[Effect of on the Drug Resistance of Diffuse Large B-Cell Lymphoma Cells by Regulating PD-1/PD-L1 Signaling Pathway].

Objective: To explore the effect of microRNA-424-5p (miR-424-5p) on the drug resistance of diffuse large B-cell lymphoma (DLBCL) cells by regulating the programmed death receptor-1 (PD-1)/programmed death ligand-1 (PD-L1) signaling pathway.

Methods: Human DLBCL cell line CRL2631 cells were induced to construct CRL2631-CHOP resistant cell line. RT-qPCR and Western blot were used to detect the expression levels of , PD-L1 mRNA and protein, and multidrug resistance gene-1 (MDR-1) protein in CRL2631 cells and CRL2631-CHOP cells, respectively.

[Gene Mutation and Clinical Characteristics of Patients with Acute Leukemia].

Objective: To investigate the characteristics of gene mutation, clinical characteristics and significance in acute leukemia (AL) patients.

Methods: The clinical data of 102 AL patients in Hebei General Hospital from September 2016 to September 2020 were collected and analyzed retrospectively, including the characteristics of gene mutation, age, peripheral blood cells, bone marrow blasts, leukemia subtypes and myeloperoxidase (MPO).

Results: The total gene mutation rate was 87.

[Visceral Vein Thrombosis of Myeloproliferative Neoplasm --Review].

Classical myeloproliferative neoplasm (MPN) related thrombosis mainly affects elderly patients and often involves arterial circulation, while, MPN-visceral venous thrombosis (SVT) mainly affects young women, and is closely associated with JAK2V617F mutation but not closely with CALR mutation. The pathogenesis of MPN-SVT is not only related to JAK2V617F mutation and vascular endothelial damage, but also needs further research to determine the machanism. JAK2V617F mutation is the most common in MPN-SVT clinically.

Pulmonary tuberculosis presenting as henoch-schönlein purpura: Case report and literature review.

Introduction: Henoch-Schönlein purpura (HSP) is an extremely rare condition in patients with pulmonary tuberculosis, with only a few reported cases. Compared to patients with typical clinical symptoms, it is difficult to make a definitive diagnosis when HSP presents as an initial manifestation in pulmonary tuberculosis patients. Herein, a case of pulmonary tuberculosis that showed HSP at first was reported, and the related literatures were reviewed.

[Effect of Arsenic Trioxide on K562 Cell Proliferation and Its Mechanism].

Objective: To investigate the molecular mechanism of arsenic trioxide(ATO) inhibiting K562 cell proliferation, and explore the new targets for treating chronic myeloid leukemia(CML).

Methods: human CML cell line K562 cells were cultured in vitro, and were treated with different concentrations of ATO; MTT was used to detect the cell proliferation; flow cytometry(FCM) was used to determine cell apoptosis, cell cycle and the expression of CD44; Transcriptional levels of β-catenin and cyclin D1 were assayed by RT-PCR.

Results: 2 µmol/L ATO could inhibit the cell proliferation obviously in a time-and-dose-dependent manner.

[Effect of Anti-CD44 Monoclonal Antibody A3D8 on Expression of AP-1 in HL-60 Cells].

Objective: To explore the effect of anti-CD44 monoclonal antibody A3D8 on expression of transcription factor AP-1 in acute myeloid leukemia cells.

Methods: After acute leukemia cell line HL-60 was treated by different concentrations of A3D8, the proliferation and cell cycle were detected by MTT and FCM respectively. The expressions of c-JUN and c-FOS at mRNA and protein level were detected by RT-PCR and Western Blot respectively.

[Research Progress on CALR Mutation in the Myeloproliterative Neoplasm -Review].

There is no gold diagnostic standard for BCR-ABL fusion gene negative chronic myeloproliterative neoplasm(cMPN). The following detection methods such as comprehensive bone marrow cell morphology, bone marrow pathology, genetic mutation, flow cytometry and immunohistochemical are needed to diagnose the BCR-ABL fusion gene positive cMPN. The JAK2 mutation can be used as a specific diagnostic criteria for polycythemia vera (PV), but there is no specific and sensitive indication for the JAK2 mutation-negative MPN.

Inhibition of multiple myeloma cell proliferation by ginsenoside Rg3 via reduction in the secretion of IGF-1.

Ginsenoside Rg3 (Rg3) is one of the primary constituents isolated from ginseng, and has been found to exhibit cytotoxic effects against cancer cells. The present study aimed to investigate the effects of Rg3 on human multiple myeloma cell proliferation and apoptosis, and to examine its underlying molecular mechanisms. Cell viability was detected using a Cell Counting kit‑8 assay, and cell cycle arrest and cell apoptosis were analyzed using flow cytometry.

[Effect of COX-2 inhibitor celecoxib on proliferation, apoptosis of HL-60 cells and its mechanism].

This study was aimed to investigate the effect of COX-2 inhibitor celecoxib on proliferation, apoptosis of human acute myeloid leukemia cell line HL-60 and its mechanism. HL-60 cells were cultured with different concentrations of celecoxib for 24 h. Cell proliferation was analyzed by CCK-8 assay, cell apoptosis and cell cycle distribution were detected by flow cytometry.

[IL-23 alone or with IL-2 induces the killing effect of hPBMNC on K562 cells].

This study was aimed to explore the killing effect of PBMNC induced by IL-23 alone or combined with IL-2 on K562 cells and its mechanism. The PBMNC were induced in vitro by IL-23 (50 ng/ml) alone or IL-23 combined with IL-2 (100 U/ml) for 72 h, and then were co-cultured with leukemia cell line K562. The CCK-8 method was used to detect the effect of PBMNC induced at different times on K562 cells, the ELISA was performed for detecting IFN-γ level in culture supernatant, and the perforin and granzymes B were detected by RQ-PCR.

Expression levels of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and focal adhesion kinase in patients with multiple myeloma and their relationship to clinical stage and extramedullary infiltration.

We explored the expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and focal adhesion kinase (FAK) mRNA and protein, and analyzed the relationship between expression levels and clinical staging and extramedullary infiltration in patients with multiple myeloma (MM). The expression levels of mRNA and protein were measured by fluorescence quantitative polymerase chain reaction (FQ-PCR) and Western blotting. Expressions of PTEN and FAK mRNA were significantly different between patients with MM and controls.

mitochondrial ceramidase overexpression up-regulates Bcl-2 protein level in K562 cells, probably through its metabolite sphingosine-1-phosphate.

Recently, a mitochondrial ceramidase has been identified and cloned, whose mitochondrial localization strongly suggests the existence of an unexpected mitochondrial pathway of ceramide metabolism that may play a key role in mitochondrial functions, especially in the regulation of apoptosis. To explore the biological effect of mitochondrial ceramidase on cells, pcDNA 3.1/His-CDase plasmid, containing mitochondrial ceramidase cDNA sequence, was transducted into K562 cells mediated by liposome, and G418 was used to screen for positive colonies.

Mutation analysis of SHIP gene in acute leukemia.

The SH2 domain containing inositol 5'-phosphatase (SHIP) was initially described as a 145 kD protein phosphorylated on tyrosines upon growth factor and cytokine stimulation. SHIP is predominately expressed in hematopoietic cells, and is a crucial negative regulator in the development of hematopoietic cells. To evaluate the role of the SHIP gene in human leukemogenesis, expression and mutation of SHIP gene in bone marrow and/or peripheral blood from 32 patients with acute myeloid leukemia (AML), 9 patients with acute lymphoblastic leukemia (ALL), as well as human hematopoietic cell lines were analyzed by reverse transcription-polymerase chain reaction (RT-PCR), single strand conformational polymorphism (SSCP) and sequencing.

[Mutation analysis of SHIP gene in acute leukemia].

Objective: The SH2 domain containing inositol 5'-phosphatase (SHIP) is predominately expressed in hematopoietic cells, and is a crucial negative regulator in the development of hematopoietic cells. This paper is to evaluate the role of the SHIP gene in human leukemogenesis.

Methods: Expression of SHIP gene in bone marrow and/or peripheral blood from 32 patients with acute myeloid leukemia (AML), 9 with acute lymphoblastic leukemia (ALL), as well as human hematopoietic cell lines was analyzed by reverse transcription-polymerase chain reaction (RT-PCR), single strand conformational polymorphism (SSCP) and DNA sequencing.

Mutation analysis of hematopoietic cell phosphatase gene in acute leukemia.

The hematopoietic cell phosphatase (HCP or SHP-1), the SH2 domain contain protein tyrosine phosphatase, is a crucial negative regulator in the process of hematopoietic cell development, proliferation and receptor-mediated mitogenic signaling pathways, and its mutation is responsible for the over-expansion and inappropriate activation of myelomonocytic population in motheaten mice. The aim of the study was to evaluate the role of the HCP gene in leukemogenesis. Bone marrow and/or peripheral blood from 32 acute myeloid leukemia (AML) patients, 9 acute lymphocytic leukemia (ALL) patients, 8 leukemia cell lines and 50 normal controls were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) based on single strand conformation polymorphism (SSCP) and sequencing.

[Effect of panax notoginseng saponin on procoagulant activity and differentiation induction in NB4 cells].

Objective: To investigate the effect of Panax notoginseng saponin (PNS) on procoagulant activity (PCA) and differentiation induction in NB4 cells.

Methods: After NB4 cells were treated with PNS, the recalcification time, PCA and TF-mRNA expression in NB4 cells were tested by RT-PCR. The inhibitory effect of PNS on NB4 cell proliferation was analysed by MTT method, NBT assay, cell morphological observation and flow cytometry.

Hyperhomocysteinemia and the MTHFR C677T mutation in Budd-Chiari syndrome.

Hyperhomocysteinemia (HH) is a factor that predisposes individuals to thrombosis, and the C677T mutation in the 5,10-methylenetetrahydrofolate reductase (MTHFR) is known to give increased plasma homocysteine. However, little is known about their roles in Budd-Chiari syndrome (BCS). This study evaluated the roles of HH and the MTHFR C677T mutation in patients with BCS.