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Sustained Complete Remission of Recurrent Acute Myeloid Correspondence 1870 evidence was provided by the detection of the TEl-AML1 (now known HG Drexler DSMZ-German Collection of Micro-organisms as EVT6-RUNX1) fusion gene which results fromthe t(12;21)(p13;q22) H Quentmeier and Cell Cultures,Braunschweig,Germany and which occurs only in primary and cultured BCP cells (including WG Dirks cell line REH);4 all three cell cultures examined showed this genetic CC Uphoff abnormality (Figure 2). Cytogenetic analysis has shown that the TEL- RAF MacLeod AML1 fusion is generated in REH by a unique four-way translocation, t(4;12;21;16)4 which we have now confirmed in WSU-CLL. Taken together, WSU-CLL is definitely only a subclone of cell line REH and References is hence a BCP cell line. It has been reported that there are significant phenotypic differences 1 Drexler HG, Dirks WG, MacLeod RAF. False human hematopo- ietic cell lines: cross-contaminations and misinterpretations. Leu- between WSU-CLL and REH. For instance, while WSU-CLL grows kemia 1999; 13: 1601–1607. very well in SCID mice, REH cells allegedly do not grow in these 2 Drexler HG (ed). The Leukemia–Lymphoma Cell Line FactsBook. animals. However, a literature search shows that different investi- Academic Press: San Diego, 2000. gators were able successfully to heterotransplant REH cells into nude 3 Mohammad RM, Mohamed AN, Hamdan MY, Vo T, Chen B, Kat- and SCID mice.6 Nevertheless, it is well known that subclones derived ato K, Abubakr YA, Dugan MC, Al-Katib A. Establishment of a explicitly or inadvertently fromtheir parental cultures can develop human B-CLL xenograft model: utility as a preclinical therapeutic quite divergent phenotypic features. A good case in point is the widely model. Leukemia 1996; 10: 130–137. distributed cell line K-562 for which quite dramatic phenotypic differ- 4 Uphoff CC, MacLeod RAF, Denkmann SA, Golub TR, Borkhardt ences between subcultures with regard to growth kinetics, cloning A, Janssen JWG, Drexler HG. Occurrence of TEL-AML1 fusion 7 efficiency and hemoglobin production have been noted. A large resulting from(12;21) translocation in humanearly B-lineage leu- panel of K-562 sublines shared several common surface antigens but kemia cell lines. Leukemia 1997; 11: 441–447. 8 expressed a marked diversity and variability of other markers. In this 5 Drexler HG, Dirks WG, MacLeod RAF, Quentmeier H, Steube KG, context, we examined the expression of a panel of immunomarkers Uphoff CC (eds). DSMZ Catalogue of Human and Animal Cell on the cell lines WSU-CLL, REH (ATCC) and REH (DSMZ) (Table 1). Lines, 8th edn. Braunschweig: Germany, 2001. It became evident that these genotypically identical cell lines express 6 Hara H, Luo Y, Haruta Y, Seon BK. Efficient transplantation of some phenotypic markers to various extents, eg CD20, CD34, CD138 human non-T-leukemia cells into nude mice and induction of (Figure 3). complete regression of the transplanted distinct tumors by ricin A- In summary, different approaches have revealed that the WSU-CLL chain conjugates of monoclonal antibodies SN5 and SN6. Cancer cell line is indeed the REH cell line and most likely resulted from Res 1988; 48: 4673–4680. an inadvertent cross-contamination during cell culture at the original 7 Dimery IW, Ross DD, Testa JR, Gupta SK, Felsted RL, Pollack A, source, presumably during the attempts to establish a B-CLL cell line. Bachur NR. Variation amongst K562 cell cultures. Exp Hematol Hence, WSU-CLL is a subclone of BCP-ALL cell line REH and it is 1983; 7: 601–610. clearly inappropriate to use WSU-CLL as a model for B-CLL. 8 Ichiki AT, Bamberger EG, Wust CJ, Lozzio CB. Diversity of cell surface hematopoietic antigens on K-562 sublines identified with monoclonal antibodies. Leukemia Res 1986; 10: 565–574. Sustainedcomplete remission of recurrent acute myeloidleukaemia with a single dose of gemtuzumab ozogamicin and low-dose interleukin-2 maintenance Leukemia (2002) 16, 1870–1871. doi:10.1038/sj.leu.2402594 tered with idarubicin, etoposide and cytarabine. This time treatment was complicated by atrial fibrillation and pneumonia during pro- TO THE EDITOR longed cytopenia. Leukocytes and platelets regenerated 22 and 26 days, respectively, after chemotherapy. Treatment of relapsed AML is difficult, especially if remission duration Another 6 months later the patient was readmitted with her second was short, if it is later than first relapse, if karyotype is unfavourable recurrence of AML and t(1;22)(p11;p11) was observed as second cyto- or if the patient is not eligible for intensive treatment. We report a case genetic aberration. Treatment with oral low-dose melphalan (2 of a 76-year-old female patient presenting with all these unfavourable mg/day) was initiated. This treatment has been shown to be well toler- predictors. Remarkably, this patient entered a third complete ated and effective in some patients with secondary AML.1 However, remission (CR) following a single dose of gemtuzumab ozogamicin re-evaluation 4 weeks later demontrated progressive pancytopenia, (CMA-676), and CR duration with low-dose interleukin-2 (IL-2) increased marrow blast counts and del(1)(q21) as the third cyto- maintenance now exceeds 11 months. genetic abnormality. The patient was first diagnosed with AML, FAB M5, with The patient was well informed about her prognosis and agreed on t(1;21)(q21;q22) in October 1998. The patient was treated with cytara- a single dose of CMA-676 (9 mg/m2), although administration of two bine, daunorubicin and the multidrug resistance modulator PSC 833 doses is generally recommended.2 CMA-676 is a humanized murine for induction resulting in CR, followed by two consolidation chemo- anti-CD33 antibody linked to the potent tumor antibiotic Nac-gamma therapies which consisted of cytarabine, daunorubicin and PSC 833 calicheamicin. Calicheamicin exerts its toxic effects only after cleav- (consolidation 1), and cytarabine, mitoxantrone and etoposide age fromthe antibody following incorporation into CD33-positive (consolidation 2). Treatment was complicated by profuse peranal cells; toxin bound to antibody is inactive.3 CD33 is brightly expressed bleeding during pancytopenia following induction. on most AML blasts and on some myeloid precursors, but scarcely Fourteen months later the patient was readmitted with first relapse expressed in non-myeloid tissues and absent on hematopoietic stem of AML. Treatment with mitoxantrone, etoposide and cytarabine, cells.4 Distribution of CD33 antigen and properties of the immuno- resulted again in CR. One cycle of consolidation therapy was adminis- toxin explain anti-AML selectivity of CMA-676 compared to conven- tional chemotherapeutic drugs. In 142 patients with CD33-positive AML in first relapse a 30% overall remission rate was achieved.5 Correspondence: C Denzlinger, Dept of Haematology/Oncology, Uni- In our patient, leukemic blasts highly expressed the CD33 antigen versity of Tu¨bingen, Medical School, Otfried-Mu¨ller-Str. 10, D-72076 and treatment with CMA-676 was effective and well tolerated: bone Tu¨bingen, Germany; Fax: +49 7071 29 5695 marrow aspirate on day 40 showed complete clearance of leukaemic Received 11 January 2002; accepted 11 April 2002 blasts. The major adverse reaction was prolonged pancytopenia asso- Leukemia Correspondence 1871 ciated with pulmonary infiltrates, which were responsive to combined patients with high-risk myelodysplastic syndromes or secondary antibiotic and antimycotic therapy. Haematological reconstitution acute myeloid leukaemia. Br J Haematol 2000; 108: 93–95. was achieved at day 48 for leukocytes (Ͼ3 × 109/l) and at day 54 for 2 Sievers EL, Linenberger M. Mylotarg: antibody-targeted chemo- platelets (Ͼ20 × 109/l, without substitution). Substitution was with 17 therapy comes of age. Curr Opin Oncol 2001; 13: 522–527. packed red blood cell concentrates and 23 pooled platelet concen- 3 Sievers EL, AppelbaumFR, Spielberger RT, FormanSJ, Flowers D, trates. CR with platelets Ͼ100 × 109/l was obtained 64 days after Smith FO, Shannon-Dorcy K, Berger MS, Bernstein ID. Selective CMA-676. ablation of acute myeloid leukemia using antibody-targeted Due to high risk of relapse, we started outpatient maintenance with chemotherapy: a phase I study of an anti-CD33 immunoconjugate. subcutaneous IL-2. Blood 1999; 93: 3678–3684. IL-2 has the potential to enhance cytotoxic activity of NK and 4 Griffin JD, Linch D, Sabbath K, Larcom P, Schlossman SF. A mono- cytotoxic T cells against AML blasts.6 Clinical trials have shown that clonal antibody reactive with normal and leukemic human treatment with IL-2 may be beneficial in the therapy of AML.7 myeloid progenitor cells. Leuk Res 1984; 8: 521–534. The initial schedule with 5 million units of IL-2 on 5 consecutive 5 Sievers EL, Larson RA, Stadtmauer EA, Estey E, Lowenberg B, Dom- days per month, was reduced to 4 Mio U and 3 Mio U in consecutive bret H, Karanes C, Theobald M, Bennett JM, Sherman ML, Berger cycles due to flu-like symptoms during treatment days. The latter dose MS, Eten CB, Loken MR, van Dongen JJ, Bernstein ID, Appelbaum was well tolerated, and our patient is still in complete remission 11 FR. Efficacy and safety of gemtuzumab ozogamicin in patients months post CMA-676 induction. with CD33-positive acute myeloid leukemia in first relapse. J Clin This case illustrates that novel treatment options such as CMA-676 Oncol 2001; 9: 3244–3254. followed by IL-2 maintenance open therapeutic perspectives and may 6 Adler A, Chervenick PA, Whiteside TL, Lotzova E, Herberman RB. save vital time of life for elderly patients even if conditions are strongly Interleukin 2 induction of lymphokine-activated killer (LAK) predictive of unfavourable outcome. We suggest that this approach activity in the peripheral blood and bone marrow of acute leuke- deserves further study. mia patients. I. Feasibility of LAK generation in adult patients with active disease and in remission.
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