A5101800252- Multiple Myeloma Research and Treatments
- Immunotherapy and Immune Responses
- Bone health and treatments
- Protein Degradation and Inhibitors
- Bone Metabolism and Diseases
- CAR-T cell therapy research
- Ubiquitin and proteasome pathways
- Cancer Mechanisms and Therapy
- T-cell and B-cell Immunology
- Chemokine receptors and signaling
- Peptidase Inhibition and Analysis
- Cancer therapeutics and mechanisms
- Immune Cell Function and Interaction
- Monoclonal and Polyclonal Antibodies Research
- Cell Adhesion Molecules Research
- Lymphoma Diagnosis and Treatment
- Lung Cancer Treatments and Mutations
- Glycosylation and Glycoproteins Research
- Cytokine Signaling Pathways and Interactions
- vaccines and immunoinformatics approaches
- Viral Infectious Diseases and Gene Expression in Insects
- Cancer Treatment and Pharmacology
- Chronic Lymphocytic Leukemia Research
- Heat shock proteins research
- Birth, Development, and Health
Qingdao University
2017-2025
Affiliated Hospital of Qingdao University
2024
Methodist Hospital
2020-2022
Shenyang Pharmaceutical University
2021-2022
Houston Methodist
2020-2022
The University of Texas MD Anderson Cancer Center
2012-2021
Guangzhou Medical University
2014-2017
Guangzhou Medical University Cancer Hospital
2014-2017
University of Nevada, Reno
2017
Sun Yat-sen University
2017
Th9 cells are a subset of CD4+ Th that produce the pleiotropic cytokine IL-9. IL-9/Th9 can function as both positive and negative regulators immune response, but role in tumor immunity is unknown. We examined model pulmonary melanoma mice. Lack IL-9 enhanced growth, while tumor-specific cell treatment promoted stronger antitumor responses prophylactic therapeutic models. also elicited strong host CD8+ CTL by promoting Ccl20/Ccr6-dependent recruitment DCs to tissues. Subsequent antigen...
Therapeutic resistance occurs in most patients with multiple myeloma (MM). One of the key mechanisms for MM drug comes from interaction between cells and adipocytes that inhibits drug-induced apoptosis cells; reprogram to morph into different characterizations, including exosomes, which are important tumor-stroma cellular communication. However, mechanism by exosomes mediate machinery vicious cycle remains unclear.Adipocytes were either isolated bone marrow aspirates healthy donors or...
// Zhiqiang Liu 1,* , Jingda Xu Jin He 1 Huan Pei Lin 2 Xinhai Wan 3 Nora M. Navone Qiang Tong 4 Larry W. Kwak Robert Z. Orlowski and Jing Yang Department of Lymphoma Myeloma, Division Cancer Medicine, Center for Immunology Research, The University Texas MD Anderson Center, Houston, Texas, USA Pathology, Genitourinary Medical Oncology-Research, Children’s Nutrition Research Baylor College * These authors have contributed equally to this work Correspondence to: Yang, email: Keywords :...
Osteolytic lesions in multiple myeloma are caused by osteoclast-mediated bone resorption and reduced formation. A unique feature of is a failure healing after successful treatment. We observed adipocytes on trabecular near the resorbed area successfully treated patients. Normal marrow adipocytes, when cocultured with cells, were reprogrammed produced adipokines that activate osteoclastogenesis suppress osteoblastogenesis. These have expression peroxisome proliferator-activated receptor γ...
p38 mitogen-activated protein kinase (MAPK), which is constitutively activated in human myeloma, has been implicated bone destruction by this cancer, but the processes it recruits are obscure. In study, we show that activity myeloma inhibits osteoblast differentiation and formation, also enhances osteoclast maturation resorption. regulated expression secretion of Wnt pathway antagonist DKK-1 monocyte chemoattractant MCP-1. Attenuating p38, DKK-1, or MCP-1 were each sufficient to reduce...
Myeloma-expressed thymidine phosphorylase enhances bone lesion formation by acting on osteoclasts and osteoblasts.
Dysregulation of MYC is frequently implicated in both early and late myeloma progression events, yet its therapeutic targeting has remained a challenge. Among key downstream targets ribosomal biogenesis, enabling increases protein translational capacity necessary to support the growth self-renewal programmes malignant cells. We therefore explored selective biogenesis with small molecule RNA polymerase (pol) I inhibitor CX-5461 myeloma. induced significant inhibition wild-type (WT) mutant...
Despite advances in therapy, multiple myeloma remains incurable, with a high frequency of relapse. This suggests the need to identify additional factors that contribute drug resistance. Our previous studies revealed bone marrow adipocytes promote resistance chemotherapy through adipocyte-secreted adipokines, but mechanism underlying this effect and specific adipokines involved are not well understood. We proposed determine role resistin, an adipokine is secreted by adipocytes, myeloma. found...
Myeloma cells repress osteoblastogenesis by inhibiting the degradation of PPARγ2 in mesenchymal stem cells.
Abstract Idiotype (Id) protein, secreted by myeloma cells, is a tumor-specific antigen. Id-based immunotherapy has been explored in patients with myeloma, and results were disappointing. Although previous studies have shown that Id-specific CTLs are able to lyse it unclear whether other types of T such as type-1 T-helper (Th1) type-2 (Th2) also suppress or kill cells. Using 5T murine model, we generated T-cell clones different subsets examined their function the context specifically lysed...
p38 MAPK signaling controls cell growth, proliferation and the cycle under stress conditions. However, function of activation in tumor metastasis is still not well understood. We report that breast cancer cells inhibits but does substantially modulate primary growth. Stable knockdown suppressed NF-κB p65 activation, inhibiting miR-365 expression resulting increased IL-6 secretion. The inhibitory effect on was mediated by suppression mesenchymal stem (MSC) migration to sites metastasis, where...