The prophylactic use of granulocyte-colony stimulating factor during remission induction is associated with increased leukaemia-free survival of adults with acute lymphoblastic leukaemia: A joint analysis of five randomised trials on behalf of the EWALL

2012 ◽  
Vol 48 (3) ◽  
pp. 360-367 ◽  
Author(s):  
Sebastian Giebel ◽  
Xavier Thomas ◽  
Helene Hallbook ◽  
Klaus Geissler ◽  
Jean-Michel Boiron ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukaemia ◽  
Lymphoblastic Leukaemia ◽  
Joint Analysis ◽  
Remission Induction ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Randomised Trials ◽  
Free Survival ◽  
Prophylactic Use ◽  
Stimulating Factor

Pilot remission induction therapy with idarubicin, plus intensified dose of Ara-C and priming with granulocyte colony-stimulating factor for acute myeloid leukemia

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 16516-16516
Author(s):  
Y. Cho ◽  
J. Baek ◽  
S. Sohn ◽  
Y. Chae ◽  
D. Kim ◽  
...  
Keyword(s):  
Myeloid Leukemia ◽  
Leukemic Cells ◽  
Remission Induction ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Dose Intensification ◽  
Standard Regimen ◽  
Free Survival ◽  
Historical Group ◽  
Stimulating Factor

16516 Background: The sensitization of leukemic cells with hematopoietic growth factors can enhance the cytotoxicity of chemotherapy in acute myeloid leukemia (AML). Intensified remission induction (RI) therapy can also improve the treatment results for AML. Therefore, the current trial attempted to evaluate the efficacy and toxicity of granulocyte colony-stimulating factor (G-CSF) priming and a dose intensification of Ara-C in RI chemotherapy for AML. Methods: A total of 29 patients with newly diagnosed AML received G-CSF-priming RI chemotherapy consisting of idarubicin (12 mg/m2, D1–3), G-CSF (150 ug/m2, D3–8), and Ara-C (500 mg/m2, bid, D4–8), and the outcomes were compared with those for a historical group treated with a standard regimen consisting of idarubicin (12 mg/m2, D1–3) and Ara-C (100 mg/m2, D1–7). Results: There was no difference in the sex, age, subtype, and cytogenetic risk between the two groups. The complete remission (CR) rate and treatment-related mortality (TRM) were 72% and 17% for G-CSF-primed group and 71% and 10% for the historical group, respectively (p = 0.89 and p = 0.32). The time to neutrophil and platelet recovery did not differ significantly between the two groups (25 days vs. 24 days, p=0.17; 24 days vs. 23 days, p = 0.23, respectively). Similarly, the duration of fever was also not significantly different (5 days vs. 7 days, p = 0.58). Thirteen patients (45%) experienced fever and 5 patients (17%) manifested skin rashes during the G-CSF priming. After a median follow-up of 336 days, the 1-year overall survival (OS), disease-free survival (DFS), and event-free survival (EFS) rates were 72% vs. 63% (p = 0.83), 74% vs. 56% (p = 0.059), and 53% vs. 38% (p = 0.32), respectively. Conclusion: The G-CSF-priming RI regimen with an intensified dose of Ara-C did not show a superior efficacy when compared with a standard regimen, yet did produce a slightly longer DFS. Therefore, the sensitization of leukemic cells with growth factors and dose intensification would only seem to be a clinically applicable means to enhance the efficacy of RI chemotherapy in selected patients with AML, thereby warranting further studies focusing on specific subgroups of AML patients. No significant financial relationships to disclose.

Use of nab-paclitaxel and gemcitabine in pancreatic cancer without granulocyte colony-stimulating factor: A multicenter real-world experience

2021 ◽  
pp. 107815522110386
Author(s):  
Angela Chen ◽  
Vincent H Ha ◽  
Sunita Ghosh ◽  
Carole R Chambers ◽  
Michael B Sawyer
Keyword(s):  
Pancreatic Cancer ◽  
Overall Survival ◽  
Median Overall Survival ◽  
Progression Free Survival ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Free Survival ◽  
Colony Stimulating Factors ◽  
Median Progression Free Survival ◽  
Stimulating Factor

Introduction The metastatic pancreatic adenocarcinoma clinical trial (MPACT) trial established gemcitabine (gem) and nab-paclitaxel (nab) as a standard treatment for pancreatic cancer utilizing granulocyte colony-stimulating factors to manage neutropenia. This was a challenge for jurisdictions that do not use granulocyte colony-stimulating factors in palliative settings. We developed dosage guidelines to dose modify gem and nab without granulocyte colony-stimulating factors. We undertook a retrospective review to determine the efficacy and safety of these dose adjustment guidelines in the real world. Methods A multi-centered, retrospective chart review was performed on pancreatic patients between December 1, 2014, and August 21, 2018. Provincial electronic medical health records were reviewed. Using Log-rank statistics we determined the patient's progression-free survival and overall survival. Results Of 248 patients, 209 met patient selection criteria. Patients were excluded if they were lost to follow-up, on gem alone prior to nab/gem combination therapy or did not receive nab or gem. Patients who received nab/gem as first-line therapy had a median progression-free survival of 6.3 months (95% CI, 5.1–7.4), and median overall survival of 11.1 months (95% CI, 9.5–12.8). Those who received gem/nab in the second line had a median progression-free survival of 4.6 months (95% CI, 2.8–6.5), and median overall survival of 19.3 months (95% CI, 12.6–26.0). Conclusions The patient’s progression-free survival and overall survival taking nab/gem using our dose modification algorithm were equivalent or superior to the MPACT trial's progression-free survival and overall survival. Gem/nab can be given by our dose modification scheme without granulocyte colony-stimulating factor.

Granulocyte colony-stimulating factor and the risk of secondary myeloid malignancy after etoposide treatment

Blood ◽  
2003 ◽  
Vol 101 (10) ◽  
pp. 3862-3867 ◽  
Author(s):  
Mary V. Relling ◽  
James M. Boyett ◽  
Javier G. Blanco ◽  
Susana Raimondi ◽  
Frederick G. Behm ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cumulative Incidence ◽  
Myeloid Leukemia ◽  
Topoisomerase Ii ◽  
Lymphoblastic Leukemia ◽  
Cranial Irradiation ◽  
Remission Induction ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Stimulating Factor

Abstract Event-free survival for children with acute lymphoblastic leukemia (ALL) now exceeds 80% in the most effective trials. Failures are due to relapse, toxicity, and second cancers such as therapy-related myeloid leukemia or myelodysplasia (t-ML). Topoisomerase II inhibitors and alkylators can induce t-ML; additional risk factors for t-ML remain poorly defined. The occurrence of t-ML among children who had received granulocyte colony-stimulating factor (G-CSF) following ALL remission induction therapy prompted us to examine this and other putative risk factors for t-ML in 412 children treated on 2 consecutive ALL protocols from 1991 to 1998. All children received etoposide and anthracyclines, 99 of whom received G-CSF; 284 also received cyclophosphamide, 58 of whom also received cranial irradiation. There were 20 children who developed t-ML at a median of 2.3 years (range, 1.0-6.0 years), including 16 cases of acute myeloid leukemia, 3 myelodysplasia, and 1 chronic myeloid leukemia. Stratifying by protocol, the cumulative incidence functions differed (P = .017) according to the use of G-CSF and irradiation: 6-year cumulative incidence (standard error) of t-ML of 12.3% (5.3%) among the 44 children who received irradiation without G-CSF, 11.0% (3.5%) among the 85 children who received G-CSF but no irradiation, 7.1% (7.2%) among the 14 children who received irradiation plus G-CSF, and 2.7% (1.3%) among the 269 children who received neither irradiation nor G-CSF. Even when children receiving irradiation were excluded, the incidence was still higher in those receiving G-CSF (P = .019). In the setting of intensive antileukemic therapy, short-term use of G-CSF may increase the risk of t-ML.

scholarly journals A double-blind controlled study of granulocyte colony-stimulating factor started two days before induction chemotherapy in refractory acute myeloid leukemia. Kohseisho Leukemia Study Group [see comments]

Blood ◽  
1994 ◽  
Vol 83 (8) ◽  
pp. 2086-2092 ◽  
Author(s):  
R Ohno ◽  
T Naoe ◽  
A Kanamaru ◽  
M Yoshida ◽  
A Hiraoka ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Controlled Study ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Double Blind ◽  
Free Survival ◽  
Refractory Acute Myeloid Leukemia ◽  
Stimulating Factor ◽  
Acute Myeloid

We conducted a prospective, double-blind controlled study to determine the efficacy of a recombinant granulocyte colony-stimulating factor (G- CSF, 200 microgram/m2) starting daily from 2 days before an induction therapy until neutrophils recovered to above 1,500/microL or until 35 days after the therapy in 58 patients with relapsed or refractory acute myeloid leukemia (AML). Twenty-eight patients in the G-CSF group showed significantly faster recovery of neutrophils (P < .001) than 30 patients in the placebo group. The incidence of febrile episodes and of documented infections was almost the same in both groups. However, among 39 patients who did not show any infectious episodes during the 2- week period after the start of chemotherapy, the incidence of documented infections after the third week tended to be lower in the G- CSF group, but not statistically significantly. There was no evidence that G-CSF stimulated the growth of AML cells in the bone marrow during the 2-day period before the chemotherapy, nor that G-CSF accelerated the regrowth of AML cells during the 5-week period after the therapy. Fifty percent of patients in the G-CSF group and 37% in the placebo group had complete remission (CR). Although the rate was higher in the G-CSF group, the difference was not statistically significant (P = .306). There was no difference between the two groups in event-free survival of all patients and in disease-free survival of patients who had achieved CR.

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