This study reports the data of 32 children with poor-prognosis solid tumors who had 78 PBSC harvests on Fenwall CS-3000plus after mobilization mainly by different treatment protocol chemotherapy regimens followed by G- or GM-CSF (92% of patients) or by G-/GM-CSF alone (8%). Timing of procedure was predicted by studying the blood count. When the white blood cell and platelet count reached a median of 8.1 (0.9-37.3) and 95 (16-338) x 10(9)/L, respectively, the median number of 2.7 (0.005-16.8) x 10(6) CD34+/kg with 1.5 (0.005-11.6) x 10(6) CD34+/kg for 1 blood volume processed was obtained per procedure. In the group of 13 patients with low body weight (median 14 [10-20] kg) 32 leukophereses were performed. The extracorporal line was primed with donor red blood cells in the patients with the weight below 15 kg. No difference was observed in CD34+ content in harvests whether GM-CSF was begun on day +1 or on day +3 after chemotherapy.
IL-6, or cytokines of the IL-6 family using gp130 as transducer chain receptor, have been suggested to play a role in certain B lymphoid neoplasia. The presence of cell membrane gp80 and gp130 IL-6 receptors was studied in 98 patients with various leukaemia and non-Hodgkin's malignant lymphoma using flow cytofluorometry and immunohistology. Except neoplasia of immature B cells which expressed neither of the receptors, the majority of B cell tumours expressed one or both of them, mantle cell lymphoma being found to express the highest density of receptors. Using IL-6-dependent XG myeloma cell lines and mAb recognizing various gp80 and gp130 functional epitopes, it has been shown that IL-6 activation leads to a modified expression of some epitopes. In particular, the decrease or the disappearance of a gp130 epitope called A1 signed gp130 dimerization which is the first step of the gp130 activation pathway. Gp80 and gp130 epitope analysis was achieved in 17 of the patients. In four, an epitope phenotype compatible with a cytokine-induced activation was found. The cells of five B-CLL patients which expressed both gp80 and gp130 receptors were incubated with IL-6 to induce activation. In three of the cases they were found to rearrange their receptors in activated forms but not in the two others, showing that cells able to be activated or not can be found. These results confirm that gp130 signalling might play an important role in the pathogenesis of certain B cell neoplasia.
We retrospectively compared the effects of two time points of G-CSF (Filgrastim) introduction for PBSC mobilization in 45 children with different malignancies. Seventeen patients received the first G-CSF dose on day 2 or 3 following chemotherapy (group 1). Twenty-eight patients received a "flexible" G-CSF injection schedule when the G-GSF was started at the time of the first platelet count rise during post-chemotherapy recovery phase (group 2). Leukapheresis was performed when WBC recovery reached >2.0 × 10 9 /l or if the peripheral blood CD34 + cell level was >0.01 × 10 9 /l. A median of 2 (1-4) leukapheresis procedures was performed in both groups to yield a median of 4.2 and 6.1 × 10 6 CD34 + cells/kg in groups 1 and 2, respectively, which was generally sufficient for auto-transplantation. The proportion of patients with a failure of PBSC collection was similar and G-CSF consumption estimated through the total cycle dose was 2.3 times less in group 2 without increasing infectious risks. The short-term hematological recovery and the early post-transplant course were similar in the two groups. Delayed introduction of G-CSF after chemotherapy allowed PBSC harvest equivalent to that obtained after early G-CSF introduction. This approach could be an interesting alternative in PBSC mobilization but should be assessed by a prospective controlled study. Am. J. Hematol. 73:225-229, 2003.
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