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Low-Dose Anti-Thymocyte Globulin (ATG) Preserves β-Cell Function and Improves HbA in New-Onset Type 1 Diabetes.
Haller MJ, Schatz DA, Skyler JS, Krischer JP, Bundy BN, Miller JL, Atkinson MA, Becker DJ, Baidal D, DiMeglio LA, Gitelman SE, Goland R, Gottlieb PA, Herold KC, Marks JB, Moran A, Rodriguez H, Russell W, Wilson DM, Greenbaum CJ, Type 1 Diabetes TrialNet ATG-GCSF Study Group
(2018) Diabetes Care 41: 1917-1925
MeSH Terms: Adolescent, Adult, Antilymphocyte Serum, C-Peptide, Child, Cytoprotection, Diabetes Mellitus, Type 1, Dose-Response Relationship, Drug, Double-Blind Method, Drug Therapy, Combination, Female, Glycated Hemoglobin A, Granulocyte Colony-Stimulating Factor, Humans, Insulin-Secreting Cells, Male, Pilot Projects, Polyethylene Glycols, Recombinant Proteins, Young Adult
Show Abstract · Added May 2, 2019
OBJECTIVE - A pilot study suggested that combination therapy with low-dose anti-thymocyte globulin (ATG) and pegylated granulocyte colony-stimulating factor (GCSF) preserves C-peptide in established type 1 diabetes (T1D) (duration 4 months to 2 years). We hypothesized that ) low-dose ATG/GCSF or ) low-dose ATG alone would slow the decline of β-cell function in patients with new-onset T1D (duration <100 days).
RESEARCH DESIGN AND METHODS - A three-arm, randomized, double-masked, placebo-controlled trial was performed by the Type 1 Diabetes TrialNet Study Group in 89 subjects: 29 subjects randomized to ATG (2.5 mg/kg intravenously) followed by pegylated GCSF (6 mg subcutaneously every 2 weeks for 6 doses), 29 to ATG alone (2.5 mg/kg), and 31 to placebo. The primary end point was mean area under the curve (AUC) C-peptide during a 2-h mixed-meal tolerance test 1 year after initiation of therapy. Significance was defined as one-sided value < 0.025.
RESULTS - The 1-year mean AUC C-peptide was significantly higher in subjects treated with ATG (0.646 nmol/L) versus placebo (0.406 nmol/L) ( = 0.0003) but not in those treated with ATG/GCSF (0.528 nmol/L) versus placebo ( = 0.031). HbA was significantly reduced at 1 year in subjects treated with ATG and ATG/GCSF, = 0.002 and 0.011, respectively.
CONCLUSIONS - Low-dose ATG slowed decline of C-peptide and reduced HbA in new-onset T1D. Addition of GCSF did not enhance C-peptide preservation afforded by low-dose ATG. Future studies should be considered to determine whether low-dose ATG alone or in combination with other agents may prevent or delay the onset of the disease.
© 2018 by the American Diabetes Association.
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Development of Aggressive Pancreatic Ductal Adenocarcinomas Depends on Granulocyte Colony Stimulating Factor Secretion in Carcinoma Cells.
Pickup MW, Owens P, Gorska AE, Chytil A, Ye F, Shi C, Weaver VM, Kalluri R, Moses HL, Novitskiy SV
(2017) Cancer Immunol Res 5: 718-729
MeSH Terms: Adenocarcinoma, Animals, Carcinoma, Pancreatic Ductal, Cell Proliferation, Disease Models, Animal, Disease Progression, Gene Expression Regulation, Neoplastic, Granulocyte Colony-Stimulating Factor, Humans, Interferon-Stimulated Gene Factor 3, gamma Subunit, Mice, Mice, Knockout, Proto-Oncogene Proteins p21(ras), Signal Transduction, T-Lymphocytes, Transforming Growth Factor beta
Show Abstract · Added July 17, 2019
The survival rate for pancreatic ductal adenocarcinoma (PDAC) remains low. More therapeutic options to treat this disease are needed, for the current standard of care is ineffective. Using an animal model of aggressive PDAC (Kras/p48), we discovered an effect of TGFβ signaling in regulation of G-CSF secretion in pancreatic epithelium. Elevated concentrations of G-CSF in PDAC promoted differentiation of Ly6G cells from progenitors, stimulated IL10 secretion from myeloid cells, and decreased T-cell proliferation via upregulation of Arg, iNOS, VEGF, IL6, and IL1b from CD11b cells. Deletion of in PDAC cells or use of a G-CSF-blocking antibody decreased tumor growth. Anti-G-CSF treatment in combination with the DNA synthesis inhibitor gemcitabine reduced tumor size, increased the number of infiltrating T cells, and decreased the number of Ly6G cells more effectively than gemcitabine alone. Human analysis of human datasets from The Cancer Genome Atlas and tissue microarrays correlated with observations from our mouse model experiments, especially in patients with grade 1, stage II disease. We propose that in aggressive PDAC, elevated G-CSF contributes to tumor progression through promoting increases in infiltration of neutrophil-like cells with high immunosuppressive activity. Such a mechanism provides an avenue for a neoadjuvant therapeutic approach for this devastating disease. .
©2017 American Association for Cancer Research.
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A Two-Biomarker Model Predicts Mortality in the Critically Ill with Sepsis.
Mikacenic C, Price BL, Harju-Baker S, O'Mahony DS, Robinson-Cohen C, Radella F, Hahn WO, Katz R, Christiani DC, Himmelfarb J, Liles WC, Wurfel MM
(2017) Am J Respir Crit Care Med 196: 1004-1011
MeSH Terms: Adult, Aged, Aged, 80 and over, Angiopoietins, Biomarkers, Cohort Studies, Critical Illness, Female, Granulocyte Colony-Stimulating Factor, Humans, Male, Middle Aged, Predictive Value of Tests, Prospective Studies, Sepsis, Systemic Inflammatory Response Syndrome, Tumor Necrosis Factor-alpha, Vascular Cell Adhesion Molecule-1
Show Abstract · Added September 19, 2017
RATIONALE - Improving the prospective identification of patients with systemic inflammatory response syndrome (SIRS) and sepsis at low risk for organ dysfunction and death is a major clinical challenge.
OBJECTIVES - To develop and validate a multibiomarker-based prediction model for 28-day mortality in critically ill patients with SIRS and sepsis.
METHODS - A derivation cohort (n = 888) and internal test cohort (n = 278) were taken from a prospective study of critically ill intensive care unit (ICU) patients meeting two of four SIRS criteria at an academic medical center for whom plasma was obtained within 24 hours. The validation cohort (n = 759) was taken from a prospective cohort enrolled at another academic medical center ICU for whom plasma was obtained within 48 hours. We measured concentrations of angiopoietin-1, angiopoietin-2, IL-6, IL-8, soluble tumor necrosis factor receptor-1, soluble vascular cell adhesion molecule-1, granulocyte colony-stimulating factor, and soluble Fas.
MEASUREMENTS AND MAIN RESULTS - We identified a two-biomarker model in the derivation cohort that predicted mortality (area under the receiver operator characteristic curve [AUC], 0.79; 95% confidence interval [CI], 0.74-0.83). It performed well in the internal test cohort (AUC, 0.75; 95% CI, 0.65-0.85) and the external validation cohort (AUC, 0.77; 95% CI, 0.72-0.83). We determined a model score threshold demonstrating high negative predictive value (0.95) for death. In addition to a low risk of death, patients below this threshold had shorter ICU length of stay, lower incidence of acute kidney injury, acute respiratory distress syndrome, and need for vasopressors.
CONCLUSIONS - We have developed a simple, robust biomarker-based model that identifies patients with SIRS/sepsis at low risk for death and organ dysfunction.
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The role of MyD88- and TRIF-dependent signaling in monophosphoryl lipid A-induced expansion and recruitment of innate immunocytes.
Hernandez A, Bohannon JK, Luan L, Fensterheim BA, Guo Y, Patil NK, McAdams C, Wang J, Sherwood ER
(2016) J Leukoc Biol 100: 1311-1322
MeSH Terms: Adaptor Proteins, Vesicular Transport, Animals, CD11b Antigen, Chemokine CXCL1, Chemokine CXCL2, Chemotaxis, Leukocyte, Granulocyte Colony-Stimulating Factor, Immunity, Innate, L-Selectin, Lipid A, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Monocytes, Myeloid Differentiation Factor 88, Myelopoiesis, Neutrophils, Receptors, Interleukin-8B, Signal Transduction, Toll-Like Receptor 4
Show Abstract · Added December 13, 2016
Treatment with the TLR4 agonist MPLA augments innate resistance to common bacterial pathogens. However, the cellular and molecular mechanisms by which MPLA augments innate immunocyte functions are not well characterized. This study examined the importance of MyD88- and TRIF-dependent signaling for leukocyte mobilization, recruitment, and activation following administration of MPLA. MPLA potently induced MyD88- and TRIF-dependent signaling. A single injection of MPLA caused rapid mobilization and recruitment of neutrophils, a response that was largely mediated by the chemokines CXCL1 and -2 and the hemopoietic factor G-CSF. Rapid neutrophil recruitment and chemokine production were regulated by both pathways although the MyD88-dependent pathway showed some predominance. In further studies, multiple injections of MPLA potently induced mobilization and recruitment of neutrophils and monocytes. Neutrophil recruitment after multiple injections of MPLA was reliant on MyD88-dependent signaling, but effective monocyte recruitment required activation of both pathways. MPLA treatment induced expansion of myeloid progenitors in bone marrow and upregulation of CD11b and shedding of L-selectin by neutrophils, all of which were attenuated in MyD88- and TRIF-deficient mice. These results show that MPLA-induced neutrophil and monocyte recruitment, expansion of bone marrow progenitors and augmentation of neutrophil adhesion molecule expression are regulated by both the MyD88- and TRIF-dependent pathways.
© Society for Leukocyte Biology.
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21 MeSH Terms
Role of G-CSF in monophosphoryl lipid A-mediated augmentation of neutrophil functions after burn injury.
Bohannon JK, Luan L, Hernandez A, Afzal A, Guo Y, Patil NK, Fensterheim B, Sherwood ER
(2016) J Leukoc Biol 99: 629-40
MeSH Terms: Animals, Burns, Granulocyte Colony-Stimulating Factor, Lipid A, Mice, Mice, Inbred BALB C, Neutrophil Infiltration, Neutrophils, Pseudomonas Infections, Pseudomonas aeruginosa, Receptors, CXCR4
Show Abstract · Added February 18, 2016
Infection is the leading cause of death in severely burned patients that survive the acute phase of injury. Neutrophils are the first line of defense against infections, but hospitalized burn patients frequently cannot mount an appropriate innate response to infection. Thus, immune therapeutic approaches aimed at improving neutrophil functions after burn injury may be beneficial. Prophylactic treatment with the TLR4 agonist monophosphoryl lipid A is known to augment resistance to infection by enhancing neutrophil recruitment and facilitating bacterial clearance. This study aimed to define mechanisms by which monophosphoryl lipid A treatment improves bacterial clearance and survival in a model of burn-wound sepsis. Burn-injured mice were treated with monophosphoryl lipid A or vehicle, and neutrophil mobilization was evaluated in the presence or absence of Pseudomonas aeruginosa infection. Monophosphoryl lipid A treatment induced significant mobilization of neutrophils from the bone marrow into the blood and sites of infection. Neutrophil mobilization was associated with decreased bone marrow neutrophil CXCR4 expression and increased plasma G-CSF concentrations. Neutralization of G-CSF before monophosphoryl lipid A administration blocked monophosphoryl lipid A-induced expansion of bone marrow myeloid progenitors and mobilization of neutrophils into the blood and their recruitment to the site of infection. G-CSF neutralization ablated the enhanced bacterial clearance and survival benefit endowed by monophosphoryl lipid A in burn-wound-infected mice. Our findings provide convincing evidence that monophosphoryl lipid A-induced G-CSF facilitates early expansion, mobilization, and recruitment of neutrophils to the site of infection after burn injury, allowing for a robust immune response to infection.
© Society for Leukocyte Biology.
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11 MeSH Terms
Granulocyte colony stimulating factor secreting hepatocellular carcinoma.
Snyder RA, Liu E, Merchant NB
(2012) Am Surg 78: 821-2
MeSH Terms: Biomarkers, Tumor, Carcinoma, Hepatocellular, Fatal Outcome, Female, Granulocyte Colony-Stimulating Factor, Humans, Leukocytosis, Liver Neoplasms, Middle Aged
Added March 7, 2014
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9 MeSH Terms
The combined expression of metaplasia biomarkers predicts the prognosis of gastric cancer.
Suh YS, Lee HJ, Jung EJ, Kim MA, Nam KT, Goldenring JR, Yang HK, Kim WH
(2012) Ann Surg Oncol 19: 1240-9
MeSH Terms: Adenocarcinoma, Biomarkers, Tumor, Cadherins, Female, Galectin 4, Gene Expression Profiling, Granulocyte Colony-Stimulating Factor, Humans, Immunohistochemistry, Keratin-20, Lectins, C-Type, Male, Metaplasia, Middle Aged, Mucin 5AC, Mucins, Neoplasm Staging, Pancreatitis-Associated Proteins, Prognosis, Stomach Neoplasms
Show Abstract · Added September 3, 2013
BACKGROUND - Our previous study indicated that gene expression profiling of intestinal metaplasia (IM) or spasmolytic polypeptide-expressing metaplasia (SPEM) can identify useful prognostic markers of early-stage gastric cancer, and seven metaplasia biomarkers (MUC13, CDH17, OLFM4, KRT20, LGALS4, MUC5AC, and REG4) were selectively expressed in 17-50% of gastric cancer tissues. We investigated whether the combined expression of these metaplasia biomarkers could predict the prognosis of advanced stage gastric cancer.
METHODS - The expression of seven metaplasia biomarkers was evaluated immunohistochemically using tissue microarrays comprised of 450 gastric cancer patients. The clinicopathologic correlations and the prognostic impact were analyzed according to the expression of multiple biomarkers.
RESULTS - MUC13, CDH17, LGALS4, and REG4 were significant prognostic biomarkers in univariate analysis. No expression of four markers was found in 56 cases (14.2%); 1 marker was seen in 67 cases (17%), 2 in 106 cases (27%), 3 in 101 cases (25.7%), and 4 in 63 cases (16%). Patients in which two or fewer proteins were expressed (group B) showed younger age, undifferentiated or diffuse type cancer, larger tumor size, larger number of metastatic lymph nodes, and more advanced stage than those in which three or more proteins were expressed (group A). In undifferentiated or stage II/III gastric cancer, the prognosis of group B was significantly poorer than that of group A by multivariate analysis.
CONCLUSIONS - The combined loss of expression of multiple metaplasia biomarkers is considered an independent prognostic indicator in undifferentiated or stage II/III gastric cancer.
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20 MeSH Terms
Comparison of outcomes after transplantation of G-CSF-stimulated bone marrow grafts versus bone marrow or peripheral blood grafts from HLA-matched sibling donors for patients with severe aplastic anemia.
Chu R, Brazauskas R, Kan F, Bashey A, Bredeson C, Camitta B, Chiang KY, Frangoul H, Gale RP, Gee A, George B, Goldman FD, Gross TG, Gupta V, Hale GA, Isola L, Ispizua AU, Lazarus H, Marsh J, Russell J, Sabloff M, Waller EK, Eapen M
(2011) Biol Blood Marrow Transplant 17: 1018-24
MeSH Terms: Adolescent, Adult, Anemia, Aplastic, Bone Marrow, Bone Marrow Transplantation, Cause of Death, Child, Female, Graft vs Host Disease, Granulocyte Colony-Stimulating Factor, HLA Antigens, Hematopoietic Stem Cell Mobilization, Histocompatibility, Humans, Leukocyte Count, Living Donors, Male, Middle Aged, Peripheral Blood Stem Cell Transplantation, Platelet Count, Postoperative Complications, Registries, Retrospective Studies, Siblings, Survival Rate, Transplantation Conditioning, Transplantation, Homologous, Treatment Outcome, Young Adult
Show Abstract · Added March 27, 2014
We compared outcomes of patients with severe aplastic anemia (SAA) who received granulocyte-colony stimulating factor (G-CSF)-stimulated bone marrow (G-BM) (n = 78), unstimulated bone marrow (BM) (n = 547), or peripheral blood progenitor cells (PBPC) (n = 134) from an HLA-matched sibling. Transplantations occurred in 1997 to 2003. Rates of neutrophil and platelet recovery were not different among the 3 treatment groups. Grade 2-4 acute graft-versus-host disease (aGVHD) (relative risk [RR] = 0.82, P = .539), grade 3-4 aGVHD (RR = 0.74, P = .535), and chronic GVHD (cGVHD) (RR = 1.56, P = .229) were similar after G-BM and BM transplants. Grade 2-4 aGVHD (RR = 2.37, P = .012) but not grade 3-4 aGVHD (RR = 1.66, P = .323) and cGVHD (RR = 5.09, P < .001) were higher after PBPC transplants compared to G-BM. Grade 2-4 (RR = 2.90, P < .001), grade 3-4 (RR = 2.24, P = .009) aGVHD and cGVHD (RR = 3.26, P < .001) were higher after PBPC transplants compared to BM. Mortality risks were lower after transplantation of BM compared to G-BM (RR = 0.63, P = .05). These data suggest no advantage to using G-BM and the observed higher rates of aGVHD and cGVHD in PBPC recipients warrants cautious use of this graft source for SAA. Taken together, BM is the preferred graft for HLA-matched sibling transplants for SAA.
2011 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
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29 MeSH Terms
Gene expression profiling of metaplastic lineages identifies CDH17 as a prognostic marker in early stage gastric cancer.
Lee HJ, Nam KT, Park HS, Kim MA, Lafleur BJ, Aburatani H, Yang HK, Kim WH, Goldenring JR
(2010) Gastroenterology 139: 213-25.e3
MeSH Terms: Aged, Biomarkers, Tumor, Cadherins, Female, Gastric Mucosa, Gene Expression Profiling, Granulocyte Colony-Stimulating Factor, Humans, Intercellular Signaling Peptides and Proteins, Male, Metaplasia, Middle Aged, Mucins, Multivariate Analysis, Neoplasm Staging, Peptides, Prognosis, Stomach Neoplasms
Show Abstract · Added October 7, 2013
BACKGROUND & AIMS - Intestinal metaplasia (IM) and spasmolytic polypeptide-expressing metaplasia (SPEM) are precursors to gastric carcinogenesis. We sought to identify molecular biomarkers of gastric metaplasias and gastric cancer by gene expression profiling of metaplastic lesions from patients.
METHODS - Complementary DNA microarray analysis was performed on IM and SPEM cells isolated from patient samples using laser capture microdissection. Up-regulated transcripts in metaplastic lesions were confirmed by immunostaining analysis in IM, SPEM, and gastric cancer tissues. Proteins that were highly expressed specifically in gastric cancer tissues were analyzed for their association with survival in a test set (n = 450) and a validation set (n = 502) of samples from gastric cancer patients.
RESULTS - Compared with normal chief cells, 858 genes were differentially expressed in IM or SPEM samples. Immunostaining was detected for 12 proteins, including 3 new markers of IM (ACE2, LGALS4, AKR1B10) and 3 of SPEM (OLFM4, LYZ, DPCR1). Of 13 proteins expressed in IM or SPEM, 8 were expressed by 17%-50% of human gastric cancer tissues (MUC13, OLFM4, CDH17, KRT20, MUC5AC, LGALS4, AKR1B10, REG4). Expression of CDH17 or MUC13 correlated with patient survival in the test and validation sets. Multivariate analysis showed that CDH17 was an independent prognostic factor in patients with stage I or node-negative disease.
CONCLUSIONS - We identified several novel biomarkers for IM, SPEM, and gastric cancer using gene expression profiling of human metaplastic lesions. Expression of CDH17 and MUC13 was up-regulated in gastric cancer tissues. CDH17 is a promising prognostic marker for early stage gastric cancer.
Copyright 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
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Autologous stem cell transplant in a patient with Down syndrome and relapsed Hodgkin lymphoma.
Eckrich MJ, Domm J, Ho R, Whitlock JA, Frangoul H
(2009) Pediatr Blood Cancer 53: 1327-8
MeSH Terms: Antineoplastic Combined Chemotherapy Protocols, Bleomycin, Carmustine, Child, Combined Modality Therapy, Cyclophosphamide, Down Syndrome, Doxorubicin, Etoposide, Granulocyte Colony-Stimulating Factor, Hodgkin Disease, Humans, Ifosfamide, Male, Mesna, Peripheral Blood Stem Cell Transplantation, Prednisone, Procarbazine, Recurrence, Remission Induction, Transplantation Conditioning, Transplantation, Autologous, Vinblastine, Vincristine, Vinorelbine
Show Abstract · Added March 5, 2014
Children with Down syndrome (DS) are at increased risk for the development of acute leukemia but they rarely develop other hematologic malignancies or solid tumors. Despite aggressive supportive care, DS patients have increased risk of treatment related morbidity and mortality compared to other children. There are few reported cases of Hodgkin disease in children with DS, and no reported cases of successful therapy for patients with relapsed disease. We report on a child with DS and relapsed Hodgkin disease who was successfully treated with high-dose chemotherapy and autologous stem cell transplant.
(c) 2009 Wiley-Liss, Inc.
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