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natural killer cell precursor acute leukemia with tetraploidy
Cancer Genetics and Cytogenetics 163 (2005) 156–159
Short communication
Myeloid/natural killer cell precursor acute leukemia with tetraploidy Gu¨nc¸ag˘ Dinc¸ola,*, Sx u¨kru¨ Palandu¨zb, Meliha Nalc¸acıa, Ali Uc¸urb, Banu Bu¨yu¨kaydına b
a Division of Hematology, Department of Internal Medicine, Istanbul Medical School, University of Istanbul, 34390, Capa, Istanbul, Turkey Division of Medical Genetics, Department of Internal Medicine, Istanbul Medical School, University of Istanbul, 34390, Capa, Istanbul, Turkey
Received 7 July 2004; received in revised form 8 March 2005; accepted 11 April 2005
Abstract
Myeloid/natural killer (NK) cell precursor acute leukemia is characterized by coexpression of myeloid and natural killer cell antigens and an aggressive clinical course. Here we report a case of myeloid/NK precursor acute leukemia in a 37-year-old woman. Clinical presentation was correlated with leukemic blast morphology, immunophenotype, and cytogenetic analysis. The patient had noted fever, weakness, purpura, peripheral lymphadenopathy, and moderate hepatosplenomegaly. Peripheral blood smears and bone marrow aspirate smears at presentation revealed blastic cells, which were generally L2 shaped, with variation in cell size, round to moderately irregular nuclei and prominent nucleoli, pale cytoplasm, and a lack of azurophilic granules. Immunophenotypic analysis of the blasts displayed coexpression of myeloid and natural killer cell antigens with relatively immature phenotype: CD71, CD331, CD341, CD561, CD571, CD162, MPO2. Cytogenetic analysis of marrow cells showed 62% of cells with a normal female karyotype; in the remaining 38%, tetraploid changes were detected, where the chromosome number was 92, with no preferential losses or gains of chromosomes. Fluorescence in situ hybridization analysis revealed the same abnormality. The patient did not respond to chemotherapy (cytosine arabinoside and idarubicin) and died of a septic complication on the 34th day after admission. To our knowledge, this is the first description of tetraploidy in myeloid/NK cell precursor acute leukemia. Ó 2005 Elsevier Inc. All rights reserved.
1. Introduction Myeloid/natural killer(NK) cell precursor acute leukemia as a new clinical entity was proposed by Suzuki et al. in 1997 [1]. It is characterized by coexpression of myeloid with natural killer cell antigens, immature lymphoblastoid morphology, a high incidence of extramedullary disease and an aggressive clinical course. According to their criteria, leukemic cells of this disease are negative for cytochemical myeloperoxidase staining, and express CD7, CD33, CD34, CD56 and frequently HLA-DR but not other NK, T-cell, and B-cell markers [1,2]. Although no recurring chromosomal abnormalities have been found, karyotype analysis of myeloid/NK cell precursor acute leukemia reveals various numerical and structural abnormalities including 7p translocation, 3p abnormalities [1,2], 7q deletion [3], inversion 7 [4], trisomy 10 [5], trisomy 8 [6], trisomy 4 [7], and 6 q abnormality in association with deletion of chromosome 12 [1,8].
* Corresponding author. Tel.: 190-212-414-2310; fax: 190-212-6311263. E-mail address: [email protected] (G. Dinc¸ol). 0165-4608/05/$ – see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.cancergencyto.2005.04.012
We report a case of myeloid/NK cell precursor acute leukemia with tetraploidy. We know of no other report of tetraploidy in myeloid/NK cell precursor acute leukemia.
2. Case report A 37-year-old woman was admitted to our division in April 2004 because of weakness, fever, and purpura. Her medical history revealed that she had never suffered a serious disease, and especially that no previous blood tests had been performed. On admission, clinical examination showed hepatosplenomegaly (both 2 cm below costal margins); cervical, axillary, and inguinal lymphadenopathy; and numerous petechiae and bruises. A computed tomography revealed mild hepatosplenomegaly and peripheral lymphadenopathy. Hemoglobin concentration was 7.4 g/ dL, white blood cell count was 1.1 109/L with 3% neutrophils, 86% lymphocytes, 11% blasts, and platelet count of 32 109/L. A bone marrow aspirate was hypercellular, with 98% blasts. As regards morphology, the cells were generally L2 shaped, with variation in cell size, round to moderately irregular nuclei and prominent nucleoli, and
G. Dinc¸ol et al. / Cancer Genetics and Cytogenetics 163 (2005) 156–159
a lack of azurophilic granules with myeloperoxidase-negative pale cytoplasm. The immunophenotype of the blasts was examined by flow cytometry: CD45 99.8%, CD1a 1.6%, CD2 1.9%, sCD3 3.1%, CD4 3.3%, CD7 98.5%, CD8 6.6%, CD10 1.2%, CD19 1.7%, CD20 2%, CD22 1.3%, CD24 2.2%, CD13 1.3%, CD33 88.8%, CD34 25.2%, CD117(c-kit) 5.3%, CD14 0.7%, CD15 0.6%, HLA-DR 18.7%, CD16 1.5%, CD161CD561 78.2%, CD56 77.6%, CD57 82.5%, CD41 0.8%, glycophorin-A 6.1%, cyCD3 1.7%, MPO (myeloperoxidase) 0.8%, cyCD22 0.9%, cyCD79a 0.9%, and TdT 1.9%. The blasts were very strongly positive for the myeloid antigen CD33. In addition, they were positive for CD7/CD56/ CD57. Cytoplasmic CD3, CD22, CD79a, and MPO were negative, as were the other B- or T-cell antigens (CD19, CD20, CD22, CD24, CD2, CD3, CD4, and CD8). Chromosome studies were performed at the time of diagnosis on unstimulated bone marrow cell cultures for 24 hour. This analysis showed 62% of cells with a normal female karyotype; in the remaining 38%, tetraploid changes were detected, where the chromosome number was 92, with no preferential losses or gains of chromosomes (Figs. 1 and 2). In the fluorescence in situ hybridization (FISH) study, signals were evaluated in 224 nuclei of uncultured bone marrow cells, 86 of which (38%) displayed four signals (Fig. 3). A diagnosis of myeloid/natural killer cell precursor acute leukemia was made. The patient underwent an acute myeloid leukemia chemotherapy protocol consisting of cytosine arabinoside (ara-c) and idarubicin (ida) (ara-c 200mg/m2, on day 1–7; ida 12 mg/m2 on day 1–3). The patient did not respond to
157
chemotherapy. Despite intensive medical care, she died as a result of a septic complication on the 34th day after admission.
3. Materials and methods Fresh bone marrow aspirates were collected into Ham’s F10 medium preservative-free heparin. Cells were cultured in RPMI 1640 medium supplemented with 15% fetal bovine serum for 24 hours; the 24-hour cultures were synchronized with methotrexate in accordance with a method previously reported [9]. Metaphase spreads were prepared by standard methods and G-banded using trypsin and Giemsa stain. Karyotypes were described according to the ISCN 1995 [10]. FISH study was performed on uncultured cells on bone marrow smears which were incubated for one night at 37 C in RPMI-1640 medium for the mechanical removal of the cells from the slide. The cells were then washed with hypotonic (0.75 mol/L) KCl solution and Carnoy’s fixative. FISH was performed as previously described by Pinkel et al. [11], using centromere-specific DNA probe chromosome 7 (D7Z1-ONCOR, Gaithersburg, MD). Hybridization and application were performed according to the manufacturer’s protocols. Chromosomes were counterstained by DAPI (4#,6-diamidino-2-phenylindole) and propidium iodide. FISH results were evaluated with microscopes equipped for epifluorescence (Nikon) and image capture software (Scientific Systems PSI, Newcastle upon Tyne, UK).
Fig. 1. Karyogram showing tetraploidy.
G. Dinc¸ol et al. / Cancer Genetics and Cytogenetics 163 (2005) 156–159
158
Fig. 3. FISH results. In the center, a tetraploid nucleus (4 signals) and a diploid nucleus (2 signals) are seen.
Fig. 2. Metaphase spread showing tetraploidy.
4. Results and discussion Here we have reported the clinical, phenotypic, and cytogenetic features of a patient with myeloid/NK cell precursor acute leukemia diagnosed in our division. The clinical, hematological, and phenotypic characteristics of this patient seemed generally in accordance with previously reported cases [1,2,5]. In addition, the leukemic cells of this patient were positive for the other natural killer–associated antigen, CD57. Notably, our patient with myeloid/NK cell precursor acute leukemia showed 38% tetraploidy as the sole cytogenetic abnormality in all 50 metaphases studied (Figs. 1 and 2). In the FISH analysis, the same ratio of cells displayed tetraploid signals (Fig. 3). Although the clinical significance of this very rare finding is not clear, numerical abnormalities are common in acute lymphocytic leukemia (ALL), found in approximately half of ALL cases, either alone or in association with structural changes. Massive hyperdiploidy is well described in ALL. It has been reported more often in cases of childhood ALL than in adult ALL [12,13]; however, near tetraploidy is rare in both adult and childhood ALL [14]. Hyperdiploidy and tetraploidy are rare cytogenetic abnormalities in myelocytic malignancies and define a prognostically unfavorable cytogenetic group in de novo AML [13,15]. Myeloid/NK cell precursor acute leukemia showed various numerical and structural chromosomal abnormalities. Six of the original seven patients studied by Suzuki et al. [1] had an abnormal karyotype, with five of them being complex. No common karyotype was present, although two reported patients had a similar karyotype, with a 6q abnormality and deletion of chromosome 12 [1,8]. The other chromosomal abnormalities reported in the literature to date are 7p translocation, 3p abnormalities [1,2], 7q
deletion [3], inversion 7 [4], trisomy 10 [5], trisomy 8 [6], and trisomy 4 [7]. The outcome of myeloid/NK cell precursor acute leukemia cases with immature phenotype reported in the literature to date has been poor. Although chemotherapy for acute myeloid leukemia was generally effective for this myeloid/NK cell precursor acute leukemia disease, the remission duration was relatively short and with a fatal outcome, despite multiagent intensive chemotherapy including bone marrow transplantation [1,2,5,6,16]. Our patient did not respond to chemotherapy and the role of tetraploidy in the leukemogenesis or the prognosis of leukemia in this patient remains unclear. To our knowledge, this is the first case of myeloid/NK cell precursor acute leukemia reported in the literature showing tetraploidy with standard cytogenetic analysis and a FISH study on uncultured bone marrow cells. References [1] Suzuki R, Yamamoto K, Seto M, Kagami Y, Ogura M, Yatabe Y, Suchi T, Kodera Y, Morishima Y, Takahashi T, Saito H, Ueda R, Nakamura S. CD71 and CD 561 myeloid/natural killer cell precursor acute leukemia: a distinct hematolymphoid disease entity. Blood 1997;90:2417–28. [2] Suzuki R, Nakamura S. Malignancies of natural killer (NK) cell precursor: myeloid/NK cell precursor acute leukemia and blastic NK cell lymphoma/leukemia. Leuk Res 1999;23:615–24. [3] Nagai M, Bandoh S, Tasaka T, Fujita M, Yamaguchi A, Kuwabara H, Funamato Y, Yamaoka G, Takahara J. Secondary myeloid/natural killer cell precursor acute leukemia following essential thrombocythemia. Hum Pathol 1999;30:868–71. [4] Tezuka K, Nakayama H, Honda K, Suzumiya J, Oshima K, Kitoh T, Ishii E. Treatment of a child with myeloid/NK cell precursor acute leukemia with L-asparaginase and unrelated cord blood transplantation. Int J Hematol 2002;75:201–6. [5] Inaba T, Shimazaki C, Sumikuma T, Ochiai N, Okano A, Hatsuse M, Ashihara E, Kobayashi Y, Rin K, Murakami S, Haruyama H, Fujita N, Nakagawa M. Clinicopathological features of myeloid/ natural killer (NK) cell precursor acute leukemia. Leuk Res 2001;25:109–13.
G. Dinc¸ol et al. / Cancer Genetics and Cytogenetics 163 (2005) 156–159 [6] Kahl C, Pelz A-F, Bartsch R, Jentsch-Ullrich K, Bru¨ckner R, Fostitsch H-P, Franke A. Myeloid/natural killer cell precursor blast crisis of chronic myelogeneous leukemia with two Philadelphia (Ph-1) chromosomes. Ann Hematol 2001;80:58–61. [7] Papadaki HA, Kosteas T, Gemetzi C, Damianaki A, Anagnou NP, Eliopoulos GD. Acute myeloid/NK precursor cell leukemia with trisomy 4 and a novel point mutation in the extracellular domain of the G-CSF receptor in a patient with chronic idiopathic neutropenia. Ann Hematol 2004;83:345–8. [8] Chen VMY, McIlroy K, Loui JPY, Fay K, Ward C. Extramedullary presentation of acute leukaemia: a case of myeloid, natural killer cell precursor leukaemia. Pathology 2003;35:325–9. [9] Barch MJ. The ACT cytogenetics laboratory manual. 2nd ed. New York: Raven Press, 1991. 427–8. [10] ISCN 1995: an international system for human cytogenetic nomenclature (1995). In: Mitelman F, editor. Basel: S. Karger, 1995. [11] Pinkel D, Straume T, Gray JW. Cytogenetic analysis using quantitative, high-sensitivity, fluorescence hybridization. Proc Natl Acad Sci U S A 1986;83:2934–8.
159
[12] Third International Workshop on Chromosomes in Leukemia. Chromosomal abnormalities and their clinical significance in acute lymphoblastic leukemia. Cancer Res 1983;43:868–73. [13] Mitelman F, Johansson B, Mertens F, editors. Mitelman database of chromosome aberrations in cancer [Internet]. Updated November 2001. Available at http://cgap.nci.nih.gov/Chromosomes/Mitelman. Accessed 2001. [14] Walters R, Kantarjian HM, Keating MJ, Estey EH, Trujillo J, Cork A, McCredie KB, Freireich EJ. The importance of cytogenetic studies in adult acute lymphocytic leukemia. Am J Med 1990;89: 579–87. [15] Iyer RV, Sait SNJ, Matsui S-I, Block AMW, Barcos M, Slack JL, Wetzler M, Baer MR. Massive hyperdiploidy and tetraploidy in acute myelocytic leukemia and myelodysplastic syndrome. Cancer Genet Cytogenet 2004;148:29–34. [16] Handa H, Motohashi S, Isozumi K, Komatsumoto S, Nara M. CD71 and CD561 myeloid/natural killer precursor acute leukemia treated with idarubicin and cytosine arabinoside. Acta Haematol 2002;108: 47–52.
Short communication
Myeloid/natural killer cell precursor acute leukemia with tetraploidy Gu¨nc¸ag˘ Dinc¸ola,*, Sx u¨kru¨ Palandu¨zb, Meliha Nalc¸acıa, Ali Uc¸urb, Banu Bu¨yu¨kaydına b
a Division of Hematology, Department of Internal Medicine, Istanbul Medical School, University of Istanbul, 34390, Capa, Istanbul, Turkey Division of Medical Genetics, Department of Internal Medicine, Istanbul Medical School, University of Istanbul, 34390, Capa, Istanbul, Turkey
Received 7 July 2004; received in revised form 8 March 2005; accepted 11 April 2005
Abstract
Myeloid/natural killer (NK) cell precursor acute leukemia is characterized by coexpression of myeloid and natural killer cell antigens and an aggressive clinical course. Here we report a case of myeloid/NK precursor acute leukemia in a 37-year-old woman. Clinical presentation was correlated with leukemic blast morphology, immunophenotype, and cytogenetic analysis. The patient had noted fever, weakness, purpura, peripheral lymphadenopathy, and moderate hepatosplenomegaly. Peripheral blood smears and bone marrow aspirate smears at presentation revealed blastic cells, which were generally L2 shaped, with variation in cell size, round to moderately irregular nuclei and prominent nucleoli, pale cytoplasm, and a lack of azurophilic granules. Immunophenotypic analysis of the blasts displayed coexpression of myeloid and natural killer cell antigens with relatively immature phenotype: CD71, CD331, CD341, CD561, CD571, CD162, MPO2. Cytogenetic analysis of marrow cells showed 62% of cells with a normal female karyotype; in the remaining 38%, tetraploid changes were detected, where the chromosome number was 92, with no preferential losses or gains of chromosomes. Fluorescence in situ hybridization analysis revealed the same abnormality. The patient did not respond to chemotherapy (cytosine arabinoside and idarubicin) and died of a septic complication on the 34th day after admission. To our knowledge, this is the first description of tetraploidy in myeloid/NK cell precursor acute leukemia. Ó 2005 Elsevier Inc. All rights reserved.
1. Introduction Myeloid/natural killer(NK) cell precursor acute leukemia as a new clinical entity was proposed by Suzuki et al. in 1997 [1]. It is characterized by coexpression of myeloid with natural killer cell antigens, immature lymphoblastoid morphology, a high incidence of extramedullary disease and an aggressive clinical course. According to their criteria, leukemic cells of this disease are negative for cytochemical myeloperoxidase staining, and express CD7, CD33, CD34, CD56 and frequently HLA-DR but not other NK, T-cell, and B-cell markers [1,2]. Although no recurring chromosomal abnormalities have been found, karyotype analysis of myeloid/NK cell precursor acute leukemia reveals various numerical and structural abnormalities including 7p translocation, 3p abnormalities [1,2], 7q deletion [3], inversion 7 [4], trisomy 10 [5], trisomy 8 [6], trisomy 4 [7], and 6 q abnormality in association with deletion of chromosome 12 [1,8].
* Corresponding author. Tel.: 190-212-414-2310; fax: 190-212-6311263. E-mail address: [email protected] (G. Dinc¸ol). 0165-4608/05/$ – see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.cancergencyto.2005.04.012
We report a case of myeloid/NK cell precursor acute leukemia with tetraploidy. We know of no other report of tetraploidy in myeloid/NK cell precursor acute leukemia.
2. Case report A 37-year-old woman was admitted to our division in April 2004 because of weakness, fever, and purpura. Her medical history revealed that she had never suffered a serious disease, and especially that no previous blood tests had been performed. On admission, clinical examination showed hepatosplenomegaly (both 2 cm below costal margins); cervical, axillary, and inguinal lymphadenopathy; and numerous petechiae and bruises. A computed tomography revealed mild hepatosplenomegaly and peripheral lymphadenopathy. Hemoglobin concentration was 7.4 g/ dL, white blood cell count was 1.1 109/L with 3% neutrophils, 86% lymphocytes, 11% blasts, and platelet count of 32 109/L. A bone marrow aspirate was hypercellular, with 98% blasts. As regards morphology, the cells were generally L2 shaped, with variation in cell size, round to moderately irregular nuclei and prominent nucleoli, and
G. Dinc¸ol et al. / Cancer Genetics and Cytogenetics 163 (2005) 156–159
a lack of azurophilic granules with myeloperoxidase-negative pale cytoplasm. The immunophenotype of the blasts was examined by flow cytometry: CD45 99.8%, CD1a 1.6%, CD2 1.9%, sCD3 3.1%, CD4 3.3%, CD7 98.5%, CD8 6.6%, CD10 1.2%, CD19 1.7%, CD20 2%, CD22 1.3%, CD24 2.2%, CD13 1.3%, CD33 88.8%, CD34 25.2%, CD117(c-kit) 5.3%, CD14 0.7%, CD15 0.6%, HLA-DR 18.7%, CD16 1.5%, CD161CD561 78.2%, CD56 77.6%, CD57 82.5%, CD41 0.8%, glycophorin-A 6.1%, cyCD3 1.7%, MPO (myeloperoxidase) 0.8%, cyCD22 0.9%, cyCD79a 0.9%, and TdT 1.9%. The blasts were very strongly positive for the myeloid antigen CD33. In addition, they were positive for CD7/CD56/ CD57. Cytoplasmic CD3, CD22, CD79a, and MPO were negative, as were the other B- or T-cell antigens (CD19, CD20, CD22, CD24, CD2, CD3, CD4, and CD8). Chromosome studies were performed at the time of diagnosis on unstimulated bone marrow cell cultures for 24 hour. This analysis showed 62% of cells with a normal female karyotype; in the remaining 38%, tetraploid changes were detected, where the chromosome number was 92, with no preferential losses or gains of chromosomes (Figs. 1 and 2). In the fluorescence in situ hybridization (FISH) study, signals were evaluated in 224 nuclei of uncultured bone marrow cells, 86 of which (38%) displayed four signals (Fig. 3). A diagnosis of myeloid/natural killer cell precursor acute leukemia was made. The patient underwent an acute myeloid leukemia chemotherapy protocol consisting of cytosine arabinoside (ara-c) and idarubicin (ida) (ara-c 200mg/m2, on day 1–7; ida 12 mg/m2 on day 1–3). The patient did not respond to
157
chemotherapy. Despite intensive medical care, she died as a result of a septic complication on the 34th day after admission.
3. Materials and methods Fresh bone marrow aspirates were collected into Ham’s F10 medium preservative-free heparin. Cells were cultured in RPMI 1640 medium supplemented with 15% fetal bovine serum for 24 hours; the 24-hour cultures were synchronized with methotrexate in accordance with a method previously reported [9]. Metaphase spreads were prepared by standard methods and G-banded using trypsin and Giemsa stain. Karyotypes were described according to the ISCN 1995 [10]. FISH study was performed on uncultured cells on bone marrow smears which were incubated for one night at 37 C in RPMI-1640 medium for the mechanical removal of the cells from the slide. The cells were then washed with hypotonic (0.75 mol/L) KCl solution and Carnoy’s fixative. FISH was performed as previously described by Pinkel et al. [11], using centromere-specific DNA probe chromosome 7 (D7Z1-ONCOR, Gaithersburg, MD). Hybridization and application were performed according to the manufacturer’s protocols. Chromosomes were counterstained by DAPI (4#,6-diamidino-2-phenylindole) and propidium iodide. FISH results were evaluated with microscopes equipped for epifluorescence (Nikon) and image capture software (Scientific Systems PSI, Newcastle upon Tyne, UK).
Fig. 1. Karyogram showing tetraploidy.
G. Dinc¸ol et al. / Cancer Genetics and Cytogenetics 163 (2005) 156–159
158
Fig. 3. FISH results. In the center, a tetraploid nucleus (4 signals) and a diploid nucleus (2 signals) are seen.
Fig. 2. Metaphase spread showing tetraploidy.
4. Results and discussion Here we have reported the clinical, phenotypic, and cytogenetic features of a patient with myeloid/NK cell precursor acute leukemia diagnosed in our division. The clinical, hematological, and phenotypic characteristics of this patient seemed generally in accordance with previously reported cases [1,2,5]. In addition, the leukemic cells of this patient were positive for the other natural killer–associated antigen, CD57. Notably, our patient with myeloid/NK cell precursor acute leukemia showed 38% tetraploidy as the sole cytogenetic abnormality in all 50 metaphases studied (Figs. 1 and 2). In the FISH analysis, the same ratio of cells displayed tetraploid signals (Fig. 3). Although the clinical significance of this very rare finding is not clear, numerical abnormalities are common in acute lymphocytic leukemia (ALL), found in approximately half of ALL cases, either alone or in association with structural changes. Massive hyperdiploidy is well described in ALL. It has been reported more often in cases of childhood ALL than in adult ALL [12,13]; however, near tetraploidy is rare in both adult and childhood ALL [14]. Hyperdiploidy and tetraploidy are rare cytogenetic abnormalities in myelocytic malignancies and define a prognostically unfavorable cytogenetic group in de novo AML [13,15]. Myeloid/NK cell precursor acute leukemia showed various numerical and structural chromosomal abnormalities. Six of the original seven patients studied by Suzuki et al. [1] had an abnormal karyotype, with five of them being complex. No common karyotype was present, although two reported patients had a similar karyotype, with a 6q abnormality and deletion of chromosome 12 [1,8]. The other chromosomal abnormalities reported in the literature to date are 7p translocation, 3p abnormalities [1,2], 7q
deletion [3], inversion 7 [4], trisomy 10 [5], trisomy 8 [6], and trisomy 4 [7]. The outcome of myeloid/NK cell precursor acute leukemia cases with immature phenotype reported in the literature to date has been poor. Although chemotherapy for acute myeloid leukemia was generally effective for this myeloid/NK cell precursor acute leukemia disease, the remission duration was relatively short and with a fatal outcome, despite multiagent intensive chemotherapy including bone marrow transplantation [1,2,5,6,16]. Our patient did not respond to chemotherapy and the role of tetraploidy in the leukemogenesis or the prognosis of leukemia in this patient remains unclear. To our knowledge, this is the first case of myeloid/NK cell precursor acute leukemia reported in the literature showing tetraploidy with standard cytogenetic analysis and a FISH study on uncultured bone marrow cells. References [1] Suzuki R, Yamamoto K, Seto M, Kagami Y, Ogura M, Yatabe Y, Suchi T, Kodera Y, Morishima Y, Takahashi T, Saito H, Ueda R, Nakamura S. CD71 and CD 561 myeloid/natural killer cell precursor acute leukemia: a distinct hematolymphoid disease entity. Blood 1997;90:2417–28. [2] Suzuki R, Nakamura S. Malignancies of natural killer (NK) cell precursor: myeloid/NK cell precursor acute leukemia and blastic NK cell lymphoma/leukemia. Leuk Res 1999;23:615–24. [3] Nagai M, Bandoh S, Tasaka T, Fujita M, Yamaguchi A, Kuwabara H, Funamato Y, Yamaoka G, Takahara J. Secondary myeloid/natural killer cell precursor acute leukemia following essential thrombocythemia. Hum Pathol 1999;30:868–71. [4] Tezuka K, Nakayama H, Honda K, Suzumiya J, Oshima K, Kitoh T, Ishii E. Treatment of a child with myeloid/NK cell precursor acute leukemia with L-asparaginase and unrelated cord blood transplantation. Int J Hematol 2002;75:201–6. [5] Inaba T, Shimazaki C, Sumikuma T, Ochiai N, Okano A, Hatsuse M, Ashihara E, Kobayashi Y, Rin K, Murakami S, Haruyama H, Fujita N, Nakagawa M. Clinicopathological features of myeloid/ natural killer (NK) cell precursor acute leukemia. Leuk Res 2001;25:109–13.
G. Dinc¸ol et al. / Cancer Genetics and Cytogenetics 163 (2005) 156–159 [6] Kahl C, Pelz A-F, Bartsch R, Jentsch-Ullrich K, Bru¨ckner R, Fostitsch H-P, Franke A. Myeloid/natural killer cell precursor blast crisis of chronic myelogeneous leukemia with two Philadelphia (Ph-1) chromosomes. Ann Hematol 2001;80:58–61. [7] Papadaki HA, Kosteas T, Gemetzi C, Damianaki A, Anagnou NP, Eliopoulos GD. Acute myeloid/NK precursor cell leukemia with trisomy 4 and a novel point mutation in the extracellular domain of the G-CSF receptor in a patient with chronic idiopathic neutropenia. Ann Hematol 2004;83:345–8. [8] Chen VMY, McIlroy K, Loui JPY, Fay K, Ward C. Extramedullary presentation of acute leukaemia: a case of myeloid, natural killer cell precursor leukaemia. Pathology 2003;35:325–9. [9] Barch MJ. The ACT cytogenetics laboratory manual. 2nd ed. New York: Raven Press, 1991. 427–8. [10] ISCN 1995: an international system for human cytogenetic nomenclature (1995). In: Mitelman F, editor. Basel: S. Karger, 1995. [11] Pinkel D, Straume T, Gray JW. Cytogenetic analysis using quantitative, high-sensitivity, fluorescence hybridization. Proc Natl Acad Sci U S A 1986;83:2934–8.
159
[12] Third International Workshop on Chromosomes in Leukemia. Chromosomal abnormalities and their clinical significance in acute lymphoblastic leukemia. Cancer Res 1983;43:868–73. [13] Mitelman F, Johansson B, Mertens F, editors. Mitelman database of chromosome aberrations in cancer [Internet]. Updated November 2001. Available at http://cgap.nci.nih.gov/Chromosomes/Mitelman. Accessed 2001. [14] Walters R, Kantarjian HM, Keating MJ, Estey EH, Trujillo J, Cork A, McCredie KB, Freireich EJ. The importance of cytogenetic studies in adult acute lymphocytic leukemia. Am J Med 1990;89: 579–87. [15] Iyer RV, Sait SNJ, Matsui S-I, Block AMW, Barcos M, Slack JL, Wetzler M, Baer MR. Massive hyperdiploidy and tetraploidy in acute myelocytic leukemia and myelodysplastic syndrome. Cancer Genet Cytogenet 2004;148:29–34. [16] Handa H, Motohashi S, Isozumi K, Komatsumoto S, Nara M. CD71 and CD561 myeloid/natural killer precursor acute leukemia treated with idarubicin and cytosine arabinoside. Acta Haematol 2002;108: 47–52.