The safety and efficacy of the re-administration of gilteritinib in a patient with FLT3-mutated R/R AML with CNS relapse: a case report.

FLT3-ITD is a type of poor prognostic factors in acute myeloid leukemia (AML) disease. Gilteritinib, the second-generation FLT3 tyrosine kinase inhibitor, improved the overall survival of patients with relapsed/refractory FLT3-mutated AML in the ADMIRAL phase III trial. However, few data are available on the efficacy and safety of gilteritinib-based therapy for FLT3-mutated AML with central nervous system (CNS) involvement.

A novel inflammation-related prognostic model for predicting the overall survival of primary central nervous system lymphoma: A real-world data analysis.

Background: Primary central nervous system lymphoma (PCNSL) is a type of extranodal non-Hodgkin lymphoma. Although there are widely used prognostic scores, their accuracy and practicality are insufficient. Thus, a novel prognostic prediction model was developed for risk stratification of PCNSL patients in our research.

A multi-center, open-label, randomized, parallel-controlled phase II study comparing pharmacokinetic, pharmacodynamics and safety of ripertamab (SCT400) to rituximab (MabThera) in patients with CD20-positive B-cell non-Hodgkin lymphoma.

Objective: This multi-center, open-label, randomized, parallel-controlled phase II study aimed to compare the pharmacokinetics (PK), pharmacodynamics (PD) and safety profile of ripertamab (SCT400), a recombinant anti-CD20 monoclonal antibody, to rituximab (MabThera) in patients with CD20-positive B-cell non-Hodgkin lymphoma (NHL).

Methods: Patients with CD20-positive B-cell NHL who achieved complete remission or unconfirmed complete remission after standard treatment were randomly assigned at a 1:1 ratio to receive a single dose of ripertamab (375 mg/m) or rituximab (MabThera, 375 mg/m). PK was evaluated using area under the concentration-time curve (AUC) from time 0 to d 85 (AUC), AUC from time 0 to week 1 (AUC), AUC from time 0 to week 2 (AUC), AUC from time 0 to week 3 (AUC), AUC from time 0 to week 8 (AUC), maximum serum concentration (C), terminal half-life (T), time to maximum serum concentration (T) and clearance (CL).

Efficacy and safety of PD-1 inhibitor alone or combined with chemotherapy in patients with relapsed or refractory extranodal natural Killer/T cell lymphoma: A retrospective study.

Extranodal natural killer/T cell lymphoma (ENKTL) patients typically face a grim prognosis after relapse or progression following asparaginase-based chemotherapy. Currently, programmed cell death protein-1 (PD-1) immune checkpoint blockade has shown promising efficacy as an optimal regimen for relapsed or refractory ENKTL (rrENKTL) patients. This study retrospectively investigated the efficacy, safety, and factors influencing the survival of 26 rrENKTL patients who underwent monoclonal antibody treatment using PD-1 (Sintilimab or Camrelizumab) alone or combined with chemotherapy from January 2018 to February 2022.

Hyperglycemia-induced PATZ1 negatively modulates endothelial vasculogenesis via repression of FABP4 signaling.

Vascular endothelial dysfunction, a central hallmark of diabetes, predisposes diabetic patients to numerous cardiovascular complications. The POZ/BTB and AT-hook-containing zinc finger protein 1 (PATZ1), is an important transcriptional regulatory factor and regulates divergent pathways depending on the cellular context, but its role in endothelial cells remains poorly understood. Herein, we report for the first time that endothelial PATZ1 expression was abnormally upregulated in diabetic endothelial cells (ECs) regardless of diabetes classification.

[Construction and expression of fusion protein TRX-hJagged1 in E.coli BL21].

This study was purposed to construct prokaryotic expression vector and to investigate the expression of Notch ligand Jagged1 in E.coli. An expression vector pET-hJagged1 was constructed, which can be inserted in Jagged1 with different lengths, but the DSL domain of human Jagged1 should be contained.

AEG-1 overexpression is essential for maintenance of malignant state in human AML cells via up-regulation of Akt1 mediated by AURKA activation.

Acute myeloid leukemia (AML) remains highly fatal, highlighting the need for improved understanding of signal pathways that can lead to the development of new therapeutic regimens targeting common molecular pathways shared across different AML subtypes. Here we demonstrate that astrocyte elevated gene-1 (AEG-1) is one of such pathways, involving in cell cycle and apoptosis regulation and contributing to enhanced proliferation and chemoresistance in HL-60 and U937 AML cells. The pleiotropic effects of AEG-1 on AML were found to correlate with two novel target genes, Aurora kinase A (AURKA) and Akt1.

[Clinical analysis of peripheral blood stem cell mobilization regimens in autologous transplantation for treating non-Hodgkin's lymphoma].

The purpose of this study was to compare the efficacy of CEP plus G-CSF and CVP plus G-CSF regimens in the mobilization and collection of peripheral blood hematopoietic stem cells (PBHSC), and in the hematopoietic recovery. 57 patients with non-Hodgkin's lymphoma (NHL) underwent autologous PBHSC transplantation were analyzed retrospectively. The PBHSC were mobilized and collected by using CEP plus G-CSF and CVP plus G-CSF respectively, and were retransfused into these NHL patients after preconditioning, then the mobilization efficacy, adverse reactions and hematopoietic recovery were analyzed.

Notch signaling maintains proliferation and survival of the HL60 human promyelocytic leukemia cell line and promotes the phosphorylation of the Rb protein.

The Notch signaling pathway has been implicated in the development of several leukemia and lymphoma. In order to investigate the relationship between Notch signaling and acute myeloid leukemia (AML), in this study, we expressed a recombinant Notch ligand protein, the DSL domain of the human Jagged1 fused with GST (GST-Jag1). GST-Jag1 could activate Notch signaling in the human promyelocytic leukemia cell line HL60, as shown by a reporter assay and the induced expression of Notch effector gene Hes1 and Hes5.

Apoptosis induction effects of EGCG in laryngeal squamous cell carcinoma cells through telomerase repression.

Epigallocatechin-3-gallate (EGCG), the major component of green tea polyphenol, has potent efficiency to prevent the growth of a variety of cancer cells. As a novel anticancer agent for treatment of cancers, EGCG is promising and the mechanism has not been fully understood. Laryngeal squamous cell carcinoma (LSCC) is one common tumor in head and neck cancers.

The BH3-only protein PUMA is involved in green tea polyphenol-induced apoptosis in colorectal cancer cell lines.

The green tea polyphenol (GTP) has been shown to possess cancer therapeutic effect through induction of apoptosis, while the underlying molecular mechanism of its anticancer effect is not well understood. PUMA (p53-upregulated modulator of apoptosis) plays an important role in the process of apoptosis induction in a variety of human tumor cells in both p53-dependent and -independent manners. However, whether or not PUMA is involved in the process of GTP-induced apoptosis in cancer cells has not been well reported.

[Nonmyleoablative allogeneic stem cell transplantation combined with imatinib in treatment of chronic myeloid leukemia: a clinical study].

Objective: To study the effect of nonmyeloablative allogeneic peripheral blood stem cell (NST) transplantation combined with imatinib in the treatment of chronic myeloid leukemia (CML).

Methods: Ten CML patients, 5 males and 5 females, aged 21-41, 3 in chronic phase (CP), 4 in accelerated phase (AP) and 3 in blast crisis phase (BP), were treated with imatinib (400-1500 mg/d) before (n = 10) and/or after (n = 6) NST transplantation. The donors were HLA-identical (n = 4), 5/6 antigen-matched (n = 2), 4/6 antigen-matched (n = 2), 3/6 antigen-matched (n = 1) siblings or haplo-identical mothers (n = 2).

[Activating effects of protein transduction domain mediated BCR/ABL protein on CML T cells].

Objective: To study the activating effect of protein transduction domain (PTD) mediated BCR/ABL protein on T cells from CML patients.

Methods: The plasmid containing PTD and b3a2 bcr/abl of CML was constructed by genetic engineering and expressed in E. coli.

[Clinical analysis of retinoic acid syndrome developed in 11 patients with acute promyelocytic leukemia].

To explore the clinical features, risk factors an d treatment of retinoic acid syndrome (RAS) in patients with acute promyelocytic leukemia (APL) treated with retinoic acid, the clinical and laboratory data of 11 APL patients with RAS were retrospectively analysed. The results showed that earlier and more common symptoms of RAS were successively dyspnea (11/11), fever (10/11) and hydrothorax (6/11). Higher WBC count (> or = 15.

[Alteration of the Cell Cycle during the Differentiation of HL-60 Cells by Induction of Retinoic Acid].

To study the alteration of the cell cycle during the differentiation of human myeloid leukemia cell line HL-60 induced with all trans-retinoic acid (RA), the flow cytometry was used to assay the various phases of cell cycle in HL-60 cells treated with RA. The results showed: (1) S + G(2)/M phase proportion kept relative invariability during the 48 hours incubation of HL-60 cells with RA, however, the proportion alteration of S-phase cells was associated with the RA concentrations. At 10(-6) mol/L RA, the proportion of S-phase cells appeared a temporarily increasing peak followed by persistent decrease of S-phase proportion.

Transcription factor EGR-1 inhibits growth of hepatocellular carcinoma and esophageal carcinoma cell lines.

Aim: The transcription factor EGR-1 (early growth response gene-1) plays an important role in cell growth, differentiation and development. It has identified that EGR-1 has significant transformation suppression activity in some neoplasms, such as fibrosarcoma, breast carcinoma. This experiment was designed to investigate the role of egr-1 in the cancerous process of hepatocellular carcinoma (HCC) and esophageal carcinoma (EC), and then to appraise the effects of EGR-1 on the growth of these tumor cells.