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Journal articles on the topic 'Leukemie'

Author: Grafiati

Published: 4 June 2021

Last updated: 31 January 2023

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1

van Sprundel, Mariska. "Leukemie." Nursing 28, no. 5 (2022): 45–51. http://dx.doi.org/10.1007/s41193-022-0063-x.

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2

BOOGAERTS MA. "Milieu en leukemie." Tijdschrift voor Geneeskunde 55, no. 3 (1999): 206–11. http://dx.doi.org/10.2143/tvg.55.3.5000346.

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3

Špaček, Martin. "Treatment of relapsed chronic lymphocytic leukemia." Onkologie 13, no. 3 (2019): 107–10. http://dx.doi.org/10.36290/xon.2019.021.

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4

VAN HOVE W. "Acute leukemie. Dertig jaar therapie." Tijdschrift voor Geneeskunde 54, no. 3 (1998): 191–94. http://dx.doi.org/10.2143/tvg.54.3.5000034.

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5

Venrooij, Twan van. "Venetoclax bij acute myeloïde leukemie." Hemato-oncologie 8, no. 4 (2021): 11–12. http://dx.doi.org/10.24078/hemato.2021.11.128202.

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6

Szotkowski, Tomáš, Martin Čerňan, Jaromír Hubáček, Milena Holzerová, and Tomáš Papajík. "Anticancer therapy - related acute myeloid leukemias." Onkologie 11, no. 3 (2017): 115–20. http://dx.doi.org/10.36290/xon.2017.023.

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7

SCHUERMANS C and VERHOEF G. "T-LGL-leukemie bij reumatoïde artritis." Tijdschrift voor Geneeskunde 62, no. 6 (2006): 445–51. http://dx.doi.org/10.2143/tvg.62.6.5002423.

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8

Brand, T. "Leukemie bij kinderen door werk ouders." Tijdschrift Voor Bedrijfs- en Verzekeringsgeneeskunde 16, no. 9 (2008): 414. http://dx.doi.org/10.1007/bf03321426.

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9

Bruijnzeel, P. L. B. "De behandeling van acute lymfatische leukemie." Medisch-Farmaceutische Mededelingen 44, no. 7 (2006): 219–20. http://dx.doi.org/10.1007/bf03058835.

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10

Cavanna, Luigi, Daniele Vallisa, Michele Di Stasi, et al. "Acute Myelocytic Leukemia and Chronic Myelomonocytic Leukemia Simultaneously with Resectable Breast Cancer: A Report of two Cases." Tumori Journal 78, no. 5 (1992): 356–58. http://dx.doi.org/10.1177/030089169207800516.

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This report describes 2 patients who developed acute myelocytic leukemie (AML) type M2 and chronic myelomonocytic leukemia (CMML) of the FAB classification, respectively 2 months and 2 weeks after diagnosis of operable breast cancer. The patient with AML showed pancytopenia 2 months before the diagnosis of AML, had a normal karyotype, and showed a good response to chemotherapy. The patient with CMML had a normal karyotype, and she was treated with hydroxyurea and supportive therapy. The 2 patients had no previous exposure to irradiation or cytotoxic therapy. These cases show that breast cancer

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11

Havlíčková, Barbora. "Autoimunne haemolytic anaemia as a complication of a Chronic Lymphocytic Leukaemia." Interní medicína pro praxi 20, no. 3 (2018): e9-e14. http://dx.doi.org/10.36290/int.2018.056.

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12

Šustková, Zuzana, and Zdeněk Ráčil. "Acute leukemia - what should general practitioners know about." Medicína pro praxi 13, no. 4 (2016): 192–95. http://dx.doi.org/10.36290/med.2016.041.

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13

de Rooij, M. L., S. S. N. de Graaf, E. S. J. M. de Bont, and G. J. L. Kaspers. "Acute promyelocytaire leukemie bij kinderen in Nederland." Tijdschrift voor Kindergeneeskunde 77, no. 1 (2009): 22–30. http://dx.doi.org/10.1007/bf03086348.

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14

Šrámková, Lucie. "New therapeutic modalities in the treatment of childhood acute lymphoblastic leukemia." Česko-slovenská pediatrie 77, no. 5 (2022): 265–71. http://dx.doi.org/10.55095/cspediatrie2022/042.

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15

Klamová, Hana. "Current approach for chronic myeloid leukemia treatment with tyrosin kinase inhibitors." Onkologie 10, no. 3 (2016): 120–26. http://dx.doi.org/10.36290/xon.2016.026.

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16

Bisschop, M. M., T. R. évész, and M. Bierings. "Chloroom als presentatie van acute niet-lymfatische leukemie." Tijdschrift voor kindergeneeskunde 69, no. 2 (2001): 184–87. http://dx.doi.org/10.1007/bf03061353.

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17

Van de Streek, Jenneke. "Studie nieuw middel chronische lymfatische leukemie stopt om succes." Mednet 6, no. 11-12 (2013): 20. http://dx.doi.org/10.1007/s12462-013-0316-0.

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18

Tomic, Welko, and André Brouwers. "Kwaliteit van leven en zingeving bij chronische lymfatische leukemie." Psychologie en Gezondheid 37, no. 3 (2009): 134–44. http://dx.doi.org/10.1007/bf03080386.

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19

Wassenaar, M., C. A. J. Brouwer, J. M. Vonk, W. A. Kamps, and A. Postma. "Overgewicht na behandeling voor acute lymfatische leukemie bij kinderen." Tijdschrift voor kindergeneeskunde 75, no. 4 (2007): 149–53. http://dx.doi.org/10.1007/bf03061683.

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20

Bose, Chinmoy K., Nirban Basu, and Mohini Basu. "Cílená léčba mutované formy isocitrát dehydrogenázy 1 u akutní myeloidní leukemie - příběh ivosidenibu." Onkologie 14, no. 6 (2021): 295–98. http://dx.doi.org/10.36290/xon.2020.097.

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21

Kingma, A., and R. Blaauwbroek. "Blijvende neuropsychologische schade na behandeling wegens leukemie of een hersentumor." Bijblijven 22, no. 8 (2006): 314–20. http://dx.doi.org/10.1007/bf03059958.

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22

Wiley, James S., Carole L. Smith, and Gary P. Jamieson. "Transport of 2′-deoxycoformycin in human leukemie and lymphoma cells." Biochemical Pharmacology 42, no. 3 (1991): 708–10. http://dx.doi.org/10.1016/0006-2952(91)90338-6.

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23

Hrabovský, Štěpán, František Folber, Barbora Jurová, Zdeněk Řehák, and Michael Doubek. "Acute lymphoblastic leukemia of adults - a case of prolonged hip pain diagnostics with a surprising conclusion: case report." Vnitřní lékařství 63, no. 5 (2017): 348–53. http://dx.doi.org/10.36290/vnl.2017.070.

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24

VAN HOOF A, SELLESLAG D, BILLIET J, HIDAYAT M, CRIEL A, and LOUWAGIE A. "Myelodysplasie en leukemie na voorafgaandelijke blootstelling aan chemotherapie en/of radiotherapie." Tijdschrift voor Geneeskunde 54, no. 12 (1998): 839–49. http://dx.doi.org/10.2143/tvg.54.12.5000149.

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25

VERHOEF G, DELFORGE M, MAERTENS J, et al. "Recente inzichten in de pathofysiologie en behandeling van chronische lymfatische leukemie." Tijdschrift voor Geneeskunde 56, no. 7 (2000): 519–25. http://dx.doi.org/10.2143/tvg.56.7.5000711.

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26

Koten, Jan-Willem. "Verhoogd risico folliculair lymfoom en chronische lymfatische leukemie bij blootstelling trichloorethyleen." TBV – Tijdschrift voor Bedrijfs- en Verzekeringsgeneeskunde 22, no. 2 (2014): 56–57. http://dx.doi.org/10.1007/s12498-014-0025-6.

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27

Faber, Edgar. "20 let klinických zkušeností s léčbou chronické myeloidní leukemie inhibitory tyrosinové kinázy." Vnitřní lékařství 66, no. 4 (2020): E4. http://dx.doi.org/10.36290/vnl.2020.072.

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28

VERHOEF G, VANDENBERGHE P, MAERTENS J, DELFORGE M, VERBURGH E, and BOOGAERTS MA. "Impact van de moleculaire biologie op de behandeling van chronische myeloïde leukemie." Tijdschrift voor Geneeskunde 57, no. 8 (2001): 601–8. http://dx.doi.org/10.2143/tvg.57.8.5001032.

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29

Lous, A. Mol, J. D. Bosch, J. E. W. M. Dongen-Melman, and J. Huisman. "Late emotionele problematiek en cognitief functioneren bij kinderen met acute lymfatische leukemie." Tijdschrift voor kindergeneeskunde 69, no. 1 (2001): 210–15. http://dx.doi.org/10.1007/bf03061359.

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30

Blink, M., T. D. Buitenkamp, J. P. van Wouwe, E. R. van Wering, V. H. J. van der Velden, and C. M. Zwaan. "Ontwikkelingen in de diagnostiek en behandeling van leukemie bij kinderen met downsyndroom." Tijdschrift voor Kindergeneeskunde 77, no. 2 (2009): 52–58. http://dx.doi.org/10.1007/bf03086357.

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31

Mihál, Vladimír, Zbyněk Novák, Petr Kamínek, Jan Hrbek, and Kamila Michálková. "Development of multifocal osteonecrosis of both ankles in a adolescent boy during the aggressive treatment of acute lymphoblastic leukemia." Pediatrie pro praxi 22, no. 1 (2021): 69–72. http://dx.doi.org/10.36290/ped.2021.013.

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32

Adam, Zdeněk, Luděk Pour, Marta Krejčí, et al. "Plasma cell neoplasms, multiple myeloma, solitary plasmocytoma a plasma cell leukemia. Clinical symptoms, diagnostic criteria and therapy." Onkologie 16, Suppl. B (2022): 7–32. http://dx.doi.org/10.36290/xon.2022.054.

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33

Yan, Ying, Peter Steinherz, Xiuqin Guan, Ann Jakubowski, Joesph P. McGuirk, and Richard J. O’Reilly. "Growth Potential of Human Leukemia Blast Cells in SCID Mice and Association with Prognosis of Human Acute Leukemias." Blood 104, no. 11 (2004): 1900. http://dx.doi.org/10.1182/blood.v104.11.1900.1900.

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Abstract We have described a severe combined immunodeficiency (SCID) mouse model that permits the subcutaneous growth of primary human acute leukemia blast cells into a measurable subcutaneous nodule which may be followed by the development of disseminated disease. Utilizing the SCID mouse model, we examined the ability of patient-derived leukemic blasts to generate leukemic growth in the animals after subcutaneous inoculation without conditioning treatment. Leukemia blasts derived from 133 patients with acute leukemias, (67 acute lymphoblastic leukemia (ALL) and 66 acute myeloid leukemia (AML

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34

Abdel-Wahab, Omar, and Ross L. Levine. "Metabolism and the leukemic stem cell." Journal of Experimental Medicine 207, no. 4 (2010): 677–80. http://dx.doi.org/10.1084/jem.20100523.

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Acute leukemias are clonal disorders of hematopoiesis wherein a leukemic stem cell (LSC) acquires mutations that confer the capacity for unlimited self-renewal, impaired hematopoietic differentiation, and enhanced proliferation to the leukemic clone. Many recent advances in understanding the biology of leukemia have come from studies defining specific genetic and epigenetic abnormalities in leukemic cells. Three recent articles, however, further our understanding of leukemia biology by elucidating specific abnormalities in metabolic pathways in leukemic hematopoiesis. These studies potentially

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35

Horton, Sarah J., Vanessa Walf-Vorderwülbecke, Steve J. Chatters, Neil J. Sebire, Jasper de Boer, and Owen Williams. "Acute myeloid leukemia induced by MLL-ENL is cured by oncogene ablation despite acquisition of complex genetic abnormalities." Blood 113, no. 20 (2009): 4922–29. http://dx.doi.org/10.1182/blood-2008-07-170480.

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Abstract Chromosomal translocations involving 11q23 are frequent in infant acute leukemia and give rise to the formation of MLL fusion genes. The mechanism of leukemic transformation by these fusions has been the subject of numerous investigations. However, the dependence of acute leukemia on MLL fusion activity in vivo and the efficacy of targeting this activity to eliminate disease have not been established. We have developed a model for conditional expression of MLL-ENL in hematopoietic progenitor cells, in which expression of the fusion oncogene is turned off by doxycycline. Conditionally

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36

Dias, Sergio, Margaret Choy, Kari Alitalo, and Shahin Rafii. "Vascular endothelial growth factor (VEGF)–C signaling through FLT-4 (VEGFR-3) mediates leukemic cell proliferation, survival, and resistance to chemotherapy." Blood 99, no. 6 (2002): 2179–84. http://dx.doi.org/10.1182/blood.v99.6.2179.

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Abstract Similar to solid tumors, growth of leukemias may also be angiogenesis dependent. Furthermore, tyrosine kinase receptors specific to endothelial cells are expressed on certain subsets of leukemias. We have previously demonstrated the existence of a VEGF/VEGFR-2 autocrine loop on leukemic cells that supports their growth and migration. Here, we demonstrate that in response to leukemia-derived proangiogenic and proinflammatory cytokines such as basic fibroblast growth factor and IL-1, endothelial cells release increasing amounts of another vascular endothelial growth factor (VEGF) family

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37

Gilliland, D. Gary, Craig T. Jordan, and Carolyn A. Felix. "The Molecular Basis of Leukemia." Hematology 2004, no. 1 (2004): 80–97. http://dx.doi.org/10.1182/asheducation-2004.1.80.

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Abstract Major strides have been made in our understanding of the molecular basis of adult and pediatric leukemias. More than one hundred disease alleles have been identified and characterized in cell culture and murine models of leukemia. In some instances, molecularly targeted therapies have been developed based on these insights that are currently in clinical trials, such as small molecule inhibitors of FLT3. In addition, it has recently been appreciated that, as with normal hematopoiesis, there is a hierarchical organization among leukemic cells that includes a rare population of leukemic

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38

Buss, Eike C., Alexander Kalinkovich, Amir Schajnovitz, et al. "In Vivo Mobilization of Leukemic Human Precursor-B-ALL Cells by the CXCR4-Antagonist AMD3100 Is Via Secretion of SDF-1 and Synergistically by Catecholamine Action." Blood 112, no. 11 (2008): 1920. http://dx.doi.org/10.1182/blood.v112.11.1920.1920.

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Abstract Introduction Mobilization of leukemic cells from the bone marrow (BM) to the circulation in order to better kill them with DNA damaging chemotherapy agents is emerging as a new experimental therapeutic intervention, however the mechanism is not entirely clear. Currently CXCR4-antagonists such as the mobilizing agent AMD3100 (AMD) are becoming available for clinical usage. The aim of this study is to explore mechanisms of human precursor-B-ALL cell mobilization from the BM in a functional, pre-clinical immune deficient mouse model. Methodology Immunodeficient mice were stably engrafted

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39

Adamaki, Maria, Spiros Vlahopoulos, George I. Lambrou, Athanasios G. Papavassiliou, and Maria Moschovi. "Aberrant AML1 gene expression in the diagnosis of childhood leukemias not characterized by AML1-involved cytogenetic abnormalities." Tumor Biology 39, no. 3 (2017): 101042831769430. http://dx.doi.org/10.1177/1010428317694308.

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The AML1 ( acute myeloid leukemia 1) gene, a necessary prerequisite of embryonic hematopoiesis and a critical regulator of normal hematopoietic development, is one of the most frequently mutated genes in human leukemia, involving over 50 chromosome translocations and over 20 partner genes. In the few existing studies investigating AML1 gene expression in childhood leukemias, aberrant upregulation seems to specifically associate with AML1 translocations and amplifications. The aim of this study was to determine whether overexpression also extends to other leukemic subtypes than the ones karyoty

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40

Kogan, Scott C., Diane E. Brown, David B. Shultz та ін. "Bcl-2 Cooperates with Promyelocytic Leukemia Retinoic Acid Receptor α Chimeric Protein (Pmlrarα) to Block Neutrophil Differentiation and Initiate Acute Leukemia". Journal of Experimental Medicine 193, № 4 (2001): 531–44. http://dx.doi.org/10.1084/jem.193.4.531.

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The promyelocytic leukemia retinoic acid receptor α (PMLRARα) chimeric protein is associated with acute promyelocytic leukemia (APL). PMLRARα transgenic mice develop leukemia only after several months, suggesting that PMLRARα does not by itself confer a fully malignant phenotype. Suppression of apoptosis can have a central role in tumorigenesis; therefore, we assessed whether BCL-2 influenced the ability of PMLRARα to initiate leukemia. Evaluation of preleukemic animals showed that whereas PMLRARα alone modestly altered neutrophil maturation, the combination of PMLRARα and BCL-2 caused a marke

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41

Jones, RJ, SJ Sharkis, CB Miller, EK Rowinsky, PJ Burke, and WS May. "Bryostatin 1, a unique biologic response modifier: anti-leukemic activity in vitro." Blood 75, no. 6 (1990): 1319–23. http://dx.doi.org/10.1182/blood.v75.6.1319.1319.

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Abstract Bryostatin 1, a macrocyclic lactone isolated from the marine bryozoan Bugula neritina, has demonstrated both antineoplastic activity against the murine P388 leukemia line in vivo and stimulatory activity against mouse and human hematopoietic progenitors. We studied the effects of bryostatin 1 on the growth of human leukemias in vitro. Bryostatin 1 inhibited 1 to 4 logs of clonogenic leukemia cell growth from three of four leukemia cell lines. Bryostatin 1 also inhibited, by at least 1 log, the proliferation of clonogenic acute nonlymphocytic leukemia (ANLL) cells from 10 to 12 patient

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42

Jones, RJ, SJ Sharkis, CB Miller, EK Rowinsky, PJ Burke, and WS May. "Bryostatin 1, a unique biologic response modifier: anti-leukemic activity in vitro." Blood 75, no. 6 (1990): 1319–23. http://dx.doi.org/10.1182/blood.v75.6.1319.bloodjournal7561319.

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Bryostatin 1, a macrocyclic lactone isolated from the marine bryozoan Bugula neritina, has demonstrated both antineoplastic activity against the murine P388 leukemia line in vivo and stimulatory activity against mouse and human hematopoietic progenitors. We studied the effects of bryostatin 1 on the growth of human leukemias in vitro. Bryostatin 1 inhibited 1 to 4 logs of clonogenic leukemia cell growth from three of four leukemia cell lines. Bryostatin 1 also inhibited, by at least 1 log, the proliferation of clonogenic acute nonlymphocytic leukemia (ANLL) cells from 10 to 12 patients with ne

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43

Swatler, Julian, Laura Turos-Korgul, Marta Brewinska-Olchowik, et al. "4-1BBL–containing leukemic extracellular vesicles promote immunosuppressive effector regulatory T cells." Blood Advances 6, no. 6 (2022): 1879–94. http://dx.doi.org/10.1182/bloodadvances.2021006195.

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Abstract Chronic and acute myeloid leukemia evade immune system surveillance and induce immunosuppression by expanding proleukemic Foxp3+ regulatory T cells (Tregs). High levels of immunosuppressive Tregs predict inferior response to chemotherapy, leukemia relapse, and shorter survival. However, mechanisms that promote Tregs in myeloid leukemias remain largely unexplored. Here, we identify leukemic extracellular vesicles (EVs) as drivers of effector proleukemic Tregs. Using mouse model of leukemia-like disease, we found that Rab27a-dependent secretion of leukemic EVs promoted leukemia engraftm

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44

Kettyle, Laura M., Charles-Étienne Lebert-Ghali, Ivan V. Grishagin, et al. "Pathways, Processes, and Candidate Drugs Associated with a Hoxa Cluster-Dependency Model of Leukemia." Cancers 11, no. 12 (2019): 2036. http://dx.doi.org/10.3390/cancers11122036.

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High expression of the HOXA cluster correlates with poor clinical outcome in acute myeloid leukemias, particularly those harboring rearrangements of the mixed-lineage-leukemia gene (MLLr). Whilst decreased HOXA expression acts as a readout for candidate experimental therapies, the necessity of the HOXA cluster for leukemia maintenance has not been fully explored. Primary leukemias were generated in hematopoietic stem/progenitor cells from Cre responsive transgenic mice for conditional deletion of the Hoxa locus. Hoxa deletion resulted in reduced proliferation and colony formation in which surv

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45

Kogan, Scott C., Suk-hyun Hong, David B. Shultz, Martin L. Privalsky та J. Michael Bishop. "Leukemia initiated by PMLRARα: the PML domain plays a critical role while retinoic acid–mediated transactivation is dispensable". Blood 95, № 5 (2000): 1541–50. http://dx.doi.org/10.1182/blood.v95.5.1541.005k28_1541_1550.

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The most common chromosomal translocation in acute promyelocytic leukemia (APL), t15;17(q22;q21), creates PMLRAR andRARPML fusion genes. We previously developed a mouse model of APL by expressing PMLRAR in murine myeloid cells. In order to examine the mechanisms by which PMLRAR can initiate leukemia, we have now generated transgenic mice expressingPMLRARm4 and RARm4, proteins that are unable to activate transcription in response to retinoic acid.PMLRARm4 transgenic mice developed myeloid leukemia, demonstrating that transcriptional activation by PMLRAR is not required for leukemic tran

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46

Gordijn, M. S., R. R. van Litsenburg, R. J. B. J. Gemke, et al. "Hypothalamus-hypofyse-bijnier-asfunctie in overlevers van acute lymfatische leukemie op de kinderleeftijd en in gezonde controles." Tijdschrift voor Kindergeneeskunde 81, no. 1 (2013): 7–14. http://dx.doi.org/10.1007/s12456-013-0002-5.

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47

Paiva, Aldair Sousa, Hugo Diogenes De Oliveira Paiva, Geraldo Barroso Cavalcanti, et al. "Contribution of Flow Cytometry Immunophenotyping in Diagnostic of Acute and Chronic Leukemias." Blood 132, Supplement 1 (2018): 5198. http://dx.doi.org/10.1182/blood-2018-99-118923.

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Abstract BACKGROUND: Today immunophenotyping by flow cytometry is an useful adjunct to cytomorphologyc analysis to correct diagnostic of leukemias. It provides objective and quantitative data allowing for a high level of sensitivity detection and better characterization of acute and chronic leukemias. The purpose of this study was to demonstrate the contribution of the immunophenotyping by monoclonal antibodies (Mo.Ab.) in leukemic cells from patients with acute and chronic leukemias. METHODS: Analyzed 76 patients with leukemias before the treatment. The diagnostic of leukemias was based on th

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48

Horton, Sarah J., Vanessa Walf-Vorderwülbecke, Steve J. Chatters, Neil J. Sebire, Jasper de Boer, and Owen Williams. "Acute Myeloid Leukemia Induced by MLL-ENL Is Cured by Oncogene Ablation despite Acquisition of Complex Genetic Abnormalities." Blood 112, no. 11 (2008): 3109. http://dx.doi.org/10.1182/blood.v112.11.3109.3109.

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Abstract Chromosomal translocations involving the Mixed-Lineage-Leukemia (MLL) gene on chromosome 11q23 are frequent in infant acute leukemia and give rise to the formation of MLL-fusion genes. Several studies have addressed the importance of MLL-fusion activity for the initiation and maintenance of hematopoietic transformation. However, the dependence of established leukemias on MLL-fusion activity has not been previously addressed. We have developed a model for conditional expression of MLL-ENL in hematopoietic progenitor cells, in which expression of the fusion oncogene is turned off by dox

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49

Matulonis, UA, C. Dosiou, C. Lamont, et al. "Role of B7-1 in mediating an immune response to myeloid leukemia cells." Blood 85, no. 9 (1995): 2507–15. http://dx.doi.org/10.1182/blood.v85.9.2507.bloodjournal8592507.

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A costimulatory signal from B7–1 (CD80) to its counter-receptor CD28 is required for T-cell activation. Many tumors, including most human leukemias, lack expression of B7–1, and this has been suggested to contribute to the failure of immune recognition of these diseases. A murine leukemia model system was developed to assess the potential role of B7–1 in the induction immunity to leukemia cells. The nonleukemic 32Dc13 myeloid cell line was transformed by transfection of the BCR/ABL gene, generating a subline (32Dp210/clone 26) that was leukemic and rapidly lethal to syngeneic, immunocompetent

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50

Facklam, N. R., and G. J. Kociba. "Cytochemical Characterization of Leukemic Cells from 20 Dogs." Veterinary Pathology 22, no. 4 (1985): 363–69. http://dx.doi.org/10.1177/030098588502200411.

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The hematopoietic cells in blood and/or bone marrow from 20 leukemic dogs and 22 control dogs were characterized using a battery of cytochemical stains. The results of cytochemical staining led to modification of the diagnoses based on clinical, hematologic and histologic findings in seven (35%) of the leukemias. Sudan black B and chloroacetate esterase served as granulocytic markers in both the control and leukemic groups. Peroxidase activity was present in the granulocytes and monocytes of control animals but not the blasts of leukemic dogs. Alkaline phosphatase-positive staining of granuloc

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