"B-cell leukemia"

Pre-B-Cell leukemia transcription factor 1 contributes to liver fibrosis by enabling IL-7 signaling in hepatic stellate cells. Liver fibrosis, when dysregulated, contributes to irreversible loss of hepatic structure and function heralding end-stage liver diseases including cirrhosis and hepatocellular carcinoma. Hepatic stellate cells (HSCs) represent the common progenitor to myofibroblasts that produce extracellular matrix (ECM) proteins to mediate liver fibrosis. In the present study, we investigated the role of Pre-B-Cell leukemia transcription factor 1 (PBX1) in this process. Liver fibrosis was induced by CCl4 injection or bile duct ligation (BDL). Cellular transcriptome was examined by RNA-seq and CUT&Tag-seq. PBX1 was screened out of mining through liver fibrosis-related single-cell RNA

The PAX5-JAK2 translocation acts as dual-hit mutation that promotes aggressive B-cell leukemia via nuclear STAT5 activation. While PAX5 is an important tumor suppressor gene in B-cell acute lymphoblastic leukemia (B-ALL), it is also involved in oncogenic translocations coding for diverse PAX5 fusion proteins. PAX5-JAK2 encodes a protein consisting of the PAX5 DNA-binding region fused

Combining nilotinib and PD-L1 blockade reverses CD4+ T-cell dysfunction and prevents relapse in acute B-cell leukemia. Patients with acute lymphoblastic leukemia have experienced significantly improved outcomes due to the advent of chimeric antigen receptor (CAR) T cells and bispecific T-cell engagers, although a proportion of patients still relapse despite these advances. T-cell exhaustion has

Immunoglobulin gene testing for B-cell leukemia Immunoglobulin gene testing for B-cell leukemia ..

Constitutive Activation of RAS/MAPK Pathway Cooperates with Trisomy 21 and Is Therapeutically Exploitable in Down Syndrome B-cell Leukemia. Children with Down syndrome (constitutive trisomy 21) that develop acute lymphoblastic leukemia (DS-ALL) have a 3-fold increased likelihood of treatment-related mortality coupled with a higher cumulative incidence of relapse, compared with other children

Integrin α6 mediates the drug resistance of acute lymphoblastic B-cell leukemia. Resistance to multimodal chemotherapy continues to limit the prognosis of acute lymphoblastic leukemia (ALL). This occurs in part through a process called adhesion-mediated drug resistance, which depends on ALL cell adhesion to the stroma through adhesion molecules, including integrins. Integrin α6 has been

Progression of progenitor B cell leukemia is associated with alterations of the bone marrow micro-environment.

CD19 chimeric antigen receptor-T cells in B-cell leukemia and lymphoma: current status and perspectives. The approval of tisagenlecleucel and axicabtagene ciloleucel represents a breakthrough in the field of immune and cellular therapy for hematologic malignancies. These anti-CD19 chimeric antigen receptor-T cells (CAR) proved to be highly effective in the treatment of relapsed/refractory B-cell

Driver mutations in Janus kinases in a mouse model of B-cell leukemia induced by deletion of PU.1 and Spi-B Precursor B-cell acute lymphoblastic leukemia (B-ALL) is associated with recurrent mutations that occur in cancer-initiating cells. There is a need to understand how driver mutations influence clonal evolution of leukemia. The E26-transformation-specific (ETS) transcription factors PU.1

Revisiting CD28 Superagonist TGN1412 as Potential Therapeutic for Pediatric B Cell Leukemia: A Review Pediatric acute lymphoblastic leukemia (ALL) represents the most common pediatric cancer diagnosis, with numbers rising gradually every year. This paper proposes a novel therapeutic agent for pediatric ALL on the basis of a failed clinical drug trial in 2006. TGN1412 was a promising therapeutic agent that yielded outstanding results in both in vitro studies and animal trials. It is a CD28 superagonist monoclonal antibody that activates T regulatory (T) cells in the absence of costimulation of the T cell receptor (TCR) by an antigen-presenting cell. This drug was intended as a solution to T cell deficient diseases such as B cell leukemia and autoimmune diseases such as rheumatoid arthritis

B-cell leukemia/lymphoma 10 promotes angiogenesis in an experimental corneal neovascularization model Corneal neovascularization (CrNV) arises from many causes including corneal inflammatory, infectious, or traumatic insult, and frequently leads to impaired vision. This study seeks to determine the role of B-cell leukemia/lymphoma 10 (BCL-10) in the development of experimental CrNV. Corneas from

Adequate concentration of B cell leukemia/lymphoma 3 (Bcl3) is required for pluripotency and self-renewal of mouse embryonic stem cells via downregulation of Nanog transcription B cell leukemia/lymphoma 3 (Bcl3) plays a pivotal role in immune homeostasis, cellular proliferation, and cell survival, as a co-activator or co-repressor of transcription of the NF-κB family. Recently, it was reported

Pre-B cell leukemia transcription factor 3 induces inflammatory responses in human umbilical vein endothelial cells and murine sepsis via acting a competing endogenous RNA for high mobility group box 1 protein The present study investigated the roles of pre-B cell leukemia transcription factor 3 (PBX3) in sepsis. Reverse transcription-quantitative polymerase chain reaction and western blot

In Vivo Expansion and Antitumor Activity of Coinfused CD28- and 4-1BB-Engineered CAR-T Cells in Patients with B Cell Leukemia. Several recent clinical trials have successfully incorporated a costimulatory domain derived from either CD28 or 4-1BB with the original CD3ζ T cell activating domain to form second-generation chimeric antigen receptors (CARs) that can increase the responsiveness and survival of CAR-engineered T (CAR-T) cells. However, a rigorous assessment of the individual benefits of these costimulatory components relative to the in vivo performance of infused T cells in patients is still lacking. Therefore, we have designed a study that allows us to investigate and compare the impact of different costimulatory signal domains on CAR-T cells in vivo. Patients with B cell leukemia

A Study of BGB-16673 Compared to Investigator's Choice in Participants With Chronic Lymphocytic Leukemia Previously Exposed to Both Bruton Tyrosine Kinase (BTK) and B-cell Leukemia/Lymphoma 2 Protein (BCL2) Inhibitors The purpose of this study is to investigate the efficacy and safety of BGB-16673 compared with investigator's choice (idelalisib plus rituximab or bendamustine plus rituximab

CAR2219 CAR-T Cells for the Treatment of R/R B Cell Leukemia and Lymphoma This is a single arm study to evaluate the safety and efficacy of CAR2219 CAR-T cells in the treatment of relapsed/refractory CD19/CD22 positive B cell Leukemia and Lymphoma. This study is an exploratory clinical trial of a single-arm, open, single-center treatment of CAR2219 CAR-T cell. 20 subjects with relapsed or refractory CD19/ CD22 positive B-cell Leukemia and Lymphoma will be enrolled and received CAR2219 CAR T cells injection therapy, and related data such as adverse reactions and therapeutic effects after medication were followed up. To evaluate its safety and efficacy.

Clinical Study on the Safety and Efficacy of BiTE-EV in Relapsed/Refractory Acute B-Cell Leukemia The goal of this clinical trial is to learn if BiTE-EV works to treat relapsed/refractory acute B-cell leukemia in adults. It will also learn about the safety of BiTE-EV. The main questions it aims to answer are: Can BiTE-EV effectively treat relapsed/refractory acute B-cell lymphoblastic leukemia

JY231(JY231) Injection for the Treatment of Relapsed or Refractory B-Cell Leukemia This study is an investigator-initiated single center, single arm clinical study with a target population of patients with relapsed or refractory B cell leukemia. It is an early exploratory clinical study of the safety, tolerability and initial efficacy of JY231 injection in the treatment of relapsed or refractory

BRAFV600E accelerates disease progression and enhances immune suppression in a mouse model of B-cell leukemia Mutated mitogen-activated protein kinase (MAPK) pathway components promote tumor survival, proliferation, and immune evasion in solid tumors. MAPK mutations occur in hematologic cancers as well, but their role is less clear and few models are available to study this. We developed an in vivo model of disseminated BRAF B-cell leukemia to determine the effects of this mutation on tumor development and immune evasion. Mice with B-cell-restricted BRAF expression crossed with the Eµ-TCL1 model of chronic lymphocytic leukemia (CLL) developed leukemia significantly earlier (median, 4.9 vs 8.1 months; < .001) and had significantly shorter lifespan (median, 7.3 vs 12.1 months; < .001

Considerations in T Cell Therapy Product Development for B cell leukemia and lymphoma immunotherapy Based on laboratory and clinical research findings and investments in immunotherapy by many institutions in academia, government-funded laboratories, and industry, there is tremendous and deserved excitement in the field of cell and gene therapy. In particular, understanding of immune-mediated