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Zajac-Spychala O.,Hematologii i Transplantologii Pediatrycznej II | Derwich K.,Hematologii i Transplantologii Pediatrycznej II | Konatkowska B.,Hematologii i Transplantologii Pediatrycznej II | MacHowska L.,Hematologii i Transplantologii Pediatrycznej II | Wachowiak J.,Hematologii i Transplantologii Pediatrycznej II
Onkologia Polska | Year: 2010

Introduction: Relapse of acute lymphoblastic leukemia (ALL) is caused by proliferation of the residual leukemic blasts clone refractory to first line chemotherapy. To choose an appropriate strategy for the treatment of relapse, it is important to investigate the biological characteristics of blasts, especially their immunophenotype. Aim of the study was to compare immunophenotypic profiles of leukemic blasts at diagnosis and at relapse of ALL in children treated between 2002-2009 according to ALL IC-BFM 2002. Material and methods: Among 134 children aged 1-18 years (median: 6 years) treated due to ALL between 2002-2009, bone marrow or/and central nervous system relapse was diagnosed in 14 (10%) patients at the age of 3-17 years (median: 8) treated previously due to ALL, including T-cell ALL (T-ALL) in 2, and B-cell precursors ALL (BCP-ALL) in 12 patients. Isolated bone marrow relapses was diagnosed in 9 patients, combined bone marrow-central nervous system - in 4, and isolated central nervous system - in 1 patient. Immunophenotyping of the leukemic blasts was performed at the Department of Immunology Poznan University of Medical Sciences. At diagnosis and at relapse immunophenotype of bone marrow cells in patients with bone marrow relapse, and of cerebrospinal fluid in one patient with isolated central nervous system relapse was tested. Time of observation from diagnosis to relapse was 3-70 months (median: 22). Results: In the study group the immunophenotype changes at relapse of acute leukemia were diagnosed in 5/14 (36%) patients (median time of observation: 3 months), including 4/12 patients with BCP-ALL and 1 out of 2 patients with T-ALL. Among children previously diagnosed with BCP-ALL immunophenotype changes occured in 3/3 of pro-B ALL and in 1/4 of pre-B ALL, whilst there was no change in patients previously diagnosed with common ALL. Among 4 previously BCP-ALL patients with immunophenotype changes, 2 conversions of cell lineage and two intra-lineage shifts were observed, as well as in child with T-ALL. Conclusions: 1. Immunophenotype changes at relapse were observed in about 1/3 of ALL patients, including All patients with previously pro-B ALL. 2. Immunophenotype shifts usually occured in very early relapses of ALL. 3. In case of ALL relapse immunophenotyping of leukemic lymphoblasts is necessary to choose the best treatment strategy for relapsed patients. Copyright © 2010 Cornetis.

Derwich K.,Hematologii i Transplantologii Pediatrycznej II | Zajac-Spychala O.,Hematologii i Transplantologii Pediatrycznej II | Mankowska M.,Hematologii i Transplantologii Pediatrycznej II | Konatkowska B.,Hematologii i Transplantologii Pediatrycznej II | And 3 more authors.
Onkologia Polska | Year: 2010

Introduction: Poor initial prednisolone response is a well established unfavorable prognostic factor in childhood acute lymphoblastic leukemia (ALL) treated according to the ALL IC-BFM 2002 trial. lymphoblastic leukemia (BCP-ALL) with poor initial prednisolone response (PPR). Material and materials: Among 134 children with newly recognized ALL enrolled from 01.10.2002 to 31.01.2010, 48 (36%) patients were stratified into a high risk (HR) group. Twenty nine (60%) HR-BCP-ALL children with exclusion of BCR/ABL and/or MLL/AF4 fusion genes have been analysed. Among them 16 (33%) (7 ?, 9 ?; aged 2-15.5 years; median age: 6 years) showed prednisolone poor response (PPR) - analysed group and 13 (27%) (8 ?, 5 ?; aged 2-12 years; median age: 4.5 years) prednisolone good response (PGR) - control group. The immunophenotype in the PPR and PGR was respectively as follows: pro-B ALL - 4 (25%)/2 (15%), common ALL - 9 (56%)/8 (62%), pre-B ALL - 2 (13%)/3 (23%) and ABL -1 (6%)/0. Allogeneic HSCT was performed in 6/29 (21%) children: MSD-HSCT - 1, MMUD-HSCT (8/10) - 1, MUD-HSCT - in 4 patients. The median observation time was 46.5 months (range 7 to 58 months) for PPR and 52 months (range 4 to 77 months) for PGR. The Kaplan-Meier method was used to estimate probability of event-free survival (pEFS) and disease-free survival (pDFS). Results: Remission on day 15 was achieved in 6/16 (38%) patients in PPR group and 3/13 (23%) patients in PGR and respectively in 16/16 (100%) and 10/13 (77%) on day 33 of induction therapy. Two relapses of ALL were observed only in PGR group after 3 and 28 months (median time: 15.5 months) respectively. In the PPR group, 3/16 (19%) children died of MODS complications; one of them after protocol II, two of them after MUD-HSCT (on day +38 and more than 100 days). In the PGR group 2/13 (15%) children died of treatment-related complications: MODS - 1, +7 days after MMUD-HSCT and hepatotoxicity - 1, more than 100 days after MUD-HSCT. In the PPR group 13/16 (81%) children are alive in remission and 11/13 (85%) patients in the PGR group. The probability of event free survival (pEFS) and disease free survival (pDFS) were 0.8 and 1.0 for the PPR group, and 0.6 and 0.7 for the PGR group. Conclusions: 1. The ALL IC-BFM 2002 trial proved to be effective in diminishing relapses in group of PPR HRBCP- ALL without BCR/ABL and/or MLL/AF4 fusion genes with PPR. 2. Results of conventional chemotherapy according to the ALL IC-BFM 2002 trial without HSCT for HR-BCP-ALL patients with PPR are successful and it seems to have a lower risk of treatment failure. Evaluation of minimal residual disease (MRD) should be only one indicator for HSCT treatment. Copyright © 2010 Cornetis.

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