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1. Balamurugan S, Sugapriya D, Shanthi P, Thilaka V, Venkatadesilalu S, Pushpa V, Madhavan M: Multidrug resistance 1 gene expression and AgNOR in childhood acute leukemias. Indian J Hematol Blood Transfus; 2007 Dec;23(3-4):73-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multidrug resistance 1 gene expression and AgNOR in childhood acute leukemias.
  • The multidrug resistance 1 (MDR1) gene product, P-glycoprotein (Pgp/p170) is a membrane protein, which acts as an ATP dependant efflux pump that expels a wide variety of organic compounds including chemotherapeutic agents from the cell.
  • AgNORs is a simple, reliable and inexpensive method of evaluating the proliferative activity of a tumor.
  • We have studied MDR1 expression and AgNORS in 41 cases of acute leukemia in children.
  • In this study, AgNOR counts in patients with acute lymphoblastic leukemia (ALL) L2 subtype (FAB classification) were significantly higher as compared to the ALL L1 subtype.
  • Similarly, mean AgNOR count in the acute myeloid Leukemia (AML) M2 subtype was significantly higher as compared to the ALL L1 subtype.
  • However, there was no correlation between AgNOR and treatment outcome or between AgNOR counts and MDR1 expression in any of the subtypes of acute leukemia included in this series.

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  • [Cites] Br J Haematol. 1976 Aug;33(4):451-8 [188440.001]
  • [Cites] Blood. 1992 Jan 15;79(2):295-8 [1346094.001]
  • [Cites] Blood. 1992 Jan 15;79(2):473-6 [1370388.001]
  • [Cites] Br J Haematol. 1991 Jan;77(1):50-3 [1671821.001]
  • [Cites] Am J Pathol. 1996 Apr;148(4):1237-47 [8644864.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1202-10 [12663440.001]
  • [Cites] Oncol Rep. 2004 Dec;12(6):1201-7 [15547738.001]
  • [Cites] J Pathol. 1989 Jul;158(3):185-8 [2475599.001]
  • [Cites] Br J Haematol. 1981 Apr;47(4):553-61 [6938236.001]
  • [Cites] Blood. 1993 May 1;81(9):2394-8 [8097634.001]
  • [Cites] Blood. 1993 Jun 15;81(12):3480-1 [8507883.001]
  • [Cites] Leuk Lymphoma. 1995 Sep;19(1-2):135-40 [8574159.001]
  • [Cites] Cancer Lett. 1996 Nov 12;108(1):87-91 [8950214.001]
  • [Cites] Leukemia. 1997 Oct;11(10):1673-80 [9324288.001]
  • [Cites] J Clin Oncol. 1998 Apr;16(4):1512-8 [9552060.001]
  • [Cites] Am J Hematol. 1999 Jun;61(2):149-52 [10367797.001]
  • [Cites] Leuk Lymphoma. 2002 Feb;43(2):309-14 [11999562.001]
  • [Cites] Mol Cancer Res. 2004 Jun;2(6):339-47 [15235109.001]
  • [Cites] Best Pract Res Clin Haematol. 2004 Dec;17(4):641-51 [15494300.001]
  • (PMID = 23100919.001).
  • [ISSN] 0971-4502
  • [Journal-full-title] Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion
  • [ISO-abbreviation] Indian J Hematol Blood Transfus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3453125
  • [Keywords] NOTNLM ; Acute leukemia / AgNOR / Multidrug Resistance 1 / P-glycoprotein
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2. Pratz KW, Cho E, Levis MJ, Karp JE, Gore SD, McDevitt M, Stine A, Zhao M, Baker SD, Carducci MA, Wright JJ, Rudek MA, Smith BD: A pharmacodynamic study of sorafenib in patients with relapsed and refractory acute leukemias. Leukemia; 2010 Aug;24(8):1437-44
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  • [Title] A pharmacodynamic study of sorafenib in patients with relapsed and refractory acute leukemias.
  • We report the results of a phase I dose escalation trial of the multikinase inhibitor sorafenib in relapsed and refractory acute leukemia patients using an intermittent dosing regimen.
  • Fifteen patients with advanced leukemia (12 with acute myeloid leukemia, 2 with acute lymphoblastic leukemia, 1 with biphenotypic) and a median age of 63 (range 37-85) years were enrolled and treated on a dose escalation trial.
  • Out of 15 patients, 11 experienced stable disease as best response.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Benzenesulfonates / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyridines / therapeutic use

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  • [Cites] Onkologie. 2002 Dec;25(6):511-8 [12566895.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4642-9 [14673054.001]
  • [Cites] Blood. 2004 May 15;103(10):3669-76 [14726387.001]
  • [Cites] Br J Clin Pharmacol. 2004 Aug;58(2):212-6 [15255805.001]
  • [Cites] Blood. 2004 Aug 15;104(4):1145-50 [15126317.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1841-9 [15166029.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7099-109 [15466206.001]
  • [Cites] J Pharm Sci. 1972 Jun;61(6):952-4 [5046120.001]
  • [Cites] Eur J Drug Metab Pharmacokinet. 1991 Oct-Dec;16(4):249-55 [1823867.001]
  • [Cites] Blood. 2005 Jan 15;105(2):812-20 [15374878.001]
  • [Cites] J Clin Oncol. 2005 Feb 10;23(5):965-72 [15613696.001]
  • [Cites] Br J Cancer. 2005 May 23;92(10):1855-61 [15870716.001]
  • [Cites] Clin Cancer Res. 2005 Aug 1;11(15):5472-80 [16061863.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1154-63 [15870183.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1543-9 [16001087.001]
  • [Cites] Ann Oncol. 2005 Oct;16(10):1688-94 [16006586.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2484-90 [15956279.001]
  • [Cites] Oncogene. 2005 Oct 20;24(46):6861-9 [16007148.001]
  • [Cites] Cancer Chemother Pharmacol. 2006 May;57(5):685-92 [16133532.001]
  • [Cites] Expert Opin Pharmacother. 2006 Mar;7(4):453-61 [16503817.001]
  • [Cites] Cytometry B Clin Cytom. 2006 May;70(3):107-14 [16498671.001]
  • [Cites] J Clin Oncol. 2006 Sep 10;24(26):4293-300 [16908937.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2358-65 [16763210.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3477-83 [16857987.001]
  • [Cites] Clin Cancer Res. 2006 Dec 15;12(24):7271-8 [17189398.001]
  • [Cites] J Chromatogr B Analyt Technol Biomed Life Sci. 2007 Feb 1;846(1-2):1-7 [16798122.001]
  • [Cites] Oncologist. 2007 Apr;12(4):426-37 [17470685.001]
  • [Cites] J Biol Chem. 2007 Oct 12;282(41):29831-46 [17698840.001]
  • [Cites] J Natl Cancer Inst. 2008 Feb 6;100(3):184-98 [18230792.001]
  • [Cites] Curr Opin Hematol. 2008 Jul;15(4):400-7 [18536580.001]
  • [Cites] Leuk Res. 2009 Feb;33(2):348-50 [18573526.001]
  • [Cites] Blood. 2009 Apr 23;113(17):3938-46 [19029442.001]
  • [Cites] Blood. 2009 Jun 25;113(26):6567-71 [19389879.001]
  • [Cites] Blood. 2010 Feb 18;115(7):1425-32 [20007803.001]
  • (PMID = 20535150.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA128864; United States / NCI NIH HHS / CA / P30 CA006973-48; United States / NCRR NIH HHS / RR / UL1 RR025005; United States / NCI NIH HHS / CA / P30CA006973; United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / K24 CA111717; United States / NCRR NIH HHS / RR / UL1 RR025005-04; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCI NIH HHS / CA / P50 CA100632-06; United States / NCI NIH HHS / CA / R01 CA128864-04; United States / NCI NIH HHS / CA / U01 CA070095-17; United States / NCI NIH HHS / CA / U01CA70095
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ NIHMS201571; NLM/ PMC2921005
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3. Karp JE, Giles FJ, Gojo I, Morris L, Greer J, Johnson B, Thein M, Sznol M, Low J: A phase I study of the novel ribonucleotide reductase inhibitor 3-aminopyridine-2-carboxaldehyde thiosemicarbazone (3-AP, Triapine) in combination with the nucleoside analog fludarabine for patients with refractory acute leukemias and aggressive myeloproliferative disorders. Leuk Res; 2008 Jan;32(1):71-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I study of the novel ribonucleotide reductase inhibitor 3-aminopyridine-2-carboxaldehyde thiosemicarbazone (3-AP, Triapine) in combination with the nucleoside analog fludarabine for patients with refractory acute leukemias and aggressive myeloproliferative disorders.
  • We designed a Phase I trial of Triapine followed by the adenosine analog fludarabine in adults with refractory acute leukemias and aggressive myeloproliferative disorders (MPD).
  • Complete and partial responses (CR, PR) occurred in Schedule A (5/24, 21%), with CR occurring at the 2 highest fludarabine doses (2/12, 17%).
  • In contrast, no CR or PR occurred in Schedule B.

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  • [Cites] N Engl J Med. 1995 Apr 27;332(17):1132-6 [7700286.001]
  • [Cites] Cancer Chemother Pharmacol. 1995;36(3):181-8 [7781136.001]
  • [Cites] J Med Chem. 1996 Jun 21;39(13):2586-93 [8691457.001]
  • [Cites] Blood. 1996 Oct 1;88(7):2480-7 [8839839.001]
  • [Cites] Blood. 1997 Jul 1;90(1):270-8 [9207462.001]
  • [Cites] J Clin Oncol. 1997 Aug;15(8):2780-5 [9256119.001]
  • [Cites] J Clin Oncol. 1998 Jul;16(7):2321-31 [9667246.001]
  • [Cites] Br J Haematol. 1998 Aug;102(3):647-55 [9722289.001]
  • [Cites] Leuk Res. 2006 Jul;30(7):813-22 [16478631.001]
  • [Cites] Leuk Res. 2007 Sep;31(9):1165-73 [17324462.001]
  • [Cites] Biochem Pharmacol. 2000 Apr 15;59(8):983-91 [10692563.001]
  • [Cites] Leukemia. 2000 Mar;14(3):379-88 [10720130.001]
  • [Cites] Blood. 2000 Dec 1;96(12):3671-4 [11090046.001]
  • [Cites] Prog Biophys Mol Biol. 2001 Nov;77(3):177-268 [11796141.001]
  • [Cites] Anticancer Res. 2002 May-Jun;22(3):1369-77 [12168813.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4272-90 [12393615.001]
  • [Cites] Cancer. 2003 Apr 15;97(8):1920-8 [12673719.001]
  • [Cites] Leuk Res. 2003 Dec;27(12):1077-83 [12921943.001]
  • [Cites] Jpn J Cancer Res. 1985 Aug;76(8):729-35 [3930450.001]
  • [Cites] J Clin Oncol. 1986 Jan;4(1):74-9 [2416889.001]
  • [Cites] Cancer Treat Rep. 1986 Oct;70(10):1225-8 [2428492.001]
  • [Cites] Cancer Res. 1988 Jan 15;48(2):329-34 [3335008.001]
  • [Cites] Anal Biochem. 1989 Aug 1;180(2):222-6 [2554751.001]
  • [Cites] J Clin Oncol. 1991 Jan;9(1):175-88 [1702143.001]
  • [Cites] Biochem Cell Biol. 1990 Dec;68(12):1364-71 [2085432.001]
  • [Cites] Blood. 1991 Dec 1;78(11):2937-44 [1954383.001]
  • [Cites] Ann Hematol. 1992 Jul;65(1):26-32 [1643157.001]
  • [Cites] J Clin Oncol. 1993 Jan;11(1):116-24 [8418222.001]
  • [Cites] Blood. 1993 Jul 15;82(2):398-407 [8329700.001]
  • [Cites] J Biol Chem. 1993 Dec 15;268(35):26200-5 [8253740.001]
  • [Cites] J Clin Oncol. 1994 Apr;12(4):671-8 [7512125.001]
  • [Cites] Biochem Pharmacol. 1994 Jul 19;48(2):335-44 [8053929.001]
  • [Cites] Anal Biochem. 1994 Oct;222(1):116-22 [7856836.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4642-9 [14673054.001]
  • [Cites] Cancer Res. 1971 Mar;31(3):235-8 [5102115.001]
  • [Cites] Blood. 1975 Jul;46(1):11-6 [1055610.001]
  • [Cites] Cancer Res. 1980 Sep;40(9):3286-92 [7427943.001]
  • [Cites] Cancer Res. 1983 Jun;43(6):2688-93 [6189585.001]
  • (PMID = 17640728.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA070095-14; United States / NCRR NIH HHS / RR / M01-RR0052; United States / NCI NIH HHS / CA / U01 CA70095; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCRR NIH HHS / RR / M01 RR000052; United States / NCI NIH HHS / CA / CA070095-14
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Pyridines; 0 / Thiosemicarbazones; 143621-35-6 / 3-aminopyridine-2-carboxaldehyde thiosemicarbazone; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ NIHMS35421; NLM/ PMC2726775
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4. Vempati S, Reindl C, Kaza SK, Kern R, Malamoussi T, Dugas M, Mellert G, Schnittger S, Hiddemann W, Spiekermann K: Arginine 595 is duplicated in patients with acute leukemias carrying internal tandem duplications of FLT3 and modulates its transforming potential. Blood; 2007 Jul 15;110(2):686-94
SciCrunch. OMIM: Data: Gene Annotation .

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  • [Title] Arginine 595 is duplicated in patients with acute leukemias carrying internal tandem duplications of FLT3 and modulates its transforming potential.
  • FLT3-internal tandem duplications (FLT3-ITDs) comprise a heterogeneous group of mutations in patients with acute leukemias that are prognostically important.
  • To characterize the mechanism of transformation by FLT3-ITDs, we sequenced the juxtamembrane region (JM) of FLT3 from 284 patients with acute leukemias.
  • Moreover, deletion or substitution of the duplicated R595 in 2 FLT3-ITD constructs as well as the deletion of wild-type R595 in FLT3-ITD substantially reduced the transforming potential and STAT5 activation, pointing to a critical role of the positive charge of R595 in stabilizing the active confirmation of FLT3-ITDs.
  • [MeSH-major] Arginine. Leukemia / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Amino Acid Substitution. Cell Transformation, Neoplastic / genetics. Female. Gene Duplication. Humans. Male. Middle Aged. Mutagenesis. Sequence Deletion

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  • (PMID = 17387224.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 94ZLA3W45F / Arginine; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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5. Lee ST, Kim HJ, Kim SH: Defining an Optimal Number of Immunophenotypic Markers for Lineage Assignment of Acute Leukemias Based on the EGIL Scoring System. Korean J Lab Med; 2006 Dec;26(6):393-9
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  • [Title] Defining an Optimal Number of Immunophenotypic Markers for Lineage Assignment of Acute Leukemias Based on the EGIL Scoring System.
  • BACKGROUND: The lineage assignment in acute leukemias is critical in therapeutic decisions.
  • MATERIALS AND METHODS: We retrospectively analyzed 321 cases of acute leukemias whose diagnoses were based on the EGIL (European Group for Immunological Classification of Acute Leukemia) scores.
  • RESULTS: The cytoplasmic antigens including MPO stain and CD79a stain contributed greatly to the lineage assignment.
  • CONCLUSIONS: To maintain diagnostic sensitivities over 95% for each lineage, at least 14 markers (including MPO stain and CD79a stain) were needed; while 16 markers were needed for a sensitivity of 100%.
  • When combined with other important markers for specific aims such as CD45, the minimum number of markers needed for the accurate diagnosis of acute leukemias would be more than about 18 to 20.

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  • (PMID = 18156757.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
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6. Smith BD, Karp JE: What are the endpoints of therapy for acute leukemias? Old definitions and new challenges. Clin Lymphoma Myeloma; 2009;9 Suppl 3:S296-301
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  • [Title] What are the endpoints of therapy for acute leukemias? Old definitions and new challenges.
  • Acute leukemias are complex diseases on multiple levels, and laboratory efforts over the past 3 decades have focused on better understanding of the molecular underpinnings and their stem cell biology.
  • We now have a panoply of technologic advances that allow us to characterize individual leukemias by molecular profiles that relate directly to clinical behavior, to detect minimal residual disease, and to begin to develop "targeted" therapeutic strategies based on molecular considerations.
  • There are a number of challenges surrounding this task: first, how to combine these agents with traditional chemotherapeutics and/or with each other to maximize leukemic cell kill and increase the cure rate; second, how to use these targeted agents in the minimal residual disease with potential curative intent; third, for patients unable to tolerate or unlikely to benefit from aggressive approaches, how to use one or more of these agents to reduce tumor bulk and either permit some restoration of normal marrow function or induce morphologic and functional differentiation of the leukemic clone to overcome the leukemia-associated bone marrow failure; and lastly, how to measure the effects of these agents on the molecular and cellular biologic levels in ways that correlate with and might even predict overall clinical outcome.
  • These challenges are further complicated by the inherent heterogeneity in host biology; disease etiology and biology; and interactions among host, disease, and treatment that ultimately determine individual clinical outcomes.
  • Toward this end, we will discuss selected issues surrounding new clinical trial designs and the development of clinically relevant molecular endpoints that might facilitate the development of new treatment approaches that will improve the outlook for adults with acute leukemias.

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  • [Cites] Blood. 2007 Apr 1;109(7):2781-90 [17179232.001]
  • [Cites] Br J Haematol. 2005 Jan;128(2):184-91 [15638852.001]
  • [Cites] Cancer Invest. 2007 Sep;25(6):484-94 [17882662.001]
  • [Cites] Science. 2007 Oct 12;318(5848):287-90 [17872411.001]
  • [Cites] J Clin Oncol. 2007 Nov 1;25(31):4982-6 [17971597.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3547-51 [17673605.001]
  • [Cites] Clin Cancer Res. 2007 Nov 15;13(22 Pt 1):6719-26 [18006773.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):7107-12 [18056190.001]
  • [Cites] Blood. 2008 Jan 1;111(1):86-93 [17893227.001]
  • [Cites] Blood. 2008 Feb 15;111(4):2170-80 [17925489.001]
  • [Cites] Blood. 2008 Mar 15;111(6):3183-9 [18187662.001]
  • [Cites] Blood. 2008 Apr 15;111(8):3941-67 [18198345.001]
  • [Cites] Leukemia. 2008 Apr;22(4):708-22 [18337766.001]
  • [Cites] Blood. 2008 May 1;111(9):4788-96 [18252861.001]
  • [Cites] Blood. 2008 May 1;111(9):4797-808 [18270328.001]
  • [Cites] Clin Cancer Res. 2008 May 1;14(9):2519-26 [18451212.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1919-28 [18450603.001]
  • [Cites] Blood. 2008 May 15;111(10):5078-85 [18337557.001]
  • [Cites] Clin Cancer Res. 2008 May 15;14(10):3077-82 [18483374.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5477-85 [18388178.001]
  • [Cites] Exp Hematol. 2001 Apr;29(4):448-57 [11301185.001]
  • [Cites] J Clin Oncol. 2001 Jul 1;19(13):3244-54 [11432892.001]
  • [Cites] Blood. 2002 May 1;99(9):3461-4 [11964319.001]
  • [Cites] J Clin Oncol. 2002 May 15;20(10):2429-40 [12011120.001]
  • [Cites] Cell Growth Differ. 2002 Jun;13(6):275-83 [12114217.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1532-42 [12176867.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1713-24 [12200686.001]
  • [Cites] Blood. 2003 Jul 15;102(2):442-8 [12560224.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2379-86 [12791647.001]
  • [Cites] Nature. 2004 Mar 18;428(6980):332-7 [15029198.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1605-16 [15084693.001]
  • [Cites] Clin Cancer Res. 2004 Jun 1;10(11):3577-85 [15173063.001]
  • [Cites] Blood. 2004 Nov 15;104(10):3078-85 [15284114.001]
  • [Cites] N Engl J Med. 2005 Feb 10;352(6):549-57 [15703420.001]
  • [Cites] Blood. 2005 Jul 1;106(1):318-27 [15784732.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1543-9 [16001087.001]
  • [Cites] Int J Hematol. 2005 Aug;82(2):100-7 [16146839.001]
  • [Cites] Cancer. 2005 Oct 1;104(7):1442-52 [16116598.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2841-8 [15998836.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4261-8 [16150937.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 Jan;12(1 Suppl 1):13-8 [16399579.001]
  • [Cites] Blood. 2006 May 1;107(9):3481-5 [16455952.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6361-9 [16778214.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2358-65 [16763210.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3271-9 [16882711.001]
  • [Cites] Blood. 2006 Dec 15;108(13):4109-17 [16931630.001]
  • [Cites] Blood. 2007 Jan 1;109(1):52-7 [16882708.001]
  • [Cites] Blood. 2007 Mar 1;109(5):1810-6 [17095617.001]
  • [Cites] Cell. 2007 Feb 23;128(4):683-92 [17320506.001]
  • [Cites] Clin Cancer Res. 2007 May 1;13(9):2728-37 [17473206.001]
  • [Cites] Clin Cancer Res. 2008 Jun 15;14(12):3658-63 [18559579.001]
  • [Cites] Clin Cancer Res. 2008 Jun 15;14(12):3664-9 [18559580.001]
  • [Cites] Clin Cancer Res. 2008 Jun 15;14(12):3675-82 [18559582.001]
  • [Cites] Clin Cancer Res. 2008 Jul 1;14(13):4032-7 [18593978.001]
  • [Cites] J Clin Oncol. 2008 Aug 1;26(22):3785-90 [18591545.001]
  • [Cites] Blood. 2008 Aug 15;112(4):981-9 [18495956.001]
  • [Cites] Blood. 2008 Aug 15;112(4):1366-73 [18523155.001]
  • [Cites] J Clin Oncol. 2007 Sep 1;25(25):3884-91 [17679729.001]
  • (PMID = 19778856.001).
  • [ISSN] 1938-0712
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973; United States / NCRR NIH HHS / RR / RR000052-466553; United States / NCI NIH HHS / CA / 2P30 CA06973-44; United States / NCI NIH HHS / CA / U01 CA70095; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCRR NIH HHS / RR / M01 RR000052; United States / NCRR NIH HHS / RR / M01 RR000052-466553
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 63
  • [Other-IDs] NLM/ NIHMS187883; NLM/ PMC2851207
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7. Aydin-Sayitoglu M, Hatirnaz O, Erensoy N, Ozbek U: Role of CYP2D6, CYP1A1, CYP2E1, GSTT1, and GSTM1 genes in the susceptibility to acute leukemias. Am J Hematol; 2006 Mar;81(3):162-70
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  • [Title] Role of CYP2D6, CYP1A1, CYP2E1, GSTT1, and GSTM1 genes in the susceptibility to acute leukemias.
  • Acute leukemias (ALs) are heterogeneous diseases.
  • Functional polymorphisms in the genes encoding detoxification enzymes cause inter-individual differences, which contribute to leukemia susceptibility.
  • The CYP2D6*3 variant allele frequency was lower in the overall acute leukemia patients (0.6%) compared to controls (P = 0.03).
  • No association was found for the studied CYP2D6*4, CYP1A1*2A, and GSTT1"null" variants and the risk of acute leuke-mia (ALL or AML).
  • This case-control study suggests a contribution of CYP2E1, CYP2D6, and GSTM1 "null" variants to the development of acute leukemias.
  • [MeSH-major] Cytochrome P-450 CYP1A1 / genetics. Cytochrome P-450 CYP2D6 / genetics. Cytochrome P-450 CYP2E1 / genetics. Genetic Predisposition to Disease. Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16493615.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.14.13.- / Cytochrome P-450 CYP2E1; EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 1.14.14.1 / Cytochrome P-450 CYP2D6; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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8. Fazlina N, Maha A, Jamal R, Zarina AL, Cheong SK, Hamidah H, Ainoon O, Zulkifli SZ, Hamidah NH: Expression of multidrug resistance (MDR) proteins and in vitro drug resistance in acute leukemias. Hematology; 2007 Feb;12(1):33-7
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  • [Title] Expression of multidrug resistance (MDR) proteins and in vitro drug resistance in acute leukemias.
  • The expression of the multidrug resistance (MDR) proteins may influence the outcome of treatment in patients with acute leukemia.
  • A total of 82 newly diagnosed acute leukemia cases (43 adult myeloid leukaemia, AML cases and 39 acute lymphoblastic leukaemia, ALL cases) and 16 relapsed cases (8 AML cases and 8 ALL cases) were studied.
  • In conclusion, we found that MTS assay is an easy, rapid and non laborious method to study in vitro drug resistance in acute leukaemia cases.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Leukemia / metabolism. Neoplasm Proteins / metabolism. P-Glycoproteins / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Cell Survival. Child. Child, Preschool. Coloring Agents / analysis. Cytarabine / pharmacology. Daunorubicin / pharmacology. Female. Humans. Infant. Inhibitory Concentration 50. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Male. Methylphenazonium Methosulfate / pharmacology. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Recurrence. Staining and Labeling / methods. Tetrazolium Salts / analysis. Thiazoles / analysis. Treatment Outcome. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / ultrastructure

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  • (PMID = 17364990.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Coloring Agents; 0 / Neoplasm Proteins; 0 / P-Glycoproteins; 0 / Tetrazolium Salts; 0 / Thiazoles; 04079A1RDZ / Cytarabine; 138169-43-4 / 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium; 299-11-6 / Methylphenazonium Methosulfate; ZS7284E0ZP / Daunorubicin
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9. Williams RT, Sherr CJ: The ARF tumor suppressor in acute leukemias: insights from mouse models of Bcr-Abl-induced acute lymphoblastic leukemia. Adv Exp Med Biol; 2007;604:107-14
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  • [Title] The ARF tumor suppressor in acute leukemias: insights from mouse models of Bcr-Abl-induced acute lymphoblastic leukemia.
  • The prototypical Bcr-Abl chimeric oncoprotein is central to the pathogenesis of chronic myelogenous leukemias (CMLs) and a subset of acute lymphoblastic leukemias (Ph+ ALLs).
  • The INK4A/ARF tumor suppressor locus is frequently deleted in both B- and T-lineage ALLs, including Ph+ ALL, whereas the locus remains intact in CML.
  • In murine bone marrow transplant models and after transfer of syngeneic Bcr-Abl-transformed pre-B cells into immunocompetent recipient animals, Arf gene inactivation dramatically decreases the latency and enhances the aggressiveness of Bcr-Abl-induced lymphoblastic leukemia.
  • Despite exquisite in vitro sensitivity of Arf-null, BCR-ABL+ pre-B cells to imatinib, these cells efficiently establish lethal leukemias when introduced into immunocompetent mice that receive continuous, maximal imatinib therapy.
  • [MeSH-major] Fusion Proteins, bcr-abl / metabolism. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Tumor Suppressor Protein p14ARF / physiology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Benzamides. Disease Models, Animal. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Interleukin-7 / metabolism. Mice. Piperazines / pharmacology. Pyrimidines / pharmacology

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  • (PMID = 17695724.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32-CA70089
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interleukin-7; 0 / Piperazines; 0 / Pyrimidines; 0 / Tumor Suppressor Protein p14ARF; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 20
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10. Mejía Aranguré JM, Ortega Alvarez MC, Fajardo Gutiérrez A: [Acute leukemias epidemiology in children. Part 1]. Rev Med Inst Mex Seguro Soc; 2005 Jul-Aug;43(4):323-33
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  • [Title] [Acute leukemias epidemiology in children. Part 1].
  • [Transliterated title] Epidemiología de las leucemias agudas en niños. Parte 1.
  • OBJECTIVE: This paper is a revision from recent studies related to acute leukemia (AL) epidemiology in children.
  • The AL are the types of cancer with more frequency in children below 15 years old and the cost of taking care of a child with cancer represents to the health institutions around 620 thousand dollars per year per case.
  • These controversies can be explained by methodological mistakes in the studies and also because these studies did not assess the interaction between the susceptibility to AL and the environmental factors, a situation that could lead to the better understanding of the causal mechanisms of the disease.
  • [MeSH-major] Leukemia / epidemiology. Leukemia / etiology
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Female. Humans. Incidence. Infant. Male. Mexico / epidemiology. Risk Factors

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  • (PMID = 16164849.001).
  • [ISSN] 0443-5117
  • [Journal-full-title] Revista médica del Instituto Mexicano del Seguro Social
  • [ISO-abbreviation] Rev Med Inst Mex Seguro Soc
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Mexico
  • [Number-of-references] 125
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11. Bai B, Wang HW, Xu YQ, Yang HN, Qiao ZH: [Fluorescence quantitative PCR detection of WT1 gene expression in peripheral blood of patients with acute leukemias and its clinical implications]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Aug;13(4):610-4
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  • [Title] [Fluorescence quantitative PCR detection of WT1 gene expression in peripheral blood of patients with acute leukemias and its clinical implications].
  • To elucidate the expression of WT1 in all types of leukemias and its implications for monitoring minimal residual disease in patients with acute leukemia, the peripheral blood from 55 leukemia patients and 10 normal voluteer was detected by using FQ-RT-PCR.
  • Follow-up monitoring of WT1 expression of peripheral blood was performed for 20 patients with acute leukemia.
  • The results showed that the expression of WT1 gene in all types of leukemias was significantly higher than that in normal control (P < 0.001).
  • Follow-up detection of the expression of WT1 in peripheral blood samples from 20 acute leukemia patients, 7 cases relapsed after complete remission has been done.
  • The expression of WT1 gene is relatively high in all types of leukemias compared with normal peripheral blood cells, the higher WT1 expression may associate with poor prognosis in acute leukemia, and the dynamics of WT1 level correlate with the disease status.
  • The quantitative assessment of WT1 expression in peripheral blood samples by FQ-RT-PCR may be a useful tool for monitoring minimal residual disease.

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  • (PMID = 16129044.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / WT1 Proteins
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12. Wang W, Ji P, Steffen B, Metzger R, Schneider PM, Halfter H, Schrader M, Berdel WE, Serve H, Müller-Tidow C: Alterations of lymphoid enhancer factor-1 isoform expression in solid tumors and acute leukemias. Acta Biochim Biophys Sin (Shanghai); 2005 Mar;37(3):173-80
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  • [Title] Alterations of lymphoid enhancer factor-1 isoform expression in solid tumors and acute leukemias.
  • In hematological malignancies, overall LEF-1 level was higher in lymphocytic leukemias compared with myeloid leukemias and normal hematopoiesis.
  • However, acute myeloid leukemia and acute lymphocytic leukemia showed a significantly increased fraction of the oncogenic LEF-1 compared with chronic lymphocytic leukemia and chronic myeloid leukemia.
  • Taken together, these data suggest that LEF-1 is abundantly expressed in human tumors and the ratio of the oncogenic and the dominant negative short isoform altered not only in carcinomas but also in leukemia.
  • [MeSH-minor] Humans. Leukemia / genetics. Leukemia / metabolism. Lymphoid Enhancer-Binding Factor 1. Protein Isoforms / genetics. Protein Isoforms / metabolism

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  • (PMID = 15756419.001).
  • [ISSN] 1672-9145
  • [Journal-full-title] Acta biochimica et biophysica Sinica
  • [ISO-abbreviation] Acta Biochim. Biophys. Sin. (Shanghai)
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / LEF1 protein, human; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / Neoplasm Proteins; 0 / Protein Isoforms; 0 / Transcription Factors
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13. Haferlach C, Rieder H, Lillington DM, Dastugue N, Hagemeijer A, Harbott J, Stilgenbauer S, Knuutila S, Johansson B, Fonatsch C: Proposals for standardized protocols for cytogenetic analyses of acute leukemias, chronic lymphocytic leukemia, chronic myeloid leukemia, chronic myeloproliferative disorders, and myelodysplastic syndromes. Genes Chromosomes Cancer; 2007 May;46(5):494-9
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  • [Title] Proposals for standardized protocols for cytogenetic analyses of acute leukemias, chronic lymphocytic leukemia, chronic myeloid leukemia, chronic myeloproliferative disorders, and myelodysplastic syndromes.
  • It was our aim to present proposals for standardized protocols to improve the diagnosis, and hence the treatment outcome, of hematologic malignancies.
  • [MeSH-major] Cytogenetic Analysis / methods. Leukemia / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics
  • [MeSH-minor] Acute Disease. Chromosome Aberrations. Diagnosis, Differential. Humans. Karyotyping


14. Zhang X, Wang M, Zhou C, Chen S, Wang J: The expression of iASPP in acute leukemias. Leuk Res; 2005 Feb;29(2):179-83
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  • [Title] The expression of iASPP in acute leukemias.
  • Inhibitory member of the ASPP family (iASPP) is an evolutionarily conserved inhibitor of p53, and its expression is upregulated in human breast carcinomas expressing wild-type p53.
  • To examine the role of iASPP in acute leukemia (AL), we analyzed iASPP mRNA expression in AL by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR).
  • There was no significant difference between acute lymphocytic leukemia (ALL) cells and acute myeloid leukemia (AML) cells (P = 0.593).
  • However, iASPP gene expression in AL cells was not associated with gender, age, initial white blood cell count or p53 type, but was associated with CD34 expression.
  • The results of the present study suggest that iASPP gene overexpression may play an important role in the leukemogenesis and/or disease progression of AL.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid, Acute / genetics. RNA, Messenger / genetics
  • [MeSH-minor] Adolescent. Adult. Cell Line, Tumor. Female. Humans. Male. Mutation. Repressor Proteins. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Suppressor Protein p53 / antagonists & inhibitors. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Up-Regulation

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  • (PMID = 15607367.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / PPP1R13L protein, human; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / Tumor Suppressor Protein p53
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15. Rao SR, Hassett M, Schwartz JH, Maloney B, Jacobson JO: Admissions for chemotherapy-related serious adverse effects (CR-SAEs) and rates of mortality among community cancer center patients. J Clin Oncol; 2009 May 20;27(15_suppl):6571

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: We conducted a prospective cohort study of adult cancer patients (excluding acute leukemia and stem cell transplant patients) admitted to a community hospital January 2003-December 2006.
  • We identified the type of SAE, outcome of each admission, time form chemotherapy to admission and from admission to discharge/death, and the disease and treatment characteristics of each patient.
  • The average time from chemotherapy to admission was shorter for fatal vs. non-fatal admissions (3.6 vs. 7.7 days; p<.01).
  • CONCLUSIONS: Fatalities during admissions for CR-SAE's in a community cancer center are relatively uncommon and are not associated with age or type of SAE/cancer.

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  • (PMID = 27963798.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Mohty M, Balere M, Socie G, Milpied N, Ifrah N, Harousseau JL, Michallet M, Blaise D, Esperou H, Yakoub-Agha I, SFGM-TC: Effect of antithymocyte globulins (ATG) as part of the myeloablative conditioning (MAC) regimen on the risk of severe graft-versus-host disease (GVHD) after allogeneic stem cell transplantation (allo-SCT) from matched-unrelated donors (MUD). J Clin Oncol; 2009 May 20;27(15_suppl):7025

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  • [Title] Effect of antithymocyte globulins (ATG) as part of the myeloablative conditioning (MAC) regimen on the risk of severe graft-versus-host disease (GVHD) after allogeneic stem cell transplantation (allo-SCT) from matched-unrelated donors (MUD).
  • : 7025 Here, we report the results of a multicenter retrospective study analyzing the effect of ATG, incorporated within the MAC regimen for MUD-transplants in leukemic patients.
  • The purpose of the study was to compare the incidence and severity of acute and chronic GVHD as well as overall outcome.
  • 171 adult patients with acute leukemia and MDS, for whom detailed allelic HLA typing (4 digits) was available, were included.
  • With a median follow-up of 30.3 (range, 2.6-68.1) months, grade 0-1 and 2-4 acute GVHD occurred in 74 (46%) and 88 patients (54%) respectively, with grade 3-4 acute GVHD being significantly lower in the ATG group (18% vs. 32%; p = 0.04).
  • In multivariate analysis, an HLA allelic mismatch and the non-use of ATG were associated with an increased risk of grade 3-4 acute GVHD (RR = 2.80, 95% CI, 1.5-5.3, p = 0.001; and RR = 2.4, 95% CI, 1.1-5.0, p = 0.02 respectively).

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  • (PMID = 27961398.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Sholl LM, Longtine J: Molecular analysis of gene rearrangements and mutations in acute leukemias and myeloproliferative neoplasms. Curr Protoc Hum Genet; 2010 Oct;Chapter 10:Unit 10.4
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  • [Title] Molecular analysis of gene rearrangements and mutations in acute leukemias and myeloproliferative neoplasms.
  • A large subset of acute leukemias and other myeloproliferative neoplasms contain specific genetic alterations, many of which are associated with unique clinical and pathologic features.
  • These alterations include chromosomal translocations leading to oncogenic fusion genes, as well as mutations leading to aberrant activation of a variety of proteins critical to hematopoietic progenitor cell proliferation and differentiation.
  • Molecular analysis is central to diagnosis and clinical management of leukemias, permitting genetic confirmation of a clinical and histologic impression, providing prognostic and predictive information, and facilitating detection of minimal residual disease.
  • This unit will outline approaches to the molecular diagnosis of the most frequent and clinically relevant genetic alterations in acute leukemias and myeloproliferative neoplasms.

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  • (PMID = 20891029.001).
  • [ISSN] 1934-8258
  • [Journal-full-title] Current protocols in human genetics
  • [ISO-abbreviation] Curr Protoc Hum Genet
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Sachdeva MU, Ahluwalia J, Das R, Varma N, Garewal G: Role of FAB classification of acute leukemias in era of immunophenotyping. Indian J Pathol Microbiol; 2006 Oct;49(4):524-7
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  • [Title] Role of FAB classification of acute leukemias in era of immunophenotyping.
  • French-American-British classification for leukemias had been widely accepted due to its objectiveness and good reproducibility.
  • WHO classification of leukemias was formulated in 1997 with a purpose of further enhancing the objectivity.
  • A retrospective analysis of all acute leukemias over a period of 2 years was done.
  • Out of total of 469 cases of acute leukemias, 193 were diagnosed as Acute Lymphoblastic Leukemia (ALL), 200 as Acute Myeloid Leukemia (AML), and 76 cases diagnosed as Acute Leukemia, cytochemically undifferentiated.
  • Hence, only 16% of all leukemias remained unclassifiable.
  • In conclusion, FAB classification, based on morphology and simple cytochemical stains, remains effective enough, although cytogenetics and immunophenotyping can add to diagnostic accuracy in some cases.
  • [MeSH-major] Histocytochemistry / methods. Leukemia / classification. Leukemia, Myeloid / classification. Leukemia, Myeloid / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Acute Disease. Adult. Child. Child, Preschool. Cytogenetics / methods. Humans. Immunophenotyping / methods

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  • (PMID = 17183842.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] India
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19. Luong NV, Kantarjian HM, Faderl SH, Thomas DA, Vu KD: Occurence of venothromboembolism (VTE) in patients (pts) with acute lymphocytic leukemia (ALL), Burkitt's leukemia/lymphoma (BL), or lymphoblastic leukemia (LL). J Clin Oncol; 2009 May 20;27(15_suppl):7059

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Occurence of venothromboembolism (VTE) in patients (pts) with acute lymphocytic leukemia (ALL), Burkitt's leukemia/lymphoma (BL), or lymphoblastic leukemia (LL).
  • Although neoplastic diseases are known risk factors for the development of VTE, little is known about the incidence and predisposing factors of VTE among leukemia patients (pts).
  • METHODS: We performed a retrospective study to determine the incidence and risk factors associated with development of VTE among pts with ALL, BL, LL at M. D.
  • Pts who used oral contraception or hormone replacement therapy (OCP/HRT) were 2 times (95% CI: 1.07-3.92) more likely to develop VTE than non-users.
  • In a multivariate model, significant predictors of VTE were age 40-59 yrs, plt count 50-99 x 10<sup>9</sup>/L, diagnosis of Ph-positive ALL, history of VTE, and OCP/HRT use.
  • In addition to traditional risk factors, disease-specific features may also predispose pts to higher VTE risk.
  • Further studies should be done in other leukemias to establish guidelines in the prevention and management of VTE in pts with leukemia.

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  • (PMID = 27961450.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Fu JF, Liang DC, Shih LY: Analysis of acute leukemias with MLL/ENL fusion transcripts: identification of two novel breakpoints in ENL. Am J Clin Pathol; 2007 Jan;127(1):24-30

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of acute leukemias with MLL/ENL fusion transcripts: identification of two novel breakpoints in ENL.
  • t(11;19)(q23;p13.3); is one of the common chromosomal translocations in acute leukemias involving MLL rearrangements.
  • In a study of acute leukemias, 148 patients were identified to have MLL rearrangements by Southern blot analysis.
  • Of 15 patients with MLL/ENL, 7 had precursor B-cell acute lymphoblastic leukemia, 4 had T-cell acute lymphoblastic leukemia, and 4 had acute myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Oncogene Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Female. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Reverse Transcriptase Polymerase Chain Reaction. Treatment Outcome

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  • (PMID = 17145626.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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21. Lee JW, Soung YH, Kim SY, Nam SW, Park WS, Lee JY, Yoo NJ, Lee SH: Mutational analysis of MYC in common epithelial cancers and acute leukemias. APMIS; 2006 Jun;114(6):436-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutational analysis of MYC in common epithelial cancers and acute leukemias.
  • To see whether the point mutations of MYC are involved in tumors besides Burkitt's lymphomas, we analyzed the N-terminal cluster region of the mutations in 507 cancers from gastric, colorectal, breast and lung carcinomas, and acute leukemias, by polymerase chain reaction-based single-strand conformation polymorphism assay.
  • [MeSH-major] Genes, myc / genetics. Leukemia / genetics. Neoplasms / genetics. Point Mutation
  • [MeSH-minor] Acute Disease. DNA, Neoplasm / chemistry. DNA, Neoplasm / genetics. Female. Humans. Polymerase Chain Reaction. Polymorphism, Single-Stranded Conformational

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  • (PMID = 16856965.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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22. Pamuk GE, Taşçi M, Oztürk E, Demir M: Successful treatment of severe gastrointestinal bleeding after chemotherapy in acute myeloblastic leukemia with recombinant activated factor VII : report on one case and review of other uses in acute leukemias. Med Oncol; 2010 Mar;27(1):16-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment of severe gastrointestinal bleeding after chemotherapy in acute myeloblastic leukemia with recombinant activated factor VII : report on one case and review of other uses in acute leukemias.
  • Hemorrhage is a frequent complication in patients with acute leukemias as a result of chemotherapy-induced myelosuppression.
  • Patients are generally managed with red blood cell, platelet suspensions, and fresh frozen plasma; and sometimes with pharmacologic and endoscopic interventions.
  • We present our 44-year-old female patient who had gastrointestinal system bleeding after remission induction therapy for acute myeloid leukemia.
  • Thrombocytopenia was refractory to apheresis platelets; and gastrointestinal bleeding could be controlled only after the administration of a single dose (35 microg/kg, total dose 2.4 mg) of rFVIIa.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Factor VIIa / administration & dosage. Gastrointestinal Hemorrhage / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Recombinant Proteins / administration & dosage

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  • [Cites] Blood Coagul Fibrinolysis. 2004 Apr;15(3):261-3 [15060424.001]
  • [Cites] Bone Marrow Transplant. 2007 Jun;39(12 ):729-35 [17417659.001]
  • [Cites] Semin Thromb Hemost. 2000;26(4):413-9 [11092217.001]
  • [Cites] Am J Hematol. 2005 Aug;79(4):344-5 [16044447.001]
  • [Cites] Gastroenterol Clin North Am. 2003 Dec;32(4):1053-78 [14696297.001]
  • [Cites] Bone Marrow Transplant. 2001 Aug;28(4):405-7 [11571515.001]
  • [Cites] Pediatr Blood Cancer. 2008 May;50(5):1013-7 [17960639.001]
  • [Cites] Arch Intern Med. 2000 Jul 24;160(14 ):2216-7 [10904466.001]
  • [Cites] Blood Coagul Fibrinolysis. 2005 Mar;16(2):145-7 [15741803.001]
  • [Cites] Br J Haematol. 2002 Jun;117(3):705-8 [12028045.001]
  • [Cites] Eur J Haematol. 2004 Jun;72 (6):455-6 [15128428.001]
  • [Cites] Gut. 2002 Oct;51 Suppl 4:iv1-6 [12208839.001]
  • [Cites] Blood Coagul Fibrinolysis. 2006 Jun;17(4):323-4 [16651877.001]
  • [Cites] Am J Gastroenterol. 1995 Apr;90(4):568-73 [7717312.001]
  • [Cites] Blood Coagul Fibrinolysis. 1998 Mar;9 Suppl 1:S61-5 [9819030.001]
  • [Cites] Haemostasis. 1996;26 Suppl 1:159-64 [8904193.001]
  • [Cites] Blood Coagul Fibrinolysis. 1998 Mar;9 Suppl 1:S15-20 [9819024.001]
  • [Cites] J Thromb Haemost. 2003 Mar;1(3):606-8 [12871480.001]
  • [Cites] BMJ. 2001 Nov 10;323(7321):1115-7 [11701581.001]
  • [Cites] Clin Lab Haematol. 2004 Jun;26(3):229-31 [15163323.001]
  • [Cites] Thromb J. 2006 Jan 18;4:1 [16420687.001]
  • [Cites] Eur J Haematol. 2007 Feb;78(2):173-4 [17313564.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 May;13(5):622-3 [17448923.001]
  • [Cites] Am J Hematol. 2006 Sep;81(9):720 [16804937.001]
  • [Cites] Br J Haematol. 1999 Jul;106(1):254-5 [10444198.001]
  • [Cites] Crit Care Med. 2005 Apr;33(4):883-90 [15818119.001]
  • [Cites] Blood Coagul Fibrinolysis. 2000 Apr;11 Suppl 1:S107-11 [10850574.001]
  • [Cites] Haemostasis. 1996;26 Suppl 1:143-9 [8904190.001]
  • [Cites] Pediatr Hematol Oncol. 2006 Jun;23 (4):339-45 [16621776.001]
  • [Cites] Bone Marrow Transplant. 2002 Dec;30(12):975-8 [12476294.001]
  • (PMID = 19137431.001).
  • [ISSN] 1559-131X
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; EC 3.4.21.21 / Factor VIIa; ZRP63D75JW / Idarubicin
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23. Chong JH, Zheng GG, Zhu XF, Guo Y, Wang L, Ma CH, Liu SY, Xu LL, Lin YM, Wu KF: Abnormal expression of P2X family receptors in Chinese pediatric acute leukemias. Biochem Biophys Res Commun; 2010 Jan 1;391(1):498-504
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Abnormal expression of P2X family receptors in Chinese pediatric acute leukemias.
  • Their distribution patterns and significance in pediatric leukemias have not been established.
  • Here we investigated the expression of P2X receptors in BMMC samples from Chinese pediatric acute leukemias.
  • Real-time PCR and Western blot results showed that P2X1, P2X4, P2X5 and P2X7 receptors were simultaneously over expressed in leukemias compared with controls, whereas P2X2, P2X3 and P2X6 were absent or marginally expressed in both groups.
  • These results suggested that P2X1, P2X4, P2X5 and P2X7 were hematopoiesis-related P2X receptors, and their signaling, especially for P2X7, might play important roles in pediatric leukemias.
  • P2X receptors might co-operatively contribute to the malignant phenotype in human pediatric leukemias.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Leukemia / metabolism. Receptors, Purinergic P2 / biosynthesis

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  • [Copyright] Copyright 2009 Elsevier Inc. All rights reserved.
  • (PMID = 19919827.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Purinergic P2; 0 / Receptors, Purinergic P2X
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24. Kern W, Kohlmann A, Schnittger S, Schoch C, Haferlach T: Role of gene expression profiling for diagnosing acute leukemias. Rev Clin Exp Hematol; 2005 Jun;9(1):E1
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of gene expression profiling for diagnosing acute leukemias.
  • Cytomorphology and cytochemistry in combination with multiparameter immunophenotyping today are the standard methods for establishing the diagnosis of acute leukemias.
  • In addition, cytogenetics, fluorescence in situ hybridization, and polymerase chain reaction based assays provide important information regarding biologically defined and prognostically relevant subgroups and allow a comprehensive diagnosis of well defined subentities.
  • With regard to the clinical setting a better understanding of the clinical course of distinct biologically defined disease subtypes is needed to select disease-specific therapeutic approaches.
  • Paralleling the increase in knowledge on deregulated pathways in leukemia the development of new therapeutics is accelerated and therefore requires a detailed and comprehensive diagnostic tool.
  • Revealing and quantifying the expression status of many ten thousands of genes in a single analysis the microarray technology holds this potential to become an essential tool for the molecular classification of leukemias.
  • Furthermore, it is anticipated that new biologically defined and clinically relevant subtypes of leukemia will be identified based on gene expression profiling.
  • [MeSH-major] Gene Expression Profiling. Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Cytogenetic Analysis. Humans. Neoplasm Proteins / analysis. Oligonucleotide Array Sequence Analysis. Prognosis

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  • (PMID = 16027103.001).
  • [ISSN] 1825-151X
  • [Journal-full-title] Reviews in clinical and experimental hematology
  • [ISO-abbreviation] Rev Clin Exp Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Number-of-references] 64
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25. Bagg A: Lineage ambiguity, infidelity, and promiscuity in immunophenotypically complex acute leukemias: genetic and morphologic correlates. Am J Clin Pathol; 2007 Oct;128(4):545-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lineage ambiguity, infidelity, and promiscuity in immunophenotypically complex acute leukemias: genetic and morphologic correlates.
  • [MeSH-major] Cell Lineage / genetics. Immunophenotyping / methods. Leukemia, Lymphoid / genetics. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Flow Cytometry. Humans. Molecular Diagnostic Techniques

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  • (PMID = 17875503.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Editorial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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26. Chung NG, Kim MS, Chung YJ, Yoo NJ, Lee SH: Tumor suppressor WTX gene mutation is rare in acute leukemias. Leuk Lymphoma; 2008 Aug;49(8):1616-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor suppressor WTX gene mutation is rare in acute leukemias.
  • [MeSH-major] Leukemia / genetics. Mutation. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Acute Disease. Adaptor Proteins, Signal Transducing. Adult. Aged. Aged, 80 and over. Bone Marrow. DNA Mutational Analysis. DNA, Neoplasm / genetics. Humans. Middle Aged

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  • (PMID = 18452086.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AMER1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / DNA, Neoplasm; 0 / Tumor Suppressor Proteins
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27. Abstracts from Acute Leukemias XI. Prognostic Factors and Treatment Strategies. February 18-22, 2006. Munich, Germany. Ann Hematol; 2006;85 Suppl 1:12-126

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Abstracts from Acute Leukemias XI. Prognostic Factors and Treatment Strategies. February 18-22, 2006. Munich, Germany.
  • [MeSH-major] Acute Disease / therapy
  • [MeSH-minor] Animals. Humans. Leukemia. Prognosis

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  • (PMID = 16456698.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Congresses; Overall
  • [Publication-country] Germany
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28. Ravandi F, Kebriaei P: Cytokines in the treatment of acute leukemias. Cancer Treat Res; 2005;126:313-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytokines in the treatment of acute leukemias.
  • [MeSH-major] Cytokines / therapeutic use. Leukemia / therapy
  • [MeSH-minor] Acute Disease. Humans

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  • (PMID = 16209072.001).
  • [ISSN] 0927-3042
  • [Journal-full-title] Cancer treatment and research
  • [ISO-abbreviation] Cancer Treat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines
  • [Number-of-references] 88
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29. Lee JW, Soung YH, Kim SY, Nam SW, Park WS, Lee JY, Yoo NJ, Lee SH: Kinase domain mutation of ERBB family genes is uncommon in acute leukemias. Leuk Res; 2006 Feb;30(2):241-2
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  • [Title] Kinase domain mutation of ERBB family genes is uncommon in acute leukemias.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Epidermal Growth Factor / genetics. Receptor, ErbB-2 / genetics

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  • (PMID = 16054688.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.10.1 / Receptor, ErbB-4
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30. Kim YR, Eom HS, Min CK, Lee S, Chung NG, Yoo NJ, Lee SH: Analysis of NOTCH1 extracellular juxtamembrane expansion mutations in acute leukemias and multiple myelomas. APMIS; 2009 Feb;117(2):147-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of NOTCH1 extracellular juxtamembrane expansion mutations in acute leukemias and multiple myelomas.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Multiple Myeloma / genetics. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics

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  • (PMID = 19239437.001).
  • [ISSN] 1600-0463
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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31. Jeong EG, Kim SH, Kim MS, Lee SH, Yoo NJ: Absence of JAK2 exon 12 mutation in acute leukemias. Acta Haematol; 2008;119(1):38-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Absence of JAK2 exon 12 mutation in acute leukemias.
  • [MeSH-major] Exons. Janus Kinase 2 / genetics. Leukemia / genetics. Mutation
  • [MeSH-minor] Acute Disease. Base Sequence. DNA Primers. Humans. Polymerase Chain Reaction

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  • (PMID = 18230964.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / DNA Primers; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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32. Devergie A: [Treatment of acute leukemias and chronic myeloid leukemias]. Soins; 2008 Mar;(723):44-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Treatment of acute leukemias and chronic myeloid leukemias].
  • [Transliterated title] Le traitement des leucémies aiguës et de la leucémie myéloïde chronique.
  • [MeSH-major] Leukemia / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation. Humans. Prognosis. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction / methods. Transplantation Conditioning. Treatment Outcome

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  • (PMID = 18380312.001).
  • [ISSN] 0038-0814
  • [Journal-full-title] Soins; la revue de référence infirmière
  • [ISO-abbreviation] Soins
  • [Language] fre
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
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33. Soung YH, Lee JW, Kim SY, Nam SW, Kim SH, Lee JY, Yoo NJ, Lee SH: Absence of the mutation of serine/threonine kinase genes AKT2 and MYLK2 in acute leukemias. Eur J Haematol; 2006 Aug;77(2):175-6
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  • [Title] Absence of the mutation of serine/threonine kinase genes AKT2 and MYLK2 in acute leukemias.
  • [MeSH-major] Leukemia / genetics. Myosin-Light-Chain Kinase / genetics. Proto-Oncogene Proteins c-akt / genetics
  • [MeSH-minor] Acute Disease. DNA Mutational Analysis. Humans. Neoplasms / enzymology. Neoplasms / genetics. Polymorphism, Single-Stranded Conformational. Protein Structure, Tertiary

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  • (PMID = 16856912.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] EC 2.7.11.1 / AKT2 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.18 / Myosin-Light-Chain Kinase
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34. Meyer C, Kowarz E, Hofmann J, Renneville A, Zuna J, Trka J, Ben Abdelali R, Macintyre E, De Braekeleer E, De Braekeleer M, Delabesse E, de Oliveira MP, Cavé H, Clappier E, van Dongen JJ, Balgobind BV, van den Heuvel-Eibrink MM, Beverloo HB, Panzer-Grümayer R, Teigler-Schlegel A, Harbott J, Kjeldsen E, Schnittger S, Koehl U, Gruhn B, Heidenreich O, Chan LC, Yip SF, Krzywinski M, Eckert C, Möricke A, Schrappe M, Alonso CN, Schäfer BW, Krauter J, Lee DA, Zur Stadt U, Te Kronnie G, Sutton R, Izraeli S, Trakhtenbrot L, Lo Nigro L, Tsaur G, Fechina L, Szczepanski T, Strehl S, Ilencikova D, Molkentin M, Burmeister T, Dingermann T, Klingebiel T, Marschalek R: New insights to the MLL recombinome of acute leukemias. Leukemia; 2009 Aug;23(8):1490-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New insights to the MLL recombinome of acute leukemias.
  • Chromosomal rearrangements of the human MLL gene are associated with high-risk pediatric, adult and therapy-associated acute leukemias.
  • These patients need to be identified, treated appropriately and minimal residual disease was monitored by quantitative PCR techniques.
  • Genomic DNA was isolated from individual acute leukemia patients to identify and characterize chromosomal rearrangements involving the human MLL gene.
  • A total of 760 MLL-rearranged biopsy samples obtained from 384 pediatric and 376 adult leukemia patients were characterized at the molecular level.
  • The distribution of MLL breakpoints for clinical subtypes (acute lymphoblastic leukemia, acute myeloid leukemia, pediatric and adult) and fused translocation partner genes (TPGs) will be presented, including novel MLL fusion genes.
  • [MeSH-major] Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Recombination, Genetic. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Biopsy. Bone Marrow / chemistry. Bone Marrow / pathology. Child. Chromosome Breakage. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 11 / ultrastructure. Computational Biology. DNA, Neoplasm / blood. DNA, Neoplasm / genetics. Gene Duplication. Histone-Lysine N-Methyltransferase. Humans. Polymerase Chain Reaction

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  • (PMID = 19262598.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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35. van den Ancker W, Terwijn M, Westers TM, Merle PA, van Beckhoven E, Dräger AM, Ossenkoppele GJ, van de Loosdrecht AA: Acute leukemias of ambiguous lineage: diagnostic consequences of the WHO2008 classification. Leukemia; 2010 Jul;24(7):1392-6
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  • [Title] Acute leukemias of ambiguous lineage: diagnostic consequences of the WHO2008 classification.
  • [MeSH-major] Cell Lineage. Leukemia / classification. Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Female. Humans. Immunophenotyping. Infant. Male. Middle Aged. World Health Organization. Young Adult

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  • (PMID = 20485373.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
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36. Kadia TM, Faderl S, Estrov Z, Konopleva M, George S, Lee W, Puzanov I, Chen A, Kantarjian H, Ravandi F: Final results of phase I and pharmacokinetic study of SJG-136 administered on a daily x 5 schedule. J Clin Oncol; 2009 May 20;27(15_suppl):e13506

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Here we report the results of a CTEP-sponsored phase I trial of SJG-136 administered on a daily x 5 schedule in pts with relapsed or refractory (R/R) leukemias.
  • METHODS: Previously treated pts with R/R acute leukemias (AML, ALL, high risk MDS, CML blast phase) or R/R CLL with adequate organ function and ECOG performance status of ≤ 2 were eligible for the study.
  • Other manifestations of vascular leak including grade I, II hypoalbuminemia, edema, and pleural effusions were seen in a number of patients starting at dose level 24 mcg/m<sup>2</sup> and above.
  • Other non-dose limiting toxicities included nausea, dyspnea, fatigue, bloating, and insomnia.
  • One pt had a PR, 8 pts had stable disease, and 6 had progression.
  • CONCLUSIONS: SJG-136 is safe and active in patients with advanced leukemias.

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  • (PMID = 27961262.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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37. Jeong EG, Kim MS, Nam HK, Min CK, Lee S, Chung YJ, Yoo NJ, Lee SH: Somatic mutations of JAK1 and JAK3 in acute leukemias and solid cancers. Clin Cancer Res; 2008 Jun 15;14(12):3716-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatic mutations of JAK1 and JAK3 in acute leukemias and solid cancers.
  • EXPERIMENTAL DESIGN: We analyzed 494 tissues from 186 acute adulthood leukemias, 30 multiple myelomas, and 278 common solid cancers, including 90 breast, 47 gastric, 47 colon, 47 lung, and 47 hepatocellular carcinomas by single-strand conformation polymorphism analysis.
  • RESULTS: Overall, we found six JAK1 mutations (four in acute leukemias, one in a lung carcinoma, and one in a breast carcinoma) and three JAK3 mutations (two in breast carcinomas and one in a gastric carcinoma).
  • We found three of the four leukemias with JAK1 mutations expressed mutated JAK1 at the mRNA level.
  • With respect to the cancer types, T-acute lymphoblastic leukemia (T-ALL) showed the highest incidence of the mutations (3 of 11; 27.3%).
  • [MeSH-major] Breast Neoplasms / genetics. Carcinoma / genetics. Janus Kinase 1 / genetics. Janus Kinase 3 / genetics. Leukemia / genetics. Mutation
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Base Sequence. Colorectal Neoplasms / genetics. DNA Mutational Analysis. Humans. Liver Neoplasms / genetics. Middle Aged. Stomach Neoplasms / genetics

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  • (PMID = 18559588.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / JAK3 protein, human; EC 2.7.010.2 / JAK1 protein, human; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 3
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38. Forestier E, Schmiegelow K, Nordic Society of Paediatric Haematology and Oncology NOPHO: The incidence peaks of the childhood acute leukemias reflect specific cytogenetic aberrations. J Pediatr Hematol Oncol; 2006 Aug;28(8):486-95
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  • [Title] The incidence peaks of the childhood acute leukemias reflect specific cytogenetic aberrations.
  • The correlation between age and karyotype was studied in 1425, 0 to 14.9 years old children who were diagnosed with acute lymphoblastic leukemia (ALL) or acute myeloblastic leukemia.
  • Almost 80% of the non-Down B-cell precursor ALL cases in the 2 to 7 years frequency peak group who had aberrant cytogenetic results had either a high-hyperdiploid clone (51 to 61 chromosomes) or a translocation t(12;21)(p13;q22).
  • Among B-cell precursor ALL cases, high white blood cell counts correlated with earlier age at diagnosis (rS=-0.23; P<0.001) being most evident for 11q23/MLL-aberrations, translocation t(12;21)(p13;q22), and high-hyperdiploidy.
  • Among acute myeloblastic leukemia patients, frequency peaks were found for those with MLL/11q23 rearrangements (peak: first year), Down syndrome (peak: second to third year), or cytogenetic abnormalities other than translocations t(8;21), t(15;17), and inv(16)/t(16;16) (peak: first to third year).
  • The epidemiology of the cytogenetic subsets of acute leukemias questions whether age as a disease-related prognostic parameter has any relevance in childhood leukemia clinical research beyond being a surrogate marker for more important, truly biologic features such as cytogenetic aberrations and white cell count at diagnosis.
  • Further research is needed to explore whether the 2 to 7 years age incidence peak in childhood ALL harbor yet unidentified cytogenetic subsets with the same natural history as the high-hyperdiploid and t(12;21)-positive leukemias.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Age Distribution. Child. Child, Preschool. Cohort Studies. Comorbidity. Cytogenetic Analysis / methods. Down Syndrome / diagnosis. Down Syndrome / epidemiology. Down Syndrome / genetics. Female. Humans. Incidence. Infant. Infant, Newborn. Karyotyping. Male. Ploidies. Recurrence. Registries / statistics & numerical data. Risk Factors. Scandinavian and Nordic Countries / epidemiology

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  • (PMID = 16912588.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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39. Nakanishi H, Nakamura T, Canaani E, Croce CM: ALL1 fusion proteins induce deregulation of EphA7 and ERK phosphorylation in human acute leukemias. Proc Natl Acad Sci U S A; 2007 Sep 4;104(36):14442-7
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  • [Title] ALL1 fusion proteins induce deregulation of EphA7 and ERK phosphorylation in human acute leukemias.
  • Erythropoietin-producing hepatoma-amplified sequence (Eph) receptor tyrosine kinases and their cell-surface-bound ligands, the ephrins, function as a unique signaling system triggered by cell-to-cell interaction and have been shown to mediate neurodevelopmental processes.
  • The ALL1 (also termed MLL) gene on human chromosome 11q23 was isolated by virtue of its involvement in recurrent chromosome translocations associated with acute leukemias with poor prognosis.
  • The most common translocations in ALL1-associated leukemias are t(4;11) and t(9;11), which generate ALL1/AF4 and ALL1/AF9 fusion protein, respectively.
  • Finally, we show apoptotic cell death, specific for leukemic cells carrying the t(4;11) chromosome translocation, after treatment of the cells with an ERK phosphorylation blocker.

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  • [Cites] Prostate. 1999 Dec 1;41(4):275-80 [10544301.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jul 18;92(15):6808-12 [7624324.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):2301-6 [11280802.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Int J Cancer. 2003 Feb 20;103(5):657-63 [12494475.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7853-8 [12782787.001]
  • [Cites] Cancer Biol Ther. 2003 Sep-Oct;2(5):544-51 [14614324.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(2):617-28 [14701735.001]
  • [Cites] Pathol Oncol Res. 2004;10(1):26-33 [15029258.001]
  • [Cites] Cell. 1992 Nov 13;71(4):701-8 [1423625.001]
  • [Cites] Oncogene. 1997 Apr 10;14(14):1635-42 [9135064.001]
  • [Cites] Blood. 1997 Nov 1;90(9):3613-22 [9345045.001]
  • [Cites] Clin Cancer Res. 1998 Mar;4(3):791-7 [9533549.001]
  • [Cites] Leukemia. 1998 May;12(5):779-87 [9593281.001]
  • [Cites] Protein Sci. 1998 Nov;7(11):2249-55 [9827991.001]
  • [Cites] J Neurosci. 1999 Jun 15;19(12):4962-71 [10366629.001]
  • [Cites] Int J Cancer. 1999 Oct 22;84(5):494-501 [10502726.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Jun;6(6):462-75 [15928710.001]
  • [Cites] Clin Cancer Res. 2005 Sep 15;11(18):6450-8 [16166419.001]
  • [Cites] Mol Biotechnol. 2005 Oct;31(2):151-74 [16170216.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3559-66 [16046533.001]
  • [Cites] J Med Genet. 2006 Jun;43(6):507-11 [16155194.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jun 26;104(26):10980-5 [17581865.001]
  • [Cites] Cancer Lett. 2001 Mar 10;164(1):97-104 [11166921.001]
  • (PMID = 17726105.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA128609; United States / NCI NIH HHS / CA / CA128609
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 24386-93-4 / 5-iodotubercidin; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / Receptor, EphA7; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; M351LCX45Y / Tubercidin
  • [Other-IDs] NLM/ PMC1964835
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40. Robazzi TC, Silva LR, Mendonça N, Barreto JH: Gastrointestinal manifestations as initial presentation of acute leukemias in children and adolescents. Acta Gastroenterol Latinoam; 2008 Jun;38(2):126-32
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  • [Title] Gastrointestinal manifestations as initial presentation of acute leukemias in children and adolescents.
  • OBJECTIVE: this study aimed to determine the prevalence and characteristics of gastrointestinal manifestations on initial clinical presentation of acute leukemias (AL) in childhood.
  • RESULTS: acute lymphoid leukemia (ALL) was diagnosed in 273 (77.1%) patients and acute non-lymphocytic leukemia (AML) in 81 (22.9%).
  • CONCLUSIONS: gastrointestinal symptoms are not very well-documented as initial manifestation of leukemia in children and should be considered on the differential diagnosis of gastrointestinal symptoms of unknown etiology in children.
  • [MeSH-major] Gastrointestinal Diseases / etiology. Leukemia, Myeloid, Acute / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • (PMID = 18697407.001).
  • [ISSN] 0300-9033
  • [Journal-full-title] Acta gastroenterologica Latinoamericana
  • [ISO-abbreviation] Acta Gastroenterol. Latinoam.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Argentina
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41. Makeshova AB, Levina AA, Mamukova IuI, Tsibul'skaia MM, Makarova PM, Romanova EA, Fevraleva IS, Sudarikov AB, Golovkina LL, Stremoukhova AG, Parovichnikova EN, Savchenko VG: [Determinants for iron overload in patients with acute leukemias and aplastic anemia]. Ter Arkh; 2010;82(7):26-9
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  • [Title] [Determinants for iron overload in patients with acute leukemias and aplastic anemia].
  • AIM: to reveal the determinants of the development of iron overload in patients with acute leukemias (AL) and aplastic anemia (AA).
  • SUBJECTS AND METHODS: The investigation included 104 patients, including 64 with various types of AL, 31 with AA, and 9 with myelodysplastic syndromes (MDS).
  • SF was 1046.1 microg/l in patients, H63D heterozygous carriers who had received less than 10 packed red blood cell transfusions and 2856 microg/l in those who had 20 transfusions (p < 0.005).
  • In patients with transfusion chimeras and a rare phenotype in terms of rhesus antigens, packed red blood cell transfusion results in a much more increase in iron stores.
  • CONCLUSION: The most important factor of iron overload acceleration is no specific choice of packed red blood cells for patients with rare combinations of red blood cell antigens and for those with artificially induced chimeras.
  • [MeSH-major] Anemia, Aplastic / blood. Erythrocyte Transfusion. Hemosiderosis / blood. Histocompatibility Antigens Class I / genetics. Iron / blood. Leukemia / blood. Membrane Proteins / genetics
  • [MeSH-minor] Acute Disease. Erythrocytes / cytology. Ferritins / blood. Heterozygote. Homozygote. Humans. Mutation. Radioimmunoassay. Rh-Hr Blood-Group System / genetics. Risk Factors


42. Meyer-Monard S: [Genetic diagnosis of acute leukemias--a practical guide]. Ther Umsch; 2006 Apr;63(4):237-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Genetic diagnosis of acute leukemias--a practical guide].
  • Acute leukemias are the consequence of accumulation of immature precursor cells.
  • Genetic alterations are cause of uncontrolled cell proliferation.
  • They can be detected by conventional cytogenetics and molecular methods at diagnosis.
  • Classification of acute leukemias according to the World Health Organization depend on the knowledge of the presence of these aberrations.
  • Detection and monitoring of genetic abnormalities in acute leukemias are of major importance for correct management of patients.
  • [MeSH-major] Leukemia / genetics
  • [MeSH-minor] Acute Disease. Chromosome Aberrations. Cytogenetics. Diagnosis, Differential. Follow-Up Studies. Genetic Markers. Humans. Karyotyping. Mutation. Polymerase Chain Reaction / methods. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. World Health Organization

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  • (PMID = 16689453.001).
  • [ISSN] 0040-5930
  • [Journal-full-title] Therapeutische Umschau. Revue thérapeutique
  • [ISO-abbreviation] Ther Umsch
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Genetic Markers
  • [Number-of-references] 11
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43. Robazzi TC, Barreto JH, Silva LR, Santiago MB, Mendonça N: Osteoarticular manifestations as initial presentation of acute leukemias in children and adolescents in Bahia, Brazil. J Pediatr Hematol Oncol; 2007 Sep;29(9):622-6
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  • [Title] Osteoarticular manifestations as initial presentation of acute leukemias in children and adolescents in Bahia, Brazil.
  • OBJECTIVE: This study was to determine the prevalence and characteristics of the osteoarticular manifestations on initial clinical presentation of acute leukemias (ALs) on childhood in the state of Bahia, Brazil.
  • RESULTS: Acute lymphocytic leukemia (ALL) was diagnosed in 313 (77.1%) patients and acute myeloid leukemia (AML), in 93 (22.9%) patients, including 241 males (59.4%) and 165 females (40.6%).
  • Prior referral to our center, the most frequent initial diagnosis was anemia (15.8%), leukemia (15.0%), amygdalitis (3.7%), and rheumatic fever (2.7%).
  • CONCLUSIONS: AL should be considered on the differential diagnosis of osteoarticular symptoms of unknown etiology in children.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Osteoarthritis / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Brazil. Child. Child, Preschool. Female. Humans. Infant. Male

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  • (PMID = 17805037.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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44. Andersson A, Ritz C, Lindgren D, Edén P, Lassen C, Heldrup J, Olofsson T, Råde J, Fontes M, Porwit-Macdonald A, Behrendtz M, Höglund M, Johansson B, Fioretos T: Microarray-based classification of a consecutive series of 121 childhood acute leukemias: prediction of leukemic and genetic subtype as well as of minimal residual disease status. Leukemia; 2007 Jun;21(6):1198-203
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  • [Title] Microarray-based classification of a consecutive series of 121 childhood acute leukemias: prediction of leukemic and genetic subtype as well as of minimal residual disease status.
  • Gene expression analyses were performed on 121 consecutive childhood leukemias (87 B-lineage acute lymphoblastic leukemias (ALLs), 11 T-cell ALLs and 23 acute myeloid leukemias (AMLs)), investigated during an 8-year period at a single center.
  • Minimal residual disease status (MRD) in T-cell ALLs with a high (>0.1%) MRD at day 29 could be classified with 100% accuracy already at the time of diagnosis.
  • In pediatric leukemias with uncharacteristic cytogenetic aberrations or with a normal karyotype, unsupervised analysis identified two novel subgroups: one consisting mainly of cases remaining in complete remission (CR) and one containing a few patients in CR and all but one of the patients who relapsed.
  • This study of a consecutive series of childhood leukemias confirms and extends further previous reports demonstrating that global gene expression profiling provides a valuable tool for genetic and clinical classification of childhood leukemias.
  • [MeSH-major] Leukemia / classification. Leukemia / genetics. Neoplasm, Residual / diagnosis. Oligonucleotide Array Sequence Analysis / methods
  • [MeSH-minor] Acute Disease. Algorithms. Child. Gene Expression Profiling. Genes, cdc. Humans. Leukemia, B-Cell. Leukemia, Myeloid. Leukemia, T-Cell. Predictive Value of Tests. Recurrence. Remission Induction

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  • (PMID = 17410184.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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45. Huh JY, Chung S, Oh D, Kang MS, Eom HS, Cho EH, Han MH, Kong SY: Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature. Korean J Lab Med; 2010 Apr;30(2):117-21
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  • [Title] Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature.
  • The translocation t(10;11)(p13;q14q21) has been found to be recurrent in acute lymphoblastic and myeloid leukemias, and results in the fusion of the clathrin assembly lymphoid myeloid leukemia (CALM) gene with the AF10 gene; these genes are present on chromosomes 11 and 10, respectively.
  • Because the CALM-AF10 rearrangement is a rare chromosomal abnormality, it is not included in routine molecular tests for acute leukemia.
  • The first patient (case 1) was diagnosed with T-cell ALL, and the second patient (case 2) was diagnosed with AML.
  • Both patient samples showed expression of the homeobox A gene cluster and the histone methyltransferase hDOT1L, which suggests that they mediate leukemic transformation in CALM-AF10-positive and mixed-lineage leukemia-AF10-positive leukemias.
  • The first patient (case 1) relapsed after double-unit cord blood transplantation; there was no evidence of relapse in the second patient (case 2) after allogenic peripheral blood stem cell transplantation.
  • Since CALM-AF10- positive leukemias have been shown to have poor prognosis with conventional therapy, molecular tests for CALM-AF10 rearrangement would be necessary to detect minimal residual disease during follow-up.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Monomeric Clathrin Assembly Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adolescent. Adult. Bone Marrow / pathology. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 11. Cord Blood Stem Cell Transplantation. Female. Histone-Lysine N-Methyltransferase / genetics. Histone-Lysine N-Methyltransferase / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Male. Recurrence. Translocation, Genetic

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  • (PMID = 20445327.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MLLT10 protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Transcription Factors; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 14
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46. Andersson A, Paulsson K, Lilljebjörn H, Lassen C, Strömbeck B, Heldrup J, Behrendtz M, Johansson B, Fioretos T: FLT3 mutations in a 10 year consecutive series of 177 childhood acute leukemias and their impact on global gene expression patterns. Genes Chromosomes Cancer; 2008 Jan;47(1):64-70
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  • [Title] FLT3 mutations in a 10 year consecutive series of 177 childhood acute leukemias and their impact on global gene expression patterns.
  • During 1995-2004, 209 children/adolescents were diagnosed with acute lymphoblastic or myeloid leukemia (ALL, AML) in Southern Sweden, of which 177 (85%), comprising 128 B-lineage ALL, 34 AML, and 15 T-cell ALL, could be analyzed for internal tandem duplications (ITD) and activating point mutations in the second tyrosine kinase domain (ATKD) of FLT3.
  • None of the T-cell ALL harbored any mutations.
  • [MeSH-major] Gene Expression Regulation, Leukemic / physiology. Leukemia, Myeloid, Acute / genetics. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 17943971.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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47. Jelinek J, Oki Y, Gharibyan V, Bueso-Ramos C, Prchal JT, Verstovsek S, Beran M, Estey E, Kantarjian HM, Issa JP: JAK2 mutation 1849G&gt;T is rare in acute leukemias but can be found in CMML, Philadelphia chromosome-negative CML, and megakaryocytic leukemia. Blood; 2005 Nov 15;106(10):3370-3
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  • [Title] JAK2 mutation 1849G>T is rare in acute leukemias but can be found in CMML, Philadelphia chromosome-negative CML, and megakaryocytic leukemia.
  • The mutation was frequent in polycythemia vera (PV) (86%) and myelofibrosis (95%) but less prevalent in acute myeloid leukemia (AML) with an antecedent PV or myelofibrosis (5 [36%] of 14 patients).
  • JAK2 mutation was also detected in 3 (19%) of 16 patients with Philadelphia-chromosome (Ph)-negative chronic myelogenous leukemia (CML), 2 (18%) of 11 patients with megakaryocytic AML, 7 (13%) of 52 patients with chronic myelomonocytic leukemia, and 1 (1%) of 68 patients with myelodysplastic syndromes.
  • No mutation was found in Ph(+)CML (99 patients), AML M0-M6 (28 patients), or acute lymphoblastic leukemia (20 patients).
  • We conclude that the JAK2 1849G>T mutation is common in Ph(-) MPD but not critical for transformation to the acute phase of these diseases and that it is generally rare in aggressive leukemias.

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  • [Cites] Anal Biochem. 2000 Apr 10;280(1):103-10 [10805527.001]
  • [Cites] Blood. 2005 Sep 15;106(6):2162-8 [15920007.001]
  • [Cites] Cancer. 2002 Oct 15;95(8):1673-84 [12365015.001]
  • [Cites] Arch Pathol Lab Med. 2003 May;127(5):601-5 [12708906.001]
  • [Cites] Cell. 1993 Jul 30;74(2):227-36 [8343951.001]
  • [Cites] Blood. 1997 Oct 1;90(7):2535-40 [9326218.001]
  • [Cites] Cell. 1998 May 1;93(3):385-95 [9590173.001]
  • [Cites] Blood. 2005 Feb 1;105(3):973-7 [15388582.001]
  • [Cites] Curr Opin Hematol. 2005 Mar;12(2):112-6 [15725900.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [Cites] J Clin Oncol. 2005 Apr 1;23(10):2224-32 [15710945.001]
  • [Cites] Cancer Res. 2005 Apr 1;65(7):2662-7 [15805263.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] J Biol Chem. 2005 Jun 17;280(24):22788-92 [15863514.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1207-9 [15860661.001]
  • [Cites] Blood. 2002 Feb 1;99(3):840-9 [11806985.001]
  • (PMID = 16037387.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50CA100632
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Other-IDs] NLM/ PMC1895065
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48. Traina F, Favaro PM, Medina Sde S, Duarte Ada S, Winnischofer SM, Costa FF, Saad ST: ANKHD1, ankyrin repeat and KH domain containing 1, is overexpressed in acute leukemias and is associated with SHP2 in K562 cells. Biochim Biophys Acta; 2006 Sep;1762(9):828-34
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  • [Title] ANKHD1, ankyrin repeat and KH domain containing 1, is overexpressed in acute leukemias and is associated with SHP2 in K562 cells.
  • In the present study, increased levels of ANKHD1 mRNA and protein expression in leukemia cell lines are reported, as compared with normal hematopoietic cells.
  • Furthermore, a higher expression of ANKHD1 mRNA was detected in primary acute leukemia samples than in normal hematopoietic cells (P=0.002).
  • ANKHD1 was detected in the cytosolic and membrane fraction of cells and was co-immunoprecipitated with SHP2 in protein extracts of K562 and LNCaP cell lines.
  • These findings suggest a role for ANKHD1 as a scaffolding protein that may be associated with the abnormal phenotype of leukemia cells.
  • [MeSH-major] Ankyrin Repeat. Gene Expression Regulation, Neoplastic. Intracellular Signaling Peptides and Proteins / metabolism. Leukemia / metabolism. Protein Tyrosine Phosphatases / metabolism. Protein-Serine-Threonine Kinases / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Case-Control Studies. Cell Line, Tumor. Cytoplasm / metabolism. HL-60 Cells. Humans. K562 Cells. Middle Aged. Protein Tyrosine Phosphatase, Non-Receptor Type 11. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16956752.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Messenger; EC 2.7.11.1 / ANKK1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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49. Kiss F, Simon A, Csáthy L, Hevessy Z, Katona E, Kiss C, Kappelmayer J: A coagulation factor becomes useful in the study of acute leukemias: studies with blood coagulation factor XIII. Cytometry A; 2008 Mar;73(3):194-201
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  • [Title] A coagulation factor becomes useful in the study of acute leukemias: studies with blood coagulation factor XIII.
  • By using 3- and 4-color flow cytometry FXIII expression was investigated in normal peripheral blood and bone marrow samples and in acute myeloblastic (AML) and lymphoblastic (ALL) leukemia cases.
  • FXIII-A was detectable in normal peripheral blood monocytes and in large quantities in platelets, but both cell types were negative for FXIII-B.
  • In samples derived from patients with AML M4 and M5, FXIII-A sensitively identified blast cells.
  • These data provide evidence that FXIII-A is a sufficiently sensitive marker in differentiating myeloblasts and monoblasts and is suitable for identifying leukemia-associated phenotypes in ALL.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Factor XIII / chemistry. Factor XIII / physiology. Leukemia / blood. Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Animals. Blood Platelets / chemistry. Blood Platelets / metabolism. Blood Platelets / pathology. Flow Cytometry / methods. Humans. Monocytes / chemistry. Monocytes / metabolism. Monocytes / pathology

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  • [Copyright] Copyright 2007 International Society for Analytical Cytology.
  • (PMID = 18000871.001).
  • [ISSN] 1552-4930
  • [Journal-full-title] Cytometry. Part A : the journal of the International Society for Analytical Cytology
  • [ISO-abbreviation] Cytometry A
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 9013-56-3 / Factor XIII
  • [Number-of-references] 56
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50. Moretta A, Locatelli F, Moretta L: Human NK cells: from HLA class I-specific killer Ig-like receptors to the therapy of acute leukemias. Immunol Rev; 2008 Aug;224:58-69
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  • [Title] Human NK cells: from HLA class I-specific killer Ig-like receptors to the therapy of acute leukemias.
  • This review traces the major advances in human NK cell biology from the original discovery of human leukocyte antigen class I-specific inhibitory receptors to recent groundbreaking clinical applications.
  • These, in turn, led to major achievements and further expectations in the cure of high risk of otherwise fatal leukemias.
  • It has become evident that there is a role of donor-derived 'alloreactive' NK cells in eradicating acute myeloid (and now also lymphoid) leukemias in the T-cell-depleted haploidentical hemopoietic stem cell transplantation setting.
  • The key role played also in preventing graft rejection and graft versus host disease renders alloreactive NK cells an ideal tool for successful haploidentical hematopoietic stem cell transplantation.
  • [MeSH-major] Histocompatibility Antigens Class I / metabolism. Killer Cells, Natural / immunology. Leukemia / therapy. Receptors, KIR / metabolism
  • [MeSH-minor] Acute Disease. Animals. Cytotoxicity, Immunologic. Graft Rejection / immunology. Graft Rejection / prevention & control. Graft vs Host Disease / immunology. Graft vs Host Disease / prevention & control. Hematopoietic Stem Cell Transplantation. Humans. Immunotherapy. Isoantigens / immunology. Transplantation Immunology. Transplantation, Homologous

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  • (PMID = 18759920.001).
  • [ISSN] 1600-065X
  • [Journal-full-title] Immunological reviews
  • [ISO-abbreviation] Immunol. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class I; 0 / Isoantigens; 0 / Receptors, KIR
  • [Number-of-references] 119
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51. Figueroa ME, Melnick A, Greally JM: Genome-wide determination of DNA methylation by Hpa II tiny fragment enrichment by ligation-mediated PCR (HELP) for the study of acute leukemias. Methods Mol Biol; 2009;538:395-407
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  • [Title] Genome-wide determination of DNA methylation by Hpa II tiny fragment enrichment by ligation-mediated PCR (HELP) for the study of acute leukemias.
  • The HELP assay allows methylation levels throughout the genome to be accurately determined so that the epigenetic state of leukemia cells can be identified, compared, and contrasted.
  • [MeSH-major] DNA / analysis. DNA Methylation. DNA-Cytosine Methylases / metabolism. Genome, Human. Leukemia / genetics. Polymerase Chain Reaction / methods
  • [MeSH-minor] Acute Disease. CpG Islands. Cytosine / chemistry. Humans. Oligonucleotide Array Sequence Analysis

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  • (PMID = 19277580.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 8J337D1HZY / Cytosine; 9007-49-2 / DNA; EC 2.1.1.- / DNA modification methylase HpaII; EC 2.1.1.- / DNA-Cytosine Methylases
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52. Schaad K, Strömbeck B, Mandahl N, Andersen MK, Heim S, Mertens F, Johansson B: FISH mapping of i(7q) in acute leukemias and myxoid liposarcoma reveals clustered breakpoints in 7p11.2: implications for formation and pathogenetic outcome of the idic(7)(p11.2). Cytogenet Genome Res; 2006;114(2):126-30
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  • [Title] FISH mapping of i(7q) in acute leukemias and myxoid liposarcoma reveals clustered breakpoints in 7p11.2: implications for formation and pathogenetic outcome of the idic(7)(p11.2).
  • Despite its high frequency, nothing is known about the formation and the pathogenetic outcome of this abnormality.
  • To address these issues, we performed a detailed fluorescence in situ hybridization (FISH) investigation of four acute lymphoblastic leukemias, one acute myeloid leukemia, and two myxoid liposarcomas with i(7q).
  • [MeSH-major] Chromosome Breakage / genetics. Chromosomes, Human, Pair 7 / genetics. Isochromosomes / genetics. Leukemia / genetics. Leukemia / pathology. Liposarcoma, Myxoid / genetics. Liposarcoma, Myxoid / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged


53. Franklin JL, Seibel NL, Krailo M, Fu C, Adamson PC, Reaman G, Children's Oncology Group: Phase 2 study of docetaxel in the treatment of childhood refractory acute leukemias: a Children's Oncology Group report. Pediatr Blood Cancer; 2008 Mar;50(3):533-6
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  • [Title] Phase 2 study of docetaxel in the treatment of childhood refractory acute leukemias: a Children's Oncology Group report.
  • BACKGROUND: To determine the response rate and toxicity of docetaxel when administered as a 60 mg/m(2) dose by 1 hr intravenous (IV) infusion weekly x 3 weeks in children with relapsed acute lymphoblastic leukemia (ALL) or acute myeloid leukemia (AML).
  • PROCEDURE: Patients who were under the age of 22-year-old at the time of the original ALL or AML diagnosis and in a second relapse were accrued from August 2002 to May 2005 for this Children's Oncology Group (COG) phase 2 study (ADVL0023).
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Leukemia / drug therapy. Salvage Therapy. Taxoids / therapeutic use
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Bone Marrow Diseases / chemically induced. Child. Child, Preschool. Drug Administration Schedule. Female. Fever / etiology. Humans. Infant. Infusions, Intravenous. Leukemia, Myeloid / drug therapy. Male. Neutropenia / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Treatment Failure

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17668867.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 98543
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel
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54. Haferlach T, Kern W, Schnittger S, Schoch C: Modern diagnostics in acute leukemias. Crit Rev Oncol Hematol; 2005 Nov;56(2):223-34
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  • [Title] Modern diagnostics in acute leukemias.
  • Acute leukemias are a heterogeneous group of diseases.
  • Improvements in patient's treatment resulting in better survival rates are closely linked to the biological understanding of the disease subtypes, which is assessed by specific diagnostic approaches.
  • Thus, several diagnostic techniques are mandatory at diagnosis for classification and for individual therapeutic decisions.
  • Furthermore they are also needed for follow up studies focusing especially on minimal residual disease (MRD) to guide further treatment decisions based on the response of the disease to given treatment protocols.
  • Only by using a comprehensive diagnostic panel including cytomorphology, cytochemistry, multiparameter flow cytometry (MFC), cytogenetics, fluorescence in situ hybridization (FISH) and molecular genetic methods the correct diagnosis in acute leukemias can be established today.
  • [MeSH-major] Biomarkers, Tumor. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Flow Cytometry / methods. Histocytochemistry / methods. Humans. In Situ Hybridization, Fluorescence / methods. Neoplasm, Residual

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  • (PMID = 16213152.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 70
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55. Sung Kim M, Ki Min C, Lee S, Gyun Chung N, Jin Yoo N, Hyung Lee S: Somatic mutation of TRAF3 gene is rare in common human cancers and acute leukemias. Acta Oncol; 2008;47(8):1615-7
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  • [Title] Somatic mutation of TRAF3 gene is rare in common human cancers and acute leukemias.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Neoplasms / genetics. TNF Receptor-Associated Factor 3 / genetics

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  • (PMID = 18607851.001).
  • [ISSN] 1651-226X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / TNF Receptor-Associated Factor 3; 0 / TRAF3 protein, human
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56. Oh JE, Chung NG, Min CK, Lee S, Yoo NJ, Lee SH: Absence of JAK1 exon 10 and 13 mutations in acute leukemias and multiple myelomas. Eur J Haematol; 2008 Nov;81(5):408-9
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  • [Title] Absence of JAK1 exon 10 and 13 mutations in acute leukemias and multiple myelomas.
  • [MeSH-major] Exons / genetics. Janus Kinase 1 / genetics. Leukemia / genetics. Multiple Myeloma / genetics. Point Mutation
  • [MeSH-minor] Acute Disease. Humans

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  • (PMID = 18691320.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] EC 2.7.010.2 / JAK1 protein, human; EC 2.7.10.2 / Janus Kinase 1
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57. Marangon E, Citterio M, Sala F, Barisone E, Lippi AA, Rizzari C, Biondi A, D'Incalci M, Zucchetti M: Pharmacokinetic profile of imatinib mesylate and N-desmethyl-imatinib (CGP 74588) in children with newly diagnosed Ph+ acute leukemias. Cancer Chemother Pharmacol; 2009 Feb;63(3):563-6
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  • [Title] Pharmacokinetic profile of imatinib mesylate and N-desmethyl-imatinib (CGP 74588) in children with newly diagnosed Ph+ acute leukemias.

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  • (PMID = 18521606.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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58. Abstracts of Acute Leukemias XII : biology and treatment strategies. February 16-20, 2008. Munich, Germany. Ann Hematol; 2008 Feb;87 Suppl 1:S1-98
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  • [Title] Abstracts of Acute Leukemias XII : biology and treatment strategies. February 16-20, 2008. Munich, Germany.
  • [MeSH-major] Leukemia / pathology. Leukemia / therapy
  • [MeSH-minor] Acute Disease. Animals. Humans

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  • (PMID = 18214480.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Congresses; Overall
  • [Publication-country] Germany
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59. Kolitz JE: Acute leukemias in adults. Dis Mon; 2008 Apr;54(4):226-41
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  • [Title] Acute leukemias in adults.
  • [MeSH-major] Leukemia. Remission Induction / methods
  • [MeSH-minor] Acute Disease. Adult. Aged. Cytogenetic Analysis. Humans. Middle Aged. Prognosis

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  • (PMID = 18346480.001).
  • [ISSN] 1557-8194
  • [Journal-full-title] Disease-a-month : DM
  • [ISO-abbreviation] Dis Mon
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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60. Adachi A, Sato S, Sasaki Y, Ghazizadeh M, Maeda M, Kaizu K, Liu XL, Fukunaga Y: Electron microscopic studies on the occurrence of activated neutrophils in peripheral blood of children with acute leukemias. J Submicrosc Cytol Pathol; 2005 Apr;37(1):13-8
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  • [Title] Electron microscopic studies on the occurrence of activated neutrophils in peripheral blood of children with acute leukemias.
  • Peripheral blood (PB) cells are examined to assess cellular maturity and the degree of bone marrow abnormality in children with acute leukemias.
  • We here report for the first time the identification of activated neutrophils in PB of children with acute leukemias.
  • To examine the impact of activated neutrophils, we compared two groups of children including 18 with acute lymphoblastic leukemia (ALL) and 7 with acute myelogenous leukemia (AML) by an ultrastructural leukocyte count method.
  • Non-leukemic hospitalized (n =3) and healthy (n = 3) control cases showed a median rate of 3.32% activated neutrophils in PB.
  • These findings reveal that a significantly high rate of activated neutrophils occurs in PB of children with ALL which may be exploited in the diagnostic assessment of children with acute leukemias.
  • [MeSH-major] Leukemia, Myeloid, Acute / blood. Neutrophil Activation. Neutrophils / immunology. Neutrophils / ultrastructure. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood

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  • (PMID = 16136725.001).
  • [ISSN] 1122-9497
  • [Journal-full-title] Journal of submicroscopic cytology and pathology
  • [ISO-abbreviation] J. Submicrosc. Cytol. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
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61. Bloomfield CD: Importance of genetic heterogeneity in curing adult acute leukemia (AL). J Clin Oncol; 2009 May 20;27(15_suppl):s1

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Importance of genetic heterogeneity in curing adult acute leukemia (AL).
  • Publication of the French-American-British classification 34 years ago resulted in acceptance that morphology and cytochemistry separated AL into two different diseases, acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL), that required separate treatment.
  • The most striking example of increased curability of AL is acute promyelocytic leukemia, in which targeted therapy combined with chemotherapy has increased survival from a 2-week median to an 80% cure rate.
  • Recognition of increased sensitivity of a genetic subtype of AML to high-dose cytarabine (HiDAC) has increased the cure rate of core-binding factor (CBF) AML from <10%-25% to 55%-60%.
  • Among adult de novo AML 40%-45% are cytogenetically normal (CN); the striking molecular heterogeneity of CN-AML is now being recognized and promises to allow individualized approaches that improve substantially upon the current cure rate of 40%.
  • New approaches to studying the leukemia genome and epigenome should improve our understanding of AL heterogeneity, identify new therapeutic targets, and allow the cure of most patients.

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  • (PMID = 27962366.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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62. Zeng H, Wang H, Chen F, Xin H, Wang G, Xiao L, Song K, Wu D, He Q, Shen G: Development of quartz-crystal-microbalance-based immunosensor array for clinical immunophenotyping of acute leukemias. Anal Biochem; 2006 Apr 1;351(1):69-76
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  • [Title] Development of quartz-crystal-microbalance-based immunosensor array for clinical immunophenotyping of acute leukemias.
  • An integrated piezoelectric immunosensor array has been developed to immunophenotype acute leukemias in clinic.
  • Each quartz crystal microbalance (QCM) was fabricated with plasma-polymerized film of n-butylamine, nanogold particles, and protein A (PA) to be used to immobilize antibodies in orientation.
  • Leukemic lineage-associated monoclonal antibodies were separately immobilized onto the nanogold-PA-modified surface of the crystals, which were constructed by a 2 x 2 type of probes forming a QCM-based immunosensor array.
  • The main detection conditions were investigated, including the immobilization amount of antibodies, pH, immunoreaction time, sample dilution ratio, etc.
  • It was found that the developed technique could readily identify leukemia samples in 5 min and might monitor dynamically the immunoreaction processes.
  • Moreover, comparison studies were carried out for CD antigens expressed on the nucleated cells isolated from 96 acute leukemic patients and 24 normal subjects using the QCM-based immunosensor method and the fluoroimmunoassay.
  • The results of specimen evaluation indicated that it might be clinically suitable for quantifying human differentiated leukocytes and immunophenotyping of acute leukemias.
  • [MeSH-major] Biosensing Techniques. Immunophenotyping / methods. Leukemia / immunology. Quartz
  • [MeSH-minor] Acute Disease. Flow Cytometry. Humans. Immunohistochemistry. Jurkat Cells

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  • (PMID = 16455039.001).
  • [ISSN] 0003-2697
  • [Journal-full-title] Analytical biochemistry
  • [ISO-abbreviation] Anal. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 14808-60-7 / Quartz
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63. Zhao Y, Li HH, Bo J, Jing Y, Gao CJ, Wang QS, Yu L: [Significance of Id4 gene methylation in monitoring efficacy of allo-PBSCT for treatment of acute leukemias]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Feb;17(1):151-4
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  • [Title] [Significance of Id4 gene methylation in monitoring efficacy of allo-PBSCT for treatment of acute leukemias].
  • This study was purposed to investigate the significance of Id4 gene methylation in monitoring the efficacy of allo-PBSCT for treatment of acute leukemias.
  • MS-PCR method was used to detect Id4 gene methylation in bone marrow samples from 29 patients with acute leukemia before and at 1, 3, 6 and 12 months after allo-PBSCT.
  • After allo-PBSCT, Id4 gene methylation status can be regarded as an indicator for predicting prognosis of acute leukemias.

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  • (PMID = 19236768.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ID4 protein, human; 0 / Inhibitor of Differentiation Proteins
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64. Batinić D, Dubravcić K, Rajić L, Mikulić M, Labar B: [Biphenotypic and bilineal acute leukemias]. Acta Med Croatica; 2008 Oct;62(4):387-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Biphenotypic and bilineal acute leukemias].
  • Human acute leukemias (AL) are classified as myeloid or lymphoid according to cytomorphology and the expression of leukocyte differentiation antigens/CD-markers.
  • However, in the minority of cases leukemic cells express markers of more than one lineage, which has led to the introduction of a new subgroup of acute leukemias termed mixed or biphenotypic acute leukemias (BAL).
  • In an effort to distinguish between BAL and those AL with aberrant expression of markers of other lineage, the European Group for the Immunological Characterization of Acute Leukemias (EGIL) has proposed a scoring system in which CD-markers are assigned a score of 0.5, 1.0 or 2.0, depending on the specificity of a particular antigen for myeloid, B- and/or T-lymphoid lineage, respectively.
  • In addition to BAL in which a single cell population expresses both myeloid and lymphoid differentiation markers, this new group of leukemias also comprises cases that present with two separate blast populations (acute bilineal leukemia, aBLL).
  • In general, BAL accounts for less than 5% of all AL cases, whereas aBLL is a rare disease constituting 1%-2% of AL cases that contains B- or T-lymphoid along with myeloid blasts.
  • Unfortunately, optimal therapy is not known, although regimens designed for acute lymphoblastic leukemia may result in a better response rate.
  • [MeSH-major] Leukemia, Biphenotypic, Acute

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  • (PMID = 19209464.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Croatia
  • [Number-of-references] 30
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65. Oto OA, Paydas S, Tanriverdi K, Seydaoglu G, Yavuz S, Disel U: Survivin and EPR-1 expression in acute leukemias: prognostic significance and review of the literature. Leuk Res; 2007 Nov;31(11):1495-501
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  • [Title] Survivin and EPR-1 expression in acute leukemias: prognostic significance and review of the literature.
  • The aim of this study is to detect the biologic and/or prognostic significance of survivin (S) and effector protease receptor 1: EPR-1 (E) expression in acute leukemias (34 ALL and 40 AML) by using RT-PCR.
  • In conclusion S expression is a bad prognostic indicator in cases with acute leukemia especially in AML.
  • S negativity and E positivity show good clinical outcome in acute leukemias.
  • [MeSH-major] Leukemia / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Receptors, Cell Surface / metabolism
  • [MeSH-minor] Acute Disease. Base Sequence. DNA Primers. Humans. Inhibitor of Apoptosis Proteins. Prognosis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17328950.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / DNA Primers; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Receptors, Cell Surface
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66. Poreba M, Jaźwiec B, Kuliczkowski K, Poreba R: [Circulating endothelial cells, endothelial precursors, VEGF and bFGF concentrations in patients with acute leukemias, lymphomas and myelomas]. Pol Arch Med Wewn; 2005 Jan;113(1):27-34
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  • [Title] [Circulating endothelial cells, endothelial precursors, VEGF and bFGF concentrations in patients with acute leukemias, lymphomas and myelomas].
  • Measurements were carried out in 20 patients with acute leukemia, 21 with malignant lymphoma and with 20 with multiple myeloma.
  • In patients with acute leukemias and lymphomas the number of CEC was significantly higher than in controls, and that high number correlated with worse prognosis in patients with lymphomas.
  • The increased number of CEP at diagnosis in patients with acute leukemia and lymphoma correlated with worse prognosis.
  • After chemotherapy the decrease in CEC and CEP numbers in patients with acute leukemia and lymphoma was observed.
  • Results suggest that in patients with acute leukemias and lymphomas CEC and CEP may be the markers of malignant process correlating with clinical outcome. aCEC may have a similar role in both diseases.
  • Also in patients with lymphoma VEGF may be a marker of disease activity. bFGF is connected with pathogenesis of acute leukemia, myeloma and lymphoma and in patients with lymphoma is a predictor of worse prognosis.
  • [MeSH-major] Endothelial Cells / metabolism. Fibroblast Growth Factor 2 / blood. Leukemia, Lymphoid / blood. Lymphoma / blood. Multiple Myeloma / blood. Vascular Endothelial Growth Factor A / blood

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  • (PMID = 16130598.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] pol
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2
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67. Kröger N, Bacher U, Bader P, Böttcher S, Borowitz MJ, Dreger P, Khouri I, Macapinlac HA, Olavarria E, Radich J, Stock W, Vose JM, Weisdorf D, Willasch A, Giralt S, Bishop MR, Wayne AS: NCI First International Workshop on the Biology, Prevention, and Treatment of Relapse after Allogeneic Hematopoietic Stem Cell Transplantation: report from the Committee on Disease-Specific Methods and Strategies for Monitoring Relapse following Allogeneic Stem Cell Transplantation. Part I: Methods, acute leukemias, and myelodysplastic syndromes. Biol Blood Marrow Transplant; 2010 Sep;16(9):1187-211
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  • [Title] NCI First International Workshop on the Biology, Prevention, and Treatment of Relapse after Allogeneic Hematopoietic Stem Cell Transplantation: report from the Committee on Disease-Specific Methods and Strategies for Monitoring Relapse following Allogeneic Stem Cell Transplantation. Part I: Methods, acute leukemias, and myelodysplastic syndromes.
  • Relapse has become the major cause of treatment failure after allogeneic stem cell transplantation.
  • To detect early relapse or minimal residual disease, sensitive methods such as molecular genetics, tumor-specific molecular primers, fluorescein in situ hybridization, and multiparameter flow cytometry (MFC) are commonly used after allogeneic stem cell transplantation to monitor patients, but not all of them are included in the commonly employed disease-specific response criteria.
  • Here, we summarize the current knowledge about the utilization of such sensitive monitoring techniques based on tumor-specific markers and donor cell chimerism and how these methods might augment the standard definitions of posttransplant remission, persistence, progression, relapse, and the prediction of relapse.
  • Critically important is the need for standardization of the different residual disease techniques and to assess the clinical relevance of minimal residual disease and chimerism surveillance in individual diseases, which in turn, must be followed by studies to assess the potential impact of specific interventional strategies.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia / therapy. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Acute Disease. Chimerism. Chromosome Banding. Disease Progression. Humans. Neoplasm Recurrence, Local / diagnosis. Transplantation Conditioning. Treatment Outcome

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  • [Copyright] Copyright (c) 2010 American Society for Blood and Marrow Transplantation. All rights reserved.
  • [ErratumIn] Biol Blood Marrow Transplant. 2010 Dec;16(12):1752. Macapintac, Homer [corrected to Macapinlac, Homer A]
  • (PMID = 20558311.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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68. Andersson A, Edén P, Olofsson T, Fioretos T: Gene expression signatures in childhood acute leukemias are largely unique and distinct from those of normal tissues and other malignancies. BMC Med Genomics; 2010;3:6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression signatures in childhood acute leukemias are largely unique and distinct from those of normal tissues and other malignancies.
  • BACKGROUND: Childhood leukemia is characterized by the presence of balanced chromosomal translocations or by other structural or numerical chromosomal changes.
  • It is well know that leukemias with specific molecular abnormalities display profoundly different global gene expression profiles.
  • However, it is largely unknown whether such subtype-specific leukemic signatures are unique or if they are active also in non-hematopoietic normal tissues or in other human cancer types.
  • METHODS: Using gene set enrichment analysis, we systematically explored whether the transcriptional programs in childhood acute lymphoblastic leukemia (ALL) and myeloid leukemia (AML) were significantly similar to those in different flow-sorted subpopulations of normal hematopoietic cells (n = 8), normal non-hematopoietic tissues (n = 22) or human cancer tissues (n = 13).
  • Moreover, the 11q23/MLL subtype of ALL showed similarities with non-hematopoietic tissues.
  • CONCLUSIONS: This study demonstrates, for the first time, that the expression profiles of childhood leukemia are largely unique, with limited similarities to transcriptional programs active in normal hematopoietic cells, non-hematopoietic normal tissues or the most common forms of human cancer.
  • In addition to providing important pathogenetic insights, these findings should facilitate the identification of candidate genes or transcriptional programs that can be used as unique targets in leukemia.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Cites] Blood. 2003 Oct 15;102(8):2951-9 [12730115.001]
  • [Cites] Best Pract Res Clin Haematol. 2001 Sep;14(3):497-529 [11640867.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1617-28 [15084694.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 20;101(16):6062-7 [15075390.001]
  • [Cites] Blood. 2004 Aug 15;104(4):923-32 [15155462.001]
  • [Cites] Genome Biol. 2004;5(10):R80 [15461798.001]
  • [Cites] Ann Med. 2004;36(7):492-503 [15513300.001]
  • [Cites] Blood. 1990 Jul 1;76(1):117-22 [2364165.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Aug 3;96(16):9212-7 [10430922.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3679-87 [15226186.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 20;102(51):18556-61 [16339305.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):19069-74 [16354839.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3339-44 [16492768.001]
  • [Cites] Cancer. 2007 Jan 1;109(1):157-63 [17133407.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1198-203 [17410184.001]
  • [Cites] Bioinformatics. 2007 Dec 1;23(23):3251-3 [17644558.001]
  • [Cites] Science. 2008 Jan 18;319(5861):336-9 [18202291.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1531-7 [10942402.001]
  • [Cites] Oncogene. 2001 Sep 10;20(40):5763-77 [11607826.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1605-16 [15084693.001]
  • (PMID = 20211010.001).
  • [ISSN] 1755-8794
  • [Journal-full-title] BMC medical genomics
  • [ISO-abbreviation] BMC Med Genomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
  • [Other-IDs] NLM/ PMC2845086
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69. Zebisch A, Linkesch W, Sill H: Bedside RNA stabilizing kit systems for gene expression analysis of acute leukemias: influence of non-neoplastic white blood cells. Leukemia; 2005 Jan;19(1):136-7
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  • [Title] Bedside RNA stabilizing kit systems for gene expression analysis of acute leukemias: influence of non-neoplastic white blood cells.
  • [MeSH-major] Gene Expression Profiling. Leukemia / genetics. Leukocytes / metabolism. RNA / genetics
  • [MeSH-minor] Acute Disease. Humans. Polymerase Chain Reaction

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  • [ErratumIn] Leukemia. 2005 Apr;19(4):685
  • (PMID = 15510197.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 63231-63-0 / RNA
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70. Pigazzi M, Manara E, Baron E, Beghin A, Basso G: The inducible cyclic adenosine 3',5'-monophosphate early repressor (ICER) enhances drug sensitivity in acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e22045

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The inducible cyclic adenosine 3',5'-monophosphate early repressor (ICER) enhances drug sensitivity in acute myeloid leukemia.
  • CREB was previously demonstrated to be overexpressed in acute leukemia, whereas ICER was found rapidly degradated being unable to control gene transcription.
  • ICER exogenous expression was demonstrated to repress CREB targets preventing leukemia progression.
  • We hypothesized that ICER restoration deserves a special consideration for playing a role in CREB oncogenic feature and in modeling leukemic cell phenotype.
  • We monitored transcription and translation of a series of genes involved in different pathways by quantitative gene expression and western blot analysis.
  • We investigate ICER's role in cell death after treatment with chemotherapic drugs.
  • RESULTS: We revealed that ICER was able to control gene expression in leukemia, principally of genes involved in cell death and survival.
  • Cell cycle analyses revealed a block in G2 phase, a lowered cell proliferation and clonogenic potential with respect to HL60 treated at the same conditions.

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  • (PMID = 27963227.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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71. Da WM, Wu T, Lu DP: [Prevention and treatment of leukemia relapse after allogeneic hematopoietic stem cell transplantation for acute leukemias]. Zhonghua Xue Ye Xue Za Zhi; 2007 Dec;28(12):793-4
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  • [Title] [Prevention and treatment of leukemia relapse after allogeneic hematopoietic stem cell transplantation for acute leukemias].
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia / therapy
  • [MeSH-minor] Acute Disease. Humans. Postoperative Period. Secondary Prevention

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  • (PMID = 18476587.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] Editorial
  • [Publication-country] China
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72. Burmeister T, Marschalek R, Schneider B, Meyer C, Gökbuget N, Schwartz S, Hoelzer D, Thiel E: Monitoring minimal residual disease by quantification of genomic chromosomal breakpoint sequences in acute leukemias with MLL aberrations. Leukemia; 2006 Mar;20(3):451-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monitoring minimal residual disease by quantification of genomic chromosomal breakpoint sequences in acute leukemias with MLL aberrations.
  • An estimated 10% of acute leukemias carry mixed-lineage leukemia (MLL) fusion genes.
  • These leukemias are commonly regarded as high-risk cases and are treated accordingly with intensified therapy regimens, including hematopoietic stem cell transplantation.
  • Monitoring minimal residual disease (MRD) is undoubtedly of great value in clinical decision making, also in the pre- and post-transplant setting.
  • Here, we describe a novel method for detecting MRD in leukemias with MLL aberrations.
  • [MeSH-major] Chromosome Fragile Sites. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm, Residual / genetics
  • [MeSH-minor] Acute Disease. Base Sequence. DNA Primers. DNA Probes. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping

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  • (PMID = 16424875.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA Probes; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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73. Zuna J, Zaliova M, Muzikova K, Meyer C, Lizcova L, Zemanova Z, Brezinova J, Votava F, Marschalek R, Stary J, Trka J: Acute leukemias with ETV6/ABL1 (TEL/ABL) fusion: poor prognosis and prenatal origin. Genes Chromosomes Cancer; 2010 Oct;49(10):873-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute leukemias with ETV6/ABL1 (TEL/ABL) fusion: poor prognosis and prenatal origin.
  • Only 19 cases of ETV6/ABL1-positive hematological malignancy have been published, diagnosed with chronic myeloid leukemia, other types of chronic myeloproliferative neoplasm, acute myeloid leukemia or acute lymphoblastic leukemia (ALL).
  • A thorough review of the literature and an analysis of all published data, including the three new cases, suggest poor prognosis of ETV6/ABL1-positive acute leukemias.
  • The course of the disease in the two pediatric patients is characterized by minimal residual disease monitoring, using quantification of both the ETV6/ABL1 transcript and immunoreceptor gene rearrangements.
  • Eosinophilia could not be confirmed as a hallmark of the ETV6/ABL1-positive disease.
  • [MeSH-major] Neoplasm, Residual / diagnosis. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein-Tyrosine Kinases / genetics

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  • (PMID = 20589932.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / TEL-ABL fusion protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases
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74. Zwaan CM, Reinhardt D, Hitzler J, Vyas P: Acute leukemias in children with Down syndrome. Hematol Oncol Clin North Am; 2010 Feb;24(1):19-34
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  • [Title] Acute leukemias in children with Down syndrome.
  • Children with Down syndrome have an increased risk for developing both acute myeloid as well as lymphoblastic leukemia.
  • These leukemias differ in presenting characteristics and underlying biology when compared with leukemias occurring in non-Down syndrome children.
  • Myeloid leukemia in children with Down syndrome is preceded by a preleukemic clone (transient leukemia or transient myeloproliferative disorder), which may disappear spontaneously, but may also need treatment in case of severe symptoms.
  • Twenty percent of children with transient leukemia subsequently develop myeloid leukemia.
  • This transition offers a unique model to study the stepwise development of leukemia and of gene dosage effects mediated by aneuploidy.
  • [MeSH-major] Down Syndrome / complications. Leukemia, Myeloid, Acute / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • [MeSH-minor] Child. Clone Cells / pathology. Humans. Leukemia

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20113894.001).
  • [ISSN] 1558-1977
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 83
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75. Zwaan MC, Reinhardt D, Hitzler J, Vyas P: Acute leukemias in children with Down syndrome. Pediatr Clin North Am; 2008 Feb;55(1):53-70, x
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  • [Title] Acute leukemias in children with Down syndrome.
  • Children with Down syndrome have an increased risk for developing both acute myeloid as well as lymphoblastic leukemia.
  • These leukemias differ in presenting characteristics and underlying biology when compared with leukemias occurring in non-Down syndrome children.
  • Myeloid leukemia in children with Down syndrome is preceded by a preleukemic clone (transient leukemia or transient myeloproliferative disorder), which may disappear spontaneously, but may also need treatment in case of severe symptoms.
  • Twenty percent of children with transient leukemia subsequently develop myeloid leukemia.
  • This transition offers a unique model to study the stepwise development of leukemia, and of gene dosage effects mediated by aneuploidy.
  • [MeSH-major] Down Syndrome / complications. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Clinical Trials as Topic. Disease Progression. Humans. Infant. Infant, Newborn. Mutation

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  • (PMID = 18242315.001).
  • [ISSN] 0031-3955
  • [Journal-full-title] Pediatric clinics of North America
  • [ISO-abbreviation] Pediatr. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 83
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76. Hu SY, Gu WY, Chen ZX, Wang XL, Cen JN, He HL, Chai YH, Chen CS: The significance of detecting WT1 expression in childhood acute leukemias. Pediatr Hematol Oncol; 2010 Nov;27(8):581-91
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  • [Title] The significance of detecting WT1 expression in childhood acute leukemias.
  • WT1 (Wilms' tumor gene 1) overexpression is implicated in the prognosis of acute leukemia.
  • The purpose of this study was to investigate WT1 expression and its clinical implication in childhood acute leukemia (AL) in Chinese population.
  • Bone marrow specimen from 200 children at different stages of acute leukemia and from 21 children without leukemia were studied.
  • The WT1 expression at diagnostic marrow specimen in both acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL) was higher than control group, whereas WT1 expression in AML was higher than in ALL, and WT1 expression level in relapse in ALL increased more significantly than in AML.
  • The WT1 expression level showed positive correlation with the hypodiploidy and BCR-ABL fusion gene in acute leukemia.
  • This study suggested that WT1 expression levels in acute leukemia can potentially be a marker for evaluating therapeutic efficacy, correlating with monitoring minimal residue disease, and predicting hematological relapse in children acute leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. WT1 Proteins / genetics
  • [MeSH-minor] Child. Child, Preschool. Cytogenetic Analysis. Female. Flow Cytometry. Fusion Proteins, bcr-abl / genetics. Humans. Immunophenotyping. Infant. Male. Neoplasm, Residual / diagnosis. Neoplasm, Residual / genetics. Prognosis. Recurrence. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20863155.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / WT1 Proteins; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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77. McNally RJ, Parker L: Environmental factors and childhood acute leukemias and lymphomas. Leuk Lymphoma; 2006 Apr;47(4):583-98
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  • [Title] Environmental factors and childhood acute leukemias and lymphomas.
  • This review considers recent studies regarding the role of environmental factors in the etiology of childhood leukemia and lymphoma.
  • Potential environmental risk factors identified for childhood leukemia include exposure to magnetic fields of more than 0.4 micro Tessla, exposure to pesticides, solvents, benzene and other hydrocarbons, maternal alcohol consumption (but only for certain genotypes), contaminated drinking water, infections, and high birth weight.
  • There is little evidence linking childhood leukemia with lifetime exposure to ionizing radiation although fetal exposures to X-rays are associated with increased risk.
  • Burkitt lymphoma (BL) is confined to areas of the world where malaria is endemic, with the additional involvement of the Epstein-Barr virus (EBV) as a co-factor.
  • Environmental risk factors suggested for other types of non-Hodgkin lymphoma (NHL) include exposure to ionizing radiation (both lifetime and antenatal), pesticides, and, in utero exposure to cigarette smoke, benzene and nitrogen dioxide (via the mother).
  • [MeSH-major] Environmental Exposure. Leukemia / diagnosis. Leukemia / etiology. Lymphoma / diagnosis. Lymphoma / etiology
  • [MeSH-minor] Acute Disease. Case-Control Studies. Child. Cohort Studies. Ecology. Electromagnetic Fields / adverse effects. Family Health. Humans. Risk. Risk Factors

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  • (PMID = 16690516.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 141
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78. Brusa G, Zuffa E, Hattinger CM, Serra M, Remondini D, Castellani G, Righi S, Campidelli C, Pileri S, Zinzani PL, Gabriele A, Mancini M, Corrado P, Barbieri E, Santucci MA: Genomic imbalances associated with secondary acute leukemias in Hodgkin lymphoma. Oncol Rep; 2007 Dec;18(6):1427-34
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  • [Title] Genomic imbalances associated with secondary acute leukemias in Hodgkin lymphoma.
  • Secondary tumors and leukemias are major complications in Hodgkin lymphoma (HL).
  • To distinguish genomic imbalances associated with the development of acute myeloid leukemia (AML) in HL we used an array-based comparative genomic hybridization (aCGH) strategy on whole lymph node biopsies of HL patient.
  • Genomic imbalances (amplifications and deletions) associated with AML outcome in 3 classic HL patients, at clinical diagnosis they exhibited a discrete individual variability.
  • They involved AFM137XA11, a 9p11.2 pericentric region; FGFR1, the FGF receptor most frequently translocated in AML; PPARBP, a co-activator of nuclear receptors RARalpha, RXR and TRbeta1; AFM217YD10, a 17q25 telomeric region; FGR, an SRC2 kinase involved in cytokine production by NK and CD4+ NKT cells; GATA3, a Th2-specific transcription factor; TOP1, involved in DNA recombination and repair; WT1, a transcription factor involved in CD8+ T cell response against leukaemic blasts.
  • Immunohistochemistry confirmed aCGH results and distinguished the distribution of either amplified or deleted gene products in neoplastic Reed Sternberg (RS) cells and non-neoplastic lymph node components.
  • [MeSH-major] Chromosome Aberrations. Hodgkin Disease / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics


79. Wananukul S, Nuchprayoon I, Siripanich H: Mucocutaneous findings in febrile neutropenic children with acute leukemias. J Med Assoc Thai; 2005 Jun;88(6):817-23
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  • [Title] Mucocutaneous findings in febrile neutropenic children with acute leukemias.
  • Febrile neutropenia is common in children with leukemia.
  • The authors prospectively examined children with fever with neutropenia in acute leukemia, aged 1-15 years, who were admitted to the Department of Pediatrics, King Chulalongkorn Memorial Hospital, between September 2000 and August 2001.
  • The prevalence of infection was found in severe neutropenia (absolute neutrophil count, ANC less than 500 cell/cu mm), moderate neutropenia (ANC, 500-1000 cell/cu mm) and mild neutropenia (ANC, 1001-1500 cell/cu mm) was 72%, 9% and 5%, respectively.
  • Daily physical examination of skin and mucous membrane are suggested for proper and prompt diagnosis and treatment of febrile neutropenic children with acute leukemia to reduce mortality and morbidity in these patients.
  • A Guideline for the use of antimicrobial agents in neutropenic patients with acute leukemia is proposed In conclusion, infection was commonly found in severe neutropenia.
  • Mucocutaneous infection was the most common site of infection infebrile neutropenia in children with leukemia.
  • [MeSH-major] Fever. Neutropenia / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Skin Diseases / etiology

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  • (PMID = 16083222.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
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80. Demir C, Demir H, Esen R, Atmaca M, Tagdemir E: Erythrocyte catalase and carbonic anhydrase activities in acute leukemias. Asian Pac J Cancer Prev; 2010;11(1):247-50
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  • [Title] Erythrocyte catalase and carbonic anhydrase activities in acute leukemias.
  • OBJECTIVE: To determine activity of catalase (CAT) as a antioxidant and carbonic anhydrase (CA) in erythrocytes from acute leukemia cases.
  • Venous blood samples were taken from a total of 67 individuals (31 with acute leukemia and 36 healthy) included in the study.
  • RESULTS: CAT activity was found to be significantly decreased (P<0.001) on average in acute leukemia cases as compared to the control group while erythrocyte CA activity was significantly increased (P<0.001).
  • CONCLUSIONS: Our findings point to malfunction of the antioxidant system in acute leukemia patients.
  • Furthermore, clarification of the relationship between the antioxidant system and CA inhibitors in the pathogenesis of acute leukemia appears warranted.
  • [MeSH-major] Carbonic Anhydrases / blood. Catalase / blood. Erythrocytes / enzymology. Leukemia / blood. Leukemia / enzymology
  • [MeSH-minor] Acute Disease. Adult. Antioxidants / metabolism. Female. Humans. Male

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  • (PMID = 20593965.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Antioxidants; EC 1.11.1.6 / Catalase; EC 4.2.1.1 / Carbonic Anhydrases
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81. Erdur B, Yilmaz S, Oren H, Demircioğlu F, Cakmakç H, Irken G: Evaluating pulmonary complications in childhood acute leukemias. J Pediatr Hematol Oncol; 2008 Jul;30(7):522-6
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  • [Title] Evaluating pulmonary complications in childhood acute leukemias.
  • SUMMARY: We evaluated the frequency, etiologic factors, outcome, and the comorbid conditions affecting the morbidity and mortality of pulmonary complications in acute childhood leukemia.
  • Acute respiratory distress syndrome, leukostasis, lymphomatoid granulomatosis, pulmonary edema, and pneumothorax were among the noninfectious causes.
  • The pulmonary complications in the induction and consolidation phase of leukemia therapy were more severe and the mortality rate was higher.
  • In conclusion, pulmonary complications are frequent in children with acute leukemia, and early diagnosis and appropriate management are important to avoid mortality owing to pulmonary complications, especially in neutropenic patients receiving induction or consolidation phase of chemotherapy.
  • [MeSH-major] Leukemia / complications. Pneumonia / complications
  • [MeSH-minor] Acute Disease. Adolescent. Anti-Bacterial Agents / therapeutic use. Antineoplastic Agents / adverse effects. Child. Child, Preschool. Comorbidity. Disseminated Intravascular Coagulation / etiology. Disseminated Intravascular Coagulation / mortality. Female. Humans. Infant. Male. Multiple Organ Failure / etiology. Multiple Organ Failure / mortality. Neutropenia / chemically induced. Neutropenia / complications. Pneumothorax / complications. Pneumothorax / epidemiology. Pulmonary Edema / complications. Pulmonary Edema / epidemiology. Respiration, Artificial / utilization. Respiratory Distress Syndrome, Adult / complications. Respiratory Distress Syndrome, Adult / epidemiology. Retrospective Studies

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  • (PMID = 18797199.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antineoplastic Agents
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82. Blum W, Klisovic RB, Becker H, Yang X, Rozewski DM, Phelps MA, Garzon R, Walker A, Chandler JC, Whitman SP, Curfman J, Liu S, Schaaf L, Mickle J, Kefauver C, Devine SM, Grever MR, Marcucci G, Byrd JC: Dose escalation of lenalidomide in relapsed or refractory acute leukemias. J Clin Oncol; 2010 Nov 20;28(33):4919-25
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  • [Title] Dose escalation of lenalidomide in relapsed or refractory acute leukemias.
  • We report results of a phase I dose-escalation trial of lenalidomide in relapsed or refractory acute leukemia.
  • PATIENTS AND METHODS: Thirty-one adults with acute myeloid leukemia (AML) and four adults with acute lymphoblastic leukemia (ALL) were enrolled.
  • Two of four patients who received lenalidomide as initial therapy for AML relapse after allogeneic transplantation achieved durable CR after development of cutaneous graft-versus-host disease, without donor leukocyte infusion.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Thalidomide / analogs & derivatives

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  • [Cites] Biol Blood Marrow Transplant. 2006 Jan;12(1):61-7 [16399569.001]
  • [Cites] Br J Cancer. 2005 Sep 19;93(6):613-9 [16222306.001]
  • [Cites] Blood. 2006 Jul 15;108(2):618-21 [16569772.001]
  • [Cites] N Engl J Med. 2006 Oct 5;355(14):1456-65 [17021321.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jul 3;104(27):11406-11 [17576924.001]
  • [Cites] J Clin Pharmacol. 2007 Dec;47(12):1466-75 [17954615.001]
  • [Cites] Br J Haematol. 2008 Jan;140(1):36-45 [17995965.001]
  • [Cites] Blood. 2008 Jan 1;111(1):86-93 [17893227.001]
  • [Cites] J Clin Invest. 2008 Jul;118(7):2427-37 [18551193.001]
  • [Cites] Clin Cancer Res. 2008 Jul 15;14(14):4650-7 [18628480.001]
  • [Cites] Cancer Immunol Immunother. 2008 Dec;57(12):1849-59 [18392823.001]
  • [Cites] J Clin Oncol. 2008 Nov 1;26(31):5078-87 [18809607.001]
  • [Cites] Blood. 2009 Jan 29;113(5):1002-5 [18824593.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Apr 14;106(15):6250-5 [19332800.001]
  • [Cites] Blood. 2009 Apr 23;113(17):3947-52 [18987358.001]
  • [Cites] J Clin Pharmacol. 2009 Jun;49(6):650-60 [19451403.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Aug 4;106(31):12974-9 [19470455.001]
  • [Cites] Blood. 2009 Nov 5;114(19):4027-33 [19710500.001]
  • [Cites] Br J Haematol. 2010 Jan;148(2):217-25 [19804455.001]
  • [Cites] J Clin Oncol. 2010 Feb 1;28(4):596-604 [20026798.001]
  • [Cites] J Clin Oncol. 2010 Feb 1;28(4):556-61 [20026803.001]
  • [Cites] J Clin Oncol. 2010 Feb 1;28(4):549-55 [20026805.001]
  • [Cites] Blood. 2010 Feb 11;115(6):1204-13 [19965644.001]
  • [Cites] Blood. 2010 Mar 11;115(10):2077-87 [20053754.001]
  • [Cites] Blood. 2010 Apr 1;115(13):2619-29 [19965642.001]
  • [Cites] Proc Natl Acad Sci U S A. 2010 Apr 20;107(16):7473-8 [20368434.001]
  • [Cites] J Clin Oncol. 2010 May 10;28(14):2389-95 [20385984.001]
  • [Cites] Bone Marrow Transplant. 2000 Dec;26(11):1157-63 [11149725.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4642-9 [14673054.001]
  • [Cites] Blood. 1997 Jun 1;89(11):4226-35 [9166868.001]
  • [Cites] Cancer Chemother Pharmacol. 1997;40 Suppl:S9-12 [9272127.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3983-93 [10339508.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1969-78 [15632409.001]
  • [Cites] Bone Marrow Transplant. 2005 May;35(10):965-70 [15806131.001]
  • [Cites] Semin Oncol. 2005 Aug;32(4 Suppl 5):S24-30 [16085014.001]
  • [Cites] Future Oncol. 2005 Oct;1(5):575-83 [16556034.001]
  • (PMID = 20956622.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA140158; United States / NCI NIH HHS / CA / K23 CA120708; United States / NCI NIH HHS / CA / P50-CA140158; United States / NCI NIH HHS / CA / K23CA120708; United States / NCRR NIH HHS / RR / UL1 RR025755; United States / NCI NIH HHS / CA / P30 CA016058
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide
  • [Other-IDs] NLM/ PMC3020696
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83. Thomas X, Campos L, Le QH, Guyotat D: Heat shock proteins and acute leukemias. Hematology; 2005 Jun;10(3):225-35
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  • [Title] Heat shock proteins and acute leukemias.
  • HSPs have also been implicated in the resistance of leukemia cells to potential therapeutic agents.
  • HSPs were shown highly expressed by acute myeloid leukemia (AML) cells as well as by acute lymphoblastic leukemia (ALL) cells.
  • [MeSH-major] Antineoplastic Agents / metabolism. Gene Expression Regulation, Leukemic / drug effects. HSP90 Heat-Shock Proteins / metabolism. Neoplasm Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Rifabutin / analogs & derivatives

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  • (PMID = 16019471.001).
  • [ISSN] 1024-5332
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / Neoplasm Proteins; 1W306TDA6S / Rifabutin; 4GY0AVT3L4 / tanespimycin
  • [Number-of-references] 122
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84. Sun XL, Fang MY, Jiang F, Jing Y: [Immunologic classification used in typing of 68 cases of acute leukemias]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Feb;14(1):39-41
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  • [Title] [Immunologic classification used in typing of 68 cases of acute leukemias].
  • To evaluate the significance of immunologic classification for typing of acute leukemia (AL).
  • 68 cases of AL were classified by morphologic and immunologic typings.
  • The results showed that the consistency rate was 94.1% between morphology and immunology, and 4 morphologic misdiagnosed cases were corrected by immunology; CD13 and CD33 were special myeloid lineage-associated antigens; AML-M(3) was often CD34 low-expressed and HLA-DR-negative; CD14 was often expressed in AML-M(4) and M(5); lymphoid lineage-associated antigens (CD7) were easily found in ANLL, and myeloid lineage-associated antigens were also found in ALL.
  • In conclusion, immunologic classification can improve the accuracy in acute leukemia diagnosis.
  • The diagnosis of some special AL, such as acute unidentified leukemia (AUL), AML-M(0) and so on, must rely on immunologic classification.

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  • (PMID = 16584588.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD14; 0 / Antigens, CD34; 0 / Antigens, CD7; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
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85. Shiozawa K, Nakanishi T, Tan M, Fang HB, Wang WC, Edelman MJ, Carlton D, Gojo I, Sausville EA, Ross DD: Preclinical studies of vorinostat (suberoylanilide hydroxamic acid) combined with cytosine arabinoside and etoposide for treatment of acute leukemias. Clin Cancer Res; 2009 Mar 1;15(5):1698-707
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preclinical studies of vorinostat (suberoylanilide hydroxamic acid) combined with cytosine arabinoside and etoposide for treatment of acute leukemias.
  • In this preclinical study, we evaluated combining cytosine arabinoside [1-beta-D-arabinofuranosylcytosine (ara-C)] and/or etoposide with vorinostat for use in the treatment of acute leukemias.
  • EXPERIMENTAL DESIGN: Cell survival was examined in vitro in HL-60 human myeloid leukemia cells and K562 myeloid blast crisis chronic myelogenous leukemia cells, using the 2,3-bis[2-methoxy-4-nitro-5-sulfophenyl]-2H-tetrazolium-5-carboxanilide inner salt and/or fluorescein diacetate/propidium iodide assays.
  • Cell cycle phase distribution was measured by flow cytometry.
  • Cell cycle analyses revealed that the sequence-dependent interaction of vorinostat and ara-C or etoposide reflected the arrest of cells in G1 or G2 phase during vorinostat treatment and recovery into S phase after removal of vorinostat.
  • CONCLUSIONS: These findings using two independent methods to assess drug combination effects provide a preclinical rationale for phase I trials of the sequential combination of vorinostat followed by ara-C and etoposide in patients with advanced or refractory leukemias.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Blast Crisis. Cell Survival / drug effects. Cytarabine / administration & dosage. Drug Evaluation, Preclinical. Drug Synergism. Etoposide / administration & dosage. G1 Phase / drug effects. Humans. Hydroxamic Acids / administration & dosage. S Phase / drug effects. Tumor Cells, Cultured

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  • (PMID = 19223502.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA106767
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hydroxamic Acids; 04079A1RDZ / Cytarabine; 58IFB293JI / vorinostat; 6PLQ3CP4P3 / Etoposide
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86. Tong W, Stevenson W, Cortes J, Needham L, Brotherton D, Davidson A, Drummond A, Garcia-Manero G: In vitro and in vivo anti-leukemia activity of CHR-2845, a cell-targeted HDAC inhibitor for use in monocytic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e14579

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro and in vivo anti-leukemia activity of CHR-2845, a cell-targeted HDAC inhibitor for use in monocytic leukemia.
  • : e14579 Background: Histone deacetylase inhibitors alter gene expression and induce apoptosis in a wide range of cancer cells including those derived from human leukemias.
  • METHODS: We studied the in vitro and in vivo anti-leukemia activity of CHR-2845 using cell proliferation assay, annexin V binding assay, cell cycle analysis, western blot and in vitro primary leukemia cell culture.
  • RESULTS: Both U937 and THP1 cells express high levels of hCE-1 whereas the myeloid cell line, HL60, does not.
  • In comparison to vorinostat, CHR-2845 showed increased anti-proliferative potency (IC<sub>50</sub>) against monocytic cell lines (THP1, 30 nM vs 700 nM and U937, 30 nM vs 475 nM), compared to a myeloid cell line (HL60, 700nM vs 470 nM).
  • In a broad panel of leukemic cell lines, the potency of CHR-2845 over vorinostat correlated completely with hCE-1 expression.
  • In monocytic cell lines, CHR-2845 induced more apoptosis than vorinostat (THP1: 45±5% vs 11±1% and U937: 23±14% vs 6±1%), as measured by flow cytometry using Annexin V.
  • Biochemical assessment of histone H3 and H4 protein acetylation by Western blot also indicateed that CHR-2845 is at least 10 times more potent than vorinostat in monocytic cell lines but not in HL-60 cells.
  • We also studied the anti-leukemia activity of CHR-2845 in primary leukemia cells from 8 patients with acute or chronic myelomonocytic leukemia.
  • CONCLUSIONS: These results indicated that CHR-2845 has potential to be efficacious in the treatment of patients with monocytic leukemia.

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  • (PMID = 27963654.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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87. Nikolic NM, Tomasevic Z, Jelic S: Secondary malignancies developing during metastatic breast cancer treatment. J Clin Oncol; 2009 May 20;27(15_suppl):e12020

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e12020 Background: Secondary malignancies (SM) developing during metastatic breast cancer (MBC) are obviously more complicated for diagnosis, potential surgery and for further MBC treatment.
  • Patients with contra-lateral BC and acute leukemia were excluded.
  • CONCLUSIONS: According to our experience, SM develops more frequently in MBC than in non MBC patients, representing 60% (30/50 patients) of all SM in BC patients; 46.6% (14/30) of SM diagnosed during MBC could be surgically resected, and does not influence further MBC treatment.

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  • (PMID = 27964310.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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88. Rangarajan B, Prabhash K, Nair R, Menon H, Jain P, Kannan S, Jeevangi NK, Bagal B, Parikh PM, Kurkure PA: Rater. J Clin Oncol; 2009 May 20;27(15_suppl):e20678

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Inclusion criteria were diagnosis of hematolymphoid malignancy, neutropenic febrile episode secondary to chemotherapy or during induction therapy of acute leukemia and more than 18 years of age All patients were risk stratified, hospitalized and treated with broad-spectrum, empiric, intravenous antibiotic therapy until recovery or outcome of the event.
  • We subsequently analyzed the subset of Acute Myeloid Leukemia (AML) patients as they were the majority comprising of 62/81 episodes.

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  • (PMID = 27961676.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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89. Mayer F, Weidmann J, Federmann B, Schwarz S, Hartmann JT, Kanz L, Bethge W: Clinical impact and follow-up of taste disturbances following myeloablative or nonmyeloablative chemotherapy and stem cell transplantation. J Clin Oncol; 2009 May 20;27(15_suppl):e20609

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical impact and follow-up of taste disturbances following myeloablative or nonmyeloablative chemotherapy and stem cell transplantation.
  • : e20609 Background: Stem cell transplantation (SCT) after myeloablative (MA) or non-myeloablative (NMA) chemotherapy is a successful treatment option for a variety of diseases.
  • Indications for SCT included acute leukemia (n=38), myeloproliferative disease (n=20), lymphoma (n=13), and others (n=29).
  • 75% of pts reported moderate to severe changes in taste perception on a semiquantitative visual analogue scale during the acute phase of SCT with no differences between the three groups (73%, 79%, 75%).
  • The lower incidence of persiting changes in taste perception after autologous SCT might be attributed to the absence of graft versus host disease or the dispensability of immunosuppression.

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  • (PMID = 27961552.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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90. Wehner S, Soerensen J, Schwabe D, Tramsen L, Quaritsch R, Esser R, Klingebiel T, Koehl U: 10-Parameter flow cytometry as a new tool to improve diagnosis and MRD follow-up of acute leukemias. Klin Padiatr; 2009 Nov-Dec;221(6):393-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 10-Parameter flow cytometry as a new tool to improve diagnosis and MRD follow-up of acute leukemias.
  • [MeSH-major] Flow Cytometry / methods. Immunophenotyping / methods. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 19890796.001).
  • [ISSN] 1439-3824
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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91. Thomas XG: Rare acute leukemias. Cancer Treat Res; 2008;142:149-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rare acute leukemias.
  • [MeSH-major] Acute Disease. Leukemia

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  • (PMID = 18283786.001).
  • [ISSN] 0927-3042
  • [Journal-full-title] Cancer treatment and research
  • [ISO-abbreviation] Cancer Treat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 237
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92. Duhoux F, Libouton J, Bahloula K, Ameye G, Poirel HA: Identification by FISH of 4 novel partner loci of PRDM16 in myeloid malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):11037

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 11037 Background: PRDM16 is a gene located on 1p36.32 that encodes for a zinc finger transcription factor and contains an N-terminal PR domain.
  • It has been shown to be involved in the reciprocal translocation t(1;3)(p36;q21) and more rarely the t(1;21)(p36;q22) which both occur in myelodysplastic syndromes (MDS) and acute myeloid leukemias (AML).
  • These translocations result in the overexpression of a truncated version of the PRDM16 protein that lacks the PR domain.
  • METHODS: We studied 35 myeloid malignancies, 12 lymphoid malignancies and 3 undifferentiated acute leukemias with 1p36 abnormalities by fluorescent in situ hybridization (FISH) with a bacterial artificial chromosomes (BAC) contig containing 50 BAC probes on 1p36.
  • We identified the respective candidate partner loci : TEL/ETV6, IKZF1, CDH4 and a non-coding unknown sequence.
  • Interestingly, the shortest isoform of MDS/EVI-1, lacking the PR domain, is supposed to have an oncogenic effect due to its translocation-induced upregulation in AML.

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  • (PMID = 27964015.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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93. Chatterjee T, Panigrahi I, Agrawal N, Naithani R, Mahapatra M, Pati HP, Wadhwa S, Saxena R: Cytochemical, immunophenotypic and ultrastructural characterization of acute leukemias: a prospective study of fifty cases: haematological malignancy. Hematology; 2006 Jun;11(3):147-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytochemical, immunophenotypic and ultrastructural characterization of acute leukemias: a prospective study of fifty cases: haematological malignancy.
  • Cytochemistry and immunophenotyping are established methods in the diagnosis of most leukemias but the role of electron microscopy in diagnosis, apart from understanding the cellular morphology is less studied.
  • We present here 50 cases of acute leukemias that were studied for morphology, conventional cytochemistry, immunophenotyping and transmission electron microscopy (TEM), including ultrastructural cytochemistry using myeloperoxidase (MPO) and platelet peroxidase activity.
  • TEM morphology using ultrastructural cytochemistry helped in definitive typing in one mixed lineage leukemia case, one AML-M5b, one AML-M6b and one microgranular variant of APML.
  • Thus, ultrastructural studies may be useful in accurate diagnosis of biphenotypic leukemia and further classification of acute leukemias.
  • Also, in cases with hypercellular marrow and with associated myelofibrosis, where the marrow aspirate gives low cell count, ultrastructural studies are a valuable aid to arriving at an accurate diagnosis.
  • [MeSH-major] Leukemia / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antigens, CD / analysis. Antigens, Neoplasm / analysis. Child. Child, Preschool. Female. Humans. Immunophenotyping. Male. Microscopy, Electron. Middle Aged. Neoplasm Proteins / analysis. Neoplastic Stem Cells / chemistry. Neoplastic Stem Cells / ultrastructure. Peroxidase / analysis. Prospective Studies

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  • (PMID = 17325954.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Neoplasm Proteins; EC 1.11.1.7 / Peroxidase
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94. Lopez-Enriquez AT: Acute promielocytic leukemia: 14 years experience at the University Hospital, San Juan, Puerto Rico. J Clin Oncol; 2009 May 20;27(15_suppl):e18006

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute promielocytic leukemia: 14 years experience at the University Hospital, San Juan, Puerto Rico.
  • : e18006 Background: Acute promielocytic leukemias (APL) are a unique example in carcinogenesis, of maturation arrest at the promielocytic stage, associated with a chromosomal reciprocal translocation of a portion of chromosome 15 and 17 with the formation of fusion proteins between the PML gene and the alpha-retinoic acid receptor site.
  • METHODS: Since 1994 when transretinoic acid (ATRA) became available to us, we developed a protocol incorporating this drug to the standard regime of induction chemotherapy for acute leukemias used in our institution of 7 days of continuous infusion of cytosine arabinoside (Ara-C) and three days of daunorubicine (7+3), starting the ATRA on day 14 at 45 mg/m2 and continued daily for 120 days.

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  • (PMID = 27963993.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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95. Wang H, Zeng H, Shen G, Yu R: Immunophenotyping of acute leukemias using a quartz crystal microbalance and monoclonal antibody-coated magnetic microspheres. Anal Chem; 2006 Apr 15;78(8):2571-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunophenotyping of acute leukemias using a quartz crystal microbalance and monoclonal antibody-coated magnetic microspheres.
  • Immunophenotyping, which utilizes panels of lineage-associated monoclonal antibodies to recognize clusters of differentiation (CD) antigens expressed on various leukocytes, plays a key role in the clinical diagnosis of acute leukemias.
  • In this paper, a rapid, simple, and automatic immunophenotyping technique for acute leukemias has been initially proposed by incorporating immunomagnetic separation and quartz crystal microbalance (QCM) measurement.
  • Results indicate that this new technique can allow for easy and clear identification of acute leukocytes of lymphoid and myeloid origins as well as their subsets.
  • It may also permit the quantitative determination of acute leukocytes with cell concentration down to approximately 10(3) cells mL(-1).
  • [MeSH-major] Biosensing Techniques. Immunophenotyping / methods. Leukemia / diagnosis. Microspheres. Quartz / chemistry
  • [MeSH-minor] Acute Disease. Antibodies, Monoclonal / immunology. Immunoassay / instrumentation. Immunoassay / methods. Magnetics. Phenotype. Reproducibility of Results. Sensitivity and Specificity. Staphylococcal Protein A / chemistry. Time Factors

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  • (PMID = 16615766.001).
  • [ISSN] 0003-2700
  • [Journal-full-title] Analytical chemistry
  • [ISO-abbreviation] Anal. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Staphylococcal Protein A; 14808-60-7 / Quartz
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96. Karp JE, Passaniti A, Gojo I, Kaufmann S, Bible K, Garimella TS, Greer J, Briel J, Smith BD, Gore SD, Tidwell ML, Ross DD, Wright JJ, Colevas AD, Bauer KS: Phase I and pharmacokinetic study of flavopiridol followed by 1-beta-D-arabinofuranosylcytosine and mitoxantrone in relapsed and refractory adult acute leukemias. Clin Cancer Res; 2005 Dec 1;11(23):8403-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I and pharmacokinetic study of flavopiridol followed by 1-beta-D-arabinofuranosylcytosine and mitoxantrone in relapsed and refractory adult acute leukemias.
  • We designed a phase I clinical trial using a timed sequential therapy approach where flavopiridol was given for the dual purpose of initial cytoreduction and enhancing cell cycle progression of the remaining leukemia cell cohort followed by cycle-dependent drugs 1-beta-D-arabinofuranosylcytosine (ara-C) and mitoxantrone.
  • In vivo correlates included pharmacokinetics, modulation of blast cycle regulators, and serum and marrow supernatant vascular endothelial growth factor levels.
  • RESULTS: Of 34 adults receiving induction therapy, 16 (47%) evinced direct leukemia cytotoxicity with > or =50% drop in peripheral blast counts and tumor lysis in 9 (26%).
  • Overall response rate was 31% in 26 acute myelogenous leukemia and 12.5% in acute lymphoblastic leukemia.
  • Vascular endothelial growth factor was detected in sera and marrow supernatant pretreatment, and sera obtained on day 3 inhibited bovine aortic endothelial cell proliferation by a mean of 32% (range, 10-80%).
  • CONCLUSIONS: Our data suggest that flavopiridol is cytotoxic to leukemic cells and, when followed by ara-C and mitoxantrone, exerts biological and clinical effects in patients with relapsed and refractory acute leukemias.
  • These findings warrant continuing development of flavopiridol at 50 mg/m2/d x 3 days in combination with cytotoxic and biological agents for acute leukemias.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Flavonoids / pharmacokinetics. Leukemia, Myeloid, Acute / drug therapy. Piperidines / pharmacokinetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adult. Aged. Animals. Bone Marrow Cells / metabolism. Cattle. Cell Proliferation. Cohort Studies. Cytarabine / administration & dosage. Endothelium, Vascular / metabolism. Female. Humans. Male. Maximum Tolerated Dose. Middle Aged. Mitoxantrone / administration & dosage. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / metabolism. Salvage Therapy. U937 Cells. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16322302.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Flavonoids; 0 / Piperidines; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 04079A1RDZ / Cytarabine; 45AD6X575G / alvocidib; BZ114NVM5P / Mitoxantrone
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97. Ravandi F: Role of cytokines in the treatment of acute leukemias: a review. Leukemia; 2006 Apr;20(4):563-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of cytokines in the treatment of acute leukemias: a review.
  • Myeloid growth factors, such as granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor, have been used to decrease the duration of chemotherapy-induced neutropenia and thereby reduce the incidence and severity of infections in various regimens used to treat acute myeloid leukemia and acute lymphoblastic leukemia.
  • These growth factors have also been used to recruit dormant myeloid leukemia cells into the S phase of cell cycle in order to increase their susceptibility to the antileukemic effects of agents such as cytarabine.
  • A reduction in the duration of neutropenia has been the most consistent finding; this has not been associated with stimulation of leukemia cells, the main concern of using this strategy.
  • Unfortunately, few studies have reported a benefit in prolonging the duration of disease-free survival or overall survival.
  • Other cytokines, including interleukins and thrombopoietin, have also been evaluated for their theoretical ability to recruit immune mechanisms to eradicate residual leukemia burden after chemotherapy, and to stimulate platelet production.
  • In this review, we summarize the clinical experience with these growth factors in treating acute leukemias.
  • [MeSH-major] Cytokines / therapeutic use. Leukemia, Myeloid / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Neutropenia / drug therapy. Prospective Studies. Randomized Controlled Trials as Topic. Treatment Outcome

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  • (PMID = 16498390.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
  • [Number-of-references] 92
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98. Styczynski J, Wysocki M, Debski R, Czyzewski K, Balwierz W, Juraszewska E, Matysiak M, Malinowska I, Stanczak E, Sońta-Jakimczyk D, Szczepanski T, Wachowiak J, Konatkowska B, Balcerska A, Ploszynska A, Kowalczyk J, Stefaniak J, Badowska W, Wieczorek M, Olejnik I, Krawczuk-Rybak M, Kuzmicz M: In vitro sensitivity of leukemic cells to nucleoside derivatives in childhood acute leukemias: good activity in leukemic relapses. Neoplasma; 2005;52(1):74-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro sensitivity of leukemic cells to nucleoside derivatives in childhood acute leukemias: good activity in leukemic relapses.
  • Nucleoside analogues such as fludarabine and cladribine are used in therapy of indolent lymphomas and leukemias in adults, while cytarabine is used mainly in protocols for acute leukemias.
  • The objective of the study was the analysis of in vitro cellular drug sensitivity in childhood acute lymphoblastic (ALL) and myeloid (AML) leukemia.
  • Isolated leukemic cells obtained from 264 patients, including 152 initial ALL, 45 relapsed ALL, 54 initial AML and 13 relapsed AML were tested for cytotoxicity for fludarabine, cladribine, and cytarabine by the MTT assay.
  • Samples of relapsed ALL and initial AML were more resistant than ALL de novo ones.
  • Unexpectedly, no differences were observed between initial and relapsed AML samples for all tested drugs, what suggests that nucleoside analogues are active drugs in relapsed AML, which is commonly regarded as a resistant disease.
  • In summary, tested nucleoside analogues presented relatively good activity against childhood leukemias at relapse stage.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cladribine / pharmacology. Cytarabine / pharmacology. Leukemia, Myeloid / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Vidarabine / analogs & derivatives. Vidarabine / pharmacology
  • [MeSH-minor] Adolescent. Adult. Cell Death. Child. Child, Preschool. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor. Female. Humans. Infant. Infant, Newborn. Male. Recurrence. Tumor Cells, Cultured

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  • (PMID = 15739031.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; 47M74X9YT5 / Cladribine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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99. Tang X, Long C, Wang C, Xiao G: [Expression of DLK1 gene in acute leukemias and its function in erythroid differentiation of K562 cell line]. Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2009 Sep;34(9):886-91
MedlinePlus Health Information. consumer health - Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of DLK1 gene in acute leukemias and its function in erythroid differentiation of K562 cell line].
  • OBJECTIVE: To determine the expression of DLK1 gene in acute leukemias (AL) and its function in erythroid differentiation of K562 cells.
  • METHODS: We detected the expression of DLK1 gene in 65 different acute leukemia categories (a test group) and 34 normal bone marrow controls (a control group) with RT-PCR.
  • The K562 cell line was induced to erythroid differentiation by hemin.
  • RESULTS: Both leukemia cells and normal marrow cells expressed DLK1.
  • The expression of DLK1 mRNA in patients in the test group was higher than that in the control group (P=0.018), while there was no significance between acute lymphoblastic leukemia and acute myelogenous leukemia (P>0.05).The expression of DLK1 mRNA in the test group at onset had no relation with the WBC and platelet count in the total peripheral blood, and the same was true for blast cell rates in bone marrow cells.The level of DLK1 protein in the test group was higher than that in the control group, which was consistent with the mRNA expression (P=0.042).
  • CONCLUSION: DLK1 gene may be involved in leukemia,but the mRNA level of DLK1 has no relation with some clinical characteristics of AL patients at onset.
  • [MeSH-major] Cell Differentiation / genetics. Cell Transformation, Neoplastic / genetics. Erythroid Cells / pathology. Intercellular Signaling Peptides and Proteins / metabolism. Leukemia / genetics. Membrane Proteins / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Case-Control Studies. Child. Child, Preschool. Erythroid Precursor Cells / pathology. Female. Humans. K562 Cells. Male. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. Young Adult

  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
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  • (PMID = 19779261.001).
  • [ISSN] 1672-7347
  • [Journal-full-title] Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
  • [ISO-abbreviation] Zhong Nan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DLK1 protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / RNA, Messenger
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100. Kohlmann A, Schoch C, Dugas M, Schnittger S, Hiddemann W, Kern W, Haferlach T: New insights into MLL gene rearranged acute leukemias using gene expression profiling: shared pathways, lineage commitment, and partner genes. Leukemia; 2005 Jun;19(6):953-64

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New insights into MLL gene rearranged acute leukemias using gene expression profiling: shared pathways, lineage commitment, and partner genes.
  • Rearrangements of the MLL gene occur in both acute lymphoblastic and acute myeloid leukemias (ALL, AML).
  • This study addressed the global gene expression pattern of these two leukemia subtypes with respect to common deregulated pathways and lineage-associated differences.
  • We analyzed 73 t(11q23)/MLL leukemias in comparison to 290 other acute leukemias and demonstrate that 11q23 leukemias combined are characterized by a common specific gene expression signature.
  • Through the use of novel biological network analyses, essential regulators of early B cell development, PAX5 and EBF, were shown to be associated with a clear B-lineage commitment in lymphoblastic t(11q23)/MLL leukemias.
  • Taken together, the identified molecular expression pattern of MLL fusion gene samples and biological networks revealed new insights into the aberrant transcriptional program in 11q23/MLL leukemias.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adult. Cell Lineage / genetics. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Multigene Family. Myeloid-Lymphoid Leukemia Protein. Oligonucleotide Array Sequence Analysis. Transcription, Genetic. Translocation, Genetic

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  • (PMID = 15815718.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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