Runqing Lu

First Affiliated Hospital of Zhengzhou University

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S. K. Joshi

McLean Hospital

Shibin Ma

Creighton University

Vipul Shukla

Northwestern University

Rong Guo

First Affiliated Hospital of Zhengzhou University

Jixin Fan

First Affiliated Hospital of Zhengzhou University

Long Trinh

Children's Hospital 1

Simanta Pathak

University of Houston

Weijie Cao

First Affiliated Hospital of Zhengzhou University

Dingming Wan

First Affiliated Hospital of Zhengzhou University

Haiqiu Zhao

First Affiliated Hospital of Chongqing Medical University

Cooperative Institutions

University of Nebraska Medical Center

First Affiliated Hospital of Zhengzhou University

Peking University

Chinese Academy of Medical Sciences & Peking Union Medical College

Peking University People's Hospital

Institute of Hematology & Blood Diseases Hospital

Zhengzhou University

Nebraska Medical Center

National Clinical Research

Chinese Academy of Sciences

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Venetoclax combined chemotherapy versus chemotherapy alone for acute myeloid leukemia: a systematic review and meta-analysis

Frontiers in Oncology (2024)

Jingkui Zhu Jixin Fan Tiantian Xie Haiqiu Zhao Runqing Lu

Objective To compare the efficacy and safety of venetoclax (VEN) in combination with chemotherapy (chemo) versus chemo alone in the treatment of acute myeloid leukemia (AML). Method To compare the efficacy and/or safety of VEN+chemo versus chemotherapy alone for AML, PubMed, Embase, Web of Science, and the Cochrane Library were used to searching up to June 2023. Comparisons included complete remission (CR), CR with incomplete hematologic recovery (CRi), morphologic leukemia-free state (MLFS), overall response rate (ORR), and adverse events (AEs). Result A total of 9 articles were included, including 3124 patients. The baseline characteristics between two patient groups were similar. The combined analysis showed that compared with the group receiving chemo alone, the VEN+chemo group exhibited higher rates of CR, CRi, MLFS and ORR. Additionally, the VEN+chemo group had longer event-free survival (EFS) and overall survival (OS) durations. The incidence rates of AEs and serious AEs (SAEs) were similar between the two groups, but the early 30-day mortality rate was lower in the VEN+chemo group than in the chemo alone group. Conclusion The VEN+chemo therapy demonstrates significant efficacy and safety profile in AML patients. However, more prospective studies are needed in the future to provide more accurate and robust evidence for treatment selection in patients. Systematic Review Registration https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42023439288 , identifier CRD42023439288.

Venetoclax

Ven

10.3389/fonc.2024.1361988

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Detection of Measurable Residual Disease May Better Predict the Outcome Rather Than Mutations Based on Next-Generation Sequencing in Acute Myeloid Leukemia with Biallelic Mutations of CEBPA

Blood (2019)

Jing Wang Hao Jiang Xiao‐Jun Huang Guo‐Rui Ruan Runqing Lu

CEBPA

Cumulative incidence

Induction chemotherapy

NPM1

Minimal Residual Disease

Chemotherapy regimen

10.1182/blood-2019-127696

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Critical role of IRF-5 in regulation of B-cell differentiation

Proceedings of the National Academy of Sciences (2010)

Chunyang Lien Chee-Mun Fang David Huso Ferenc Livák Runqing Lu

IFN-regulatory factor 5 (IRF-5), a member of the IRF family, is a transcription factor that has a key role in the induction of the antiviral and inflammatory response. When compared with C57BL/6 mice, Irf5(-/-) mice show higher susceptibility to viral infection and decreased serum levels of type I IFN and the inflammatory cytokines IL-6 and TNF-alpha. Here, we demonstrate that IRF-5 is involved in B-cell maturation and the stimulation of Blimp-1 expression. The Irf5(-/-) mice develop an age-related splenomegaly, associated with a dramatic accumulation of CD19(+)B220(-) B cells and a disruption of normal splenic architecture. Splenic B cells from Irf5(-/-) mice also exhibited a decreased level of plasma cells. The CD19(+) Irf5(-/-) B cells show a defect in Toll-like receptor (TLR) 7- and TLR9-induced IL-6 production, and the aged Irf5(-/-) mice have decreased serum levels of natural antibodies; however, the antigen-specific IgG1 primary response was already dependent in IRF-5 in young mice, although the IgM response was not. Analysis of the profile of transcription factors associated with plasma cell differentiation shows down-regulation of Blimp-1 expression, a master regulator of plasma cell differentiation, which can be reconstituted with ectopic IRF-5. IRF-5 stimulates transcription of the Prdm1 gene encoding Blimp-1 and binds to the IRF site in the Prdm1 promoter. Collectively, these results reveal that the age-related splenomegaly in Irf5(-/-) mice is associated with an accumulation of CD19(+)B220(-) B cells with impaired functions and show the role of IRF-5 in the direct regulation of the plasma cell commitment factor Blimp-1 and in B-cell terminal differentiation.

IRF5

TLR9

Ectopic expression

10.1073/pnas.0911193107

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Effects of post-transplant maintenance therapy with decitabine prophylaxis on the relapse for acute lymphoblastic leukemia

Bone Marrow Transplantation (2023)

Jixin Fan Runqing Lu Jingkui Zhu Xiao Guo Dingming Wan

Decitabine

Cumulative incidence

10.1038/s41409-023-01948-y

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A Role for Interferon Regulatory Factor 4 in Receptor Editing

Molecular and Cellular Biology (2008)

Simanta Pathak Shibin Ma Long Trinh Runqing Lu

Receptor editing is the primary means through which B cells revise antigen receptors and maintain central tolerance. Previous studies have demonstrated that interferon regulatory factor 4 (IRF-4) and IRF-8 promote immunoglobulin light-chain rearrangement and transcription at the pre-B stage. Here, the roles of IRF-4 and -8 in receptor editing were analyzed. Our results show that secondary rearrangement was impaired in IRF-4 but not IRF-8 mutant mice, suggesting that receptor editing is defective in the absence of IRF-4. The role of IRF-4 in receptor editing was further examined in B-cell-receptor (BCR) transgenic mice. Our results show that secondary rearrangement triggered by membrane-bound antigen was defective in the IRF-4-deficient mice. Our results further reveal that the defect in secondary rearrangement is more severe at the immunoglobulin lambda locus than at the kappa locus, indicating that IRF-4 is more critical for the lambda rearrangement. We provide evidence demonstrating that the expression of IRF-4 in immature B cells is rapidly induced by self-antigen and that the reconstitution of IRF-4 expression in the IRF-4 mutant immature B cells promotes secondary rearrangement. Thus, our studies identify IRF-4 as a nuclear effector of a BCR signaling pathway that promotes secondary rearrangement at the immature B-cell stage.

Gene rearrangement

10.1128/mcb.01946-07

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Stimulation of IRF-7 Gene Expression by Tumor Necrosis Factor α

Journal of Biological Chemistry (2002)

Runqing Lu Paul A. Moore Paula M. Pitha

Interferon regulatory factor 7 (IRF-7) plays an important role in innate immunity, where, together with IRF-3, it controls the expression of interferon A/B genes as well as chemokine RANTES (regulated on activation normal T cell expressed and secreted). Previously, we characterized human IRF-7 promoter and showed that an interferon-stimulated response element site in the first intron binds interferon-stimulated gene factor 3 (ISGF3) and confers the response to interferon. Here we report the stimulation of IRF-7 expression by 12-O-tetradecanoylphorbol-13-acetate (TPA) and tumor necrosis factor α (TNFα) in human peripheral blood monocytes. Using promoter analysis in combination with electrophoretic mobility shift assays, we have demonstrated that an NFκB site located next to the TATA box, binds p50 and p65 heterodimer and is required for the induction of the IRF-7 gene by TPA and TNFα. In addition, we report stimulation of IRF-7 gene expression by topoisomerase II (TOPII) inhibitors. We show by chromatin immunoprecipitation assay that treatment with the TOPII inhibitor etoposide induces association of acetylated histone 3 with the promoter of IRF-7 gene, indicating that TOPII-mediated changes in chromatin structure could be responsible for the induction. This suggests that the IRF-7 gene is localized in the condensed area of the chromosome where it is inaccessible to transcription factors that would promote its constitutive expression.

Chromatin immunoprecipitation

IRF8

IRF1

TATA box

IRF4

Interferon-stimulated gene

10.1074/jbc.m111440200

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Evaluation of Nutritional Interventions in Preventing Type 2 Diabetes Mellitus: A Randomized Controlled Trial

Current Topics in Nutraceutical Research (2024)

Qiuyu Li Xin Wang Runqing Lu Jiaoyang Zheng Jingjing Chen

This study aimed to evaluate the effectiveness of the structured dietary intervention in reducing the risk of developing type 2 diabetes mellitus and improving associated metabolic health indicators. We included 530 participants randomly assigned to an intervention group with a Mediterranean-style diet and a control group with generic dietary guidelines. The incidence of type 2 diabetes mellitus was the primary outcome, whereas changes in fasting plasma glucose, lipid profiles, and body composition were the secondary outcomes. After 24 months, the incidence of type 2 diabetes mellitus was significantly lower among participants in the intervention group than those in the control group (P < 0.05). Fasting glucose, hemoglobin A1c, total cholesterol, and low-density lipoprotein levels were decreased (P < 0.05), and high-density lipoprotein levels were increased among participants in the intervention group than in those in the control group (P < 0.05). Also, body weight, blood pressure, and body mass index, major negative predictors of fasting glucose levels, were significantly decreased in participants in the intervention group than in those in the control group (P < 0.05), irrespective of other covariates. Dietary intervention substantially reduced the risk of developing type 2 diabetes mellitus and improved glycemic control, lipid profiles, and overall metabolic health.

10.37290/ctnr2641-452x.22:424-430

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[Significance of ST2 in the Early Diagnosis and Treatment of Graft-Versus-Host Disease--Review].

PubMed (2016)

Runqing Lu Rong Guo

Graft-versus-host disease (GVHD) is a major complication of allo-hematopoietic stem cell transplantation. It is reported that IL-2R, TNFR1, elafin (for skin GVHD) and REG-3α (for gastrointestinal GVHD) can be used in the early diagnosis of acute GVHD, but they cannot predict the response to therapy independently. Therefore, it is urgent to find a biomarker to predict GVHD and glucocorticoid resistance. ST2 is a member of IL-1 receptor family and specially binds to IL-33. Researchers have found that higher ST2 level is associated with increased GVHD risk, glucocorticoid resistance and transplantation-related mortality. This review focuses on the structure, function, signal transduction pathway of ST2/IL-33, and its roles in diagnosis and treatment of autoimmune diseases and GVHD.

10.7534/j.issn.1009-2137.2016.01.060

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The Impact of Anti-HLA Antibodies on the Prognosis of Allogeneic Hematopoietic Stem Cell Transplantation in Myelodysplastic Syndrome

Blood (2024)

Tiantian Xie Runqing Lu Weijie Cao Bian Zhilei Wei Li

10.1182/blood-2024-206974

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Background: A genome-wide SNP association study has linked low levels of IRF4 with the development of CLL. Results: Low levels of IRF4 disrupt homeostasis of B1 B cells and promote survival of CLL cell. Conclusion: Our results demonstrate a causal relationship between low levels of IRF4 and the development of CLL. Significance: We establish IRF4 as a critical regulator in the pathogenesis of CLL.

Shibin Ma Vipul Shukla Leilei Fang Karen A. Gould S. K. Joshi

A recent genome-wide SNP association study identified IRF4 as a major susceptibility gene for chronic lymphocytic leukemia (CLL). Moreover, the SNPs located in the 3 UTR of the IRF4 gene have been linked to a down-regulation of IRF4. However, whether a low level of IRF4 is critical for CLL development remains unclear. New Zealand Black (NZB) mice are a naturally occurring, late-onset mouse model of CLL. To examine the role of a reduced level of IRF4 in CLL development, we generated, through breeding, IRF4 heterozygous mutant mice in the NZB background (NZB IRF4 / ). Our results show that CLL development is accelerated dramatically in the NZB IRF4 / mice. The average onset of CLL in NZB mice is 12 months, but CLL cells can be detected in NZB IRF4 / mice at 3 months of age. By 5 months of age, 80% of NZB IRF4 / mice developed CLL. CLL cells are derived from B1 cells in mice. Interestingly, NZB IRF4 / B1 cells exhibit prolonged survival, accelerated selfrenewal, and defects in differentiation. Although NZB IRF4 / CLL cells are resistant to apoptosis, high levels of IRF4 inhibit their survival. High levels of IRF4 also reduce the survival of MEC-1 human CLL cells. Our analysis further reveals that high levels of IRF4 suppress Akt activity and can do so without the IRF4 DNA binding domain. Thus, our findings reveal a causal relationship between a low level of IRF4 and the development of CLL and establish IRF4 as a novel regulator in the pathogenesis of CLL.

IRF4

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