Research Topics
Species | E ShacterSummaryAffiliation: Food and Drug Administration Country: USA Publications
| Collaborators
|
Detail Information
Publications
Oxidative stress interferes with cancer chemotherapy: inhibition of lymphoma cell apoptosis and phagocytosisE Shacter
Laboratory of Immunology, Division of Therapeutic Proteins, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD, USA
Blood 96:307-13. 2000..The results suggest that chemotherapy-induced apoptosis and phagocytosis of cancer cells may be enhanced by including certain antioxidant agents in the treatment protocol...
Re-processing of biological products: regulatory considerations from the CBER perspectiveE Shacter
Division of Therapeutic Proteins, CBER, FDA, Rockville, Maryland 20852, USA
Dev Biol (Basel) 113:105-7; discussion 115-6. 2003
Chronic inflammation and cancerEmily Shacter
Laboratory of Immunology, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892 4555, USA
Oncology (Williston Park) 16:217-26, 229; discussion 230-2. 2002..A thorough understanding of the molecular basis of inflammation-associated neoplasia and progression can lead to novel approaches to the prevention and treatment of cancer...
Oxidative stress inhibits the phagocytosis of apoptotic cells that have externalized phosphatidylserineH A Anderson
Laboratory of Immunology, Division of Therapeutic Proteins, Bethesda, MD 20892, USA
Cell Death Differ 9:616-25. 2002..Another phagocytosis recognition factor must therefore exist to facilitate uptake of apoptotic cells, and this factor is sensitive to modification by H(2)O(2)...
Oxidant-induced apoptosis is mediated by oxidation of the actin-regulatory protein cofilinFabio Klamt
Laboratory of Biochemistry, Division of Therapeutic Proteins, Center for Drug Evaluation and Research, Food and Drug Administration, Bethesda, MD 20892, USA
Nat Cell Biol 11:1241-6. 2009..Exposure of cofilin to TnCl results in intramolecular disulphide bonding and oxidation of Met residues to Met sulphoxide, but only Cys oxidation causes cofilin to induce mitochondrial damage...
Rac1 inhibits apoptosis in human lymphoma cells by stimulating Bad phosphorylation on Ser-75Baolin Zhang
Laboratory of Biochemistry, Division of Therapeutic Proteins, Office of Biotechnology Products, Center for Drug Evaluation and Research, Food and Drug Administration, Bethesda, MD 20892 4555, USA
Mol Cell Biol 24:6205-14. 2004..These findings define a mechanism by which active Rac1 promotes lymphoma cell survival and inhibits apoptosis in response to cancer chemotherapy drugs...
Caspase 3-mediated inactivation of rac GTPases promotes drug-induced apoptosis in human lymphoma cellsBaolin Zhang
Laboratory of Biochemistry, Division of Therapeutic Proteins, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA
Mol Cell Biol 23:5716-25. 2003..Thus, proteolytic inactivation of Rac GTPases represents a novel, irreversible mechanism of Rac downregulation that allows maximal cell death following drug treatment...
Rho GDP dissociation inhibitor protects cancer cells against drug-induced apoptosisBaolin Zhang
Laboratory of Biochemistry, Division of Therapeutic Proteins, Office of Biotechnology Products, Center for Drug Evaluation and Research, Food and Drug Administration, Bethesda, Maryland, USA
Cancer Res 65:6054-62. 2005..Taken together, the data show that RhoGDI is an anti-apoptotic molecule that mediates cellular resistance to these chemotherapy agents...
Mechanism of the guanine nucleotide exchange reaction of Ras GTPase--evidence for a GTP/GDP displacement modelBaolin Zhang
Laboratory of Biochemistry, Division of Therapeutic Proteins, Office of Biotechnology Products, Center for Drug Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA
Biochemistry 44:2566-76. 2005..These results strongly support a GEF reaction mechanism by which nucleotide exchange occurs on Ras through a direct GTP/GDP displacement model...
Desferal inhibits breast tumor growth and does not interfere with the tumoricidal activity of doxorubicinEileen M Hoke
Department of Pediatrics, Uniformed Services University of the Health Sciences, Bethesda, MD 20815, USA
Free Radic Biol Med 39:403-11. 2005..Furthermore, desferal may have utility as an adjunctive chemotherapy due to its ability to inhibit breast tumor growth and cardiotoxic side effects without compromising the tumor-killing activity of an anthracycline chemotherapy drug...
Auto-oxidation and oligomerization of protein S on the apoptotic cell surface is required for Mer tyrosine kinase-mediated phagocytosis of apoptotic cellsHiroshi Uehara
Laboratory of Biochemistry, Division of Therapeutic Proteins, Center for Drug Evaluation and Research, Food and Drug Administration, 29 Lincoln Drive, Bethesda, MD 20892
J Immunol 180:2522-30. 2008..The requirement for oxidative modification of protein S can explain why this abundant blood protein does not constitutively activate MerTK in circulating monocytes and tissue macrophages...
Regulation of macrophage interleukin-6 (IL-6) and IL-10 expression by prostaglandin E2: the role of p38 mitogen-activated protein kinaseJ A Williams
Laboratory of Immunology, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda MD 20892, USA
J Interferon Cytokine Res 20:291-8. 2000..These results indicate that macrophage IL-10 and IL-6 expression is differentially regulated by PGE2 and p38 MAP kinase in murine inflammatory macrophages...
Fas aggregation does not correlate with Fas-mediated apoptosisY Lee
Laboratory of Immunology, Division of Therapeutic Proteins, Food and Drug Administration, Center for Biologics and Evaluation and Research, Bethesda, MD 20892, USA
J Immunol 167:82-9. 2001..These results show that Fas aggregation and Fas-mediated apoptosis are not directly correlated and may even be inversely correlated...
Taurine chloramine, an oxidant derived from neutrophils, induces apoptosis in human B lymphoma cells through mitochondrial damageFabio Klamt
Laboratory of Biochemistry, Division of Therapeutic Proteins, Center of Drug Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA
J Biol Chem 280:21346-52. 2005..The data suggest that TN-Cl causes apoptosis through direct damage to the mitochondria...
Pharmacologic ascorbic acid concentrations selectively kill cancer cells: action as a pro-drug to deliver hydrogen peroxide to tissuesQi Chen
Molecular and Clinical Nutrition Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 102:13604-9. 2005..These findings give plausibility to i.v. ascorbic acid in cancer treatment, and have unexpected implications for treatment of infections where H(2)O(2) may be beneficial...
The antioxidant transcription factor Nrf2 negatively regulates autophagy and growth arrest induced by the anticancer redox agent mitoquinoneV Ashutosh Rao
Laboratory of Biochemistry, Center for Drug Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA
J Biol Chem 285:34447-59. 2010..Keap1 and Nrf2 act as redox sensors for oxidative perturbations that lead to autophagy. MitoQ and similar compounds should be further evaluated for novel anticancer activity...
Serum-derived protein S binds to phosphatidylserine and stimulates the phagocytosis of apoptotic cellsHoward A Anderson
Laboratory of Biochemistry, Division of Therapeutic Proteins, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD 20892, USA
Nat Immunol 4:87-91. 2003..Protein S acted by binding to phosphatidylserine expressed on the apoptotic cell surface. Protein S is thus a multifunctional protein that can facilitate clearance of early apoptotic cells in addition to regulating blood coagulation...
Induction of apoptosis by chemotherapeutic drugs without generation of reactive oxygen speciesSema Senturker
Laboratory of Immunology, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA
Arch Biochem Biophys 397:262-72. 2002..The results demonstrate that, at least in B lymphoma cells, chemotherapy-induced apoptosis occurs using a mechanism that does not involve oxidants...
The FDA's assessment of follow-on protein products: a historical perspectiveJanet Woodcock
Food and Drug Administration, 5600 Fishers Lane, Rockville, Maryland 20857, USA
Nat Rev Drug Discov 6:437-42. 2007....
Natural anticoagulant proteins in the regulation of autoimmunity: potential role of protein SHoward A Anderson
Laboratory of Biochemistry, Division of Therapeutic Proteins, Center for Drug Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA
Curr Pharm Des 10:929-37. 2004..This article will review the dual roles of protein S as an anticoagulant and in regulating phagocytosis of apoptotic cells, with emphasis on exposing a possible novel role in regulating autoimmunity...
Distinct modes of cell death induced by different reactive oxygen species: amino acyl chloramines mediate hypochlorous acid-induced apoptosisRobert P Englert
Department of Pediatrics, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20815, USA
J Biol Chem 277:20518-26. 2002....
Changes to biological source materialsK Sewerin
Biologics Consulting Group, Skaldev 17, 16771 Bromma, Sweden
Biologicals 34:71-2. 2006
