A5058403613- Cytokine Signaling Pathways and Interactions
- Lymphoma Diagnosis and Treatment
- Chronic Lymphocytic Leukemia Research
- Phagocytosis and Immune Regulation
- Galectins and Cancer Biology
- CAR-T cell therapy research
- Immune Cell Function and Interaction
- T-cell and Retrovirus Studies
- Acute Lymphoblastic Leukemia research
- Multiple Myeloma Research and Treatments
- Monoclonal and Polyclonal Antibodies Research
- Peptidase Inhibition and Analysis
- Protein Degradation and Inhibitors
- Cancer Immunotherapy and Biomarkers
- Viral-associated cancers and disorders
- Histone Deacetylase Inhibitors Research
- Cancer-related gene regulation
- Protein Tyrosine Phosphatases
- Cholangiocarcinoma and Gallbladder Cancer Studies
- Chemokine receptors and signaling
- Cancer Mechanisms and Therapy
- Lung Cancer Treatments and Mutations
- Click Chemistry and Applications
- Immunotherapy and Immune Responses
- 14-3-3 protein interactions
University of Michigan
2013-2024
Ann Arbor VA Medical Center
2020
Avery Dennison (United States)
2017
University of Minnesota
2010
Abstract Purpose: T-cell lymphomas are a molecularly heterogeneous group of non-Hodgkin (NHL) that account for disproportionate number NHL disease-related deaths due to their inherent and acquired resistance standard multiagent chemotherapy regimens. Despite molecular heterogeneity frequent loss various T cell–specific receptors, the antigen receptor is retained in majority these lymphomas. As (TCR) engagement activates signaling pathways transcription factors regulate growth survival, we...
Peripheral T-cell lymphomas are clinically aggressive and usually fatal, as few complete or durable remissions achieved with currently available therapies. Recent evidence supports a critical role for lymphoma-associated macrophages during lymphoma progression, but the specific signals involved in cross-talk between malignant T cells their microenvironment poorly understood. Colony-stimulator factor 1 receptor (CSF1R, CD115) is required homeostatic survival of tissue-resident macrophages....
Monocytes and their progeny are abundant constituents of the tumor microenvironment in lymphoproliferative disorders, including chronic lymphocytic leukemia (CLL). Monocyte-derived cells, nurse-like cells (NLC) CLL, promote lymphocyte proliferation survival, confer resistance to chemotherapy, associated with more rapid disease progression. Colony-stimulating factor-1 receptor (CSF-1R) regulates homeostatic survival tissue-resident macrophages. Therefore, we sought determine whether CSF-1R is...
The transcription factor GATA-3, highly expressed in many cutaneous T-cell lymphoma (CTCL) and peripheral lymphomas (PTCL), confers resistance to chemotherapy a cell-autonomous manner. As GATA-3 is transcriptionally regulated by NF-κB, we sought determine the extent which proteasomal inhibition impairs NF-κB activation expression cell viability malignant T cells. Proteasome inhibition, activity, expression, were examined patient-derived lines primary specimens ex vivo treated with oral...
// Carlos Murga-Zamalloa 1, 2 , Avery Polk 1 Walter Hanel Pinki Chowdhury Noah Brown Alexandra C. Hristov Nathanael G. Bailey 3 Tianjiao Wang Tycel Phillips Sumana Devata Pradeep Poonnen Juan Gomez-Gelvez 4 Kedar V. Inamdar and Ryan A. Wilcox Department of Internal Medicine, Division Hematology Oncology, University Michigan, Ann Arbor, MI, USA Pathology, Hematopathology, Pittsburgh, PA, Henry Ford Hospital, Detroit, Correspondence to: Wilcox, email: rywilcox@med.umich.edu Keywords: PLK-1;...
Peripheral T-cell lymphomas (PTCL) are agressive that develop from mature T cells. The most common PTCLs genetically, molecularly, and clinically diverse generally associated with dismal outcomes. While Notch signaling plays a critically important role in both the development of immature cells their malignant transformation, its PTCL is poorly understood, despite increasingly appreciated function regulating proliferation differentiation Here, we demonstrate receptors Delta-like family...
7081 Background: PMBCL is an aggressive form of large B-cell lymphoma (LBCL) but has a unique gene expression profiling signature that more closely resembles Hodgkin’s lymphoma. Treatment R/R largely extrapolated from trials in LBCL with few patients included. Randomized leading to use CART as second line treatment for primary refractory or early relapsed enrolled ≤ 10% (ZUMA-7 and TRANSFORM). In the rituximab era, there paucity data on efficacy outcomes salvage therapy followed by high-dose...
<div>AbstractPurpose:<p>Peripheral T-cell lymphomas are clinically aggressive and usually fatal, as few complete or durable remissions achieved with currently available therapies. Recent evidence supports a critical role for lymphoma-associated macrophages during lymphoma progression, but the specific signals involved in cross-talk between malignant T cells their microenvironment poorly understood. Colony-stimulator factor 1 receptor (CSF1R, CD115) is required homeostatic...
<div>Abstract<p>Peripheral T-cell lymphomas (PTCL) are agressive that develop from mature T cells. The most common PTCLs genetically, molecularly, and clinically diverse generally associated with dismal outcomes. While Notch signaling plays a critically important role in both the development of immature cells their malignant transformation, its PTCL is poorly understood, despite increasingly appreciated function regulating proliferation differentiation Here, we demonstrate...
<div>Abstract<p>Peripheral T-cell lymphomas (PTCL) are agressive that develop from mature T cells. The most common PTCLs genetically, molecularly, and clinically diverse generally associated with dismal outcomes. While Notch signaling plays a critically important role in both the development of immature cells their malignant transformation, its PTCL is poorly understood, despite increasingly appreciated function regulating proliferation differentiation Here, we demonstrate...
Supplementary Data from Notch Signaling Promotes Mature T-Cell Lymphomagenesis
Supplementary Data from Notch Signaling Promotes Mature T-Cell Lymphomagenesis