Can adding plerixafor to granulocyte colony-stimulating factor (G-CSF) improve outcomes in people undergoing autologous transplantation for multiple myeloma or non-Hodgkin lymphoma?

2018 ◽  
Author(s):  
Simone Mocellin
Keyword(s):  
Multiple Myeloma ◽  
Hodgkin Lymphoma ◽  
Autologous Transplantation ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Non Hodgkin Lymphoma ◽  
Stimulating Factor ◽  
Factor G

Safe administration of granulocyte colony-stimulating factor (G-CSF) to a patient with G-CSF–producing multiple myeloma

2020 ◽  
Vol 99 (7) ◽  
pp. 1667-1668
Author(s):  
Taku Kikuchi ◽  
Jun Kato ◽  
Yuya Koda ◽  
Masatoshi Sakurai ◽  
Yuichiro Hayashi ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Stimulating Factor ◽  
Factor G

Granulocyte-Colony Stimulating Factor (G-CSF) in Combination with Bortezomib, Cyclophosphamide and Dexamethasone in Patients with Multiple Myeloma

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 5768-5768
Author(s):  
Bingzong Li ◽  
Ping Chen ◽  
Xueping Ge ◽  
Xiaohui Zhang ◽  
Jinxiang Fu
Keyword(s):  
Multiple Myeloma ◽  
Adverse Events ◽  
Plasma Cells ◽  
Conflicts Of Interest ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Eligibility Criteria ◽  
Grade 3 ◽  
Stimulating Factor ◽  
Factor G

Abstract Background: Proteasome inhibition with bortezomib has revolutionized the treatment of multiple myeloma, but the vast majority of patients eventually develop clinical bortezomib resistance through poorly understood mechanisms. Long-lived plasma cells, which are supported by niche environments, are postulated to be an important mediator of resistance to chemotherapy and disease relapse. CXCR4/CXCL12 (SDF-1) axis plays an important role in the interaction of long-lived plasma cells and the microenvironment. Granulocyte-Colony Stimulating Factor (G-CSF) is reported to possess the potential to inhibit the expression of SDF-1, thus to suppress the CXCR4/SDF-1 axis and mobilize long-lived plasma cells from the niche environments. Bortezomib is reported to be able to eliminate both short- and long-lived plasma cells. In this trial we hypothesized that inhibition of the CXCR4/SDF-1 axis by G-CSF would disrupt the interaction of plasma cells with the environment and increase the sensitivity of myeloma cells to bortezomib. Methods: GBCD-001 (G-CSF, Bortezomib, Cyclophosphamide and Dexamethasone), a registered phase II study clinical trial (NCT02027220), engaged to both bortezomib-naïve and bortezomib-exposed myeloma patients. All the patients received G-BCD regimen at least one cycle. Dosing schedule consisted 28-day cycles of G-CSF 150µg, intracutaneously injection (IC) on days 0, 1, 7, 8, 14, 15, 21 and 22; Bortezomib 1.3mg/m2, intravenously injection (IV) on days 1, 8, 15 and 22; Cyclophosphamide 300 mg/m2, IV on days 1, 8, 15 and 22; and Dexamethasone 20mg/d, IV on days 1, 2, 8, 9, 15, 16, 22 and 23. Response was assessed by the IMWG criteria and toxicity was graded using the CTCAE v4.0. Results: From July 2013 to July 2014, 22 patients (10 females and 12 males; median age 63, range 44-80) meeting eligibility criteria have beed enrolled onto this study and are evaluated for response and toxicity, with 21 patients presenting with Durie-Salmon stage ¢ò/¢ó, 15 presenting with ISS stage ¢ò/¢ó disease. The median plasma cells is 32%, ranging from 5%-90%. Of the 22 pts, 19 are primary ones who had received no therapy and 3 are refractory ones who had received regimens including bortezomib. The response was listed in table 1. Of 19 primary pts, the ORR (¨RPR) was17/19 (89.5%) after one cycle and 10 pts received four cycles, among which, 7 (70%) achieved nCR/CR, 2 (20%) VGPR and 1 (10%) PR. Of 3 pts who received six cycles, all (100%) achieved CR. Of 3 refractory pts, the ORR was 2/3 (67%) after one cycle, 2 CR and 1 PR after 3 cycles. The most common adverse events observed included thrombocytopenia (40.9%, with 1 grade 4, 3 grade 3, 3 grade 2 and 2 grade 1), fatigue (40.9%, with 9 grade 1), neutropenia (22.7%, with 1 grade 4, 2 grade 2 and 2 grade 1), constipation (22.7%, with 2 grade 2 and 3 grade 1) and diarrhea (18.2%, with 1 grade 3, 1 grade 2 and 2 grade 1). Peripheral neuropathy possibly related to the drug was seen in 5 patients with grade 1 and 1 patient with grade 2, respectively. There were no deaths on study. Conclusions: In this study, among patients completing four cycles of G-BCD therapy, both primary and refractory ones, 100% have achieved PR or better. CR rate was 70% and 66.7% in primary pts and refractory ones, respectively. The adverse events were well tolerated and without special intervention. The study is currently recruiting more participants and updated results will be presented at the meeting. Large clinical studies and control studies are needed to replicate this promising results.Table 1 Response 1 cycle n/N (%) 4 cyclesn/N (%)6 cyclesn/N (%)PrimaryRefractoryPrimaryRefractoryPrimaryORR (¨RPR)17/19 (89.5)2/3(66.7)10/10 (100)3/3(100)3/3(100)nCR/CR1/19(5.3)07/10(70)2/3(66.7)3/3(100)VGPR1/19(5.3)02/10(20)00PR15/19(78.9)2/3(66.7)1/10(10)1/3(33.3)0 Disclosures No relevant conflicts of interest to declare.

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