58Jan Styczynski et al.analyzed patients. We did not observe an intra-lineageshift, however, myeloid markers were usually nottested. Our results show that the lineage of leukemiausually remained unchanged while other individualphenotypic features frequently changed. Phenotypicchanges in ALL from diagnosis to relapse <strong>and</strong> subsequentsecond relapse, seemed to present a certain limitationfor the immunological detection of minimalresidual disease. Introduction of new generation, 6-8-color flow cytometers will probably overcome thisproblem.There are three general mechanisms for immunophenotypechanges in leukemia. First, chemotherapyappears to eradicate the dominant clone present atdiagnosis, permitting expansion of a secondary clonewith a different phenotype. The second mechanism isrelated to drug-induced changes in the original clone,which may either amplify or suppress differentiationprograms so that phenotypic shift is possible [13]. Thethird mechanism is based on the clonal evolution ofsubclones within a single cell population [6, 11, 12].Our analysis shows that relapsed leukemia seems totend to present blasts with immunophenotype beingclose to the leukemia initiating cell in ALL. Leukemicstem cells (LCSs) present immunophenotype based onCD34+/CD38- expression, both in AML [12] <strong>and</strong> ALL[14]. The next stage of immunophenotype isCD34+/CD38+, followed by subsequent differentiation.Although myeloid leukemias have been the provingground for most of the theories concerning LSCs, recentstudies suggest that lymphoid leukemias may alsoarise from a subset of cells with stem/progenitor cellcharacteristics. ALL, like AML, is a heterogeneousdisease with close to 80% of ALL involving B lineagecells. Reports studying the involvement of the HSCcompartment in these B-ALLs have failed to providean unequivocal demonstration that LSCs are derivedfrom normal hematopoietic stem cells, though studiesin different types of ALL suggest that ALL originatesfrom a primitive cell rather than from committed progenitors[15].CONCLUSIONS1. Second relapse of acute lymphoblastic leukemiareveals tendency to occurrence of more immaturephenotype of blasts.2. Phenotypic changes in ALL from diagnosis torelapse <strong>and</strong> subsequent second relapse, mightindicate a certain limitation for the immunologicaldetection of minimal residual disease.REFERENCES1. Gaynon P.S., Qu R.P., Chappell R.J., et al. Survival afterrelapse in childhood acute lymphoblastic leukemia: impactof site <strong>and</strong> time to first relapse - the Children's CancerGroup Experience. Cancer 1998; 82: 1387-1395.2. Gaynon P.S. Childhood acute lymphoblastic leukaemia<strong>and</strong> relapse. Br J Haematol 2005; 131: 579-587.3. van Wering E.R., Beishuizen A., Roeffen E.T., et al.Immunophenotypic changes between diagnosis <strong>and</strong>relapse in childhood acute lymphoblastic leukemia. Leukemia1995; 9: 1523-1533.4. Chucrallah A.E., Stass S.A., Huh Y.O., et al. Adult acutelymphoblastic leukemia at relapse. Cytogenetic, immunophenotypic,<strong>and</strong> molecular changes. Cancer 1995;76: 985-991.5. Borella L., Casper J.T., Lauer S.J. Shifts in expression ofcell membrane phenotypes in childhood lymphoid malignanciesat relapse. Blood 1979; 54: 64-71.6. Raghavachar A., Thiel E., Bartram CR. Analyses ofphenotype <strong>and</strong> genotype in acute lymphoblastic leukemiasat first presentation <strong>and</strong> in relapse. Blood 1987; 70:1079-1083.7. ALL-REZ B. Program leczenia wznów ostrej białaczkilimfoblastycznej u dzieci. Polska Pediatryczna Grupa dsLeczenia Białaczek i Chłoniaków. Wrocław, 1997.8. Kubicka M., Rafinska B., Kolodziej B., et al. Profildiagnostyczny wznowy ostrej bialaczki limfoblastycznej.Pediatr Pol 2008; 83: 135-142.9. Wysocki M., Styczynski J., Kubicka M., et al. Immunophenotype<strong>and</strong> morphology of blasts in children acutelymphoblastic leukemia at first relapse. Acta HaematolPol 1998; 30: 59-66.10. Jiang J.G., Roman E., N<strong>and</strong>ula S.V., et al. CongenitalMLL-positive B-cell acute lymphoblastic leukemia (B-ALL) switched lineage at relapse to acute myelocyticleukemia (AML) with persistent t(4; 11) <strong>and</strong> t(1; 6)translocations <strong>and</strong> JH gene rearrangement. Leuk Lymphoma2005; 46: 1223-1227.11. Muroi K., Yoshida M., Hatake K., et al. Phenotypicalanalysis of acute lymphoblastic leukaemia at first relapse.Leuk Res 1994; 18: 555-556.12. Lapidot T., Sirard C., Vormoor J., et al. A cell initiatinghuman acute myeloid leukaemia after transplantation intoSCID mice. Nature 1994; 367: 645-648.13. Stass S., Mirro J., Melvin S., et al. Lineage switch inacute leukemia. Blood 1984; 64: 701-706.
Analysis of immunophenotype at second relapse of acute lymphoblastic leukemia in children 5914. Hong D., Gupta R., Ancliff P., et al. Initiating <strong>and</strong> cancer-propagatingcells in TEL-AML1-associated childhoodleukemia. Science 2008; 319: 336-339.15. Cox C.V., Martin H.M., Kearns P.R., et al. Characterizationof a progenitor cell population in childhood T-cellacute lymphoblastic leukemia. Blood 2007; 109: 674-682.Address for correspondence:Jan Styczyński, MD, PhD,Chair <strong>and</strong> Clinic of Pediatric Hematology<strong>and</strong> OncologyNicolaus Copernicus University<strong>Collegium</strong> <strong>Medicum</strong> in Bydgoszczul. Curie-Sklodowskiej 985-094 BydgoszczPol<strong>and</strong>e-mail: jstyczynski@cm.umk.pltel: +48 52 585 4860fax: +48 52 585 4867Received: 16.09.2008Accepted for publication: 9.10.2008
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