Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/18218
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dc.contributor.authorYeo, Belinda-
dc.contributor.authorRedfern, Andrew D-
dc.contributor.authorMouchemore, Kellie A-
dc.contributor.authorHamilton, John A-
dc.contributor.authorAnderson, Robin L-
dc.date2018-07-02-
dc.date.accessioned2018-08-24T06:49:09Z-
dc.date.available2018-08-24T06:49:09Z-
dc.date.issued2018-04-
dc.identifier.citationClinical & experimental metastasis 2018; 35(4): 255-267-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/18218-
dc.description.abstractGranulocyte-colony stimulating factor (G-CSF) is one of several cytokines that can expand and mobilize haematopoietic precursor cells from bone marrow. In particular, G-CSF mobilizes neutrophils when the host is challenged by infection or tissue damage. Severe neutropenia, or febrile neutropenia is a life-threatening event that can be mitigated by administration of G-CSF. Consequently, G-CSF has been used to support patients undergoing chemotherapy who would otherwise require dose reduction due to neutropenia. Over the past 10-15 years it has become increasingly apparent, in preclinical tumour growth and metastasis models, that G-CSF can support tumour progression by mobilization of tumour-associated neutrophils which consequently promote tumour dissemination and metastasis. With the increasing use of G-CSF in the clinic, it is pertinent to ask if there is any evidence of a similar promotion of tumour progression in patients. Here, we have reviewed the preclinical and clinical data on the potential contribution of G-CSF to tumour progression. We conclude that, whilst the evidence for a promotion of metastasis is strong in preclinical models and that limited data indicate that high serum G-CSF levels in patients are associated with poorer prognosis, no studies published so far have revealed evidence of increased tumour progression associated with supportive G-CSF use during chemotherapy in patients. Analysis of G-CSF receptor positive cohorts within supportive trials, as well as studies of the role of G-CSF blockade in appropriate tumours in the absence of chemotherapy could yield clinically translatable findings.-
dc.language.isoeng-
dc.subjectG-CSF-
dc.subjectMetastasis-
dc.subjectTherapy-
dc.subjectTumourigenesis-
dc.titleThe dark side of granulocyte-colony stimulating factor: a supportive therapy with potential to promote tumour progression.-
dc.typeJournal Article-
dc.identifier.journaltitleClinical & experimental metastasis-
dc.identifier.affiliationOlivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australia-
dc.identifier.affiliationSchool of Cancer Medicine, La Trobe University, Melbourne, Victoria, Australia -
dc.identifier.affiliationAustin Health, Heidelberg, Victoria, Australia-
dc.identifier.affiliationFiona Stanley Hospital, Perth, WA, Australia-
dc.identifier.affiliationPeter MacCallum Cancer Centre, Parkville, Victoria, Australia-
dc.identifier.affiliationDepartment of Biochemistry & Molecular Biology, Monash University, Clayton, Victoria, Australia-
dc.identifier.affiliationArthritis and Inflammation Research Centre, Department of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville, Victoria, Australia-
dc.identifier.affiliationAustralian Institute for Musculoskeletal Science (AIMSS), The University of Melbourne and Western Health, St. Albans, Victoria, Australia-
dc.identifier.doi10.1007/s10585-018-9917-7-
dc.identifier.orcid0000-0002-6841-7422-
dc.identifier.orcid0000-0002-9218-9917-
dc.identifier.pubmedid29968171-
dc.type.austinJournal Article-
local.name.researcherAnderson, Robin L
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptOlivia Newton-John Cancer Research Institute-
crisitem.author.deptMedical Oncology-
crisitem.author.deptOlivia Newton-John Cancer Wellness and Research Centre-
crisitem.author.deptOlivia Newton-John Cancer Research Institute-
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