The Experts below are selected from a list of 270 Experts worldwide ranked by ideXlab platform

John A Hamilton - One of the best experts on this subject based on the ideXlab platform.

  • Colony-Stimulating Factors in inflammation and autoimmunity.
    Nature reviews. Immunology, 2008
    Co-Authors: John A Hamilton
    Abstract:

    Although they were originally defined as haematopoietic-cell growth Factors, Colony-Stimulating Factors (CSFs) have been shown to have additional functions by acting directly on mature myeloid cells. Recent data from animal models indicate that the depletion of CSFs has therapeutic benefit in many inflammatory and/or autoimmune conditions and as a result, early-phase clinical trials targeting granulocyte/macrophage Colony-Stimulating factor and macrophage Colony-Stimulating factor have now commenced. The distinct biological features of CSFs offer opportunities for specific targeting, but with some associated risks. Here, I describe these biological features, discuss the probable specific outcomes of targeting CSFs in vivo and highlight outstanding questions that need to be addressed.

  • the colony stimulating Factors and collagen induced arthritis exacerbation of disease by m csf and g csf and requirement for endogenous m csf
    Journal of Leukocyte Biology, 2000
    Co-Authors: Ian K. Campbell, Robert J. Bischof, Melissa J Rich, John A Hamilton
    Abstract:

    There is increasing evidence that the Colony-Stimulating Factors (CSFs) may play a part in chronic inflammatory autoimmune diseases, such as rheumatoid arthritis (RA). We examined the involvement of macrophage CSF (M-CSF or CSF-1) and granulocyte CSF (G-CSF) in collagen-induced arthritis (CIA), a murine model of RA. Daily injections of M-CSF or G-CSF, 20-24 days postprimary immunization with type II collagen, exacerbated disease symptoms in suboptimally immunized DBA/1 mice. Support for the involvement of endogenous M-CSF in CIA was obtained by studies in which neutralizing monoclonal antibody reduced the severity of established CIA and also by studies showing the resistance of M-CSF-deficient op/op mice to CIA induction. These studies show that M-CSF and G-CSF can be proinflammatory in CIA and provide evidence that macrophage- and granulocyte-lineage cells can exacerbate CIA. Our results also show that M-CSF-dependent cells are essential for CIA development, suggesting M-CSF may be a suitable target for therapeutic intervention in RA.

  • proliferation of a subpopulation of human peripheral blood monocytes in the presence of colony stimulating Factors may contribute to the inflammatory process in diseases such as rheumatoid arthritis
    Immunobiology, 2000
    Co-Authors: Suzanne T Moss, John A Hamilton
    Abstract:

    Apart from acting on hemopoietic progenitor cells, colony stimulating Factors (CSFs) have been shown to be involved in the activation, survival, proliferation and differentiation of more mature cells of the monocyte/macrophage lineage. There is evidence that a proportion of human peripheral blood monocytes can proliferate in response to CSF-1, (also known as M-CSF) and granulocyte-macrophage-CSF (GM-CSF). CSFs have been shown to be at elevated levels in the synovial fluid of RA patients and thus local proliferation of monocyte/macrophage within an inflamed lesion may contribute to the local tissue hyperplasia evident in inflammatory conditions. Flow cytometric analysis of surface antigen expression and cytokine production in response to lipopolysaccharide stimulation has been used to characterise the proliferating subpopulation of monocytes. Further characterization and subsequent isolation of this subpopulation of monocytes may provide new and important information necessary in understanding inflammatory diseases such as rheumatoid arthritis, where local proliferation at the site of inflammation may be a key factor contributing to the chronicity of the disease.

  • Exacerbation of acute inflammatory arthritis by the Colony-Stimulating Factors CSF-1 and granulocyte macrophage (GM)-CSF: evidence of macrophage infiltration and local proliferation.
    Clinical and experimental immunology, 2000
    Co-Authors: Robert J. Bischof, John A Hamilton, D Zafiropoulos, Ian K. Campbell
    Abstract:

    CSF-1 and GM-CSF have been implicated in the pathogenesis of rheumatoid arthritis. We report the effects of CSF-1 and GM-CSF in the development of an acute methylated bovine serum albumin (mBSA)-induced murine arthritis model. Examination of histopathological features revealed that the systemic administration of CSF-1 or GM-CSF following mBSA administration into the knee resulted in the exacerbation of arthritis. This included synovial hyperplasia and joint inflammation, most evident at 7 and 14 days post-mBSA administration, and the appearance of erosive pannus tissue. The exacerbation by CSF-1 and GM-CSF was not sustained but declined in incidence and severity by 21 days post-mBSA administration, similar to the effects of IL-1β in this model, reported here and previously. Macrophages expressing Mac-2 and F4/80 were a prominent feature of the pathology observed, particularly the infiltration of Mac-2+ macrophages seen in all mice administered CSF-1, GM-CSF or IL-1β. Present in inflamed knees was a locally dividing population of cells which included Mac-2+ and F4/80+ macrophages. These studies demonstrate that CSF-1 and GM-CSF can exacerbate and prolong the histopathology of acute inflammatory arthritis and lend support to monocytes/macrophages being a driving influence in the pathogenesis of inflammatory arthritis.

  • regulation of pinocytosis in murine macrophages by colony stimulating Factors and other agents
    Journal of Leukocyte Biology, 1992
    Co-Authors: Kenneth R Knight, Gino Vairo, John A Hamilton
    Abstract:

    Lucifer yellow (LY) accumulation was used to measure macrophage pinocytosis. The hematopoietic growth Factors, macrophage Colony-Stimulating factor (CSF-1), granulocyte-macrophage CSF (GM-CSF), and interleukin 3, and the macrophage activators, lipopoly- saccharide and zymosan, all stimulated LY uptake in both murine bone marrow-derived macrophages (BMMs) and resident peritoneal macrophages (RPMs) without affecting LY efflux. The stimulation of pinocytosis in the poorly cycling RPMs and in BMMs by nonmitogens dis- sociates stimulation of pinocytosis from subsequent DNA synthesis. Regulation of pinocytosis in BMMs appears to be independent of that of urokinase-type plasminogen ac- tivator expression. The increases in CSF-mediated BMM pinocytosis were not inhibited by pertussis toxin, by ele- vations in intracellular CAMP, or by glucocorticoids and were only partially inhibited by inhibitors of Na�/W an- tiport and Na�/K�-ATPase activities. Protein kinase C ac- tivation could be involved in regulating BMM pinocyto- sis because phorbol myristate acetate, oleoylacyglycerol, and exogenously added phospholipase C can all stimulate it. Ca2� ionophores were inactive, whereas the Na�/W ionophore monensin potently inhibited BMM pinocytosis. J. Leu.koc. Biol. 51: 350-359; 1992.

G. P. Dutta - One of the best experts on this subject based on the ideXlab platform.

  • comparative evaluation of the colony stimulating Factors induction potential of plasmodium cynomolgi infected monkey erythrocytes and soluble antigens
    Acta Tropica, 1992
    Co-Authors: P P Singh, G. P. Dutta
    Abstract:

    Plasmodium cynomolgi total antigens soluble in culture medium (P.c.SA), and noninfective P. cynomolgi-infected monkey erythrocytes (P.c.IE) were compared for their potential to induce Colony-Stimulating Factors (CSFs). When injected intravenously in monkeys, both preparations induced an increase in the serum CSFs levels; P.c.IE appeared to be 1.6-fold more potent than the P.c.SA. In vitro P.c.IE induced 1.8-fold more CSF by monkey blood monocyte-derived macrophages than P.c. However, both in vivo and in vitro, the peak CSFs levels induced by P.c.SA were attained apparently 8 h earlier. CSF generated by P.c.SA and P.c.IE induced the formation of macrophage, granulocyte and granulocyte-macrophage colonies, in vitro; P.c.IE-generated CSF induced the formation of significantly (P<0.01) higher numbers of granulocyte-macrophage colonies, indicating that the CSF induced by them stimulated different biological responses. The CSF induction appeared to be LPS-independent.

  • Comparative evaluation of the Colony-Stimulating Factors induction potential of Plasmodium cynomolgi-infected monkey erythrocytes and soluble antigens.
    Acta tropica, 1992
    Co-Authors: P P Singh, G. P. Dutta
    Abstract:

    Plasmodium cynomolgi total antigens soluble in culture medium (P.c.SA), and noninfective P. cynomolgi-infected monkey erythrocytes (P.c.IE) were compared for their potential to induce Colony-Stimulating Factors (CSFs). When injected intravenously in monkeys, both preparations induced an increase in the serum CSFs levels; P.c.IE appeared to be 1.6-fold more potent than the P.c.SA. In vitro P.c.IE induced 1.8-fold more CSF by monkey blood monocyte-derived macrophages than P.c. However, both in vivo and in vitro, the peak CSFs levels induced by P.c.SA were attained apparently 8 h earlier. CSF generated by P.c.SA and P.c.IE induced the formation of macrophage, granulocyte and granulocyte-macrophage colonies, in vitro; P.c.IE-generated CSF induced the formation of significantly (P

  • induction of colony stimulating Factors by plasmodium cynomolgi components
    Journal of Biological Regulators and Homeostatic Agents, 1991
    Co-Authors: P P Singh, G. P. Dutta
    Abstract:

    Plasmodium cynomolgi total parasite antigens soluble in culture medium (P.c.SA), when injected in monkeys (Macaca mulatta) intravenously, induced the synthesis and secretion of serum Colony-Stimulating Factors (CSFs). In vitro cultured monkey splenic macrophages and blood monocytes, following incubation with P.c.SA, also elaborated CSFs: the splenic macrophages responded more. Peak CSFs levels, both in vivo and in vitro, were attained after 8 hours of P.c.SA stimulation, and thereafter declined to baseline values within 48 hours. CSFs, both in serum and in conditioned medium, induced the formation of macrophage, granulocyte and granulocyte-macrophage colonies in vitro, in the same proportion, indicating that committed progenitor cells responded to CSF from both sources in a similar way. Polymyxin B treatment had no effect on P.c.SA stimulated CSF elaboration by macrophages, suggesting an LPS-independent mechanism of CSF induction. CSF synthesis appeared to be de novo, as cycloheximide treatment of macrophages completely inhibited CSF production. These observations indicate that P. cynomolgi components can induce CSF synthesis.

  • Enkephalins-modulation of Plasmodium cynomolgi antigens-induced Colony-Stimulating Factors elaboration by macrophages.
    Journal of biological regulators and homeostatic agents, 1991
    Co-Authors: Pal Singh, G. P. Dutta, Savita Singh, V.c. Dhawan, W. Haq, K. B. Mathur, R.c. Srimal
    Abstract:

    Methionine-enkephalin (M-Enk) and its analogue compound 82/205 (10(-5) and 10(-6) M) inhibited elaboration of Plasmodium cynomolgi total antigens soluble in culture medium (P.c.SA)-induced Colony-Stimulating Factors (CSFs) by monkey blood monocyte-derived macrophages, in vitro. Paradoxically, lower concentrations (10(-7)-10(-9) M) of both the peptides greatly augmented CSFs elaboration; 82/205 appeared to be nearly 2.3-fold more potent. Naloxone (10(-5) M) pretreatment of macrophages inhibited only the M-Enk- and 82/205-induced enhanced CSFs elaboration, suggesting an opiate receptors-mediated mechanism of action. None of the peptides or naloxone (10(-5)-10(-9) M) had any direct effect on the CSF elaboration by unstimulated macrophages.

Thomas J Smith - One of the best experts on this subject based on the ideXlab platform.

  • recommendations for the use of wbc growth Factors american society of clinical oncology clinical practice guideline update
    Journal of Clinical Oncology, 2015
    Co-Authors: Thomas J Smith, Gary H Lyman, Jeffrey Crawford, Kari Bohlke, Kenneth R Carson, Scott J Cross, John M Goldberg, James Khatcheressian, Natasha B Leighl, Cheryl L Perkins
    Abstract:

    Purpose To update the 2006 American Society of Clinical Oncology guideline on the use of hematopoietic Colony-Stimulating Factors (CSFs). Methods The American Society of Clinical Oncology convened an Update Committee and conducted a systematic review of randomized clinical trials, meta-analyses, and systematic reviews from October 2005 through September 2014. Guideline recommendations were based on the review of the evidence by the Update Committee. Results Changes to previous recommendations include the addition of tbo-filgrastim and filgrastim-sndz, moderation of the recommendation regarding routine use of CSFs in older patients with diffuse aggressive lymphoma, and addition of recommendations against routine dose-dense chemotherapy in lymphoma and in favor of high–dose-intensity chemotherapy in urothelial cancer. The Update Committee did not address recommendations regarding use of CSFs in acute myeloid leukemia or myelodysplastic syndromes in adults. Recommendations Prophylactic use of CSFs to reduce ...

  • THE ASCO EXPERIENCE WITH EVIDENCE-BASED CLINICAL PRACTICE GUIDELINES
    Oncology, 1997
    Co-Authors: Thomas J Smith, Mark R. Somerfield
    Abstract:

    After strong demand from members, the American Society of Clinical Oncology (ASCO) began, in 1992, to formulate clinical practice guidelines. Guidelines were written for the following: outcomes from cancer treatment, hematopoietic Colony-Stimulating Factors, tumor markers for breast and colorectal cancer, surveillance of breast cancer patients, and management of non-small-cell lung cancer. Further guidelines are being drafted for management of advanced prostate cancer, antiemetics, bisphosphonates in breast cancer and myeloma, chemoprotectants, and surveillance of colorectal cancer patients. This article explores the process by which ASCO guidelines are drafted, as well problems with these guidelines. Suggestions are made for ASCO and other professional groups that anticipate framing a set of guidelines.

  • Economic analysis of the clinical uses of the Colony-Stimulating Factors.
    Current opinion in hematology, 1996
    Co-Authors: Thomas J Smith
    Abstract:

    Colony-Stimulating Factors can reduce the morbidity and possibly the mortality from some types of cancer treatment. Reductions in hospitalization and supportive care, eg, transfusion requirements and antibiotics, have been documented in several clinical trials and can lead to lower total care costs. However, the high cost of Colony-Stimulating Factors and the necessity to treat large numbers of patients who do not benefit can offset the economic gains, unless the savings in hospitalization and supportive care are substantial. Primary prophylaxis with Colony-Stimulating Factors is cost-saving only if the rate of hospitalization for febrile neutropenia is 40% or more; no current standard regimens are near that figure. In general, the American Society of Clinical Oncology clinical practice guide-lines for the use of Colony-Stimulating Factors lead to effective and cost-conscious use of these expensive growth Factors. Colony-Stimulating Factors are not recommended for primary prophylaxis of febrile neutropenia, are recommended for secondary prophylaxis if dose-reduction is not appropriate, and are recommended for stimulation of hematopoietic progenitor cells and reconstitution after high-dose chemotherapy. Further expansion of use based on economic Factors will depend on documented survival benefit, major improvements in supportive care due to Colony-Stimulating Factors, or markedly lower costs of Colony-Stimulating Factors.

P P Singh - One of the best experts on this subject based on the ideXlab platform.

  • comparative evaluation of the colony stimulating Factors induction potential of plasmodium cynomolgi infected monkey erythrocytes and soluble antigens
    Acta Tropica, 1992
    Co-Authors: P P Singh, G. P. Dutta
    Abstract:

    Plasmodium cynomolgi total antigens soluble in culture medium (P.c.SA), and noninfective P. cynomolgi-infected monkey erythrocytes (P.c.IE) were compared for their potential to induce Colony-Stimulating Factors (CSFs). When injected intravenously in monkeys, both preparations induced an increase in the serum CSFs levels; P.c.IE appeared to be 1.6-fold more potent than the P.c.SA. In vitro P.c.IE induced 1.8-fold more CSF by monkey blood monocyte-derived macrophages than P.c. However, both in vivo and in vitro, the peak CSFs levels induced by P.c.SA were attained apparently 8 h earlier. CSF generated by P.c.SA and P.c.IE induced the formation of macrophage, granulocyte and granulocyte-macrophage colonies, in vitro; P.c.IE-generated CSF induced the formation of significantly (P<0.01) higher numbers of granulocyte-macrophage colonies, indicating that the CSF induced by them stimulated different biological responses. The CSF induction appeared to be LPS-independent.

  • Comparative evaluation of the Colony-Stimulating Factors induction potential of Plasmodium cynomolgi-infected monkey erythrocytes and soluble antigens.
    Acta tropica, 1992
    Co-Authors: P P Singh, G. P. Dutta
    Abstract:

    Plasmodium cynomolgi total antigens soluble in culture medium (P.c.SA), and noninfective P. cynomolgi-infected monkey erythrocytes (P.c.IE) were compared for their potential to induce Colony-Stimulating Factors (CSFs). When injected intravenously in monkeys, both preparations induced an increase in the serum CSFs levels; P.c.IE appeared to be 1.6-fold more potent than the P.c.SA. In vitro P.c.IE induced 1.8-fold more CSF by monkey blood monocyte-derived macrophages than P.c. However, both in vivo and in vitro, the peak CSFs levels induced by P.c.SA were attained apparently 8 h earlier. CSF generated by P.c.SA and P.c.IE induced the formation of macrophage, granulocyte and granulocyte-macrophage colonies, in vitro; P.c.IE-generated CSF induced the formation of significantly (P

  • induction of colony stimulating Factors by plasmodium cynomolgi components
    Journal of Biological Regulators and Homeostatic Agents, 1991
    Co-Authors: P P Singh, G. P. Dutta
    Abstract:

    Plasmodium cynomolgi total parasite antigens soluble in culture medium (P.c.SA), when injected in monkeys (Macaca mulatta) intravenously, induced the synthesis and secretion of serum Colony-Stimulating Factors (CSFs). In vitro cultured monkey splenic macrophages and blood monocytes, following incubation with P.c.SA, also elaborated CSFs: the splenic macrophages responded more. Peak CSFs levels, both in vivo and in vitro, were attained after 8 hours of P.c.SA stimulation, and thereafter declined to baseline values within 48 hours. CSFs, both in serum and in conditioned medium, induced the formation of macrophage, granulocyte and granulocyte-macrophage colonies in vitro, in the same proportion, indicating that committed progenitor cells responded to CSF from both sources in a similar way. Polymyxin B treatment had no effect on P.c.SA stimulated CSF elaboration by macrophages, suggesting an LPS-independent mechanism of CSF induction. CSF synthesis appeared to be de novo, as cycloheximide treatment of macrophages completely inhibited CSF production. These observations indicate that P. cynomolgi components can induce CSF synthesis.

Gary H Lyman - One of the best experts on this subject based on the ideXlab platform.

  • recommendations for the use of wbc growth Factors american society of clinical oncology clinical practice guideline update
    Journal of Clinical Oncology, 2015
    Co-Authors: Thomas J Smith, Gary H Lyman, Jeffrey Crawford, Kari Bohlke, Kenneth R Carson, Scott J Cross, John M Goldberg, James Khatcheressian, Natasha B Leighl, Cheryl L Perkins
    Abstract:

    Purpose To update the 2006 American Society of Clinical Oncology guideline on the use of hematopoietic Colony-Stimulating Factors (CSFs). Methods The American Society of Clinical Oncology convened an Update Committee and conducted a systematic review of randomized clinical trials, meta-analyses, and systematic reviews from October 2005 through September 2014. Guideline recommendations were based on the review of the evidence by the Update Committee. Results Changes to previous recommendations include the addition of tbo-filgrastim and filgrastim-sndz, moderation of the recommendation regarding routine use of CSFs in older patients with diffuse aggressive lymphoma, and addition of recommendations against routine dose-dense chemotherapy in lymphoma and in favor of high–dose-intensity chemotherapy in urothelial cancer. The Update Committee did not address recommendations regarding use of CSFs in acute myeloid leukemia or myelodysplastic syndromes in adults. Recommendations Prophylactic use of CSFs to reduce ...

  • Agents under investigation for the treatment and prevention of neutropenia.
    Expert Opinion on Investigational Drugs, 2007
    Co-Authors: Alissa Huston, Gary H Lyman
    Abstract:

    Neutropenia, and most notably febrile neutropenia, represents a significant complication following chemotherapy administration. Present agents used for the treatment of neutropenia include G-CSF, GM-CSF and G-CSF conjugated to polyethylene glycol (PEG) as pegylated G-CSF. Despite the availability and considerable efficacy of the above approved agents in reducing the risk of neutropenia and its complications remain significant issues in oncology. This article explores some of the biology behind the Colony-Stimulating Factors and the recent advances in agents for the treatment and prevention of neutropenia, including the development of additional G-CSF agonists, chemoprotectants, retinoic receptor agonists and CXC chemokine receptor 4 antagonists.

  • impact of primary prophylaxis with granulocyte colony stimulating factor on febrile neutropenia and mortality in adult cancer patients receiving chemotherapy a systematic review
    Journal of Clinical Oncology, 2007
    Co-Authors: Nicole M Kuderer, D C Dale, Jeffrey Crawford, Gary H Lyman
    Abstract:

    Purpose Randomized controlled trials (RCTs) of prophylactic granulocyte Colony-Stimulating Factors (G-CSF) have demonstrated a significant reduction in febrile neutropenia (FN) after systemic chemotherapy. Several RCTs have been published recently that investigate the impact of G-CSF on mortality and relative dose-intensity (RDI). Methods A comprehensive systematic review and meta-analysis of all reported RCTs comparing primary prophylactic G-CSF with placebo or untreated controls in adult solid tumor and malignant lymphoma patients was undertaken without language restrictions, using electronic databases, conference proceedings, and hand-searching techniques. Two reviewers extracted data independently. Summary estimates of relative risk (RR) with 95% CIs were estimated based on the method of Mantel-Haenszel and DerSimonian and Laird. Results Seventeen RCTs were identified including 3,493 patients. For infection-related mortality, RR reduction with G-CSF compared with controls was 45% (RR = 0.55; 95% CI, 0...

  • A cost analysis of hematopoietic Colony-Stimulating Factors.
    Oncology (Williston Park N.Y.), 1995
    Co-Authors: Gary H Lyman, Frcp, Lodovico Balducci
    Abstract:

    The administration of hematopoietic Colony-Stimulating Factors (CSFs) to reduce the severity and duration of neutropenia associated with systemic chemotherapy has become widespread, although the appropriate use of