{"title":"Human granulocyte colony-stimulating factor (G-CSF), the premier granulopoietin: biology, clinical utility, and receptor structure and function.","authors":"L S Tkatch, D J Tweardy","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>In summary, both G-CSF and GM-CSF have been identified, cloned, and produced for pharmacologic use in humans. While both G-CSF and GM-CSF have had significant impact in the treatment of neutropenic states, G-CSF appears to be more advantageous than GM-CSF in overall efficacy and paucity of side effects. Much has been discovered about the structure of the G-CSF receptor but further work is necessary to determine its mechanism of signal transduction. As our understanding of G-CSF signaling advances, the therapeutic impact of our knowledge about G-CSF biology will evolve from the current focus on enhancing its effects in hematologic and oncologic illnesses to decreasing its effects in inflammatory conditions where overexhuberant neutrophil infiltration and activation cause disease.</p>","PeriodicalId":77246,"journal":{"name":"Lymphokine and cytokine research","volume":"12 6","pages":"477-88"},"PeriodicalIF":0.0000,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Lymphokine and cytokine research","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
In summary, both G-CSF and GM-CSF have been identified, cloned, and produced for pharmacologic use in humans. While both G-CSF and GM-CSF have had significant impact in the treatment of neutropenic states, G-CSF appears to be more advantageous than GM-CSF in overall efficacy and paucity of side effects. Much has been discovered about the structure of the G-CSF receptor but further work is necessary to determine its mechanism of signal transduction. As our understanding of G-CSF signaling advances, the therapeutic impact of our knowledge about G-CSF biology will evolve from the current focus on enhancing its effects in hematologic and oncologic illnesses to decreasing its effects in inflammatory conditions where overexhuberant neutrophil infiltration and activation cause disease.