Impact on Acute Myeloid Leukemia Relapse in Granulocyte Colony Stimulating Factor Application: A Meta-Analysis

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 5169-5169
Author(s):  
Xiaoqin Feng ◽  
Chunfu Li
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Conflicts Of Interest ◽  
Meta Analysis ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Significant Difference ◽  
The Impact ◽  
Stimulating Factor ◽  
Acute Myeloid

Abstract Objective: This meta-analysis evaluated the impact of granulocyte colony-stimulating factor (G-CSF) added to chemotherapy on treatment outcomes including survival and disease recurrence in patients with acute myeloid leukemia (AML). Methods: Medline, Cochrane, EMBASE,Google Scholar databases were searched until December 7, 2015 using the following search terms. Randomized control trials (RCTs), two-arm, and prospective studies that investigated patients with AML who underwent stem-cell transplantation were included. Results: The overall analysis revealed significant improvement in overall survival (OS) (pooled HR= 0.90; 95%CI, 0.83 to 0.98; P = 0.017) and disease free survival (DFS) (pooled HR = 0.85; 95% CI, 0.77 to 0.94; P = 0.002) for patients receiving G-CSF with chemotherapy. Among patients without prior AML treatment, there was significant improvement in DFS (pooled HR = 0.87; 95% CI, 0.77 to 0.98; P = 0.021) and reduction in incidence of relapse (pooled HR = 0.81; 95% CI, 0.68 to 0.96; P = 0.015) for those who received G-CSF. However, subgroup analyses found no significant difference between G-CSF (+) and G-CSF (-) treatments in rates of OS (P = 0.135) and complete remission (CR) (P = 0.357) for patients without prior AML treatment. Among patients with relapsed/refractory AML, there was no significant difference found between G-CSF(+) and G-CSF(-)groups for OS (P = 0.225), DFS (P = 0.209) and CR (P = 0.208).[EG1] Discussion and Co nclusion: Treatment with chemotherapy plus G-CSF appears to provide better survival and treatment responses compared with chemotherapy alone, particularly for patients with previously untreated AML. Disclosures No relevant conflicts of interest to declare.

Granulocyte Colony-Stimulating Factor (G-CSF) Treatment of Childhood Acute Myeloid Leukemias That Overexpress the Differentiation-Defective G-CSF Receptor Isoform IV Is Associated With a Higher Incidence of Relapse

2010 ◽  
Vol 28 (15) ◽  
pp. 2591-2597 ◽  
Author(s):  
Stephanie Ehlers ◽  
Christin Herbst ◽  
Martin Zimmermann ◽  
Nicole Scharn ◽  
Manuela Germeshausen ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Children And Adolescents ◽  
Cumulative Incidence ◽  
Myeloid Leukemia ◽  
Cell Surface Expression ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Stimulating Factor ◽  
Acute Myeloid ◽  
Factor G

Purpose This prospective, multicenter Acute Myeloid Leukemia Berlin-Frankfurt-Muenster (AML-BFM) 98 study randomly tested the ability of granulocyte colony-stimulating factor (G-CSF) to reduce infectious complications and to improve outcomes in children and adolescents with acute myeloid leukemia (AML). However, a trend toward an increased incidence of relapses in the standard-risk (SR) group after G-CSF treatment was observed. Patients and Methods Of 154 SR patients in the AML-BFM 98 cohort, 50 patients were tested for G-CSF receptor (G-CSFR) RNA isoform I and IV expression, G-CSFR cell surface expression, and acquired mutations in the G-CSFR gene. Results In patients randomly assigned to receive G-CSF after induction, 16 patients overexpressing the G-CSFR isoform IV showed an increased 5-year cumulative incidence of relapse (50% ± 13%) compared with 14 patients with low-level isoform IV expression (14% ± 10%; log-rank P = .04). The level of G-CSFR isoform IV had no significant effect in patients not receiving G-CSF (P = .19). Multivariate analyses of the G-CSF–treated subgroup, including the parameters G-CSFR isoform IV overexpression, sex, and favorable cytogenetics as covariables, revealed the prognostic relevance of G-CSFR isoform IV overexpression for 5-year event-free survival (P = .031) and the 5-year cumulative incidence of relapse (P = .049). Conclusion Our results demonstrate that children and adolescents with AMLs that overexpress the differentiation-defective G-CSFR isoform IV respond to G-CSF administration after induction, but with a significantly higher incidence of relapse.

scholarly journals A point mutation in the granulocyte colony-stimulating factor receptor (G-CSF-R) gene in a case of acute myeloid leukemia results in the overexpression of a novel G-CSF-R isoform

Blood ◽  
1995 ◽  
Vol 85 (4) ◽  
pp. 902-911 ◽  
Author(s):  
F Dong ◽  
M van Paassen ◽  
C van Buitenen ◽  
LH Hoefsloot ◽  
B Lowenberg ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Point Mutation ◽  
Myeloid Leukemia ◽  
Receptor Gene ◽  
Splice Donor Site ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Cytoplasmic Region ◽  
Stimulating Factor ◽  
Acute Myeloid

A novel human granulocyte colony-stimulating factor (G-CSF) receptor isoform, designated SD, has been identified in which the distal C- terminal cytoplasmic region, previously shown to be essential for maturation signalling, is substituted by an altered C-terminus. The SD receptor has a high affinity for G-CSF and retains the membrane- proximal cytoplasmic region known to be sufficient for proliferative signalling. Nonetheless, the SD isoform lacks the ability to transduce growth signals in murine BAF3 cells and, in contrast to the wild-type G- CSF receptor, is scarcely capable of activating JAK2 kinase. Expression of SD receptor was found to be low in normal granulocytes, but was significantly increased in a patient with acute myeloid leukemia (AML). The leukemic cells of this patient harbour a point mutation in the SD splice donor site of the G-CSF receptor gene. These findings provide the first evidence that mutations in the G-CSF receptor gene can occur in certain cases of clinical de novo AML. The possible contribution of defective G-CSF receptor signalling to leukemogenesis is discussed.

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