymphoma (aggressive B-NHL) in China, where HBV is endemic. HBV was present in 39 aggressive B-NHL patients (10.46%), 13 indolent B-NHL patients (5.

A novel epigenetic mini-circuitry contributes to t(8;21) leukaemogenesis.

DNA methylation patterns are frequently deregulated in t(8;21) acute myeloid leukaemia (AML), but little is known of the mechanisms by which specific gene sets become aberrantly methylated. Here, we found that the promoter DNA methylation signature of t(8;21) AML blasts differs from that of t(8;21) AMLs. This study demonstrated that a novel hypermethylated zinc finger-containing protein, THAP10, is a target gene and can be epigenetically suppressed by AML1-ETO at the transcriptional level in t(8;21) AML.

SIRT2 is an unfavorable prognostic biomarker in patients with acute myeloid leukemia.

SIRT2 is a member of the NAD+ dependent deacetylases. In this study, the associations between SIRT2 expression and molecular and clinical characteristics of patients with acute myeloid leukemia (AML) were evaluated by data from The Cancer Genome Atlas. SIRT2 was overexpressed in the intermediate- and poor-risk groups of patients, compared to the favorable-risk group of patients (P = 0.

Increased PRAME-specific CTL killing of acute myeloid leukemia cells by either a novel histone deacetylase inhibitor chidamide alone or combined treatment with decitabine.

As one of the best known cancer testis antigens, PRAME is overexpressed exclusively in germ line tissues such as the testis as well as in a variety of solid and hematological malignant cells including acute myeloid leukemia. Therefore, PRAME has been recognized as a promising target for both active and adoptive anti-leukemia immunotherapy. However, in most patients with PRAME-expressing acute myeloid leukemia, PRAME antigen-specific CD8(+) CTL response are either undetectable or too weak to exert immune surveillance presumably due to the inadequate PRAME antigen expression and PRAME-specific antigen presentation by leukemia cells.

A histone acetyltransferase p300 inhibitor C646 induces cell cycle arrest and apoptosis selectively in AML1-ETO-positive AML cells.

AML1-ETO fusion protein (AE) is generated by t(8;21)(q22;q22) chromosomal translocation, which is one of the most frequently observed structural abnormalities in acute myeloid leukemia (AML) and displays a pivotal role in leukemogenesis. The histone acetyltransferase p300 promotes self-renewal of leukemia cells by acetylating AE and facilitating its downstream gene expression as a transcriptional coactivator, suggesting that p300 may be a potential therapeutic target for AE-positive AML. However, the effects of p300 inhibitors on leukemia cells and the underlying mechanisms have not been extensively investigated.