Belinda R. Avalos

Levine Cancer Institute

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Edward A. Copelan

Levine Cancer Institute

111

Lawrence J. Druhan

Levine Cancer Institute

Nilanjan Ghosh

Levine Cancer Institute

Michael R. Grunwald

Levine Cancer Institute

Nury Steuerwald

Levine Cancer Institute

James T. Symanowski

Levine Cancer Institute

Ryan Jacobs

Levine Cancer Institute

Jai N. Patel

Levine Cancer Institute

Jing Ai

First Bethune Hospital of Jilin University

Saad Z. Usmani

Memorial Sloan Kettering Cancer Center

Cooperative Institutions

Levine Cancer Institute

175

Carolinas Healthcare System

The Ohio State University

Atrium Medical Cente

Wake Forest University

Carolinas Medical Center

Mayo Clinic in Florida

Medical College of Wisconsin

Cleveland Clinic

The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute

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Dissociation of the Jak kinase pathway from G-CSF receptor signaling in neutrophils.

PubMed (1997)

Belinda R. Avalos J. M. R. Parker D A Ware Melissa Hunter K A Sibert

Tyrosine kinase 2

Janus kinase 2

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Citations (36)

LRG-accelerated differentiation defines unique G-CSFR signaling pathways downstream of PU.1 and C/EBPε that modulate neutrophil activation

Journal of Leukocyte Biology (2008)

Jing Ai Lawrence J. Druhan Melissa Hunter Megan Loveland Belinda R. Avalos

Abstract Expression of leucine-rich α2 glycoprotein (LRG), a member of the leucine-rich repeat family of proteins, was recently shown to be up-regulated during neutrophil differentiation. Its precise role in granulopoiesis, however, remains unknown. In this paper, we show that the transcription factors PU.1 and C/EBPε that regulate the expression of multiple myeloid-specific genes also bind to the LRG promoter. We also demonstrate that LRG localizes to the same cytoplasmic compartment as myeloperoxidase and that G-CSF treatment of the 32Dcl3 myeloid cell line induces nuclear translocation of LRG. Stable transfection of LRG into 32Dcl3 cells resulted in accelerated, G-CSF-mediated neutrophil differentiation and induction of CD11b expression. In contrast, constitutive expression of LRG in 32Dwt18 cells, expressing a chimeric erythropoietin (Epo)/G-CSFR consisting of the EpoR extracellular domain fused to the G-CSFR transmembrane and cytoplasmic domains, failed to induce accelerated neutrophil differentiation and CD11b expression in response to Epo stimulation. LRG-mediated accelerated differentiation and CD11b expression were found to correlate with an increased level of phospho-Stat3 but not with PU.1 or p27kip1 levels. Hence, similar to other genes involved in neutrophil differentiation, the expression of LRG also appears to be regulated by PU.1 and C/EBPε. Collectively, these findings suggest a role for LRG in modulating neutrophil differentiation and expression of CD11b via nonredundant G-CSFR signals.

Granulopoiesis

Myelopoiesis

10.1189/jlb.1107751

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Citations (29)

Optimizing Progenitor Cell Mobilization in Patients with Myeloma: Effect of a Pre-Emptive Day 4 Plerixafor-Based Mobilization Algorithm

Blood (2016)

Omotayo Fasan Saad Z. Usmani Danyu Sun Ryan Jacobs Carlos Lee

Plerixafor

Mobilization

Autologous stem-cell transplantation

10.1182/blood.v128.22.2184.2184

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Citations (1)

New Germline Syndrome Discovery: Heterozygous CSF3R Mutations May Predispose to Myeloid and Lymphoid Malignancies

Blood (2019)

Amy M. Trottier Ira L. Kraft Lawrence J. Druhan Amanda Lance Belinda R. Avalos

10.1182/blood-2019-129492

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Citations (0)

Validation of Dynamic Biomarker-Based Risk Progression Model for Smoldering Multiple Myeloma

Blood (2017)

Shebli Atrash Myra Robinson Amanda Aneralla Taylor Brown Reed Friend

10.1182/blood.v130.suppl_1.1779.1779

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Citations (1)

T618I CSF3R mutations in chronic neutrophilic leukemia induce oncogenic signals through aberrant trafficking and constitutive phosphorylation of the O-glycosylated receptor form

Biochemical and Biophysical Research Communications (2019)

Andrea E. Price Lawrence J. Druhan Amanda Lance Gavin I. Clark C. Greer Vestal

Internalization

10.1016/j.bbrc.2019.12.030

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Citations (12)

How Many Stem Cells Are Sufficient for Engraftment?

Humana Press eBooks (2000)

Lynn O’Donnell Patrick Elder Belinda R. Avalos

The past 15 yr have witnessed an explosion of advances leading to important information regarding hematopoietic stem cells (HSCs), which has been directly applicable to the clinical setting. Mobilized peripheral blood (PB) and umbilical cord blood (CB) have been identified as alternatives to bone marrow (BM) as sources of human HSCs for clinical transplantation. Currently, BM remains the predominant stem cell source for allogeneic transplants (allotransplant); most autologous transplants (autotransplants) are now performed solely with mobilized PB stem cells (PBSC). Although experience with CB as a source of stem cells has been limited, it is expected to have its greatest application in the unrelated allotransplant setting. Recent observations that stem cells from each of these sources have biologically distinct properties, and that stem cell doses affect outcomes in clinical transplantation, underscore the importance of stem cell enumeration in predicting transplant outcomes.

Cord blood

10.1007/978-1-59259-657-7_1

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Citations (5)

Allogeneic hematopoietic cell transplantation; the current renaissance

Blood Reviews (2018)

Edward A. Copelan Aleksander L. Chojecki Hillard M. Lazarus Belinda R. Avalos

Hematologic Neoplasms

Hematologic disorders

10.1016/j.blre.2018.11.001

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Citations (90)

Real-World Analysis of Barriers to Timely Administration of Chimeric Antigen Receptor T cell (CAR T) Therapy in Diffuse Large B-cell Lymphoma

Transplantation and Cellular Therapy (2024)

Bei Hu Rakhee Vaidya Ferdous Ahmed Hamid Ehsan Tamara K. Moyo

10.1016/j.jtct.2024.09.007

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Citations (0)

G-CSFR Ubiquitination Critically Regulates Myeloid Cell Survival and Proliferation

PLoS ONE (2008)

Jing Ai Lawrence J. Druhan Megan Loveland Belinda R. Avalos

The granulocyte colony-stimulating factor receptor (G-CSFR) is a critical regulator of granulopoiesis. Mutations in the G-CSFR in patients with severe congenital neutropenia (SCN) transforming to acute myelogenous leukemia (AML) have been shown to induce hypersensitivity and enhanced growth responses to G-CSF. Recent studies have demonstrated the importance of the ubiquitin/proteasome system in the initiation of negative signaling by the G-CSFR. To further investigate the role of ubiquitination in regulating G-CSFR signaling, we generated a mutant form of the G-CSFR (K762R/G-CSFR) which abrogates the attachment of ubiquitin to the lysine residue at position 762 of the G-CSFR that is deleted in the Delta716 G-CSFR form isolated from patients with SCN/AML. In response to G-CSF, mono-/polyubiquitination of the G-CSFR was impaired in cells expressing the mutant K762R/G-CSFR compared to cells transfected with the WT G-CSFR. Cells stably transfected with the K762R/G-CSFR displayed a higher proliferation rate, increased sensitivity to G-CSF, and enhanced survival following cytokine depletion, similar to previously published data with the Delta716 G-CSFR mutant. Activation of the signaling molecules Stat5 and Akt were also increased in K762R/G-CSFR transfected cells in response to G-CSF, and their activation remained prolonged after G-CSF withdrawal. These results indicate that ubiquitination is required for regulation of G-CSFR-mediated proliferation and cell survival. Mutations that disrupt G-CSFR ubiquitination at lysine 762 induce aberrant receptor signaling and hyperproliferative responses to G-CSF, which may contribute to leukemic transformation.

10.1371/journal.pone.0003422

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Citations (15)