Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/18218
Title: The dark side of granulocyte-colony stimulating factor: a supportive therapy with potential to promote tumour progression.
Authors: Yeo, Belinda;Redfern, Andrew D;Mouchemore, Kellie A;Hamilton, John A;Anderson, Robin L
Affiliation: Olivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australia
La Trobe University School of Cancer Medicine, Heidelberg, VIC, Australia
Austin Health, Heidelberg, Victoria, Australia
Fiona Stanley Hospital, Perth, WA, Australia
Peter MacCallum Cancer Centre, Parkville, VIC, Australia
Department of Biochemistry & Molecular Biology, Monash University, Clayton, VIC, Australia
Arthritis and Inflammation Research Centre, Department of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC, Australia
Australian Institute for Musculoskeletal Science (AIMSS), The University of Melbourne and Western Health, St. Albans, VIC, Australia
Issue Date: Apr-2018
EDate: 2018-07-02
Citation: Clinical & experimental metastasis 2018; 35(4): 255-267
Abstract: Granulocyte-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.
URI: http://ahro.austin.org.au/austinjspui/handle/1/18218
DOI: 10.1007/s10585-018-9917-7
ORCID: 0000-0002-6841-7422
0000-0002-9218-9917
PubMed URL: 29968171
Type: Journal Article
Subjects: G-CSF
Metastasis
Therapy
Tumourigenesis
Appears in Collections:Journal articles

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