Rogersgriffin8356

To investigate the clinical characteristics of relapsed or refractory (R/R) diffuse large B-cell lymphoma (DLBCL) and the factors affecting overall survival (OS) time.

The clinical data of 14 R/R DLBCL patients admitted to the Hainan Hospital of Chinese PLA General Hospital from April 2012 to March 2019 were analyzed retrospectively and the overall response rate (ORR) after the end of different treatments was estimated. Kaplan-Meier method was used to describe the survival curve, and Log-rank test was used to compare whether different survival curves showed statistically different.

There were 8 males and 6 females with a median age of 51 (26-75) years old and the median course of treatment before R/R was 7 (4-13). Finally, 11 patients achieved remission, 6 patients of which showed complete remission, and 5 patients showed partial remission, with the median ORR duration at 2.5 (0-51) months. FUT-175 supplier All patients in the group of ibrutinib combined with second-line chemotherapy achieved remission (4/4), it was equort and the prognosis is very poor. The survival time of patients with high level of lactate dehydrogenase, IPI score≥3 at diagnosis and SD/PD after treatment is significantly shortened. Ibrutinib combined second-line chemotherapy and HDC-AHSCT can improve the efficacy and survival of R/R DLBCL patients.

To investigate the expression and mechanism of histone acetyltransferase 2A (KAT2A) and cyclin D1 dependent kinase 4/6 (CDK4/CDK6) in children with acute leukemia(AL).

Seventy-one children with leukemia were selected from June 2017 to November 2018 and were enrolled in AL children group. 59 persons of healthy physical examination were selected and enrolled in control group. Real-time fluorescent quantification PCR chip was used to determine the expression of histone-modified genes and the expression levels of CDK4, CDK6 and CDK4/CDK6 mRNA; Western blot was used to validated KAT2A-positive expression; SPSS Pearson correlation analysis software was used to analyze the correlation between KAT2A and CDK4/CDK6 expression in children with acute leukemia.

By comprehensive analysis of the existing chip data, the positive expression of KAT2A in the AL children group was 78.87%, which was higher than that in the control group (8.47%) (P<0.05). The expression level of CDK4 and CDK6 mRNA in the AL children group in AL children, there is a significant correlation between of them, which is expected to become a new target for the treatment of acute leukemia children.

To detect the expression level of LncRNA XLOC_109948 in bone marrow and serum of patients with acute myeloid Leukemia (AML), to verify the consistency between the expression in bone marrow and serum and to explore the role of LncRNA XLOC_109948 expression in the occurrence a development of AML.

Bone marrow and peripheral blood samples were collected from 62 patients with AML, including 36 patients with AML (AML group), 26 AML patients with complete remission (AML-CR group), and peripheral blood from 20 healthy persons (control group) were also collected. The expression level of LncRNA XLOC_109948 was detected by real-time quantitative fluorescence PCR (qRT-PCR), and the relationship between its expression and clinical characteristics was analyzed.

The expression of LncRNA XLOC_109948 in bone marrow and serum of AML patients was higher than that of AML patients with complete remission and healthy people (P<0.001). And there was no statistically significant difference between the AML-CR group and control group (P>0.05). The expression of LncRNA XLOC_109948 significantly decreased when AML patients reached to CR, and significantly increased when the disease relapsed (P<0.05). The expression of LncRNA XLOC_109948 significantly correlated with the clinicopathologic parameters of cytogenetics (P<0.05), but not significantly correlated with sex, age, WBC count, blast in bone marrow, FAB classification and other clinical characteristics (P>0.05).

The expression of LncRNA XLOC_109948 in bone marrow and serum of AML patients is high, and its expression in time and sequence is consistent between bone marrow and serum, which can reflect the occurrence, development, chemotherapy efficacy and prognosis of AML patients.

The expression of LncRNA XLOC_109948 in bone marrow and serum of AML patients is high, and its expression in time and sequence is consistent between bone marrow and serum, which can reflect the occurrence, development, chemotherapy efficacy and prognosis of AML patients.

To explore the effect of nuclear factor kappa-B (NF-κB) inhibitor pyrrolidine dithiocarbamate (PDTC) on the proliferation and apoptosis of acute leukemia cell HL-60.

HL-60 cells were cultured with PDTC of 0, 25, 50, 100 μmol/L for 24, 48, 72 h. The inhibition rate of cell proliferation was detected by CCK-8 assay. Cell apoptosis was detected by Hoechst staining. Cell cycle was detected by flow cytometry. The expression of B-cell lymphoma-2 (BCL-2), BCL-2 associated X protein (BAX), cyclinD1, activated cysteinyl aspartate specific proteinase (cleaved caspase 3), cleaved caspase 8 and activation of NF-κB signal pathway related protein was detected by Western blot.

After the HL-60 cells were cultured with PDTC of 25, 50, 100 μmol/L for 24, 48, 72 h, the inhibition rate of cell proliferation increased with the enhancement of PDTC concentration at the same time point (r=0.924, P<0.01). At the same PDTC concentration, the inhibition rate of cell proliferation increased with prolonging of time (r=0.952, P<0.01). After HL-60 cell was cultured with PDTC of 25, 50, 100 μmol/L for 48 h, compared with control group, PDTC of 25, 50, 100 μmol/L increased the cell apoptotic rate, arrested cell cycle at G1 phase (P<0.01), the expression of BCL-2, cyclinD1 and p-NF-κB p65 was down-regulated(P<0.05), the expression of BAX, cleaved caspase 3, cleaved caspase 8 was up-regulated(P<0.01). PDTC of 50, 100 μmol/L down-regulated the expression of p-inhibitor of NF-κB (p-IκBα)(P<0.01).

PDTC can inhibit acute leukemia HL-60 cell proliferation and induce cell apoptosis.

PDTC can inhibit acute leukemia HL-60 cell proliferation and induce cell apoptosis.