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©Ferrata Storti Foundation Acute Leukemias original paper haematologica 2001; 86:154-161 Impact of CD133 (AC133) and CD90 http://www.haematologica.it/2001_02/0154.htm expression analysis for acute leukemia immunophenotyping CHRISTIAN WUCHTER,* RICHARD RATEI,* GÜNTHER SPAHN,* CLAUDIA SCHOCH,° JOCHEN HARBOTT,# SUSANNE SCHNITTGER,° TORSTEN HAFERLACH,° URSULA CREUTZIG,@ CHRISTIAN SPERLING,* LEONID KARAWAJEW,* WOLF-DIETER LUDWIG* *Dept. of Hematology, Oncology and Tumor Immunology, Robert- Rössle-Clinic, Charité, Humboldt-University of Berlin, °Dept. of Internal Medicine III, Ludwig-Maximilians-University of München, Correspondence: Christian Wuchter, M.D., Robert-Rössle-Clinic, Charité, #Oncogenetic Laboratory, Children’s Hospital, Justus-Liebig-Uni- Humboldt University of Berlin, Lindenberger Weg 80, 13125 Berlin, Ger- versity of Gießen, @Dept. of Hematology-Oncology, University Chil- many. Phone: international +0049-30-94171362 - Fax: international +0049-30-94171308 - E-mail: [email protected] dren's Hospital, Münster, Germany Background and Objectives. AC133 is a novel monoclonal cute leukemias derive from either malignant, antibody (Moab) reacting with a population of imma- transformed, uncommitted multipotent stem cells ture/primitive or granulo-monocytic committed CD34+ve Aor lineage-restricted progenitor cells.1-3 So far, cells. Up to now, only few studies with small numbers of cas- CD34 is the most commonly used antigen to define es have examined AC133 (recently designated CD133) immature hematopoietic progenitor cells.4 In acute expression in acute leukemia. To determine the value of this leukemia immunophenotyping, CD34 is not lineage- Moab for acute leukemia immunophenotyping, we investi- restricted and thus not useful for distinguishing acute gated a large series of leukemic cell samples for their reac- myeloid leukemia (AML) from acute lymphoblastic tivity with Moab AC133. leukemia (ALL).5 Therefore, new Moabs, recognizing sub- Design and Methods. A total of 298 cell samples from sets of CD34 leukemic cells with the potential to dis- patients with de novo acute myeloid leukemia (AML) tinguish uncommitted multipotential stem cells from (n=142), acute lymphoblastic leukemia (ALL) (n=119), lineage-restricted progenitor cells are of special inter- CD34+ve biphenotypic acute leukemia (n=13), and CD34+ve CML blast crisis (=BC; 21 myeloid BC/3 lymphoid BC) were est for acute leukemia immunophenotyping. Moab investigated by flow cytometry for Moab AC133 reactivity. AC133 reacts with a population of non-committed or CD133 expression was compared with CD90(Thy-1) expres- granulomonocytic (GM)-committed CD34+ve cells in nor- sion, another CD34-associated antigen. mal hematopoiesis.6,7 Recently it was shown that among the CD34-veCD38-veLin-ve subset of human cord blood an Results. Fifteen (5%) samples expressed CD90, whereas +ve -ve 114 (38%) samples were positive for Moab AC133 (20% extremely rare population of AC133 CD7 cells is cut-off level). No significant differences in CD133 and CD90 highly enriched for progenitor activity and capable of expression levels between AML and ALL were observed. In differentiation into CD34+ve cells.8 So far, it is not clear AML, but not ALL, CD133 was more often expressed in which molecule is detected by Moab AC133, recently CD34+ve cases than in CD34–ve ones (p<0.00001). Howev- designated CD133 by the 7th Workshop and Conference er, CD133 expression was not restricted to CD34+ve leukemic on Human Leukocyte Differentiation (June 2000). The cells in individual cell samples. All 8 pro-B-ALL cell samples AC133-antigen may be the human homolog of the with 11q23-anomalies and MLL (mixed lineage leukemia) mouse kidney prominin, which is preferentially found gene translocations were positive for CD133, whereas only on the apical surface of various murine embryonic and 2 of 9 pro-B-ALL without MLL gene translocations expressed 9-11 CD133 (p<0.002). In contrast, none of the 5 AML cell sam- adult epithelia. Recent data suggest that CD133 ples with a t(9;11) and MLL gene translocation reacted with expression also defines a subset of circulating endothe- Moab AC133. CD34+ve CML cells in myeloid BC were less lial cells that may play a role in neoangiogenesis.12 often positive for CD133 than CD34+ve de novo AML cells Up to now, only a few studies with small numbers of (p <0.0001). cases have examined CD133 expression in acute Interpretation and Conclusions. CD133 and CD90 expres- leukemia: in one study, CD133 expression was mainly sion analysis is not helpful for lineage determination in acute restricted to immature AML FAB subtypes.13 However, leukemia immunophenotyping. However, Moab AC133 may in another study the highest CD133 expression levels be an informative marker for the detection and further char- were found in myelomonocytic differentiated AML FAB acterization of immature AML cells, as well as pro-B-ALL M4/M5 cases.6 Two other studies revealed no correla- cells with MLL gene translocations, by flow cytometry. tion between CD133 expression, FAB subtypes and ©2001, Ferrata Storti Foundation cytogenetics in AML.14,15 AC133 reactivity was observed Key words: acute leukemia, CD133 (AC133), CD90, flow cytom- in 56-67% of ALL cell samples examined.6,15,16 In con- etry, immunophenotyping trast, another study could not detect CD133 expression in any of 17 ALL samples tested.13 In AML, some stud- haematologica vol. 86(2):February 2001 CD133 (AC133) and CD90 expression in acute leukemia 155 ies have found that Moab AC133 reacts preferentially son). Cell samples were considered positive for a specif- with CD34+ve leukemic cells,13,14,17 although another ic antigen if the antigen was expressed on at least 20% study found no clear difference in CD133 expression of the leukemic cells/sample (= 20 % cut-off level).5,22 levels between CD34+ve and CD34-ve AML.15 A recent Detection of CD133 and CD90 expression in study revealed disconcordant CD133 expression in acute leukemia by flow cytometry patients with AML or myelodysplastic syndrome (MDS) Cells were stained by direct immunofluorescence compared with precursor cells from normal marrow or using the phycoerythrin (PE)-conjugated Moab AC1336 peripheral blood stem cells.18 (IgG1; Miltenyi Biotech, Auburn, CA, USA) and the FITC- To determine the value of CD133 expression analysis conjugated anti-CD90 Moab 5E1019 (IgG1; PharMingen, for acute leukemia immunophenotyping on a large num- San Diego, CA, USA) as recommended by the manufac- ber of acute leukemia samples, we investigated 298 cell turers. Non-specific binding of Fcγ-receptors was samples from children and adults with acute leukemia blocked by pre-incubation of the cells with a polyclon- for their reactivity with Moab AC133 by flow cytome- al rabbit serum (Gibco BRL, Paisley, UK). At least 10,000 try. Furthermore, CD133 expression was compared with cells per sample were acquired and analyzed by flow CD90(Thy-1) expression, an epitope found on approxi- cytometry as described above. Freshly obtained cell sam- mately 25% of CD34+ve cells with enhanced proliferative ples were analyzed by three-color immunophenotyping, and self-renewal capabilities.19 Finally, we correlated using CD90-FITC, CD133-PE and CD34-PECy5 (clone CD133 and CD90 expression with immunophenotypic QBend10; Beckman Coulter, Marseille, France). Non- features, FAB morphology and cyto-/molecular genetic viable cells were excluded by scatter gating. Previously data of the examined patients. cryopreserved cell samples were analyzed by two-color Design and Methods immunophenotyping using the combinations CD90- FITC/CD34-PE, CD34-FITC/CD133-PE, and CD90/CD133- Patients and cell samples PE. In each of these samples, non-viable cells were We examined either freshly obtained or cryopreserved excluded from analysis by propidium iodide co-staining bone marrow or peripheral blood samples from 298 (0.3 µg/mL; Sigma, Deisenhofen, Germany). No differ- patients with acute leukemia for their reactivity with ences in CD133 and CD90 expression patterns between Moab AC1336 and anti-CD90 Moab 5E10.19 In our series, freshly obtained and previously cryopreserved cell sam- 110 children with ALL (90 B-lineage ALL, 20 T-lineage ples were observed. Cell samples were considered posi- ALL), 38 children and 104 adults with de novo AML, and tive for CD90 or CD133 if at least 20% of the leukemic 9 adults with ALL (8 B-lineage ALL, 1 T-lineage ALL) cells/sample specifically stained with Moabs 5E10 or were included. Moreover, cell samples from 13 patients AC133 revealed a higher fluorescence intensity than (2 adults, 11 children) with biphenotypic acute leukemia cells stained with the isotype-matched control antibody (=BAL), and 24 adults with CD34+ve CML blast crisis (=20% cut-off level).5,22 (=BC; 21 myeloid BC/3 B-lymphoid BC) were examined Cytogenetics in this study. The age of the patients examined ranged Chromosome analyses were performed on metaphas- between 10 months and 78 years (median 51 years) for es from short-term (24h, 48h) cultures of pretreatment those with de novo AML, between 1 month and 59 years bone marrow and/or peripheral blood cells. Cell cultiva- (median 5 years) for those with ALL, between 1 year and tion and chromosome preparation were carried out 70 years (median 12 years) for BAL, and between 32 according to standard protocols. G-banding was used years and 83 years (median 53 years) for those in CML and the chromosomes interpreted according to ISCN blast crisis. Diagnosis of acute leukemia was based on (1995) nomenclature.23 Patients with adult AML were immunologic criteria according to EGIL recommenda- grouped into three different risk categories: good: tions5 and morphologically in accordance with FAB cri- t(8;21), inv(16)/t(16;16), t(15;17); intermediate: normal teria.20 B-lineage ALL cases were subgrouped into pro- karyotype, other abnormalities; poor: -5/5q-, -7/7q-, B-ALL, common-ALL, pre-B-ALL, and mature B-ALL, and 11q23-abnormalities, inv(3)/t(3;3), t(9;22), t(6;9), 17p- T-lineage ALL cases into pro-/pre-T-ALL, cortical T-ALL, abnormalities, complex aberrant karyotype (three or and mature T-ALL.5 The diagnosis of BAL was based on more numerical or structural abnormalities).
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