However, overexpression of G-CSF has been implicated in several important processes in tumor biology such as tumor growth, angiogenesis, and metastasis.
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.
As a high neutrophil-to-lymphocyte ratio in patients predicts poor outcome, while mild neutropenia predicts an improved outcome, we urge caution in the use of G-CSF in neutrophil recovery following chemotherapy as there is increasing evidence in preclinical models that G-CSF can promote metastasis.
However, in a previous meta-analysis, G-CSF prophylaxis was associated with an increased risk of secondary malignancies while reducing long-term mortality.
<i>In vitro</i> and <i>in vivo</i> investigations revealed that MDSCs produced in response to tumor-derived G-CSF are involved in premetastatic niche formation, which promotes visceral organ metastasis of TRL-positive cancer.
It has been shown that Granulocyte colony-stimulating factor (G-CSF) has a higher expression in malignant tumors, and anti-G-CSF therapy considerably decreases tumor growth, tumor vascularization and metastasis.
The levels of spontaneous production of interleukin (IL)-10 and granulocyte colony-stimulating factor (G-CSF) and the amounts of IL-2, IL-10, G-CSF and monocyte chemoattractant protein-1 (MCP-1) produced during stimulation by PAs, as well as the index of stimulation by polyclonal activators (ISPA) for IL-2 production, were lower for MAC with LN metastasis than for MAC without LN metastasis.
Circulating concentrations of the cytokines interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF) and chemokines monocyte chemotatic protein 1 (MCP-1)/CCL2 and growth-regulator oncogene α (GROα)/chemokine C-X-C motif ligand 1 are commonly increased in cancer patients and they are increasingly recognised as important promoters, via divergent mechanisms, of cancer progression and metastasis.
Thus, we advance the hypothesis that G-CSF expression is serving as a marker of a more generalized trans-dominant pathway linked to tumor progression and metastasis.
High-dose paclitaxel with granulocyte colony-stimulating factor in patients with advanced breast cancer refractory to anthracycline therapy: a European Cancer Center trial.