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1. Figueroa ME, Skrabanek L, Li Y, Jiemjit A, Fandy TE, Paietta E, Fernandez H, Tallman MS, Greally JM, Carraway H, Licht JD, Gore SD, Melnick A: MDS and secondary AML display unique patterns and abundance of aberrant DNA methylation. Blood; 2009 Oct 15;114(16):3448-58
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  • [Title] MDS and secondary AML display unique patterns and abundance of aberrant DNA methylation.
  • Increasing evidence shows aberrant hypermethylation of genes occurring in and potentially contributing to pathogenesis of myeloid malignancies.
  • To determine the extent of promoter hypermethylation in such tumors, we compared the distribution of DNA methylation of 14 000 promoters in MDS and secondary acute myeloid leukemia (AML) patients enrolled in a phase 1 trial of 5-azacytidine and the histone deacetylase inhibitor entinostat against de novo AML patients and normal CD34(+) bone marrow cells.
  • The MDS and secondary AML patients displayed more extensive aberrant DNA methylation involving thousands of genes than did the normal CD34(+) bone marrow cells or de novo AML blasts.
  • Aberrant methylation in MDS and secondary AML tended to affect particular chromosomal regions, occurred more frequently in Alu-poor genes, and included prominent involvement of genes involved in the WNT and MAPK signaling pathways.
  • [MeSH-major] Azacitidine / administration & dosage. DNA Methylation / drug effects. DNA, Neoplasm / metabolism. Enzyme Inhibitors / administration & dosage. Leukemia, Myeloid, Acute. Myelodysplastic Syndromes. Neoplasms, Second Primary / drug therapy. Neoplasms, Second Primary / metabolism

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  • [Cites] Mol Pharmacol. 2001 Apr;59(4):751-7 [11259619.001]
  • [Cites] Lancet Oncol. 2009 Mar;10(3):223-32 [19230772.001]
  • [Cites] Blood. 2009 Feb 5;113(6):1315-25 [18832655.001]
  • [Cites] Blood. 2009 Sep 24;114(13):2764-73 [19546476.001]
  • [Cites] Nucleic Acids Res. 2002 Jan 1;30(1):207-10 [11752295.001]
  • [Cites] J Clin Oncol. 2002 May 15;20(10):2429-40 [12011120.001]
  • [Cites] Nat Rev Genet. 2002 Jun;3(6):415-28 [12042769.001]
  • [Cites] Hum Mol Genet. 2002 Oct 1;11(20):2479-88 [12351584.001]
  • [Cites] Leukemia. 2003 May;17(5):910-8 [12750705.001]
  • [Cites] Leukemia. 2003 Sep;17(9):1813-9 [12970781.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2042-54 [14627790.001]
  • [Cites] J Biol Chem. 2004 Apr 9;279(15):15161-6 [14722112.001]
  • [Cites] Nat Med. 2004 May;10(5):481-3 [15048110.001]
  • [Cites] Genome Biol. 2004;5(10):R80 [15461798.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):103-7 [9916800.001]
  • [Cites] Bioinformatics. 2005 Jun 1;21(11):2789-90 [15797915.001]
  • [Cites] Br J Haematol. 2005 Jul;130(2):209-17 [16029449.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7086-90 [16103056.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):305-19 [16075461.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 1;102(44):15785-90 [16243968.001]
  • [Cites] Nat Clin Pract Oncol. 2005 Dec;2 Suppl 1:S36-44 [16341239.001]
  • [Cites] Eur J Haematol. 2006 Jan;76(1):23-32 [16343268.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6361-9 [16778214.001]
  • [Cites] BMC Genomics. 2006;7:133 [16740159.001]
  • [Cites] Genome Res. 2006 Aug;16(8):1046-55 [16809668.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3895-903 [16921040.001]
  • [Cites] Blood. 2007 Jan 1;109(1):52-7 [16882708.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1937-44 [17611569.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):8248-54 [17804739.001]
  • [Cites] Mol Cell. 2007 Oct 26;28(2):337-50 [17964271.001]
  • [Cites] Mol Cell Biol. 2008 Jan;28(2):752-71 [17991895.001]
  • [Cites] Semin Hematol. 2008 Jan;45(1):23-30 [18179966.001]
  • [Cites] Nucleic Acids Res. 2008 Jan;36(Database issue):D773-9 [18086701.001]
  • [Cites] PLoS One. 2008;3(3):e1882 [18365023.001]
  • [Cites] Bioinformatics. 2008 May 1;24(9):1161-7 [18353789.001]
  • [Cites] Mol Cancer Ther. 2008 Sep;7(9):2998-3005 [18790780.001]
  • [CommentIn] Blood. 2009 Oct 15;114(16):3363-4 [19833849.001]
  • (PMID = 19652201.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00101179
  • [Grant] United States / NCI NIH HHS / CA / R21 CA110507; United States / NCI NIH HHS / CA / U10 CA021115; United States / NCI NIH HHS / CA / U54 CA143876-01; United States / NCI NIH HHS / CA / K24 CA111717; United States / NCI NIH HHS / CA / R01 CA125635; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCI NIH HHS / CA / U54 CA143876; United States / NICHD NIH HHS / HD / R01 HD044078; United States / NCI NIH HHS / CA / CA21115; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / R01 CA104348; United States / NCI NIH HHS / CA / U01CA70095
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / DNA, Neoplasm; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Wnt Proteins; EC 3.5.1.98 / Histone Deacetylases; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC2765680
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2. Rizzieri DA, O'Brien JA, Broadwater G, Decastro CM, Dev P, Diehl L, Beaven A, Lagoo A, Gockerman JP, Chao NJ, Moore JO: Outcomes of patients who undergo aggressive induction therapy for secondary acute myeloid leukemia. Cancer; 2009 Jul 1;115(13):2922-9
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  • [Title] Outcomes of patients who undergo aggressive induction therapy for secondary acute myeloid leukemia.
  • BACKGROUND: Response and survival in 96 patients with secondary acute myeloid leukemia (sAML) who received aggressive induction chemotherapy was reviewed.
  • Patients with AML after previous chemotherapy or radiation therapy had a higher morphologic remission rate compared with those arising from myelodysplastic syndrome or myeloproliferative disease (82% vs 62%; P = .027).
  • In this population of patients who received aggressive chemotherapy, Charlson comorbidity index or a higher number of factors recognized as high risk in leukemia patients did not affect the chance of OS, DFS, and EFS, although having more recognized leukemia risk factors was related to a lower chance of surviving 1 year.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Neoplasms, Second Primary / drug therapy

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  • (PMID = 19452542.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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3. Ducastelle S, Adès L, Gardin C, Dombret H, Prébet T, Deconinck E, Rio B, Thomas X, Debotton S, Guerci A, Gratecos N, Stamatoullas A, Fegueux N, Dreyfus F, Fenaux P, Wattel E: Long-term follow-up of autologous stem cell transplantation after intensive chemotherapy in patients with myelodysplastic syndrome or secondary acute myeloid leukemia. Haematologica; 2006 Mar;91(3):373-6
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  • [Title] Long-term follow-up of autologous stem cell transplantation after intensive chemotherapy in patients with myelodysplastic syndrome or secondary acute myeloid leukemia.
  • We report on the outcomes of 53 patients with myelodysplastic syndromes (MDS) or acute myeloid leukemia secondary to MDS, autografted in first complete remission.
  • [MeSH-major] Leukemia, Myeloid, Acute / surgery. Myelodysplastic Syndromes / surgery. Stem Cell Transplantation


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4. Willems L, Suarez F, Messas E, Baubion N, Decaudin D, Fourquet A, Ghez D, Delarue R, Hermine O, Buzyn A, Varet B, Rubio MT: [High risk of cardiac dysfunction after treatment of secondary acute myeloid leukemia following chemotherapy and radiotherapy for breast cancer]. Bull Cancer; 2010 Feb;97(2):245-54
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  • [Title] [High risk of cardiac dysfunction after treatment of secondary acute myeloid leukemia following chemotherapy and radiotherapy for breast cancer].
  • Secondary acute myeloid leukaemia (AML) occurring after breast cancer is a rare long-term complication of the chemo- and/or radiation therapy required to treat breast cancer.
  • The usually recognized curative option of these secondary AML includes courses of anthracycline-based chemotherapy followed by haematopoietic stem cell transplantation (HSCT).
  • Cardiac dysfunction during AML treatment of these patients previously treated with anthracyclines for breast cancer has not been reported to date.
  • We evaluated the evolution of cardiac function in seven patients treated with anthracyclines and/or autologous or allogeneic bone marrow transplantation for secondary AML occurring after breast cancer.
  • All of the patients who received a cumulative anthracycline dose above the cardiac toxicity threshold developed cardiac symptoms during AML chemotherapy courses.
  • Thus, the risk of severe cardiac dysfunction after treatment of secondary AML following breast cancer must be taken in account as part of the therapeutic strategy of those patients.
  • As discussed here, an accurate evaluation of risk factors, the use of sensitive detection tests and of cardioprotective drugs as well as that of non-cardiotoxic chemotherapy might decrease the occurrence and severity of this life-threatening complication.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Breast Neoplasms. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid / therapy. Neoplasms, Second Primary / therapy
  • [MeSH-minor] Acute Disease. Adult. Chemotherapy, Adjuvant / adverse effects. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Epirubicin / administration & dosage. Epirubicin / adverse effects. Female. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Heart Diseases / chemically induced. Heart Diseases / drug therapy. Heart Diseases / physiopathology. Humans. Middle Aged. Remission Induction. Stroke Volume / drug effects. Stroke Volume / physiology

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  • (PMID = 19819776.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; U3P01618RT / Fluorouracil; ZS7284E0ZP / Daunorubicin; FEC protocol
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5. Koh Y, Kim I, Bae JY, Song EY, Kim HK, Yoon SS, Lee DS, Park SS, Park MH, Park S, Kim BK: Prognosis of secondary acute myeloid leukemia is affected by the type of the preceding hematologic disorders and the presence of trisomy 8. Jpn J Clin Oncol; 2010 Nov;40(11):1037-45
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  • [Title] Prognosis of secondary acute myeloid leukemia is affected by the type of the preceding hematologic disorders and the presence of trisomy 8.
  • BACKGROUND: Differences in the clinical course of secondary acute myeloid leukemia according to the type of the preceding disorders are not defined.
  • We compared the outcomes of therapy-related acute myeloid leukemia, acute myeloid leukemia following myelodysplastic syndrome and acute myeloiod leukemia following myeloproliferative neoplasm.
  • We also intended to find prognostic factors in secondary acute myeloid leukemia overall.
  • RESULTS: Ninety-five secondary acute myeloid leukemia patients (median age of 56.4 years) were analyzed.
  • Twenty-six, 57 and 12 patients had therapy-related leukemia, leukemia following myelodysplastic syndrome and myeloproliferative neoplasm, respectively.
  • Compared to therapy-related leukemia (P = 0.027) and leukemia following myelodysplastic syndrome (P = 0.050), leukemia following myeloproliferative neoplasm had shorter overall survival.
  • In secondary leukemia, presence of trisomy 8 had a prognostic impact (P = 0.003) along with cytogenetic risk group (P = 0.016).
  • CONCLUSIONS: Prognosis of secondary acute myeloid leukemia was different according to the type of the preceding disorders with the worst prognosis in leukemia following myeloprolfierative neoplasm.
  • Along with cytogenetic risk grouping, trisomy 8 had a poor prognostic impact in secondary acute myeloid leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / complications. Myeloproliferative Disorders / complications. Trisomy

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  • (PMID = 20587614.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin; ZS7284E0ZP / Daunorubicin
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6. Ostgård LS, Kjeldsen E, Holm MS, Brown Pde N, Pedersen BB, Bendix K, Johansen P, Kristensen JS, Nørgaard JM: Reasons for treating secondary AML as de novo AML. Eur J Haematol; 2010 Sep;85(3):217-26
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  • [Title] Reasons for treating secondary AML as de novo AML.
  • In a Danish bi-regional registry-based study, we conducted an analysis of the incidence and clinical importance of secondary acute myeloid leukaemia (AML).
  • In a total of 630 cases of AML, we found 157 (25%) cases of secondary AML.
  • The secondary leukaemia arose from MDS (myelodysplastic syndrome) in 77 cases (49%), CMPD (chronic myeloproliferative disorder) in 43 cases (27%) and was therapy-related AML (t-AML) in 37 cases (24%).
  • Median age at diagnosis of AML was 69 yr in secondary cases when compared to 66 yr in de novo cases (P = 0.006).
  • In univariate analyses, secondary AML was associated with an inferior complete remission (CR) rate (P = 0.008) and poorer overall survival (OS, P = 0.003) whereas in complete remitters, disease-free survival (DFS) of secondary cases was equal to that of de novo cases.
  • Interestingly, in all further analyses of CR-rates, OS and DFS, when correcting for the influence of age, cytogenetic abnormalities, performance status and leucocyte count (WBC), presence of secondary AML completely lost prognostic significance.
  • We conclude that the presence of secondary AML does not per se convey an unfavourable prognosis and that patients with secondary AML should be offered the chance of benefiting from treatment according to current frontline AML protocols.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / complications


7. Owatari S, Otsuka M, Uozumi K, Takeshita T, Hanada S: Two cases of secondary acute myeloid leukemia accompanying adult T-cell leukemia/lymphoma. Int J Hematol; 2007 Jan;85(1):32-5
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  • [Title] Two cases of secondary acute myeloid leukemia accompanying adult T-cell leukemia/lymphoma.
  • We identified 2 cases of secondary acute myeloid leukemia (AML) following adult T-cell leukemia/lymphoma (ATL) in patients who had previously received chemotherapy.
  • Both cases were thought to represent therapy-related AML because the patients had previously received combination chemotherapy including epipodophyllotoxin, anthracycline, and alkylating agents for the ATL.
  • The cases were diagnosed as AML M4 with eosinophilia and AML M2, with the chromosomal abnormalities inv(16)(p13q22) and t(8;21)(q22;q22), respectively.
  • In our hospital, only these 2 cases of secondary AML accompanying ATL were identified among 90 cases of acute- or lymphoma-type ATL diagnosed from October 1999 to July 2006.
  • The frequency of coexisting AML and ATL is lower than that reported for acute leukemia coexisting with other lymphoid malignancies.
  • The low frequency of secondary leukemia with ATL may be associated with the short survival times of ATL patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia-Lymphoma, Adult T-Cell / complications. Neoplasms, Second Primary / chemically induced
  • [MeSH-minor] Acute Disease. Alkylating Agents / therapeutic use. Anthracyclines / therapeutic use. Chromosome Aberrations. Female. Humans. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myelomonocytic, Acute / chemically induced. Male. Middle Aged. Podophyllotoxin / therapeutic use

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  • (PMID = 17261499.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Anthracyclines; L36H50F353 / Podophyllotoxin
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8. Kuptsova-Clarkson N, Ambrosone CB, Weiss J, Baer MR, Sucheston LE, Zirpoli G, Kopecky KJ, Ford L, Blanco J, Wetzler M, Moysich KB: XPD DNA nucleotide excision repair gene polymorphisms associated with DNA repair deficiency predict better treatment outcomes in secondary acute myeloid leukemia. Int J Mol Epidemiol Genet; 2010;1(4):278-94
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  • [Title] XPD DNA nucleotide excision repair gene polymorphisms associated with DNA repair deficiency predict better treatment outcomes in secondary acute myeloid leukemia.
  • We evaluated these polymorphisms and XPD haplotypes in adult de novo (n=214) and secondary (n=79) acute myeloid leukemia (AML) patients treated with cytarabine and anthracycline chemotherapy.
  • Differential responses were observed in secondary, but not de novo, AML.
  • Among secondary AML patients, the odds of achieving complete remission (CR) were higher for the XPD 312Asn/Asn (OR= 11.23; 95% CI, 2.23-56.63) and XPD 751Gln/Gln (OR= 7.07; 95% CI, 1.42-35.18) genotypes.
  • If validated, these findings could support stratification of chemotherapy in secondary AML.

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  • (PMID = 21394217.001).
  • [ISSN] 1948-1756
  • [Journal-full-title] International journal of molecular epidemiology and genetics
  • [ISO-abbreviation] Int J Mol Epidemiol Genet
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA108353-02; United States / NCI NIH HHS / CA / R03 CA108353; United States / NCI NIH HHS / CA / CA108353-01; United States / NCI NIH HHS / CA / R03 CA108353-02; United States / NCI NIH HHS / CA / R03 CA108353-01
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS247623; NLM/ PMC3049908
  • [Keywords] NOTNLM ; Acute Myeloid Leukemia (AML) / DNA repair gene polymorphisms / pharmacogenetics/pharmacogenomics / secondary AML
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9. Gombos DS, Hungerford J, Abramson DH, Kingston J, Chantada G, Dunkel IJ, Antoneli CB, Greenwald M, Haik BG, Leal CA, Medina-Sanson A, Schefler AC, Veerakul G, Wieland R, Bornfeld N, Wilson MW, Yu CB: Secondary acute myelogenous leukemia in patients with retinoblastoma: is chemotherapy a factor? Ophthalmology; 2007 Jul;114(7):1378-83
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  • [Title] Secondary acute myelogenous leukemia in patients with retinoblastoma: is chemotherapy a factor?
  • PURPOSE: To describe a series of patients with secondary acute myelogenous leukemia (sAML) and retinoblastoma (RB).
  • MAIN OUTCOME MEASURES: History of RB and development of sAML, management of RB (surgery, radiotherapy, chemotherapy), age at diagnosis of RB and leukemia, French-American-British (FAB) subtype, and current status of patient (alive or dead).
  • Mean latent period from RB to AML diagnosis was 9.8 years (median, 42 months).
  • Ten children died of their leukemia.
  • CONCLUSIONS: Acute myelogenous leukemia is a rare secondary malignancy among retinoblastoma patients, many of whom were treated with primary or adjuvant chemotherapy.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / adverse effects. Enzyme Inhibitors / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Neoplasms, Second Primary / chemically induced. Podophyllotoxin / adverse effects. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy. Topoisomerase II Inhibitors


10. Park TS, Choi JR, Yoon SH, Song J, Kim J, Kim SJ, Kwon O, Min YH: Acute promyelocytic leukemia relapsing as secondary acute myelogenous leukemia with translocation t(3;21)(q26;q22) and RUNX1-MDS1-EVI1 fusion transcript. Cancer Genet Cytogenet; 2008 Dec;187(2):61-73
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  • [Title] Acute promyelocytic leukemia relapsing as secondary acute myelogenous leukemia with translocation t(3;21)(q26;q22) and RUNX1-MDS1-EVI1 fusion transcript.
  • Acute promyelocytic leukemia (APL) is a subtype of acute myelogenous leukemia (AML) that is characterized by peculiar clinical and biologic features, including severe hemorrhagic diathesis, specific recurrent chromosomal aberration, and distinct morphologic features with predominant pathologic promyelocytes.
  • A reciprocal translocation involving chromosomes 15 and 17, t(15;17)(q22;q21), is a characteristic feature of APL that represents approximately 5-8% of AML.
  • In contrast to other AML subtypes, APL is particularly sensitive to treatment with all trans-retinoic acid (ATRA) combined with chemotherapy, converting this once fatal leukemia to a highly curable disease.
  • Nonetheless, therapy-related myelodysplastic syndrome-acute myelogenous leukemia (t-MDS/AML) has been reported as a rare complication of chemotherapy in APL.
  • Of 30 APL cases described as t-MDS/AML in the literature, only 1 case relapsed as acute leukemia with t(3;21)(q26;q22).
  • Here we describe a rare case of APL relapsing as secondary AML with t(3;21)(q26;q22) and clinically characterize this patient using the RUNX1 (previously AML1)-MDS1-EVI1 fusion transcript (with follow-up for 55 months), and review the relevant literature.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Promyelocytic, Acute / genetics. Neoplasms, Second Primary / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 19027486.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human; 0 / Transcription Factors; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin
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11. Suzuki K, Ohishi K, Sekine T, Masuya M, Katayama N: Selective blast cell reduction in elderly patients with acute myeloid leukemia secondary to myelodysplastic syndrome treated with methylprednisolone. Int J Hematol; 2007 May;85(4):344-9
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  • [Title] Selective blast cell reduction in elderly patients with acute myeloid leukemia secondary to myelodysplastic syndrome treated with methylprednisolone.
  • The management of elderly patients with acute myeloid leukemia (AML) and a poor performance status is challenging.
  • An 89-year-old man with AML secondary to myelodysplastic syndrome (MDS) and a poor performance status (4) underwent treatment with methylprednisolone (mPSL) (125 mg/body), which resulted in a remarkable reduction of blast cells in the peripheral blood.
  • On the basis of this experience, we gave the same mPSL dose to other elderly patients with MDS/AML (n=5) or AML-M4 (n=1) who had a poor performance status (3 or higher) and appeared unable to tolerate standard cytotoxic chemotherapies.
  • Selective and significant blast cell reduction was observed in 4 of the 5 patients with MDS/AML, whereas no effects were seen in the AML patient.
  • Although our experience is limited, these findings may provide a clue to understanding the mechanisms regulating the survival of blast cells of MDS/AML and indicate that mPSL may provide a benefit to a subset of these patients.
  • [MeSH-major] Blast Crisis / drug therapy. Blast Crisis / etiology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / etiology. Methylprednisolone / administration & dosage. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / drug therapy


12. Maris MB, Ravandi F, Stuart R, Stone R, Cripe L, Cooper M, Strickland S, Turturro F, Stock W, Berman C: A phase II study of voreloxin as single agent therapy for elderly patients (pts) with newly diagnosed acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of voreloxin as single agent therapy for elderly patients (pts) with newly diagnosed acute myeloid leukemia (AML).
  • Interim results of REVEAL-1, a phase II study of single agent voreloxin in newly diagnosed elderly AML pts, are reported.
  • Eligibility: newly diagnosed AML (de novo or secondary AML), pts age ≥ 60 and ≥ 1 additional adverse risk factor (age ≥ 70, secondary AML, intermediate or unfavorable cytogenetics, or PS 2).
  • Voreloxin PK were similar to those in an earlier single agent phase I study in relapsed/refractory AML.
  • CONCLUSIONS: In REVEAL-1, voreloxin demonstrates clinical activity with 2 dosing schedules in previously untreated elderly (age ≥ 60) patients with AML who are unlikely to benefit from standard chemotherapy.

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  • (PMID = 27961427.001).
  • [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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13. Bello CM, Yu D, Zhu W, Wetzstein GA, Lancet JE: Outcomes following induction chemotherapy in patients with AML arising from MDS: Analysis of prognostic factors. J Clin Oncol; 2009 May 20;27(15_suppl):7088

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcomes following induction chemotherapy in patients with AML arising from MDS: Analysis of prognostic factors.
  • : 7088 Background: Secondary acute myeloid leukemia (sAML) arising from myelodysplasia (MDS) or a myeloproliferative neoplasm (MPN) has a poor prognosis.
  • METHODS: Retrospective chart review of patients with untreated AML from MDS/MPN treated with standard induction therapy from January 2004 to September 2008.
  • Multivariable analysis indicated that the same three factors were significantly negatively associated with CR/CRp as well as OS: PR cytogenetics, prior treatment with DM/L, and long transformation to AML on log scale.
  • Only 32% of the group that received prior treatment with a DM/L achieved CR/CRp compared to 78% in non DM/L-treated patients (OR = 0.13, 95% CI: 0.04-0.42).
  • The median OS for those treated with a DM/L was 3.7 mo compared to 10.5 mo for non DM/L-treated patients (p < 0.0001).
  • CONCLUSIONS: Prior MDS treatment with a DM/L, PR cytogenetics and long transformation to AML are independent negative prognostic factors for response and OS in patients with sAML following induction therapy, suggesting that such patients may be better served by novel approaches, and that stratification for these risk factors should be considered in future clinical trials.

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  • (PMID = 27961482.001).
  • [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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14. Villano JL, Letarte N, Yu JM, Shakir AR, Bressler L: Hematologic adverse events associated with temozolomide (TMZ). J Clin Oncol; 2009 May 20;27(15_suppl):2053

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 2053 Background: Secondary acute myeloid leukemia (AML) is reported to occur in 3%-10% of patients treated with alkylating agents for Hodgkin's lymphoma, non-Hodgkin's lymphoma, ovarian cancer, breast cancer, and multiple myeloma.
  • The incidence of secondary AML is greatest at 5-10 years after treatment, and AML often follows myelodysplastic syndrome (MDS).
  • Among these patients, we identified 140 cases that we labeled as major hematologic adverse events: agranulocytosis (8 cases), aplasia (42), aplastic anemia (52), leukemia (26), MDS (6), and lymphoma (6).
  • Risk of leukemia/MDS from our review may also be significant, but length of follow-up is insufficient and the real risk is likely still unknown.

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  • (PMID = 27964671.001).
  • [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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15. Kröger N, Shimoni A, Zabelina T, Schieder H, Panse J, Ayuk F, Wolschke C, Renges H, Dahlke J, Atanackovic D, Nagler A, Zander A: Reduced-toxicity conditioning with treosulfan, fludarabine and ATG as preparative regimen for allogeneic stem cell transplantation (alloSCT) in elderly patients with secondary acute myeloid leukemia (sAML) or myelodysplastic syndrome (MDS). Bone Marrow Transplant; 2006 Feb;37(4):339-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reduced-toxicity conditioning with treosulfan, fludarabine and ATG as preparative regimen for allogeneic stem cell transplantation (alloSCT) in elderly patients with secondary acute myeloid leukemia (sAML) or myelodysplastic syndrome (MDS).
  • We investigated a dose-reduced conditioning regimen consisting of treosulfan and fludarabine followed by allogeneic stem cell transplantation (SCT) in 26 patients with secondary AML or MDS.
  • Acute graft-versus-host disease (GvHD) grade II-IV was seen in 23% and severe grade III GvHD in 12% of the patients.
  • No patients experienced grade IV acute GvHD.
  • [MeSH-major] Antilymphocyte Serum / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Busulfan / analogs & derivatives. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adult. Aged. Disease-Free Survival. Female. Graft vs Host Disease / drug therapy. Graft vs Host Disease / prevention & control. HLA Antigens / analysis. Humans. Male. Middle Aged. Prospective Studies. Recurrence. Siblings. Survival Rate. Transplantation, Homologous. Treatment Outcome


16. Czibere A, Prall WC, Zerbini LF, Grall F, Craigie EC, Ulrich SD, Giagounidis AA, Haas R, Libermann TA, Aivado M: The nonsteroidal anti-inflammatory drug Exisulind selectively induces apoptosis via JNK in secondary acute myeloid leukemia after myelodysplastic syndrome. Cell Cycle; 2005 Jun;4(6):812-7
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  • [Title] The nonsteroidal anti-inflammatory drug Exisulind selectively induces apoptosis via JNK in secondary acute myeloid leukemia after myelodysplastic syndrome.
  • Treatment of patients suffering from myelodysplastic syndromes and secondary acute myeloid leukemia after MDS is often unsuccessful.
  • Exisulind is another potentially pro-apoptotic agent, and therefore, we investigated its influence on proliferation, differentiation, cell cycle and apoptosis in two sAML/MDS cell lines, one de-novo AML cell line and healthy CD34+ bone marrow cells.
  • Exisulind had no effect on de-novo AML or normal CD34+ cells.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Apoptosis / drug effects. JNK Mitogen-Activated Protein Kinases / metabolism. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / complications. Sulindac / analogs & derivatives


17. Nemoto N, Suzukawa K, Shimizu S, Shinagawa A, Takei N, Taki T, Hayashi Y, Kojima H, Kawakami Y, Nagasawa T: Identification of a novel fusion gene MLL-MAML2 in secondary acute myelogenous leukemia and myelodysplastic syndrome with inv(11)(q21q23). Genes Chromosomes Cancer; 2007 Sep;46(9):813-9
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  • [Title] Identification of a novel fusion gene MLL-MAML2 in secondary acute myelogenous leukemia and myelodysplastic syndrome with inv(11)(q21q23).
  • We have identified a novel fusion partner of MLL, namely the mastermind like 2 (MAML2 gene), in secondary acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) with inv(11)(q21q23).
  • RT-PCR and sequencing revealed that exon 7 of MLL was fused to exon 2 of MAML2 in the AML and MDS cells.
  • MLL-MAML2 in secondary AML/MDS and MECT1-MAML2 in mucoepithelioid carcinoma, benign Wartin's tumor, and clear cell hidradenoma consist of the same COOH-terminal part of MAML2.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. Transcription Factors / genetics


18. Hallemeier CL, Girgis MD, Blum WG, Brown RA, Khoury HJ, Devine SM, Vij R, Lin HS, DiPersio JF, Adkins DR: Long-term remissions in patients with myelodysplastic syndrome and secondary acute myelogenous leukemia undergoing allogeneic transplantation following a reduced intensity conditioning regimen of 550 cGy total body irradiation and cyclophosphamide. Biol Blood Marrow Transplant; 2006 Jul;12(7):749-57
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  • [Title] Long-term remissions in patients with myelodysplastic syndrome and secondary acute myelogenous leukemia undergoing allogeneic transplantation following a reduced intensity conditioning regimen of 550 cGy total body irradiation and cyclophosphamide.
  • We analyzed outcomes of patients with myelodysplastic syndrome (MDS) or secondary acute myelogenous leukemia (sAML) that were treated at our institution with a reduced intensity conditioning (RIC) regimen of 550-cGy total body irradiation and cyclophosphamide followed by related donor (RD) or unrelated donor (URD) transplantation.
  • [MeSH-major] Bone Marrow Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Neoplasms, Second Primary / therapy. Peripheral Blood Stem Cell Transplantation / methods. Transplantation Conditioning / methods


19. Al-Ali HK, Brand R, van Biezen A, Finke J, Boogaerts M, Fauser AA, Egeler M, Cahn JY, Arnold R, Biersack H, Niederwieser D, de Witte T: A retrospective comparison of autologous and unrelated donor hematopoietic cell transplantation in myelodysplastic syndrome and secondary acute myeloid leukemia: a report on behalf of the Chronic Leukemia Working Party of the European Group for Blood and Marrow Transplantation (EBMT). Leukemia; 2007 Sep;21(9):1945-51
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  • [Title] A retrospective comparison of autologous and unrelated donor hematopoietic cell transplantation in myelodysplastic syndrome and secondary acute myeloid leukemia: a report on behalf of the Chronic Leukemia Working Party of the European Group for Blood and Marrow Transplantation (EBMT).
  • Hematopoietic cell transplantation (HCT) is an effective treatment for myelodysplasia (MDS) and secondary acute myeloid leukemia (sAML).
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / mortality. Leukemia, Myeloid / mortality. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / mortality. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Distribution. Aged. Disease-Free Survival. Female. Humans. Incidence. Male. Middle Aged. Recurrence. Retrospective Studies. Survival Analysis. Tissue Donors. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome


20. Szotkowski T, Muzik J, Voglova J, Koza V, Maaloufova J, Kozak T, Jarosova M, Michalova K, Zak P, Steinerova K, Vydra J, Lanska M, Katrincsakova B, Sicova K, Pavlik T, Dusek L, Indrak K: Prognostic factors and treatment outcome in 1,516 adult patients with de novo and secondary acute myeloid leukemia in 1999-2009 in 5 hematology intensive care centers in the Czech Republic. Neoplasma; 2010;57(6):578-89
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic factors and treatment outcome in 1,516 adult patients with de novo and secondary acute myeloid leukemia in 1999-2009 in 5 hematology intensive care centers in the Czech Republic.
  • Acute myeloid leukemia (AML) is a severe condition with a high mortality.
  • The study represents a detailed analysis of the role of these factors and treatment outcomes based on a long-term follow-up of patients treated in 5 hematology intensive care centers in the Czech Republic.The studied group comprised 1,188 patients with de novo AML and 328 patients with secondary AML.
  • Curatively treated patients achieved fewer complete remissions and relapsed more often than those with de novo AML.
  • Patients with secondary AML had lower rates of allogeneic transplantation as part of consolidation therapy and a significantly shorter median overall survival.
  • However, the treatment outcome of de novo AML patients is not satisfactory, the only exception being those with acute promyelocytic leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Neoplasms, Second Primary / mortality


21. Römermann D, Hasemeier B, Metzig K, Schlegelberger B, Länger F, Kreipe H, Lehmann U: [Methylation status of LINE-1 sequences in patients with MDS or secondary AML]. Verh Dtsch Ges Pathol; 2007;91:338-42
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  • [Title] [Methylation status of LINE-1 sequences in patients with MDS or secondary AML].
  • [Transliterated title] Methylierungszustand von LINE-1-Sequenzen bei Patienten mit MDS oder sekundärer AML.
  • [MeSH-minor] Humans. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18314632.001).
  • [ISSN] 0070-4113
  • [Journal-full-title] Verhandlungen der Deutschen Gesellschaft für Pathologie
  • [ISO-abbreviation] Verh Dtsch Ges Pathol
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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22. Preudhomme C, Renneville A, Bourdon V, Philippe N, Roche-Lestienne C, Boissel N, Dhedin N, André JM, Cornillet-Lefebvre P, Baruchel A, Mozziconacci MJ, Sobol H: High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder. Blood; 2009 May 28;113(22):5583-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder.
  • Familial platelet disorder (FPD), a rare autosomal dominant disorder characterized by quantitative and qualitative platelet abnormalities, is considered as a model of genetic predisposition to acute myeloid leukemia (AML).
  • So far, monoallelic RUNX1 germline mutations have been found in 19 of 20 families with reported FPD, and the analysis of blast cells from only 5 patients at acute leukemia (AL) stage has shown no additional RUNX1 abnormality.
  • In addition to the germline RUNX1 mutation, we identified a second RUNX1 alteration in 6 AML cases (acquired point mutations in 4 cases and duplication of the altered RUNX1 allele associated with acquired trisomy 21 in 2 other cases).
  • Although haploinsufficiency of RUNX1 causes FPD, our findings suggest that a second genetic event involving RUNX1 is often associated with progression to AML.
  • [MeSH-major] Blood Platelet Disorders / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics


23. Rodriguez V, Erlandson L, Arndt CA, Wiseman GA, Anderson PM: Low toxicity and efficacy of (153)samarium-EDTMP and melphalan as a conditioning regimen for secondary acute myelogenous leukemia. Pediatr Transplant; 2005 Feb;9(1):122-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low toxicity and efficacy of (153)samarium-EDTMP and melphalan as a conditioning regimen for secondary acute myelogenous leukemia.
  • We report the case of a 15-yr-old girl who developed secondary acute myelogenous leukemia (AML) 4 yr after completion of therapy for metastatic Ewing sarcoma (primary right acetabulum with metastatic disease to the lungs).
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Melphalan. Organometallic Compounds / therapeutic use. Organophosphorus Compounds / therapeutic use. Radioisotopes. Samarium. Transplantation Conditioning / methods

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  • (PMID = 15667625.001).
  • [ISSN] 1397-3142
  • [Journal-full-title] Pediatric transplantation
  • [ISO-abbreviation] Pediatr Transplant
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Organometallic Compounds; 0 / Organophosphorus Compounds; 0 / Radioisotopes; 122575-21-7 / samarium ethylenediaminetetramethylenephosphonate; 42OD65L39F / Samarium; Q41OR9510P / Melphalan
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24. Lim Z, Brand R, Martino R, van Biezen A, Finke J, Bacigalupo A, Beelen D, Devergie A, Alessandrino E, Willemze R, Ruutu T, Boogaerts M, Falda M, Jouet JP, Niederwieser D, Kroger N, Mufti GJ, De Witte TM: Allogeneic hematopoietic stem-cell transplantation for patients 50 years or older with myelodysplastic syndromes or secondary acute myeloid leukemia. J Clin Oncol; 2010 Jan 20;28(3):405-11
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  • [Title] Allogeneic hematopoietic stem-cell transplantation for patients 50 years or older with myelodysplastic syndromes or secondary acute myeloid leukemia.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy


25. Burmeister T, Meyer C, Thiel G, Reinhardt R, Thiel E, Marschalek R: A MLL-KIAA0284 fusion gene in a patient with secondary acute myeloid leukemia and t(11;14)(q23;q32). Blood Cells Mol Dis; 2008 Sep-Oct;41(2):210-4
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  • [Title] A MLL-KIAA0284 fusion gene in a patient with secondary acute myeloid leukemia and t(11;14)(q23;q32).
  • MLL aberrations are found in approximately 10% of acute leukemias.
  • We describe here the case of a patient who developed secondary acute myeloid leukemia five years after the patient had received adjuvant radiochemotherapy because of breast cancer.
  • The expression of KIAA0284 in various tissues and hematologic diseases was investigated by real time quantitative PCR and turned out to be very low in all lymphatic and myeloid diseases investigated.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasms, Second Primary / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 18640063.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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26. Allen SL, Kolitz JE, Lundberg AS, Bennett JM, Capizzi RL, Budman DR: Phase I trials of amonafide as monotherapy and in combination with cytarabine in patients with poor-risk acute myeloid leukemia. Leuk Res; 2010 Apr;34(4):487-91
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  • [Title] Phase I trials of amonafide as monotherapy and in combination with cytarabine in patients with poor-risk acute myeloid leukemia.
  • Amonafide-l-malate (amonafide) is a unique DNA intercalator that maintains activity in the presence of MDR mechanisms, a frequent cause of treatment-failure in secondary AML.
  • 43 patients with relapsed/refractory or secondary AML or CML blast crisis were enrolled into two phase I dose-escalation studies investigating amonafide as monotherapy or in combination with cytarabine.
  • Between both trials responses occurred in 9/20 patients with secondary AML.
  • Both trials demonstrated an acceptable safety profile and significant antileukemic activity in patients with poor-risk AML, especially those with secondary AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Naphthalimides / administration & dosage

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19748672.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Naphthalimides; 04079A1RDZ / Cytarabine; 1Q8D39N37L / amonafide
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27. de Witte T, Hagemeijer A, Suciu S, Belhabri A, Delforge M, Kobbe G, Selleslag D, Schouten HC, Ferrant A, Biersack H, Amadori S, Muus P, Jansen JH, Hellström-Lindberg E, Kovacsovics T, Wijermans P, Ossenkoppele G, Gratwohl A, Marie JP, Willemze R: Value of allogeneic versus autologous stem cell transplantation and chemotherapy in patients with myelodysplastic syndromes and secondary acute myeloid leukemia. Final results of a prospective randomized European Intergroup Trial. Haematologica; 2010 Oct;95(10):1754-61
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  • [Title] Value of allogeneic versus autologous stem cell transplantation and chemotherapy in patients with myelodysplastic syndromes and secondary acute myeloid leukemia. Final results of a prospective randomized European Intergroup Trial.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy

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  • [Cites] Mod Pathol. 2000 Feb;13(2):193-207 [10697278.001]
  • [Cites] Br J Haematol. 2000 Sep;110(3):620-30 [10997974.001]
  • [Cites] Blood. 2001 Oct 15;98(8):2326-31 [11588026.001]
  • [Cites] Br J Haematol. 2002 Aug;118(2):385-400 [12139722.001]
  • [Cites] Blood. 2002 Aug 15;100(4):1201-7 [12149198.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1997-2004 [12200358.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1615-21 [12200672.001]
  • [Cites] Leukemia. 2003 May;17(5):859-68 [12750698.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1232-40 [12714526.001]
  • [Cites] Blood. 2004 Apr 15;103(8):2908-13 [15070662.001]
  • [Cites] Blood. 2004 Jul 15;104(2):579-85 [15039286.001]
  • [Cites] Ann Hematol. 2004 Aug;83(8):498-503 [15156346.001]
  • [Cites] Br J Haematol. 1985 Mar;59(3):425-33 [3970861.001]
  • [Cites] Br J Haematol. 1991 Apr;77(4):497-501 [2025575.001]
  • [Cites] Blood. 1995 Nov 15;86(10):3660-7 [7579331.001]
  • [Cites] Leukemia. 1995 Nov;9(11):1805-11 [7475266.001]
  • [Cites] Leukemia. 1996 Oct;10(10):1648-52 [8847900.001]
  • [Cites] Blood. 1997 Mar 15;89(6):2079-88 [9058730.001]
  • [Cites] Blood. 1997 Nov 15;90(10):3853-7 [9354651.001]
  • [Cites] Br J Haematol. 1997 Dec;99(4):939-44 [9432047.001]
  • [Cites] Br J Haematol. 1998 Sep;102(4):1015-24 [9734653.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Leukemia. 1999 Apr;13(4):524-9 [10214857.001]
  • [Cites] Ann Oncol. 1999 Jul;10(7):825-9 [10470430.001]
  • [Cites] Leukemia. 2005 Mar;19(3):396-401 [15674354.001]
  • [Cites] Bone Marrow Transplant. 2006 Jan;37(2):183-9 [16299545.001]
  • [Cites] Haematologica. 2006 Mar;91(3):373-6 [16531261.001]
  • [Cites] Blood. 2007 May 1;109(9):3658-66 [17213292.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1945-51 [17611571.001]
  • [Cites] Br J Haematol. 1982 Jun;51(2):189-99 [6952920.001]
  • [CommentIn] Haematologica. 2010 Oct;95(10):1623-7 [20884716.001]
  • (PMID = 20494931.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00002926
  • [Grant] United States / NCI NIH HHS / CA / 5U10 CA11488-32; United States / NCI NIH HHS / CA / 5U10 CA11488-27; United States / NCI NIH HHS / CA / 5U10 CA11488-38; United States / NCI NIH HHS / CA / 5U10 CA11488-28; United States / NCI NIH HHS / CA / 5U10 CA11488-35; United States / NCI NIH HHS / CA / 5U10 CA11488-31; United States / NCI NIH HHS / CA / 5U10 CA11488-26; United States / NCI NIH HHS / CA / 5U10 CA11488-37; United States / NCI NIH HHS / CA / U10 CA011488; United States / NCI NIH HHS / CA / 5U10 CA11488-29; United States / NCI NIH HHS / CA / 5U10 CA11488-36; United States / NCI NIH HHS / CA / 5U10 CA11488-33; United States / NCI NIH HHS / CA / 5U10 CA11488-34; United States / NCI NIH HHS / CA / 5U10 CA11488-30
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2948102
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28. Weintraub M, Revel-Vilk S, Charit M, Aker M, Pe'er J: Secondary acute myeloid leukemia after etoposide therapy for retinoblastoma. J Pediatr Hematol Oncol; 2007 Sep;29(9):646-8
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  • [Title] Secondary acute myeloid leukemia after etoposide therapy for retinoblastoma.
  • Most chemotherapy regimens used in retinoblastoma include etoposide, an epipodophyllotoxin associated with a risk of secondary myeloid leukemia.
  • The use of etoposide in patients with a cancer predisposition syndrome such as retinoblastoma is potentially harmful, however, reports of secondary acute myeloid leukemia in patients treated with etoposide for retinoblastoma are rare.
  • We report a case of a patient who developed secondary acute myeloid leukemia after etoposide treatment for retinoblastoma.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / adverse effects. Etoposide / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / diagnosis. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy
  • [MeSH-minor] Acute Disease. Female. Humans. Infant. Treatment Outcome

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  • [ErratumIn] J Pediatr Hematol Oncol. 2007 Oct;29(10):728. Pèer, Jacob [corrected to Pe'er, Jacob]
  • (PMID = 17805043.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide
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29. Sumrall A, Dreiling B: Therapy-related acute nonlymphoblastic leukemia following mitoxantrone therapy in a patient with multiple sclerosis. J Miss State Med Assoc; 2007 Jul;48(7):206-7
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  • [Title] Therapy-related acute nonlymphoblastic leukemia following mitoxantrone therapy in a patient with multiple sclerosis.
  • A 58-year-old male with migraine headaches, complex partial epilepsy, and secondary progressive multiple sclerosis treated with mitoxantrone was admitted to our facility in August 2005 with febrile neutropenia, worsening ataxia, aphasia, cough, and declining mental status.
  • Bone marrow aspirate was consistent with acute nonlymphoblastic leukemia.
  • Review of the literature reveals ten reported cases of nonlymphoblastic leukemias following treatment with mitoxantrone.
  • Although de novo leukemia cannot be fully excluded, the likelihood of de novo disease is low given the patient's medical history.
  • Although leukemia is rarely seen, the potential for this outcome warrants careful consideration before initiating this therapy.
  • [MeSH-major] Analgesics / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Mitoxantrone / adverse effects. Multiple Sclerosis / drug therapy

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  • (PMID = 17939254.001).
  • [ISSN] 0026-6396
  • [Journal-full-title] Journal of the Mississippi State Medical Association
  • [ISO-abbreviation] J Miss State Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Analgesics; BZ114NVM5P / Mitoxantrone
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30. Szotkowski T, Rohon P, Zapletalova L, Sicova K, Hubacek J, Indrak K: Secondary acute myeloid leukemia - a single center experience. Neoplasma; 2010;57(2):170-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary acute myeloid leukemia - a single center experience.
  • Secondary acute myeloid leukemia (sAML) may arise from the previous clonal disorder of hematopoiesis, usually from myelodysplastic syndrome (MDS) or from chronic myeloproliferative neoplasia (cMPN) or after exposure to a leukemogenic agent (previous chemotherapy or radiotherapy, some immunosuppressive drugs or environmental leukemogenic agents).
  • Secondary origin of AML is associated with unfavorable prognosis and it is not considered to be conventionally curable (with the exception of secondary acute promyelocytic leukemia).
  • Over that period of time, a total 574 patients with AML were diagnosed.
  • Of those, 430 patients were diagnosed as having primary AML; in 86 patients, sAML transformed from myelodysplastic syndrome and 58 patients were followed or treated for various malignancies or were treated with potentially leukemogenic agents because of non-malignant disorders.
  • Patients with secondary AML are older and less commonly treated with curative intention than those with primary AML.
  • With the exception of secondary acute promyelocytic leukemia, the prognosis of which does not differ from very good prognosis of the primary forms, secondary AML is not considered a conventionally curable disease.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / complications. Myeloproliferative Disorders / complications. Neoplasm Recurrence, Local / etiology. Neoplasms, Second Primary / etiology


31. Mihailov G, Ganeva P, Vassileva N, Guenova M, Balacenko G, Toshkov S, Hodjadjik D: Secondary acute myeloid leukemia early after therapy for Hodgkin's disease--a case report. J BUON; 2007 Jul-Sep;12(3):403-6
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  • [Title] Secondary acute myeloid leukemia early after therapy for Hodgkin's disease--a case report.
  • A case of acute myeloid leukemia (AML) after successful therapy for Hodgkin's disease (HD) is reported.
  • Seven months after the CR was obtained the patient developed AML.
  • Knowing that the prognosis of patients with secondary AML (sAML) after primary HD is poor we decided to perform autologous peripheral stem cells' transplantation.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / surgery. Neoplasms, Second Primary / diagnosis. Neoplasms, Second Primary / surgery

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  • (PMID = 17918297.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
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32. Varet B, Ifrah N: [Criteria for suspecting a myelodysplastic syndrome]. Rev Prat; 2010 Dec 20;60(10):1404-7
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  • The myelodysplastic syndromes are a group of heterogeneous acquired and clonal disorders that are characterized by the intramedullar, abnormal death of myeloid progenitors leading to peripheral variable cytopenias.
  • It is predictive for the risk of transformation in secondary acute myeloid leukemia.

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  • (PMID = 21425539.001).
  • [ISSN] 0035-2640
  • [Journal-full-title] La Revue du praticien
  • [ISO-abbreviation] Rev Prat
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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33. Larson RA: Is secondary leukemia an independent poor prognostic factor in acute myeloid leukemia? Best Pract Res Clin Haematol; 2007 Mar;20(1):29-37
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is secondary leukemia an independent poor prognostic factor in acute myeloid leukemia?
  • Secondary leukemia is a poorly defined term that often refers to the development of acute myeloid leukemia (AML) following the history of a previous disease, such as a myelodysplastic syndrome or a chronic myeloproliferative disorder.
  • Secondary leukemia can also be a consequence of treatment with chemotherapy, including alkylating agents and topoisomerase II inhibitors, and/or radiotherapy, or due to exposure to environmental carcinogens.
  • Outcomes for this large and variable group of patients with secondary AML have been poor compared to people who develop AML de novo.
  • The question arises whether a diagnosis of secondary leukemia per se indicates a poor prognosis or whether their bad outcomes result from an association with certain morphologic and biologic characteristics.
  • Morphologic dysplasia in de novo AML is related to unfavorable cytogenetics, but has no independent prognostic relevance under the conditions of intensive chemotherapy.
  • While there is no significant correlation between cytogenetic risk groups and dysplasia, cytogenetic features do have an impact on outcome among both de novo and secondary AML patients.
  • In various subgroups of secondary AML, the spectrum of cytogenetic abnormalities is similar to de novo AML, but the frequency of abnormalities associated with unfavorable and intermediate risk cytogenetics, such as a complex karyotype, trisomy 8, monosomy 7, and others, is higher in secondary AML.
  • The survival of patients with therapy-related myeloid leukemia (t-AML) is generally shorter than for those with de novo AML within the same cytogenetic risk group.
  • Across the population of t-AML, however, survival varies according to cytogenetic risk group, with longer survival in patients with favorable-risk karyotypes.
  • The term secondary AML is too broad and imprecise to be of importance and should not be used.
  • These AML patients should be enrolled on front-line chemotherapy trials and should be stratified by pretreatment disease status and exposure history, if necessary.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Humans. Myelodysplastic Syndromes. Myeloproliferative Disorders. Neoplasms, Second Primary / drug therapy. Neoplasms, Second Primary / genetics. Prognosis. Survival Analysis

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  • (PMID = 17336252.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 23
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34. Borthakur G, Lin E, Jain N, Estey EE, Cortes JE, O'Brien S, Faderl S, Ravandi F, Pierce S, Kantarjian H: Survival is poorer in patients with secondary core-binding factor acute myelogenous leukemia compared with de novo core-binding factor leukemia. Cancer; 2009 Jul 15;115(14):3217-21
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  • [Title] Survival is poorer in patients with secondary core-binding factor acute myelogenous leukemia compared with de novo core-binding factor leukemia.
  • BACKGROUND: Therapy related secondary acute myelogenous leukemia (AML) was commonly associated with prior exposure to alkylating agents or topoisomerase inhibitor.
  • The long-term outcome of such patients with secondary AML was found to be worse than that of patients with de novo AML.
  • Earlier reports suggested similar outcomes for patients with de novo and secondary AML associated with core-binding factor (CBF) abnormalities.
  • METHODS: A total of 188 patients with CBF AML were analyzed.
  • The frequency of secondary CBF AML was 9%.
  • RESULTS: Patients with secondary CBF AML were found to have significantly worse overall (OS) and event-free survival (EFS) compared with patients with de novo CBF AML.
  • Secondary CBF AML status appeared to have only marginal significance in multivariate analysis.
  • CONCLUSIONS: Matched analysis (by age, Eastern Cooperative Oncology Group performance status, and additional cytogenetic abnormality) indicated worse OS and EFS in patients with secondary CBF AML.
  • [MeSH-major] Core Binding Factors / metabolism. Leukemia, Myeloid, Acute / mortality. Neoplasms, Second Primary / mortality

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  • [Cites] Leukemia. 1999 Nov;13(11):1735-40 [10557046.001]
  • [Cites] Leuk Lymphoma. 2008 Mar;49(3):517-23 [18297529.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Apr;33(4):395-400 [11921273.001]
  • [Cites] Br J Haematol. 2002 Aug;118(2):385-400 [12139722.001]
  • [Cites] Eur J Haematol. 2003 Sep;71(3):143-54 [12930314.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4413-22 [14645432.001]
  • [Cites] J Clin Oncol. 2004 Mar 15;22(6):1087-94 [15020610.001]
  • [Cites] J Clin Oncol. 2004 Sep 15;22(18):3741-50 [15289486.001]
  • [Cites] Blood. 1992 Oct 1;80(7):1825-31 [1391946.001]
  • [Cites] Science. 1993 Aug 20;261(5124):1041-4 [8351518.001]
  • [Cites] J Clin Oncol. 1993 Dec;11(12):2370-9 [8246025.001]
  • [Cites] J Clin Oncol. 1998 May;16(5):1890-6 [9586906.001]
  • [Cites] Cancer Res. 1998 Sep 15;58(18):4173-9 [9751631.001]
  • [Cites] Biochim Biophys Acta. 1998 Oct 1;1400(1-3):233-55 [9748598.001]
  • [Cites] Br J Haematol. 2006 Oct;135(2):165-73 [16939487.001]
  • [Cites] Leukemia. 2007 Apr;21(4):725-31 [17287858.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Apr;33(4):379-94 [11921272.001]
  • (PMID = 19441109.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factors; 04079A1RDZ / Cytarabine
  • [Other-IDs] NLM/ NIHMS629439; NLM/ PMC4184418
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35. Stifter G, Heiss S, Gastl G, Tzankov A, Stauder R: Over-expression of tumor necrosis factor-alpha in bone marrow biopsies from patients with myelodysplastic syndromes: relationship to anemia and prognosis. Eur J Haematol; 2005 Dec;75(6):485-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Enhanced bone marrow (BM) angiogenesis is regarded as an essential cofactor in the progression of MDS to acute myelogenous leukemia (AML) and microvessel formation may be induced by TNF-alpha as well.
  • METHODS: TNF-alpha expression and BM vessels were immunohistochemically analyzed on 89 paraffin-embedded BM biopsies from patients with MDS and secondary AML, including 12 control samples.
  • MVD was increased in MDS and secondary AML and correlated with marrow cellularity and expression of TNF-alpha, but was not of prognostic significance.
  • CONCLUSIONS: TNF-alpha expression and MVD are elevated in MDS and secondary AML.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Erythroid Precursor Cells / metabolism. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism. Tumor Necrosis Factor-alpha / biosynthesis


36. Chen YC, Sheen JM, Huang LT, Wu KS, Hsiao CC: Disseminated tuberculous myositis in a child with acute myelogenous leukemia. Pediatr Neonatol; 2009 Apr;50(2):74-7
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  • [Title] Disseminated tuberculous myositis in a child with acute myelogenous leukemia.
  • We present a case of disseminated tuberculous myositis in a girl with secondary acute myelogenous Leukemia following successful chemotherapy for undifferentiated sarcoma of the maxillary sinus.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Myositis / complications. Tuberculosis / complications


37. Bacher U, Haferlach T, Schoch C: Gain of 9p due to an unbalanced rearrangement der(9;18): a recurrent clonal abnormality in chronic myeloproliferative disorders. Cancer Genet Cytogenet; 2005 Jul 15;160(2):179-83
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  • Three cases were diagnosed as polycythemia vera; one case presented with secondary acute myeloid leukemia following idiopathic osteomyelofibrosis.

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  • (PMID = 15993276.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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38. Schoen C, Unzicker C, Stuhler G, Elias J, Einsele H, Grigoleit GU, Abele-Horn M, Mielke S: Life-threatening infection caused by daptomycin-resistant Corynebacterium jeikeium in a neutropenic patient. J Clin Microbiol; 2009 Jul;47(7):2328-31
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  • Here we report, for the first time, the isolation of a highly daptomycin-resistant strain of Corynebacterium jeikeium causing a life-threatening infection in a neutropenic patient undergoing cord blood transplantation for secondary acute myeloid leukemia.
  • [MeSH-minor] Cord Blood Stem Cell Transplantation / adverse effects. Humans. Leukemia, Myeloid, Acute / complications. Male. Microbial Sensitivity Tests. Middle Aged

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  • [Cites] Scand J Infect Dis. 2006;38(4):290-2 [16709529.001]
  • [Cites] J Clin Microbiol. 2006 Feb;44(2):655-6 [16455939.001]
  • [Cites] J Clin Microbiol. 2006 Nov;44(11):4009-13 [17005748.001]
  • [Cites] JAMA. 2007 Oct 17;298(15):1763-71 [17940231.001]
  • [Cites] J Antimicrob Chemother. 2008 Feb;61(2):461-2 [18156605.001]
  • [Cites] Antimicrob Agents Chemother. 2008 Mar;52(3):1167-70 [18180351.001]
  • [Cites] Lancet. 2002 May 25;359(9320):1819-27 [12044378.001]
  • [Cites] Microbiology. 2003 Jan;149(Pt 1):67-75 [12576581.001]
  • [Cites] Clin Microbiol Infect. 2003 Dec;9(12):1179-86 [14686982.001]
  • [Cites] J Antimicrob Chemother. 2004 Apr;53(4):669-74 [14985278.001]
  • [Cites] Antimicrob Agents Chemother. 2004 Jun;48(6):2149-52 [15155214.001]
  • [Cites] Antimicrob Agents Chemother. 1989 Oct;33(10):1783-90 [2556079.001]
  • [Cites] Clin Microbiol Rev. 1997 Jan;10(1):125-59 [8993861.001]
  • [Cites] Chemotherapy. 1998 Jul-Aug;44(4):230-7 [9681199.001]
  • [Cites] J Antimicrob Chemother. 2005 Mar;55(3):283-8 [15705644.001]
  • [Cites] J Bacteriol. 2005 Jul;187(13):4671-82 [15968079.001]
  • [Cites] Clin Infect Dis. 2005 Aug 15;41(4):565-6 [16028170.001]
  • [Cites] Curr Opin Microbiol. 2005 Oct;8(5):510-7 [16098786.001]
  • [Cites] Antimicrob Agents Chemother. 2006 Jun;50(6):2137-45 [16723576.001]
  • (PMID = 19420177.001).
  • [ISSN] 1098-660X
  • [Journal-full-title] Journal of clinical microbiology
  • [ISO-abbreviation] J. Clin. Microbiol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; NWQ5N31VKK / Daptomycin
  • [Other-IDs] NLM/ PMC2708472
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39. Monreal MB, Pardo ML, Pavlovsky MA, Fernandez I, Corrado CS, Giere I, Sapia S, Pavlovsky S: Increased immature hematopoietic progenitor cells CD34+/CD38dim in myelodysplasia. Cytometry B Clin Cytom; 2006 Mar;70(2):63-70
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  • METHODS: We analyzed the expression of CD38 and HLA-DR on CD34+ cells by flow cytometry in 36 patients with MDS, as well as in healthy donors (n = 12) and patients with other hematological disorders: non-Hodgkin lymphomas and multiple myeloma, both in complete remission (CR) (n = 32); acute lymphoblastic leukemia in CR (n = 17); de novo acute myeloblastic leukemia (AML) at diagnosis (n = 22) and in CR (n = 37); and AML secondary to MDS at diagnosis (n = 19).
  • RESULTS: Compared to normal BM, the fraction of immature HPC, characterized as CD34+bright, intermediate FSC/SSC, and CD38dim, was significantly increased in high risk MDS and secondary AML, but not in low risk MDS, (P < or = 0.001, P = 0.03, and P = 0.7).
  • De novo AML showed decreased immature HPC.
  • Increased immature HPC in high risk MDS and secondary AML may reflect blocked differentiation of CD34+ cells in these diseases.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation. Disease Progression. Female. Flow Cytometry. HLA-DR Antigens / immunology. Humans. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / immunology. Male. Middle Aged. Multiple Myeloma / diagnosis. Multiple Myeloma / immunology. Observer Variation. Phenotype. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Prognosis. Reproducibility of Results. Risk Factors

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  • [Copyright] Copyright 2005 International Society for Analytical Cytology.
  • (PMID = 16470534.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / HLA-DR Antigens; EC 3.2.2.5 / Antigens, CD38
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40. Sonneck K, Mannhalter C, Krauth MT, Sperr WR, Schwarzinger I, Fonatsch C, Haas O, Geissler K, Valent P: An unusual case of myelodysplastic syndrome with prolonged clonal stability, indolent clinical course over a decade, and spontaneous regression of AML in the terminal phase. Eur J Haematol; 2005 Jul;75(1):73-7
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  • [Title] An unusual case of myelodysplastic syndrome with prolonged clonal stability, indolent clinical course over a decade, and spontaneous regression of AML in the terminal phase.
  • An unusual case of secondary acute myeloid leukemia (AML) with indolent clinical course is described.
  • In 2001, transformation to secondary AML with an increase in bone marrow blasts (>20%) and thrombocytopenia, was found.
  • However, the bone marrow still showed AML with >20% blasts.
  • [MeSH-major] Leukemia, Myeloid, Acute / physiopathology. Myelodysplastic Syndromes / complications

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  • [Copyright] (c) Blackwell Munksgaard 2005.
  • (PMID = 15946315.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Receptors, Androgen
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41. Delhommeau F, Dupont S, Della Valle V, James C, Trannoy S, Massé A, Kosmider O, Le Couedic JP, Robert F, Alberdi A, Lécluse Y, Plo I, Dreyfus FJ, Marzac C, Casadevall N, Lacombe C, Romana SP, Dessen P, Soulier J, Viguié F, Fontenay M, Vainchenker W, Bernard OA: Mutation in TET2 in myeloid cancers. N Engl J Med; 2009 May 28;360(22):2289-301
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutation in TET2 in myeloid cancers.
  • BACKGROUND: The myelodysplastic syndromes and myeloproliferative disorders are associated with deregulated production of myeloid cells.
  • METHODS: We conducted a combination of molecular, cytogenetic, comparative-genomic-hybridization, and single-nucleotide-polymorphism analyses to identify a candidate tumor-suppressor gene common to patients with myelodysplastic syndromes, myeloproliferative disorders, and acute myeloid leukemia (AML).
  • RESULTS: We initially identified deletions or mutations in TET2 in three patients with myelodysplastic syndromes, in three of five patients with myeloproliferative disorders, in two patients with primary AML, and in one patient with secondary AML.
  • We selected the six patients with myelodysplastic syndromes or AML because they carried acquired rearrangements on chromosome 4q24; we selected the five patients with myeloproliferative disorders because they carried a dominant clone in hematopoietic progenitor cells that was positive for the V617F mutation in the Janus kinase 2 (JAK2) gene.
  • TET2 defects were observed in 15 of 81 patients with myelodysplastic syndromes (19%), in 24 of 198 patients with myeloproliferative disorders (12%) (with or without the JAK2 V617F mutation), in 5 of 21 patients with secondary AML (24%), and in 2 of 9 patients with chronic myelomonocytic leukemia (22%).
  • CONCLUSIONS: Somatic mutations in TET2 occur in about 15% of patients with various myeloid cancers.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics. Proto-Oncogene Proteins / genetics


42. Barresi V, Palumbo GA, Musso N, Consoli C, Capizzi C, Meli CR, Romano A, Di Raimondo F, Condorelli DF: Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML. Leuk Res; 2010 Nov;34(11):1539-42
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  • [Title] Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML.
  • By conventional metaphase and SNP array cytogenetics we serially studied a patient affected by high-risk myelodysplastic syndrome (MDS), documenting the conversion from partial trisomy 8q to trisomy 8 and partial tetrasomy 8q during progression to acute myeloid leukemia (AML).
  • Moreover, the serial application of high resolution genomic array analysis at different disease stages allowed the description of cryptic abnormalities and the demonstration of their enrichment in the AML phase.
  • In particular the detection and quantification of a copy-neutral loss of heterozygosity region located in chromosome 11q guided the search for point mutations in the CBL gene, thus allowing the escription of the novel missense mutation K382E and the demonstration of its selection during progression to secondary AML.
  • [MeSH-major] Chromosomes, Human, Pair 11. Leukemia, Myeloid, Acute / genetics. Loss of Heterozygosity. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins c-cbl / genetics

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20674974.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
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43. Park MJ, Park YH, Ahn HJ, Choi W, Paik KH, Kim JM, Chang YH, Ryoo BY, Yang SH: Secondary hematological malignancies after breast cancer chemotherapy. Leuk Lymphoma; 2005 Aug;46(8):1183-8
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  • [Title] Secondary hematological malignancies after breast cancer chemotherapy.
  • According to several reports, the 10 year incidence of secondary acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS) after systemic chemotherapy is approximately 1.5%.
  • We detected 2 cases of secondary AML and 1 case of MDS, 19, 52 and 12 months, respectively, after systemic chemotherapy for breast cancer.
  • Published data on the occurrence of secondary hematological malignancies other than AML or MDS in this setting are scarce.
  • We encountered diffuse large B-cell lymphoma, angioimmunoblastic lymphoma and mantle cell lymphoma as secondary hematological malignancies after systemic chemotherapy for breast cancer.


44. Karp JE, Smith BD, Gojo I, Lancet JE, Greer J, Klein M, Morris L, Levis MJ, Gore SD, Wright JJ, Garrett-Mayer E: Phase II trial of tipifarnib as maintenance therapy in first complete remission in adults with acute myelogenous leukemia and poor-risk features. Clin Cancer Res; 2008 May 15;14(10):3077-82
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  • [Title] Phase II trial of tipifarnib as maintenance therapy in first complete remission in adults with acute myelogenous leukemia and poor-risk features.
  • PURPOSE: Acute myelogenous leukemia (AML) does not have a high cure rate, particularly in patients with poor-risk features.
  • Tipifarnib is an oral farnesyltransferase inhibitor with activity in AML.
  • We conducted a phase II trial of maintenance tipifarnib monotherapy for 48 adults with poor-risk AML in first CR.
  • Comparison of CR durations for 25 patients who received two-cycle timed sequential therapy followed by tipifarnib maintenance with 23 historically similar patients who did not receive tipifarnib showed that tipifarnib was associated with DFS prolongation for patients with secondary AML and adverse cytogenetics.
  • CONCLUSIONS: This study suggests that some patients with poor-risk AML, including patients with secondary AML and adverse cytogenetics, may benefit from tipifarnib maintenance therapy.

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  • [Cites] J Clin Oncol. 1999 Dec;17(12):3835-49 [10577857.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1964-70 [17581608.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3361-9 [11369625.001]
  • [Cites] Blood. 2001 Aug 1;98(3):548-53 [11468148.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1302-11 [11520775.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1312-20 [11520776.001]
  • [Cites] Leuk Res. 2003 Apr;27(4):313-21 [12531222.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1692-7 [12411300.001]
  • [Cites] Am J Clin Pathol. 2003 May;119(5):672-80 [12760285.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3880-9 [12920034.001]
  • [Cites] Blood. 2003 Dec 15;102(13):4527-34 [12947010.001]
  • [Cites] Blood Rev. 2004 Mar;18(1):39-63 [14684148.001]
  • [Cites] J Clin Oncol. 2004 Apr 1;22(7):1287-92 [15051776.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1605-16 [15084693.001]
  • [Cites] Blood. 1989 Oct;74(5):1499-506 [2676014.001]
  • [Cites] Blood. 1992 Apr 15;79(8):1924-30 [1562720.001]
  • [Cites] Blood. 1997 Oct 15;90(8):2952-61 [9376575.001]
  • [Cites] J Clin Oncol. 1998 Mar;16(3):872-81 [9508168.001]
  • [Cites] Leukemia. 1999 Jun;13(6):843-9 [10360370.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1969-78 [15632409.001]
  • [Cites] Eur J Haematol. 2005 May;74(5):418-23 [15813916.001]
  • [Cites] J Clin Oncol. 2006 Jun 1;24(16):2480-9 [16735702.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1677-83 [16670265.001]
  • [Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1387-94 [17082323.001]
  • [Cites] Blood. 2007 May 15;109(10):4158-63 [17264294.001]
  • [Cites] J Clin Oncol. 2007 May 10;25(14):1908-15 [17488990.001]
  • [Cites] Hematol Oncol Clin North Am. 2000 Feb;14(1):251-67 [10680081.001]
  • (PMID = 18483374.001).
  • [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 / CA 69854; United States / NCI NIH HHS / CA / U01 CA069854-07; United States / NCI NIH HHS / CA / U01 CA069854; United States / NCI NIH HHS / CA / U01 CA70095; United States / NCI NIH HHS / CA / U01 CA070095
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinolones; 192185-72-1 / tipifarnib
  • [Other-IDs] NLM/ NIHMS281726; NLM/ PMC3074480
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45. D'Andrea AD: Targeting DNA repair pathways in AML. Best Pract Res Clin Haematol; 2010 Dec;23(4):469-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting DNA repair pathways in AML.
  • DNA repair inhibitors, such as poly-ADP-ribose polymerase (PARP) inhibitors, may be useful in a small subset of acute myeloid leukemia (AML) patients, especially those who have complex karyotypes or those with secondary AML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. DNA Repair / drug effects. Enzyme Inhibitors / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21130409.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Enzyme Inhibitors; 0 / Poly(ADP-ribose) Polymerase Inhibitors; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
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46. Preiss BS, Bergmann OJ, Friis LS, Sørensen AG, Frederiksen M, Gadeberg OV, Mourits-Andersen T, Oestergaard B, Kerndrup GB, AML Study Group of Southern Denmark: Cytogenetic findings in adult secondary acute myeloid leukemia (AML): frequency of favorable and adverse chromosomal aberrations do not differ from adult de novo AML. Cancer Genet Cytogenet; 2010 Oct 15;202(2):108-22
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  • [Title] Cytogenetic findings in adult secondary acute myeloid leukemia (AML): frequency of favorable and adverse chromosomal aberrations do not differ from adult de novo AML.
  • During a 15-year period, 161 adult patients were diagnosed with secondary acute myeloid leukemia (s-AML) in the region of Southern Denmark.
  • In 73 patients, the AML diagnosis was preceded by myelodysplastic syndrome (MDS-AML), in 31 patients by an antecedent hematologic disease, and in 57 patients by treatment with chemotherapy and/or irradiation (t-AML).
  • MDS-AML correlated to a normal karyotype (P < 0.001).
  • t-AML correlated to abnormal clones with numerical and structural aberrations (P = 0.03), five or more unrelated aberrations (P = 0.03), marker chromosomes (P = 0.006), abnormal mitoses only (P = 0.01), female sex (P < 0.001), and -7 (P = 0.006).
  • The frequencies of aberrations in s-AML patients were compared with an age-matched group of de novo AML patients diagnosed in the same area and period.
  • In this comparison, s-AML only correlated to -7 (P = 0.02).
  • In 42 patients, we found that MDS patients with an abnormal karyotype were more likely to show cytogenetic evolution during progression to AML than MDS patients with a normal karyotype (P = 0.01).
  • We conclude that population-based cytogenetic studies of adult s-AML and age- and sex-matched de novo AML show comparable distributions of chromosome abnormalities.
  • [MeSH-major] Chromosome Aberrations. Cytogenetic Analysis. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics


47. Then Bergh F, Niklas A, Strauss A, von Ahsen N, Niederwieser D, Schwarz J, Wagner A, Al-Ali HK: Rapid progression of Myelodysplastic syndrome to acute myeloid leukemia on sequential azathioprine, IFN-beta and copolymer-1 in a patient with multiple sclerosis. Acta Haematol; 2006;116(3):207-10
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  • [Title] Rapid progression of Myelodysplastic syndrome to acute myeloid leukemia on sequential azathioprine, IFN-beta and copolymer-1 in a patient with multiple sclerosis.
  • Within several months, unusually rapid for this subtype, MDS progressed to secondary acute myeloid leukemia.
  • [MeSH-major] Azathioprine / adverse effects. Interferon-beta / adverse effects. Leukemia, Myeloid / chemically induced. Multiple Sclerosis / complications. Multiple Sclerosis / drug therapy. Myelodysplastic Syndromes / complications. Peptides / adverse effects
  • [MeSH-minor] Acute Disease. Disease Progression. Fatal Outcome. Female. Glatiramer Acetate. Humans. Middle Aged


48. Tam CS, Seymour JF, Prince HM, Kenealy M, Wolf M, Januszewicz EH, Westerman D: Treatment-related myelodysplasia following fludarabine combination chemotherapy. Haematologica; 2006 Nov;91(11):1546-50
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  • Although myelodysplasia (MDS) and secondary acute myeloid leukemia (sAML) are rare following fludarabine monotherapy, the risk of these diseases may potentially be increased when fludarabine is combined with cyclophosphamide or mitoxantrone due to synergistic effects on the inhibition of DNA repair.

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  • (PMID = 17082012.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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49. Nakai K, Kanda Y, Fukuhara S, Sakamaki H, Okamoto S, Kodera Y, Tanosaki R, Takahashi S, Matsushima T, Atsuta Y, Hamajima N, Kasai M, Kato S: Value of chemotherapy before allogeneic hematopoietic stem cell transplantation from an HLA-identical sibling donor for myelodysplastic syndrome. Leukemia; 2005 Mar;19(3):396-401
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  • The cumulative incidence of grade II-IV acute GVHD was 33%.
  • OS at 5 years was 57% for patients who underwent allo-SCT as a primary treatment for refractory anemia with excess blasts in transformation (RAEB-t) or secondary acute myeloid leukemia (AML) and 54% for those who underwent allo-SCT in remission after induction chemotherapy (P=0.81).
  • Although only a randomized controlled trial will be able to establish a definite conclusion, these results do not support the administration of induction chemotherapy for patients with RAEB-t or secondary AML before allo-SCT.


50. Hussein K, Bock O, Theophile K, Schulz-Bischof K, Porwit A, Schlue J, Jonigk D, Kreipe H: MPLW515L mutation in acute megakaryoblastic leukaemia. Leukemia; 2009 May;23(5):852-5
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  • [Title] MPLW515L mutation in acute megakaryoblastic leukaemia.
  • A series of primary and secondary acute myeloid leukaemias (AML) with megakaryoblastic phenotype and myelofibrosis unrelated to PMF (n=12) was analysed for the MPL(W515K/L) mutation by pyrosequencing.
  • None of the secondary AML cases evolving from pre-existing PMF showed MPL(W515K/L) (n=4).
  • We conclude that MPL(W515L) occurs in a considerable proportion of acute megakaryoblastic leukaemias with myelofibrosis unrelated to PMF.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mutation / genetics. Primary Myelofibrosis / genetics. Receptors, Thrombopoietin / genetics

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  • [CommentIn] Leukemia. 2009 Nov;23(11):2159-60 [19657363.001]
  • (PMID = 19194467.001).
  • [ISSN] 1476-5551
  • [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 / Receptors, Thrombopoietin; 143641-95-6 / MPL protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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51. Récher C, Beyne-Rauzy O, Demur C, Chicanne G, Dos Santos C, Mas VM, Benzaquen D, Laurent G, Huguet F, Payrastre B: Antileukemic activity of rapamycin in acute myeloid leukemia. Blood; 2005 Mar 15;105(6):2527-34
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  • [Title] Antileukemic activity of rapamycin in acute myeloid leukemia.
  • In this study, we show that mTOR inhibition by rapamycin strongly inhibits the growth of the most immature acute myeloid leukemia (AML) cell lines through blockade in G0/G1 phase of the cell cycle.
  • Accordingly, 2 downstream effectors of mTOR, 4E-BP1 and p70S6K, are phosphorylated in a rapamycin-sensitive manner in a series of 23 AML cases.
  • Interestingly, the mTOR inhibitor markedly impairs the clonogenic properties of fresh AML cells while sparing normal hematopoietic progenitors.
  • Moreover, rapamycin induces significant clinical responses in 4 of 9 patients with either refractory/relapsed de novo AML or secondary AML.
  • Overall, our data strongly suggest that mTOR is aberrantly regulated in most AML cells and that rapamycin and analogs, by targeting the clonogenic compartment of the leukemic clone, may be used as new compounds in AML therapy.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. G0 Phase / drug effects. G1 Phase / drug effects. Leukemia, Myeloid, Acute / metabolism. Protein Kinases / metabolism. Sirolimus / pharmacology

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  • (PMID = 15550488.001).
  • [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] 0 / Adaptor Proteins, Signal Transducing; 0 / Antibiotics, Antineoplastic; 0 / EIF4EBP1 protein, human; 0 / Phosphoproteins; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
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52. Eguchi M, Eguchi-Ishimae M, Knight D, Kearney L, Slany R, Greaves M: MLL chimeric protein activation renders cells vulnerable to chromosomal damage: an explanation for the very short latency of infant leukemia. Genes Chromosomes Cancer; 2006 Aug;45(8):754-60
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  • [Title] MLL chimeric protein activation renders cells vulnerable to chromosomal damage: an explanation for the very short latency of infant leukemia.
  • MLL fusion genes are a predominant feature of acute leukemias in infants and in secondary acute myeloid leukemia (AML) associated with prior chemotherapy with topo-II poisons.
  • [MeSH-major] Chromosome Aberrations. DNA Damage. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. Oncogene Proteins, Fusion / metabolism

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  • (PMID = 16688745.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Antagonists; 0 / MLL-ENL oncoprotein, human; 0 / Oncogene Proteins, Fusion; 094ZI81Y45 / Tamoxifen; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 17197F0KYM / afimoxifene
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53. Seedhouse CH, Grundy M, White P, Li Y, Fisher J, Yakunina D, Moorman AV, Hoy T, Russell N, Burnett A, Pallis M, National Cancer Research Network: Sequential influences of leukemia-specific and genetic factors on p-glycoprotein expression in blasts from 817 patients entered into the National Cancer Research Network acute myeloid leukemia 14 and 15 trials. Clin Cancer Res; 2007 Dec 1;13(23):7059-66
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  • [Title] Sequential influences of leukemia-specific and genetic factors on p-glycoprotein expression in blasts from 817 patients entered into the National Cancer Research Network acute myeloid leukemia 14 and 15 trials.
  • PURPOSE: P-glycoprotein (Pgp) is a major prognostic factor for chemotherapy failure in acute myeloid leukemia (AML).
  • This study compared the influence of genetic and leukemia-specific factors on Pgp.
  • RESULTS: Age, low WBC count, high bcl-2, secondary AML and myelodysplastic syndrome, and adverse cytogenetics all correlated strongly with high Pgp (MRK16) protein expression.
  • Moreover, leukemia-specific factors, such as low WBC count and poor risk cytogenetics, have a much greater effect than genetic polymorphisms on Pgp expression in AML blasts.
  • [MeSH-major] Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. P-Glycoprotein / biosynthesis

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  • (PMID = 18056183.001).
  • [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, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / Proto-Oncogene Proteins c-bcl-2
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54. Natelson EA: Benzene-induced acute myeloid leukemia: a clinician's perspective. Am J Hematol; 2007 Sep;82(9):826-30
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  • [Title] Benzene-induced acute myeloid leukemia: a clinician's perspective.
  • Benzene-induced acute myeloid leukemia (AML) is considered a secondary form of AML, based both in theory and on limited cohort observations.
  • Its latency, cytogenetic aberrations, and clinical features are thought similar to, or identical with, AML resulting from the use of modern day cytotoxic agents for chemotherapy and immunotherapy.
  • Although distinction between secondary AML and the far more common de novo AML is difficult to establish with certainty in any given case, latency from toxic therapeutic and environmental exposure and certain clinical and pathological features generally separate these two entities.
  • AML is the only human neoplasm proven to be potentially caused by benzene, which actually is an obsolete form of chemotherapy.
  • A review of benzene-induced AML suggests that, in developed countries, this entity should no longer merit serious consideration among workers in the modern petrochemical industry and related fields.
  • [MeSH-major] Attitude of Health Personnel. Benzene / adverse effects. Developed Countries. Drug-Related Side Effects and Adverse Reactions. Leukemia, Myeloid / etiology
  • [MeSH-minor] Acute Disease. Chromosome Aberrations / chemically induced. Chromosome Inversion. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Humans. Occupational Diseases / chemically induced. Occupational Diseases / epidemiology. Occupational Exposure / adverse effects. Occupational Exposure / analysis. Petroleum / adverse effects. Translocation, Genetic

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  • [Copyright] 2007 Wiley-Liss, Inc
  • (PMID = 17506065.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Petroleum; J64922108F / Benzene
  • [Number-of-references] 79
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55. Klepin HD, Balducci L: Acute myelogenous leukemia in older adults. Oncologist; 2009 Mar;14(3):222-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myelogenous leukemia in older adults.
  • The incidence of acute myelogenous leukemia (AML) increases with age.
  • Older AML patients, generally defined by age > or = 60 years, have worse treatment outcomes than younger patients.
  • Older patients are more likely to present with unfavorable cytogenetic abnormalities, multidrug resistance phenotypes, and secondary AML.
  • Investigations of hypomethylating agents and signal transduction inhibitors hold promise for the treatment of AML patients.
  • [MeSH-major] Geriatrics / methods. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 19282349.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 72
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56. Brakensiek K, Länger F, Schlegelberger B, Kreipe H, Lehmann U: Hypermethylation of the suppressor of cytokine signalling-1 (SOCS-1) in myelodysplastic syndrome. Br J Haematol; 2005 Jul;130(2):209-17
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  • In contrast to acute myeloid leukaemia (AML), comparably little is known about aberrant methylation in myelodysplastic syndrome (MDS), a heterogeneous clonal stem cell disorder with a risk of transformation into secondary AML of up to 30%.
  • Demethylation experiments provided direct evidence that aberrant methylation of SOCS-1 induces transcriptional silencing in myeloid cells.
  • [MeSH-minor] Acute Disease. Cell Differentiation. DNA Methylation. Down-Regulation. Granulocytes / metabolism. Humans. Leukemia, Myeloid / genetics. Leukemia, Myeloid / metabolism. Neoplasm Proteins / metabolism. Polymerase Chain Reaction / methods. Protein-Tyrosine Kinases / metabolism. Signal Transduction. Suppressor of Cytokine Signaling Proteins. Tumor Cells, Cultured

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  • (PMID = 16029449.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Neoplasm Proteins; 0 / Repressor Proteins; 0 / SOCS1 protein, human; 0 / Suppressor of Cytokine Signaling Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases
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57. Dale DC: Advances in the treatment of neutropenia. Curr Opin Support Palliat Care; 2009 Sep;3(3):207-12
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  • Current guidelines recommend the prophylactic use of the myeloid growth factors for the first cycle of chemotherapy for patients with more than a 20% risk of febrile neutropenia.
  • Meta analysis from randomized trials shows that granulocyte colony-stimulating factor prophylaxis is associated with patients receiving more intensive chemotherapy, having better survival, but also having a higher risk of secondary acute myeloid leukemia.
  • SUMMARY: The myeloid growth factor granulocyte colony-stimulating factor has radically changed our approach to the prevention of febrile neutropenia.

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  • [Cites] Crit Rev Oncol Hematol. 2008 Jun;66(3):237-47 [18243010.001]
  • [Cites] Niger J Med. 2008 Jan-Mar;17(1):57-60 [18390135.001]
  • [Cites] Ann Oncol. 2008 May;19 Suppl 2:ii116-8 [18456747.001]
  • [Cites] J Support Oncol. 2008 May-Jun;6(5):199-208 [18551855.001]
  • [Cites] Infection. 2008 Jun;36(3):250-5 [18458815.001]
  • [Cites] Am J Med. 2008 Aug;121(8):709-14 [18691485.001]
  • [Cites] Scand J Infect Dis. 2008;40(4):301-7 [17918015.001]
  • [Cites] Drugs. 2008;68(14):1941-62 [18778118.001]
  • [Cites] Clin Infect Dis. 2008 Nov 1;47(9):1176-84 [18808352.001]
  • [Cites] J Clin Pharm Ther. 2008 Oct;33(5):459-64 [18834359.001]
  • [Cites] Eur J Clin Microbiol Infect Dis. 2008 Oct;27(10):969-76 [18449581.001]
  • [Cites] Cochrane Database Syst Rev. 2008;(4):CD003189 [18843642.001]
  • [Cites] Am J Clin Oncol. 2008 Aug;31(4):369-74 [18845996.001]
  • [Cites] Pediatr Blood Cancer. 2008 Dec;51(6):778-83 [18726920.001]
  • [Cites] Br J Haematol. 2008 Oct;143(2):222-9 [18713253.001]
  • [Cites] Int J Antimicrob Agents. 2008 Nov;32 Suppl 2:S119-23 [19013335.001]
  • [Cites] Blood. 2008 Dec 1;112(12):4445-51 [18799726.001]
  • [Cites] Bone Marrow Transplant. 2008 Nov;42(10):679-84 [18695660.001]
  • [Cites] Lancet Oncol. 2008 Dec;9(12):1157-65 [19038762.001]
  • [Cites] Curr Opin Hematol. 2009 Jan;16(1):1-2 [19057197.001]
  • [Cites] N Engl J Med. 2009 Jan 1;360(1):3-5 [19118300.001]
  • [Cites] J Natl Compr Canc Netw. 2009 Jan;7(1):92-8 [19176209.001]
  • [Cites] J Natl Compr Canc Netw. 2009 Jan;7(1):99-108 [19176210.001]
  • [Cites] Br J Haematol. 2009 Feb;144(4):459-67 [19120359.001]
  • [Cites] Br J Haematol. 2009 Mar;144(5):677-85 [19055662.001]
  • [Cites] Support Care Cancer. 2009 Jun;17(6):735-44 [19096882.001]
  • [Cites] Am J Hematol. 2009 Jul;84(7):414-7 [19415727.001]
  • [Cites] Value Health. 2009 Mar-Apr;12(2):217-25 [18673353.001]
  • [Cites] Blood. 1996 Jul 1;88(1):335-40 [8704192.001]
  • [Cites] Am J Hematol. 1998 Jan;57(1):7-15 [9423810.001]
  • [Cites] J Clin Oncol. 2006 Jul 1;24(19):3187-205 [16682719.001]
  • [Cites] J Natl Compr Canc Netw. 2007 Feb;5(2):188-202 [17335688.001]
  • [Cites] Pharmacoeconomics. 2007;25(4):343-51 [17402806.001]
  • [Cites] Ann Intern Med. 2007 May 1;146(9):657-65 [17470834.001]
  • [Cites] Curr Opin Hematol. 2008 Jan;15(1):15-21 [18043241.001]
  • [Cites] Support Care Cancer. 2008 Jan;16(1):47-56 [17619911.001]
  • [Cites] Vox Sang. 2007 Nov;93(4):363-9 [18070282.001]
  • [Cites] Ann Hematol. 2008 Feb;87(2):139-45 [17938926.001]
  • [Cites] Br J Haematol. 2008 Jan;140(2):210-3 [18028488.001]
  • [Cites] Eur J Cancer Care (Engl). 2008 Jan;17(1):19-25 [18181887.001]
  • [Cites] J Clin Oncol. 2008 Jan 10;26(2):290-6 [18182670.001]
  • [Cites] Support Care Cancer. 2008 Feb;16(2):181-91 [17943327.001]
  • [Cites] J Natl Compr Canc Netw. 2008 Feb;6(2):109-18 [18319047.001]
  • [Cites] Value Health. 2008 Mar-Apr;11(2):172-9 [18380630.001]
  • [Cites] Eur J Oncol Nurs. 2008 Feb;12(1):14-25 [18291720.001]
  • (PMID = 19550332.001).
  • [ISSN] 1751-4266
  • [Journal-full-title] Current opinion in supportive and palliative care
  • [ISO-abbreviation] Curr Opin Support Palliat Care
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R24 AI049393; United States / NIAID NIH HHS / AI / R24 AI049393-09
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor
  • [Number-of-references] 48
  • [Other-IDs] NLM/ NIHMS202938; NLM/ PMC3390973
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58. Grudeva-Popova J, Yaneva M, Zisov K, Ananoshtev N: Therapy-related acute promyelocytic leukemia after treatment with radioiodine for thyroid cancer: case report with literature review. J BUON; 2007 Jan-Mar;12(1):129-32
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  • [Title] Therapy-related acute promyelocytic leukemia after treatment with radioiodine for thyroid cancer: case report with literature review.
  • Therapy-related acute promyelocytic leukemia (t-APL) is a rare but known complication of chemotherapy and/or radiation therapy.
  • The patient's excellent response to treatment supports the data of the relevant literature that t-APL is associated with a better therapeutic result than the other subtypes of secondary acute myeloid leukemia (AML).
  • [MeSH-major] Iodine Radioisotopes / adverse effects. Leukemia, Promyelocytic, Acute / etiology. Neoplasms, Radiation-Induced / etiology. Thyroid Neoplasms / radiotherapy

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  • (PMID = 17436415.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Iodine Radioisotopes
  • [Number-of-references] 19
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59. Qian SX, Li JY, Tian T, Shen YF, Jiang YQ, Lu H, Wu HX, Zhang SJ, Xu W: Effect of low-dose cytarabine and aclarubicin in combination with granulocyte colony-stimulating factor priming (CAG regimen) on the outcome of elderly patients with acute myeloid leukemia. Leuk Res; 2007 Oct;31(10):1383-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of low-dose cytarabine and aclarubicin in combination with granulocyte colony-stimulating factor priming (CAG regimen) on the outcome of elderly patients with acute myeloid leukemia.
  • The aim of this study was to evaluate the efficacy and toxicity of low-dose cytarabine and aclarubicin in combination with granulocyte colony-stimulating factor (G-CSF) protocol in elderly patients with acute myeloid leukemia (AML).
  • The overall response rate was 72.0%, and 29 of 50 (58.0%) patients achieved complete remission, including 23 of 35 (65.8%) with previously untreated AML, 6 of 15 (40.0%) with refractory, relapsed or secondary AML, 4 of 8 (50.0%) aged over 70 years, 4 of 10 (40.0%) with unfavorable cytogenetic aberrations.
  • Thus CAG priming regimen as the induction therapy is well tolerated and effective in elderly patients with AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Aclarubicin / therapeutic use. Acute Disease. Aged. Aged, 80 and over. Cytarabine / therapeutic use. Female. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Treatment Outcome

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  • (PMID = 17420048.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 74KXF8I502 / Aclarubicin; CAG protocol
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60. Rubio S, Martins C, Lacerda JF, Carmo JA, Lourenço F, Lacerda JM: Allogeneic stem cell transplantation in patients with myelodysplastic syndrome: outcome analysis according to the International Prognostic Scoring System. Acta Med Port; 2006 Sep-Oct;19(5):343-7
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  • We determined the outcome of patients with myelodysplastic syndrome (MDS) and secondary acute myeloid leukemia (sAML) after allogeneic stem cell transplantation according to their international prognostic scoring system (IPSS) risk categories at diagnosis.
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Female. Humans. Leukemia, Myeloid / surgery. Male. Middle Aged. Prognosis. Recurrence. Risk Assessment. Treatment Outcome


61. Kornblau SM, Minden MD, Rosen DB, Putta S, Cohen A, Covey T, Spellmeyer DC, Fantl WJ, Gayko U, Cesano A: Dynamic single-cell network profiles in acute myelogenous leukemia are associated with patient response to standard induction therapy. Clin Cancer Res; 2010 Jul 15;16(14):3721-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dynamic single-cell network profiles in acute myelogenous leukemia are associated with patient response to standard induction therapy.
  • PURPOSE: Complete response to induction chemotherapy is observed in approximately 60% of patients with newly diagnosed non-M3 acute myelogenous leukemia (AML).
  • However, no methods exist to predict with high accuracy at the individual patient level the response to standard AML induction therapy.
  • EXPERIMENTAL DESIGN: We applied single-cell network profiling (SCNP) using flow cytometry, a tool that allows a comprehensive functional assessment of intracellular signaling pathways in heterogeneous tissues, to two training cohorts of AML samples (n = 34 and 88) to predict the likelihood of response to induction chemotherapy.
  • Results were independent of cytogenetics, FLT3 mutational status, and diagnosis of secondary AML.
  • SCNP provides information distinct from other known prognostic factors such as age, secondary AML, cytogenetics, and molecular alterations and is potentially combinable with the latter to improve clinical decision making.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism

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  • [Copyright] Copyright 2010 AACR.
  • [Cites] Blood. 1998 Feb 15;91(4):1101-34 [9454740.001]
  • [Cites] J Clin Oncol. 2010 Feb 1;28(4):596-604 [20026798.001]
  • [Cites] Cancer Res. 1998 Sep 15;58(18):4173-9 [9751631.001]
  • [Cites] Cytokines Cell Mol Ther. 1998 Sep;4(3):187-98 [9825844.001]
  • [Cites] N Engl J Med. 1999 Sep 30;341(14):1051-62 [10502596.001]
  • [Cites] Crit Care. 2004 Dec;8(6):508-12 [15566624.001]
  • [Cites] Curr Opin Hematol. 2005 Jan;12(1):68-75 [15604894.001]
  • [Cites] Science. 2005 Apr 22;308(5721):523-9 [15845847.001]
  • [Cites] Crit Rev Oncol Hematol. 2005 Nov;56(2):195-221 [16236521.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3733-9 [16076867.001]
  • [Cites] Nat Rev Cancer. 2006 Feb;6(2):146-55 [16491074.001]
  • [Cites] Blood. 2006 May 1;107(9):3481-5 [16455952.001]
  • [Cites] Nat Methods. 2006 May;3(5):361-8 [16628206.001]
  • [Cites] Leukemia. 2006 Jun;20(6):965-70 [16598313.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2358-65 [16763210.001]
  • [Cites] Br J Haematol. 2006 Nov;135(4):438-49 [16965385.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3898-905 [16912223.001]
  • [Cites] Front Biosci. 2007;12:800-15 [17127321.001]
  • [Cites] Crit Rev Oncol Hematol. 2007 Jun;62(3):214-26 [17368038.001]
  • [Cites] J Clin Oncol. 2007 Aug 1;25(22):3337-43 [17577018.001]
  • [Cites] Blood. 2008 Feb 15;111(4):1903-12 [18042804.001]
  • [Cites] Leuk Res. 2008 Jun;32(6):913-8 [17928050.001]
  • [Cites] Leuk Res. 2008 Jun;32(6):944-53 [18206229.001]
  • [Cites] Blood. 2008 May 1;111(9):4490-5 [18309032.001]
  • [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] J Immunol. 2008 Jun 1;180(11):7358-67 [18490735.001]
  • [Cites] Blood. 2008 Jun 1;111(11):5371-9 [18378853.001]
  • [Cites] Front Biosci. 2008;13:4605-16 [18508532.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4595-602 [18559874.001]
  • [Cites] J Clin Oncol. 2008 Nov 20;26(33):5429-35 [18591546.001]
  • [Cites] Blood. 2009 Jan 1;113(1):28-36 [18827183.001]
  • [Cites] Blood. 2009 Jan 1;113(1):154-64 [18840713.001]
  • [Cites] Blood. 2009 Mar 26;113(13):3088-91 [19171880.001]
  • [Cites] Br J Haematol. 2009 Jun;145(5):555-68 [19344393.001]
  • [Cites] J Clin Oncol. 2009 Jul 1;27(19):3198-204 [19451432.001]
  • [Cites] Hematology. 2009 Aug;14(4):204-12 [19635183.001]
  • [Cites] Cancer Res. 2001 Oct 1;61(19):7233-9 [11585760.001]
  • [Cites] Nat Immunol. 2002 Dec;3(12):1129-34 [12447370.001]
  • [Cites] Semin Hematol. 2002 Oct;39(4 Suppl 3):6-11 [12447846.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Blood. 2003 Feb 1;101(3):837-45 [12393383.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1613-8 [12750167.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4642-9 [14673054.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]
  • [Cites] Cell. 2004 Jul 23;118(2):217-28 [15260991.001]
  • [Cites] Radiology. 1982 Apr;143(1):29-36 [7063747.001]
  • [Cites] Radiology. 1983 Sep;148(3):839-43 [6878708.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • (PMID = 20525753.001).
  • [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 / P01 CA108631
  • [Publication-type] Journal Article
  • [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
  • [Other-IDs] NLM/ NIHMS378349; NLM/ PMC3385931
  •  go-up   go-down


62. Bielorai B, Meyer C, Trakhtenbrot L, Golan H, Rozner E, Amariglio N, Izraeli S, Marschalek R, Toren A: Therapy-related acute myeloid leukemia with t(2;11)(q37;q23) after treatment for osteosarcoma. Cancer Genet Cytogenet; 2010 Dec;203(2):288-91
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  • [Title] Therapy-related acute myeloid leukemia with t(2;11)(q37;q23) after treatment for osteosarcoma.
  • As the number of pediatric cancer survivors increases, there is a concern about the development of secondary malignant neoplasms.
  • Secondary acute myeloid leukemia (AML) has been rarely reported after treatment for OS.
  • We describe a 14-year-old boy with OS of the left ileum who developed secondary AML 15 months after completion of treatment.
  • Only the addition of the long-distance inverse polymerase chain reaction technique identified the SEPT2 as the MLL fusion partner resulting in t(2;11)(q37;q23) that was reported in a very few secondary AML cases.
  • Because long-distance inverse polymerase chain reaction is not available in most molecular laboratories, the true incidence of t(2;11)(q37;q23) and the involvement of SEPT2 as the MLL translocation partner could be more prevalent in secondary AML.
  • [MeSH-major] Bone Neoplasms / drug therapy. Bone Neoplasms / genetics. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 2. Leukemia, Myeloid, Acute / genetics. Osteosarcoma / drug therapy. Osteosarcoma / genetics. Translocation, Genetic


63. Gyurkocza B, Storb R, Storer BE, Chauncey TR, Lange T, Shizuru JA, Langston AA, Pulsipher MA, Bredeson CN, Maziarz RT, Bruno B, Petersen FB, Maris MB, Agura E, Yeager A, Bethge W, Sahebi F, Appelbaum FR, Maloney DG, Sandmaier BM: Nonmyeloablative allogeneic hematopoietic cell transplantation in patients with acute myeloid leukemia. J Clin Oncol; 2010 Jun 10;28(17):2859-67
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nonmyeloablative allogeneic hematopoietic cell transplantation in patients with acute myeloid leukemia.
  • PURPOSE: Allogeneic hematopoietic cell transplantation (HCT) after high-dose conditioning regimens imposes prohibitively high risks of morbidity and mortality for patients with high-risk acute myeloid leukemia (AML) who are older or have comorbid conditions.
  • PATIENTS AND METHODS: Two hundred seventy-four patients (median age, 60 years) with de novo or secondary AML underwent allogeneic HCT from related (n = 118) or unrelated donors (n = 156) after conditioning with 2 Gy of total-body irradiation (TBI) with or without fludarabine.
  • The cumulative incidences of grades 2, 3, and 4 acute graft-versus-host disease (GVHD) were 38%, 9%, and 5%, respectively.
  • CONCLUSION: Allogeneic HCT from related or unrelated donors after conditioning with low-dose TBI and fludarabine, relying almost exclusively on graft-versus-leukemia effects, can result in long-term remissions in older or medically infirm patients with AML.

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  • [Cites] Blood. 2009 Mar 26;113(13):3110-8 [19059878.001]
  • [Cites] J Clin Oncol. 2008 Feb 1;26(4):577-84 [18086801.001]
  • [Cites] Blood. 2009 Sep 10;114(11):2220-31 [19587375.001]
  • [Cites] N Engl J Med. 2009 Sep 24;361(13):1235-48 [19776405.001]
  • [Cites] J Clin Oncol. 2009 Sep 20;27(27):4570-7 [19652066.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4075-83 [11110676.001]
  • [Cites] Blood. 2002 Dec 1;100(12):3869-76 [12393614.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1620-9 [12393457.001]
  • [Cites] Bone Marrow Transplant. 2003 Jun;31(12):1089-95 [12796788.001]
  • [Cites] Biol Blood Marrow Transplant. 2003 Aug;9(8):489-95 [12931117.001]
  • [Cites] Blood. 2003 Sep 15;102(6):2021-30 [12791654.001]
  • [Cites] Blood. 2003 Nov 1;102(9):3447-54 [12855572.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4642-9 [14673054.001]
  • [Cites] Blood. 2004 Aug 1;104(3):865-72 [15090449.001]
  • [Cites] Blood. 1988 Oct;72(4):1300-4 [3048439.001]
  • [Cites] Blood. 1991 Apr 15;77(8):1666-74 [2015395.001]
  • [Cites] N Engl J Med. 1994 Oct 6;331(14):896-903 [8078551.001]
  • [Cites] Blood. 1994 Nov 15;84(10):3558-66 [7524741.001]
  • [Cites] Blood. 1995 Dec 1;86(11):4376-81 [7492799.001]
  • [Cites] Bone Marrow Transplant. 1995 Jun;15(6):825-8 [7581076.001]
  • [Cites] Leukemia. 1996 Jan;10(1):13-9 [8558917.001]
  • [Cites] Blood. 1996 Mar 1;87(5):1710-7 [8634416.001]
  • [Cites] Blood. 1997 Apr 15;89(8):3048-54 [9108426.001]
  • [Cites] Blood. 1998 May 15;91(10):3607-15 [9572995.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3515-20 [9808542.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1969-78 [15632409.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Apr;11(4):272-9 [15812392.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3439-46 [15824415.001]
  • [Cites] Leukemia. 2005 Jun;19(6):990-7 [15800667.001]
  • [Cites] Leukemia. 2005 Jun;19(6):916-20 [15843817.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5728-38 [16009946.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2912-9 [15994282.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Dec;11(12):945-56 [16338616.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9387-93 [16314618.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):444-53 [16344316.001]
  • [Cites] Leukemia. 2006 Feb;20(2):322-8 [16307018.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3959-66 [16880451.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 Oct;12(10):1047-55 [17067911.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2744-8 [17595333.001]
  • [Cites] Br J Haematol. 2009 Jun;145(5):598-605 [19344426.001]
  • (PMID = 20439626.001).
  • [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 / CA18029; United States / NHLBI NIH HHS / HL / HL36444; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / P30 CA015704; United States / NCI NIH HHS / CA / CA78902; United States / NCI NIH HHS / CA / R21 CA106177; United States / NCI NIH HHS / CA / CA15704; United States / NHLBI NIH HHS / HL / P01 HL036444; United States / NCI NIH HHS / CA / CA106177; United States / NCI NIH HHS / CA / P01 CA078902
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2903320
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64. Büchner T, Berdel WE, Schoch C, Haferlach T, Serve HL, Kienast J, Schnittger S, Kern W, Tchinda J, Reichle A, Lengfelder E, Staib P, Ludwig WD, Aul C, Eimermacher H, Balleisen L, Sauerland MC, Heinecke A, Wörmann B, Hiddemann W: Double induction containing either two courses or one course of high-dose cytarabine plus mitoxantrone and postremission therapy by either autologous stem-cell transplantation or by prolonged maintenance for acute myeloid leukemia. J Clin Oncol; 2006 Jun 1;24(16):2480-9
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  • [Title] Double induction containing either two courses or one course of high-dose cytarabine plus mitoxantrone and postremission therapy by either autologous stem-cell transplantation or by prolonged maintenance for acute myeloid leukemia.
  • PURPOSE: Intensification by high-dose cytarabine in postremission or induction therapy and prolonged maintenance are established strategies to improve the outcome in patients with acute myeloid leukemia (AML).
  • PATIENTS AND METHODS: A total of 1,770 patients (age 16 to 85 years) with de novo or secondary AML or high-risk myelodysplastic syndrome (MDS) were randomly assigned upfront for induction therapy containing one course with standard dose and one course with high-dose cytarabine, or two courses with high-dose cytarabine, and in the same step received postremission prolonged maintenance or busulfan/cyclophosphamide chemotherapy with autologous stem-cell transplantation.
  • There was no significant difference in any prognostic subgroup according to secondary AML/MDS, cytogenetics, WBC, lactate dehydrogenase, and early blast clearance.
  • CONCLUSION: The regimen of one course with standard-dose cytarabine and one course with high-dose cytarabine for induction, and prolonged maintenance for postremission chemotherapy in patients with AML is not improved by additional escalation in cytotoxic treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / surgery. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / surgery
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Cytarabine / administration & dosage. Drug Administration Schedule. Female. Humans. L-Lactate Dehydrogenase / blood. Leukocyte Count. Male. Middle Aged. Mitoxantrone / administration & dosage. Multivariate Analysis. Prognosis. Prospective Studies. Remission Induction. Risk Factors. Transplantation, Autologous. Treatment Outcome

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  • [CommentIn] J Clin Oncol. 2006 Dec 1;24(34):5471-2; author reply 5472-3 [17135654.001]
  • [ErratumIn] J Clin Oncol. 2011 Jul 1;29(19):2739
  • (PMID = 16735702.001).
  • [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; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; EC 1.1.1.27 / L-Lactate Dehydrogenase
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65. Schwarz J, Pytlík R, Doubek M, Brychtová Y, Dulícek P, Campr V, Kren L, Penka M: Analysis of risk factors: the rationale of the guidelines of the Czech Hematological Society for diagnosis and treatment of chronic myeloproliferative disorders with thrombocythemia. Semin Thromb Hemost; 2006 Apr;32(3):231-45
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  • The histopathology-based nosological distinction provided by these classifications yields valuable information on prognosis (including the risks of transition into secondary acute myeloid leukemia and myelofibrosis).

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  • (PMID = 16673277.001).
  • [ISSN] 0094-6176
  • [Journal-full-title] Seminars in thrombosis and hemostasis
  • [ISO-abbreviation] Semin. Thromb. Hemost.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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66. Döhner K, Schlenk RF, Habdank M, Scholl C, Rücker FG, Corbacioglu A, Bullinger L, Fröhling S, Döhner H: Mutant nucleophosmin (NPM1) predicts favorable prognosis in younger adults with acute myeloid leukemia and normal cytogenetics: interaction with other gene mutations. Blood; 2005 Dec 1;106(12):3740-6
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  • [Title] Mutant nucleophosmin (NPM1) predicts favorable prognosis in younger adults with acute myeloid leukemia and normal cytogenetics: interaction with other gene mutations.
  • To assess the prognostic relevance of mutations in the NPM1 gene encoding a nucleocytoplasmic shuttle protein in younger adults with acute myeloid leukemia (AML) and normal cytogenetics, sequencing of NPM1 exon 12 was performed in diagnostic samples from 300 patients entered into 2 consecutive multicenter trials of the AML Study Group (AMLSG).
  • Multivariable analysis for OS revealed combined NPM1-mutated/FLT3 ITD-negative status, CEBPA mutation status, availability of a human leukocyte antigen (HLA)-compatible donor, secondary AML, and lactate dehydrogenase (LDH) as prognostic factors.
  • In conclusion, NPM1 mutations in the absence of FLT3 ITD define a distinct molecular and prognostic subclass of young-adult AML patients with normal cytogenetics.
  • [MeSH-major] Leukemia, Myeloid / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Amino Acid Sequence. Base Sequence. CCAAT-Binding Factor / genetics. Clinical Trials as Topic. Female. Humans. Male. Middle Aged. Molecular Sequence Data. Mutation. Polymerase Chain Reaction. Prognosis. Survival Analysis. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16051734.001).
  • [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] 0 / CCAAT-Binding Factor; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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67. Olivieri A, Capelli D, Troiani E, Poloni A, Montanari M, Offidani M, Discepoli G, Leoni P: A new intensive induction schedule, including high-dose Idarubicin, high-dose Aracytin and Amifostine, in older AML patients: feasibility and long-term results in 42 patients. Exp Hematol; 2007 Jul;35(7):1074-82
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  • [Title] A new intensive induction schedule, including high-dose Idarubicin, high-dose Aracytin and Amifostine, in older AML patients: feasibility and long-term results in 42 patients.
  • OBJECTIVE: We evaluated the feasibility of a new regimen in elderly patients with acute myeloid leukemia (AML).
  • The main end points were overall response rate (ORR) and toxicity; secondary end points were feasibility of peripheral blood stem cells (PBSC) collection, leukemia-free survival, and overall survival (OS).
  • Patients with unfavorable cytogenetic and those with secondary AML had poorer OS; about 40% of patients could mobilize a sufficient amount of PBSC for autologous stem cell transplantation.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 17588476.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; M487QF2F4V / Amifostine; ZRP63D75JW / Idarubicin
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68. Crump M, Hedley D, Kamel-Reid S, Leber B, Wells R, Brandwein J, Buckstein R, Kassis J, Minden M, Matthews J, Robinson S, Turner R, McIntosh L, Eisenhauer E, Seymour L: A randomized phase I clinical and biologic study of two schedules of sorafenib in patients with myelodysplastic syndrome or acute myeloid leukemia: a NCIC (National Cancer Institute of Canada) Clinical Trials Group Study. Leuk Lymphoma; 2010 Feb;51(2):252-60
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  • [Title] A randomized phase I clinical and biologic study of two schedules of sorafenib in patients with myelodysplastic syndrome or acute myeloid leukemia: a NCIC (National Cancer Institute of Canada) Clinical Trials Group Study.
  • In this randomized phase I study, eligible patients had relapsed/refractory acute myeloid leukemia (AML), and one prior induction regimen, or were age >65 with untreated myelodysplastic syndrome (MDS) or secondary AML.
  • One CR was seen in a patient with AML with FLT3-ITD.
  • The recommended phase II dose in AML is 300 mg BID continuously, and testing in combination and in FLT3-ITD AML is warranted.
  • [MeSH-major] Benzenesulfonates / therapeutic use. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. Pyridines / therapeutic use
  • [MeSH-minor] Abdominal Pain / chemically induced. Acute Disease. Adult. Aged. Aged, 80 and over. Area Under Curve. Diarrhea / chemically induced. Dose-Response Relationship, Drug. Drug Administration Schedule. Extracellular Signal-Regulated MAP Kinases / metabolism. Female. Humans. Male. Metabolic Clearance Rate. Middle Aged. Nausea / chemically induced. Niacinamide / analogs & derivatives. Phenylurea Compounds. Phosphorylation / drug effects. Protein Kinase Inhibitors / adverse effects. Protein Kinase Inhibitors / pharmacokinetics. Protein Kinase Inhibitors / therapeutic use. Treatment Outcome


69. Tavil B, Cetin M, Tuncer M: CD34/CD117 positivity in assessment of prognosis in children with myelodysplastic syndrome. Leuk Res; 2006 Feb;30(2):222-4
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  • Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal stem cell disorders that are characterized by morphology identifying dysplastic changes in one or more cell lineages, peripheral blood cytopenias and a propensity to evolve into secondary acute myeloid leukemia (AML).
  • CD34 is commonly expressed in all types of childhood leukemias, whereas CD117 is a reliable and specific marker to detect leukemia cells committed to myeloid lineage.
  • Co-expression of CD34/CD117 may strongly suggest the diagnosis of AML (Rytting ME.
  • May; Uçkan D, Hiçsönmez G, Yetgin S, Gürgey A, Cetin M, Karaağaoğlu E, et al. CD34/CD117 co-expression in childhood acute leukemia.
  • Leukemia Res 2000;24:201-6.).
  • We describe the case of a 22 month-old-girl with MDS and Down syndrome who was presented with severe anemia and thrombocytosis at diagnosis, transformed into AML-M7.
  • As the disease progressed, CD34/117 co-existence was increased and MDS transformed into AML.
  • [MeSH-minor] Bone Marrow Examination. Female. Humans. Infant. Leukemia, Myeloid, Acute / etiology. Prognosis

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  • (PMID = 16098587.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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70. Ko M, Huang Y, Jankowska AM, Pape UJ, Tahiliani M, Bandukwala HS, An J, Lamperti ED, Koh KP, Ganetzky R, Liu XS, Aravind L, Agarwal S, Maciejewski JP, Rao A: Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2. Nature; 2010 Dec 9;468(7325):839-43
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  • [Title] Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2.
  • The gene encoding TET2 resides at chromosome 4q24, in a region showing recurrent microdeletions and copy-neutral loss of heterozygosity (CN-LOH) in patients with diverse myeloid malignancies.
  • Somatic TET2 mutations are frequently observed in myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), MDS/MPN overlap syndromes including chronic myelomonocytic leukaemia (CMML), acute myeloid leukaemias (AML) and secondary AML (sAML).
  • We show here that TET2 mutations associated with myeloid malignancies compromise catalytic activity.
  • Our results demonstrate that Tet2 is important for normal myelopoiesis, and suggest that disruption of TET2 enzymatic activity favours myeloid tumorigenesis.
  • Measurement of 5hmC levels in myeloid malignancies may prove valuable as a diagnostic and prognostic tool, to tailor therapies and assess responses to anticancer drugs.


71. Ayala RM, Martínez-López J, Albízua E, Diez A, Gilsanz F: Clinical significance of Gata-1, Gata-2, EKLF, and c-MPL expression in acute myeloid leukemia. Am J Hematol; 2009 Feb;84(2):79-86
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  • [Title] Clinical significance of Gata-1, Gata-2, EKLF, and c-MPL expression in acute myeloid leukemia.
  • The aim of this study was to evaluate the biological correlation and prognostic impact of Gata-1, Gata-2, EKLF, and c-MPL transcript level in a group of 41 acute myeloid leukemia (AML) patients.
  • Expression of c-MPL was associated with CD34+ AML and M2 FAB AML subtype.
  • A higher expression of EKLF was found in secondary AML versus primary AML.
  • Our study has identified expression of EKLF as a factor with a favorable impact on prognosis in AML.
  • [MeSH-major] GATA1 Transcription Factor / physiology. GATA2 Transcription Factor / physiology. Gene Expression Regulation, Neoplastic. Kruppel-Like Transcription Factors / physiology. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / physiology. Receptors, Thrombopoietin / physiology

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  • (PMID = 19097174.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / GATA2 Transcription Factor; 0 / GATA2 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / Neoplasm Proteins; 0 / Receptors, Thrombopoietin; 0 / erythroid Kruppel-like factor; 143641-95-6 / MPL protein, human
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72. Gondek LP, Dunbar AJ, Szpurka H, McDevitt MA, Maciejewski JP: SNP array karyotyping allows for the detection of uniparental disomy and cryptic chromosomal abnormalities in MDS/MPD-U and MPD. PLoS One; 2007 Nov 21;2(11):e1225
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  • We applied single nucleotide polymorphism arrays (SNP-A) to study karyotypic abnormalities in patients with atypical myeloproliferative syndromes (MPD), including myeloproliferative/myelodysplastic syndrome overlap both positive and negative for the JAK2 V617F mutation and secondary acute myeloid leukemia (AML).
  • Transformation to AML was observed in 8/30 patients.
  • In 5 V617F+ patients who progressed to AML, we show that SNP-A can allow for the detection of two modes of transformation: leukemic blasts evolving from either a wild-type jak2 precursor carrying other acquired chromosomal defects, or from a V617F+ mutant progenitor characterized by UPD9p.

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  • [Cites] Blood. 2008 Feb 1;111(3):1534-42 [17954704.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3365-73 [17634407.001]
  • [Cites] Nat Biotechnol. 2000 Sep;18(9):1001-5 [10973224.001]
  • [Cites] Am J Pathol. 2001 Apr;158(4):1253-62 [11290543.001]
  • [Cites] Nucleic Acids Res. 2001 Sep 1;29(17):E88-8 [11522844.001]
  • [Cites] Blood. 2002 Jan 1;99(1):375-7 [11756195.001]
  • [Cites] Exp Hematol. 2002 Mar;30(3):229-36 [11882360.001]
  • [Cites] Br J Haematol. 2002 Nov;119(2):558-66 [12406101.001]
  • [Cites] Hematol Oncol Clin North Am. 2003 Oct;17(5):1129-49 [14560778.001]
  • [Cites] Nat Genet. 2004 Sep;36(9):949-51 [15286789.001]
  • [Cites] Cancer Res. 2005 Jan 15;65(2):375-8 [15695375.001]
  • [Cites] Leuk Res. 2005 Apr;29(4):365-70 [15725469.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [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] Cancer Res. 2005 Jul 15;65(14):6071-9 [16024607.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1207-9 [15860661.001]
  • [Cites] Biochem J. 2005 Aug 15;390(Pt 1):359-66 [15833084.001]
  • [Cites] Blood. 2005 Sep 15;106(6):2162-8 [15920007.001]
  • [Cites] Cancer. 2005 Oct 15;104(8):1656-60 [16104040.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3377-9 [16081687.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1242-3 [16434499.001]
  • [Cites] Oncogene. 2006 Mar 2;25(9):1434-6 [16247455.001]
  • [Cites] Cancer. 2006 May 1;106(9):1985-9 [16568439.001]
  • [Cites] Leukemia. 2006 Jun;20(6):971-8 [16598306.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1865-7 [16728702.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Oct 1;170(1):65-8 [16965958.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2173-81 [16741247.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3548-55 [16873677.001]
  • [Cites] Carcinogenesis. 2007 Jan;28(1):38-48 [16774939.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1678-86 [17038539.001]
  • [Cites] Am J Hum Genet. 2007 Jul;81(1):114-26 [17564968.001]
  • [Cites] Blood. 2007 Jul 1;110(1):375-9 [17363731.001]
  • [Cites] Leukemia. 2007 Aug;21(8):1648-57 [17554386.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2058-61 [17525728.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3835-49 [10577857.001]
  • (PMID = 18030353.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K24 HL077522; United States / NHLBI NIH HHS / HL / R01 HL082983; United States / NCRR NIH HHS / RR / S10 RR019391; United States / NCRR NIH HHS / RR / U54 RR019391
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers
  • [Other-IDs] NLM/ PMC2075364
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73. Wadehra N, Farag S, Bolwell B, Elder P, Penza S, Kalaycio M, Avalos B, Pohlman B, Marcucci G, Sobecks R, Lin T, Andrèsen S, Copelan E: Long-term outcome of Hodgkin disease patients following high-dose busulfan, etoposide, cyclophosphamide, and autologous stem cell transplantation. Biol Blood Marrow Transplant; 2006 Dec;12(12):1343-9
Hazardous Substances Data Bank. BUSULFAN .

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  • Five patients died between 5.3 and 9.3 years of late complications, including secondary myelodysplasia or acute myeloid leukemia, secondary solid malignancies, and pulmonary toxicity.

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  • [CommentIn] Biol Blood Marrow Transplant. 2007 Jun;13(6):746-7 [17531785.001]
  • (PMID = 17162217.001).
  • [ISSN] 1083-8791
  • [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] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; G1LN9045DK / Busulfan
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74. Infante-Rivard C, Vermunt JK, Weinberg CR: Excess transmission of the NAD(P)H:quinone oxidoreductase 1 (NQO1) C609T polymorphism in families of children with acute lymphoblastic leukemia. Am J Epidemiol; 2007 Jun 1;165(11):1248-54
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  • [Title] Excess transmission of the NAD(P)H:quinone oxidoreductase 1 (NQO1) C609T polymorphism in families of children with acute lymphoblastic leukemia.
  • Topoisomerase II is a DNA-processing enzyme, and secondary acute myeloid leukemia has been associated with exposure to drugs that inhibit its action.
  • Hence, prenatal exposure to chemicals that inhibit topoisomerase II could plausibly contribute to the incidence of childhood leukemia.
  • To assess its role in the etiology of childhood acute lymphoblastic leukemia, the authors studied transmission of the variant T allele in the families (parents and grandparents) of 657 affected children in Québec, Canada (1980-2000).
  • [MeSH-major] Family Health. Inheritance Patterns. NAD(P)H Dehydrogenase (Quinone) / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Cites] Crit Rev Toxicol. 2002 May;32(3):155-210 [12071572.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4590-3 [12393620.001]
  • [Cites] Am J Epidemiol. 2003 Jan 15;157(2):176-82 [12522025.001]
  • [Cites] Am J Hum Genet. 2003 Feb;72(2):438-47 [12533786.001]
  • [Cites] J Biol Chem. 2003 Mar 21;278(12):10368-73 [12529318.001]
  • [Cites] Int J Epidemiol. 2003 Feb;32(1):1-22 [12689998.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):639-49 [12951583.001]
  • [Cites] Methods Enzymol. 2004;382:115-44 [15047100.001]
  • [Cites] Mutat Res. 2004 Mar;566(2):99-130 [15164977.001]
  • [Cites] Pediatr Blood Cancer. 2004 Oct;43(5):568-70 [15382274.001]
  • [Cites] Nature. 1993 May 27;363(6427):358-60 [8497319.001]
  • [Cites] Am J Hum Genet. 1993 Nov;53(5):1114-26 [8213835.001]
  • [Cites] Biotechniques. 1998 Feb;24(2):206-8, 210, 212 [9494715.001]
  • [Cites] Am J Hum Genet. 1998 Apr;62(4):969-78 [9529360.001]
  • [Cites] Am J Epidemiol. 1998 Nov 1;148(9):893-901 [9801020.001]
  • [Cites] Annu Rev Genet. 1998;32:495-519 [9928489.001]
  • [Cites] Am J Hum Genet. 1999 Apr;64(4):1186-93 [10090904.001]
  • [Cites] Pharmacogenetics. 1999 Feb;9(1):113-21 [10208650.001]
  • [Cites] Lancet. 1999 May 29;353(9167):1816-7 [10359403.001]
  • [Cites] Cancer Res. 1999 Aug 15;59(16):4095-9 [10463613.001]
  • [Cites] Epidemiology. 1999 Sep;10(5):481-7 [10468419.001]
  • [Cites] Haematologica. 2004 Dec;89(12):1492-7 [15590400.001]
  • [Cites] Eur J Hum Genet. 2005 Jan;13(1):79-85 [15470368.001]
  • [Cites] Leukemia. 2005 Feb;19(2):214-6 [15618957.001]
  • [Cites] Environ Health Perspect. 2005 Jun;113(6):787-92 [15929905.001]
  • [Cites] Chem Biol Interact. 2005 May 30;153-154:137-46 [15935810.001]
  • [Cites] Haematologica. 2005 Nov;90(11):1511-5 [16266898.001]
  • [Cites] J Biol Chem. 2006 Jul 21;281(29):19798-808 [16682409.001]
  • [Cites] Am J Hum Genet. 2000 Jan;66(1):251-61 [10631155.001]
  • [Cites] Am J Hum Genet. 2000 Jan;66(1):335-8 [10631165.001]
  • [Cites] Cancer Causes Control. 2000 Jul;11(6):547-53 [10880037.001]
  • [Cites] Am J Epidemiol. 2000 Sep 1;152(5):480-6 [10981463.001]
  • [Cites] Br J Cancer. 2000 Dec;83(11):1559-64 [11076669.001]
  • [Cites] Epidemiology. 2001 Jan;12(1):13-9 [11138808.001]
  • [Cites] Cancer Chemother Biol Response Modif. 2001;19:129-47 [11686011.001]
  • [Cites] Int J Cancer. 2002 Jan 10;97(2):230-6 [11774269.001]
  • [Cites] BMJ. 2002 Feb 2;324(7332):283-7 [11823363.001]
  • (PMID = 17332311.001).
  • [ISSN] 0002-9262
  • [Journal-full-title] American journal of epidemiology
  • [ISO-abbreviation] Am. J. Epidemiol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 ES045005-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; J64922108F / Benzene
  • [Other-IDs] NLM/ NIHMS33454; NLM/ PMC2080583
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75. Boehm A, Sperr WR, Leitner G, Worel N, Oehler L, Jaeger E, Mitterbauer M, Haas OA, Valent P, Kalhs P, Rabitsch W: Comorbidity predicts survival in myelodysplastic syndromes or secondary acute myeloid leukaemia after allogeneic stem cell transplantation. Eur J Clin Invest; 2008 Dec;38(12):945-52
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  • [Title] Comorbidity predicts survival in myelodysplastic syndromes or secondary acute myeloid leukaemia after allogeneic stem cell transplantation.
  • PATIENTS AND METHODS: We examined the overall survival (OS) and underlying risk factors in 45 adult patients with MDS (n = 38), chronic myelomonocytic leukaemia (n = 1), or secondary acute myeloid leukaemia (AML) arising from MDS (n = 6), who underwent allogeneic SCT at our Institution.
  • CONCLUSIONS: Based on these data and similar published data we recommend selecting patients with MDS or secondary AML for SCT according to the presence of comorbidities.
  • [MeSH-major] Disease-Free Survival. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / mortality. Leukemia, Myelomonocytic, Chronic / mortality. Neoplasms, Second Primary / mortality


76. Clavio M, Vignolo L, Albarello A, Varaldo R, Pierri I, Catania G, Balocco M, Michelis G, Miglino M, Manna A, Balleari E, Carella AM, Sessarego M, Van Lint MT, Bacigalupo A, Gobbi M: Adding low-dose gemtuzumab ozogamicin to fludarabine, Ara-C and idarubicin (MY-FLAI) may improve disease-free and overall survival in elderly patients with non-M3 acute myeloid leukaemia: results of a prospective, pilot, multi-centre trial and comparison with a historical cohort of patients. Br J Haematol; 2007 Jul;138(2):186-95
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  • [Title] Adding low-dose gemtuzumab ozogamicin to fludarabine, Ara-C and idarubicin (MY-FLAI) may improve disease-free and overall survival in elderly patients with non-M3 acute myeloid leukaemia: results of a prospective, pilot, multi-centre trial and comparison with a historical cohort of patients.
  • FLAI) followed by low-dose gemtuzumab ozogamicin (GO), for induction treatment of patients with CD33+ acute myeloid leukaemia (AML).
  • However, patients with de novo AML receiving GO (n = 26) had a significantly lower risk of relapse at 2 years when compared with patients not receiving GO (n = 35) (40% vs. 80%, P = 0.01) and significantly better overall 2-year survival (40% vs. 14%P = 0.02).
  • Patients with secondary AML had comparable outcome whether or not they received GO.
  • [MeSH-major] Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antineoplastic Agents / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Antibodies, Monoclonal, Humanized. Cytarabine / administration & dosage. Drug Administration Schedule. Female. Humans. Idarubicin / administration & dosage. Male. Middle Aged. Neoplasm Recurrence, Local. Pilot Projects. Prospective Studies. Survival Analysis. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 17593025.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / gemtuzumab; 04079A1RDZ / Cytarabine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; ZRP63D75JW / Idarubicin
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77. Chaoui D, Peffault De Latour R, Legrand O, Marie JP: Acute myeloid leukemia in the elderly: etoposide when anthracyclins are contraindicated. Leuk Lymphoma; 2005 Mar;46(3):401-4
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  • [Title] Acute myeloid leukemia in the elderly: etoposide when anthracyclins are contraindicated.
  • We investigated whether etoposide might be a suitable alternative to anthracyclins for the treatment of elderly patients with acute myeloid leukemia (AML) in whom anthracyclins are contraindicated.
  • In total, 88 patients over 60 years old were treated in our department between 1988 and 2000 for de novo or secondary AML.
  • Etoposide combined with a standard dose of cytosine arabinoside is relatively safe and effective in elderly patients with AML and offers an alternative approach to patients with cardiac contraindications to anthracyclin treatment.
  • [MeSH-major] Anthracyclines / contraindications. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Etoposide / administration & dosage. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 15621830.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracyclines; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; ZS7284E0ZP / Daunorubicin
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78. Mead AJ, Linch DC, Hills RK, Wheatley K, Burnett AK, Gale RE: FLT3 tyrosine kinase domain mutations are biologically distinct from and have a significantly more favorable prognosis than FLT3 internal tandem duplications in patients with acute myeloid leukemia. Blood; 2007 Aug 15;110(4):1262-70
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  • [Title] FLT3 tyrosine kinase domain mutations are biologically distinct from and have a significantly more favorable prognosis than FLT3 internal tandem duplications in patients with acute myeloid leukemia.
  • The prognostic impact of tyrosine kinase domain (TKD) mutations of the fms-like tyrosine kinase-3 (FLT3) gene in acute myeloid leukemia (AML) is currently uncertain.
  • To resolve this issue we screened 1107 young adult nonacute promyelocytic leukemia AML patients with known FLT3 internal tandem duplication (ITD) status for FLT3/TKDs; they were detected in 127 (11%) cases.
  • Mutations were associated with a high white cell count (P =.006) and patients with inv(16) (P = .005) but were infrequent in patients with adverse cytogenetics and secondary AML.
  • The novel finding that biologically distinct activating mutations of the same gene can be associated with markedly different clinical outcomes has implications for risk stratification and therapy and is significant to the understanding of chemoresistance in AML.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid / genetics. Mutation / genetics. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Alleles. Amino Acid Substitution. Antimetabolites, Antineoplastic / therapeutic use. Cytarabine / therapeutic use. DNA Mutational Analysis. Female. Follow-Up Studies. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Prognosis. Survival Rate. Treatment Outcome

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  • (PMID = 17456725.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MRC/ G0300133; United Kingdom / Medical Research Council / / MRC/ G84/6443
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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79. Verma D, O'Brien S, Thomas D, Faderl S, Koller C, Pierce S, Kebriaei P, Garcia-Manero G, Cortes J, Kantarjian H, Ravandi F: Therapy-related acute myelogenous leukemia and myelodysplastic syndrome in patients with acute lymphoblastic leukemia treated with the hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone regimens. Cancer; 2009 Jan 1;115(1):101-6
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  • [Title] Therapy-related acute myelogenous leukemia and myelodysplastic syndrome in patients with acute lymphoblastic leukemia treated with the hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone regimens.
  • BACKGROUND: Secondary malignancies including myeloid neoplasms occur infrequently in acute lymphoblastic leukemia (ALL) and to the authors' knowledge have not been as well documented in adults as in children.
  • RESULTS: Sixteen patients (2.49%) developed secondary acute myelogenous leukemia (AML) (6 patients) or myelodysplastic syndrome (MDS) (10 patients).
  • Karyotype at time of AML/MDS diagnosis was -5, -7 in 9 patients, normal in 1 patient, complex in 1 patient, inv(11) in 1 patient, t(4;11) in 1 patient, del(20) in 1 patient, and unavailable in 2 patients.
  • Secondary AML/MDS developed at a median of 32 months after ALL diagnosis.
  • Cytarabine plus anthracycline-based treatment was given to 12 patients with AML and high-risk MDS.
  • Eight patients (1 with AML and 7 with MDS) underwent allogeneic stem cell transplantation, and all but 2 died at a median of 3 months (range, 0.5-11 months) after transplantation.
  • The median overall survival after a diagnosis of secondary AML and MDS was 9.25 months (range, 1+ to 26+ months).
  • CONCLUSIONS: Secondary AML and MDS occur infrequently in adult patients with de novo ALL treated with the hyper-CVAD regimens, and response to therapy is poor.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


80. Wang H, Wang XQ, Xu XP, Lin GW: ID4 methylation predicts high risk of leukemic transformation in patients with myelodysplastic syndrome. Leuk Res; 2010 May;34(5):598-604
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  • Epigenetic gene silencing due to promoter methylation is observed in human cancers like acute myeloid leukemia (AML).
  • Little is known about aberrant methylation in myelodysplastic syndrome (MDS), a heterogeneous clonal stem cell disorder with a approximately 30% risk of transformation into secondary AML.
  • Multivariate analysis indicated that ID4 methylation status was the independent factor that impacted leukemia-free survival (LFS).
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. DNA Methylation / genetics. Inhibitor of Differentiation Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


81. Lu GH: Clinical cytogenetic diagnosis of therapy-related acute myeloid leukemia. Beijing Da Xue Xue Bao; 2005 Feb 18;37(1):10-3
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  • [Title] Clinical cytogenetic diagnosis of therapy-related acute myeloid leukemia.
  • Therapy-related acute myeloid leukemia (tAML) is one of the two forms of secondary acute myeloid leukemia, with one derived from de novo myelodysplastic syndrome (MDS) and the other from exposure to environmental or therapeutic agents such as radiation and toxins.
  • There has been a marked increase in the number of incidences of therapy-related acute myeloid leukemia.
  • In this study, an interesting case with therapy-related myelodysplastic syndrome and acute myeloid leukemia (tMDS/tAML) will be presented.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / diagnosis. Lymphoma, B-Cell / drug therapy. Neoplasms, Second Primary / diagnosis

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  • (PMID = 15719033.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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82. Rohatiner AZ, Nadler L, Davies AJ, Apostolidis J, Neuberg D, Matthews J, Gribben JG, Mauch PM, Lister TA, Freedman AS: Myeloablative therapy with autologous bone marrow transplantation for follicular lymphoma at the time of second or subsequent remission: long-term follow-up. J Clin Oncol; 2007 Jun 20;25(18):2554-9
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  • However, use of CY+TBI was associated with a significant risk of secondary myelodysplasia and secondary acute myeloblastic leukemia, resulting in 15 patient deaths.


83. van den Heuvel-Eibrink MM, van der Holt B, Burnett AK, Knauf WU, Fey MF, Verhoef GE, Vellenga E, Ossenkoppele GJ, Löwenberg B, Sonneveld P: CD34-related coexpression of MDR1 and BCRP indicates a clinically resistant phenotype in patients with acute myeloid leukemia (AML) of older age. Ann Hematol; 2007 May;86(5):329-37
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  • [Title] CD34-related coexpression of MDR1 and BCRP indicates a clinically resistant phenotype in patients with acute myeloid leukemia (AML) of older age.
  • Clinical resistance to chemotherapy in acute myeloid leukemia (AML) is associated with the expression of the multidrug resistance (MDR) proteins P-glycoprotein, encoded by the MDR1/ABCB1 gene, multidrug resistant-related protein (MRP/ABCC1), the lung resistance-related protein (LRP), or major vault protein (MVP), and the breast cancer resistance protein (BCRP/ABCG2).
  • The clinical value of MDR1, MRP1, LRP/MVP, and BCRP messenger RNA (mRNA) expression was prospectively studied in 154 newly diagnosed AML patients >or=60 years who were treated in a multicenter, randomized phase 3 trial.
  • Higher BCRP mRNA was associated with secondary AML (p < 0.05).
  • When adjusted for other prognostic actors, only CD34-related MDR1/BCRP coexpression remained significantly associated with a lower CR rate (p = 0.03), thereby identifying a clinically resistant subgroup of elderly AML patients.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Drug Resistance, Neoplasm / genetics. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Multidrug Resistance-Associated Proteins / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Acute Disease. Age Factors. Aged. Antigens, CD34 / metabolism. Disease-Free Survival. Humans. Middle Aged. Phenotype. Prospective Studies. RNA, Messenger / metabolism. Vault Ribonucleoprotein Particles / metabolism


84. Balgobind BV, Lugthart S, Hollink IH, Arentsen-Peters ST, van Wering ER, de Graaf SS, Reinhardt D, Creutzig U, Kaspers GJ, de Bont ES, Stary J, Trka J, Zimmermann M, Beverloo HB, Pieters R, Delwel R, Zwaan CM, van den Heuvel-Eibrink MM: EVI1 overexpression in distinct subtypes of pediatric acute myeloid leukemia. Leukemia; 2010 May;24(5):942-9
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  • [Title] EVI1 overexpression in distinct subtypes of pediatric acute myeloid leukemia.
  • Overexpression of the ecotropic virus integration-1 (EVI1) gene (EVI1+), localized at chromosome 3q26, is associated with adverse outcome in adult acute myeloid leukemia (AML).
  • In pediatric AML, 3q26 abnormalities are rare, and the role of EVI1 is unknown.
  • We studied 228 pediatric AML samples for EVI1+ using gene expression profiling and RQ-PCR.
  • EVI1+ was found in 20/213 (9%) of children with de novo AML, and in 4/8 with secondary AML.
  • It was predominantly found in MLL-rearranged AML (13/47), monosomy 7 (2/3), or FAB M6/7 (6/10), and mutually exclusive with core-binding factor AML, t(15;17), and NPM1 mutations.
  • Although significant differences in 4 years pEFS for EVI1+ and EVI1- pediatric AML were observed (28%+/-11 vs 44%+/-4, P=0.04), multivariate analysis did not identify EVI1+ as an independent prognostic factor.
  • We conclude that EVI1+ can be found in approximately 10% of pediatric AML.
  • Although EVI1+ was not an independent prognostic factor, it was predominantly found in subtypes of pediatric AML that are related with an intermediate to unfavorable prognosis.
  • Remarkably, no 3q26 abnormalities were identified in EVI1+ pediatric AML.
  • [MeSH-major] Biomarkers, Tumor / genetics. Chromosomes, Human, Pair 3 / genetics. DNA-Binding Proteins / genetics. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics

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  • (PMID = 20357826.001).
  • [ISSN] 1476-5551
  • [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 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / RNA, Messenger; 0 / Transcription Factors
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85. Harousseau JL, Martinelli G, Jedrzejczak WW, Brandwein JM, Bordessoule D, Masszi T, Ossenkoppele GJ, Alexeeva JA, Beutel G, Maertens J, Vidriales MB, Dombret H, Thomas X, Burnett AK, Robak T, Khuageva NK, Golenkov AK, Tothova E, Mollgard L, Park YC, Bessems A, De Porre P, Howes AJ, FIGHT-AML-301 Investigators: A randomized phase 3 study of tipifarnib compared with best supportive care, including hydroxyurea, in the treatment of newly diagnosed acute myeloid leukemia in patients 70 years or older. Blood; 2009 Aug 6;114(6):1166-73
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  • [Title] A randomized phase 3 study of tipifarnib compared with best supportive care, including hydroxyurea, in the treatment of newly diagnosed acute myeloid leukemia in patients 70 years or older.
  • This phase 3, multicenter, open-label study evaluated the efficacy and safety of tipifarnib compared with best supportive care (BSC), including hydroxyurea, as first-line therapy in elderly patients (>or=70 years) with newly diagnosed, de novo, or secondary acute myeloid leukemia.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Hydroxyurea / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / mortality. Quinolones / administration & dosage

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  • (PMID = 19470696.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00093990
  • [Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinolones; 192185-72-1 / tipifarnib; X6Q56QN5QC / Hydroxyurea
  • [Investigator] Bezares R; Calahonra R; Fernandez I; Bosly J; Bries G; Bron D; Demuynck H; Ferrant A; Maertens J; Noens L; Selleslag D; Zachee P; Del Giglio; Figueiras R; Hungria V; Brandwein J; Kassis J; Sheridan D; Van der Jagt R; Mayer J; Dufva I; Juul Nielsen O; Friis L; Scholer Kristensen J; Bordessoule D; Dombret H; Fenaux P; Harousseau JL; Huguet F; Ifrah N; Pigneaux A; Quesnel B; Randriamalala E; Rossi JF; Thomas X; Vey N; Ganser A; Germing U; Hänel M; Moritz T; Niederwieser; Noppeney R; Borbényi Z; Losonczy H; Masszi T; Radványi G; Udvardy M; Conneally E; O'Dwyer M; Alimena G; Baccarani M; De Fabritiis P; Fanin R; Martinelli G; Kim I; Lee KH; Min YH; Garcés O; Plasencia A; Sobrevilla P; Vela J; Dmoszynska A; Jedrzejczak W; Kloczko J; Kuliczkowski K; Robak T; Skotnicki A; Sulek K; Alexeeva JA; Abdulkadyrov KM; Domnikova N; Dunaev YA; Gaisarova G; Gavrilenko A; Golenkov AK; Khuageva NK; Khlevnaya N; Loginov AB; Patrin VF; Pristupa A; Rossiev VA; Samoilova OS; Shneider TV; Suvorov A; Yablokova VV; Demeckova E; Tothova E; Wild A; Brunet S; Esteve J; Garcia J; Laraña; San Miguel J; Björkholm M; Mollgard L; Tidefelt U; Chou WC; Hsiao LT; Kuo CY; Lin TL; Löwenberg B; Van Marwijk Kooy M; Muus P; Ossenkoppele GJ; Schipperus MR; Schouten HC; Wittebol S; Gülbas Z; Burnett AK; Carr R; El-Agnaf M; Mufti GJ; Rudin C; Kaplan PE; Kryachok IA; Lysa I; Masliak ZV; Pylypenko HV; Stulginskaya MA; Manges RF
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86. Nevill TJ, Shepherd JD, Sutherland HJ, Abou Mourad YR, Lavoie JC, Barnett MJ, Nantel SH, Toze CL, Hogge DE, Forrest DL, Song KW, Power MM, Nitta JY, Dai Y, Smith CA: IPSS poor-risk karyotype as a predictor of outcome for patients with myelodysplastic syndrome following myeloablative stem cell transplantation. Biol Blood Marrow Transplant; 2009 Feb;15(2):205-13
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  • A retrospective review was performed of 156 patients who underwent SCT (114 BM, 42 BSC) for MDS or secondary acute myelogenous leukemia (sAML) at our institution.
  • Multivariate analysis showed IPSS poor-risk cytogenetics (P< .001), time from diagnosis to SCT (P< .001), FAB subgroup (P= .001), recipients not in complete remission (CR1) at SCT (P= .005), and the development of acute graft-versus-host disease (aGVHD) (P= .04) were all predictive of an inferior EFS.
  • The FAB subgroup (P= .002), poor-risk karyotype (P= .004), and non-CR1 status also correlated with ROR in multivariate analysis.


87. Sakai R, Fujimaki K, Yamazaki E, Sakamoto H, Kanamori H, Miura I, Ishigatsubo Y: Acute myelomonocytic leukemia with dysplastic bone marrow eosinophils showing t(5;17)(q13;q11) and a secondary chromosomal aberration, inv(16)(p13q22). Int J Hematol; 2006 Dec;84(5):417-20
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  • [Title] Acute myelomonocytic leukemia with dysplastic bone marrow eosinophils showing t(5;17)(q13;q11) and a secondary chromosomal aberration, inv(16)(p13q22).
  • inv(16)(p13q22) is associated with de novo acute myelomonocytic leukemia with dysplastic bone marrow eosinophils (AMML Eo), which has a relatively favorable clinical course with a longer remission duration and better survival prospects.
  • On the other hand, t(5; 17)(q13;q11), although relatively rare, has been reported to be a component of complex chromosomal abnormalities in myelodysplastic syndromes and secondary acute myeloid leukemia (AML).
  • In general, certain secondary chromosomal abnormalities are associated with the phenotype of the disease, which retains its essential biologic characteristics established by the primary abnormality.
  • Accordingly, the primary nature of the leukemic cells in this case differs from the findings for core-binding factor AML with inv(16)(p13q22).
  • We believe this report is the first of de novo AMML Eo with t(5; 17)(q13;q11) showing as a secondary chromosomal aberration with inv(16)(p13q22).
  • [MeSH-major] Bone Marrow Cells / pathology. Chromosome Inversion. Chromosomes, Human / genetics. Eosinophils / pathology. Leukemia, Myelomonocytic, Acute. Translocation, Genetic

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  • (PMID = 17189222.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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88. Rihani R, Bazzeh F, Faqih N, Sultan I: Secondary hematopoietic malignancies in survivors of childhood cancer: an analysis of 111 cases from the Surveillance, Epidemiology, and End Result-9 registry. Cancer; 2010 Sep 15;116(18):4385-94
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  • [Title] Secondary hematopoietic malignancies in survivors of childhood cancer: an analysis of 111 cases from the Surveillance, Epidemiology, and End Result-9 registry.
  • BACKGROUND: Studying secondary hematological malignancies in a large cohort of patients can help predict risks and trends associated with current therapies.
  • METHODS: The authors analyzed data from the Surveillance, Epidemiology, and End Resultsecondary 9 (SEER-9) database on patients with a primary malignancy (diagnosed before the age of 20 years) between 1973 and 2005 who developed a secondary hematological malignancy.
  • Primary cancer and histological subtype, incidence, risk factors, outcomes, and changes in risk patterns of secondary hematological malignancies were analyzed for 1973 to 1985, 1986 to 1995, and 1996 to 2005.
  • RESULTS: Of 34,867 patients with a histology-confirmed primary malignancy, 111 developed secondary hematological malignancies (median, 44 months).
  • The main histological subtype of secondary hematological malignancy was acute myeloid leukemia (AML) (49%), which had the shortest median latency time and the worst 5-year survival (18% ± 5.3%; P = .044).
  • Secondary Hodgkin lymphoma had the best 5-year survival (83% ± 15%).
  • The 5-year overall survival for patients with secondary hematological malignancies was 31% ± 4.7%.
  • The risk of secondary AML steadily increased from 1986 to 2005, whereas SIRs for acute lymphoblastic leukemia did not change over time.
  • Non-Hodgkin lymphoma, the second most common secondary hematological malignancy, occurred at a median of 112 months, and its risk steadily increased over time periods.
  • CONCLUSIONS: Childhood cancer survivors are at increased risk of developing secondary hematological malignancies, particularly secondary AML.
  • This risk has continued to rise even in recent years, emphasizing the need to study other factors contributing to secondary hematological malignancies and closely monitor these patients.

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  • [Copyright] © 2010 American Cancer Society.
  • (PMID = 20549819.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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89. Creutzig U, Diekamp S, Zimmermann M, Reinhardt D: Longitudinal evaluation of early and late anthracycline cardiotoxicity in children with AML. Pediatr Blood Cancer; 2007 Jun 15;48(7):651-62
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  • [Title] Longitudinal evaluation of early and late anthracycline cardiotoxicity in children with AML.
  • BACKGROUND: Anthracyclines are effective antineoplastic drugs in acute myelogenous leukemia (AML).
  • PROCEDURE: To evaluate anthracycline-associated cardiomyopathy in pediatric AML-patients, the incidence of early and late (>1 year after intensive AML chemotherapy) clinical and subclinical cardiotoxicity was analyzed out of a total of 1,207 patients <18 years treated between 1993 and 2003 in trials AML-BFM93/98: 1,010 protocol patients with de novo AML, 121 with Down syndrome (DS)-AML, and 76 with secondary AML.
  • RESULTS: Thirty-eight patients (4.3%), including 3 DS-AML and 1 secondary AML, suffered from early cardiomyopathy.
  • After 5 years, four patients showed temporarily or persistently a reduced shortening fraction, which led to death in one DS-AML patient.
  • Late clinical cardiomyopathy mainly affected patients with a second anthracycline therapy (secondary malignancy) and those with early cardiotoxicity.
  • CONCLUSION: In spite of a highly intensive and effective treatment, the frequency of anthracycline-associated cardiomyopathy was low in the AML-BFM studies.
  • [MeSH-major] Anthracyclines / adverse effects. Heart / drug effects. Heart Diseases / chemically induced. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Dose-Response Relationship, Drug. Drug-Related Side Effects and Adverse Reactions. Echocardiography / methods. Female. Follow-Up Studies. Humans. Infant. Longitudinal Studies. Male. Pilot Projects. Risk Factors. Survivors. Time. Treatment Outcome

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • [CommentIn] Pediatr Blood Cancer. 2007 Jun 15;48(7):649-50 [17318875.001]
  • (PMID = 17183582.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines
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90. Bug G, Ritter M, Wassmann B, Schoch C, Heinzel T, Schwarz K, Romanski A, Kramer OH, Kampfmann M, Hoelzer D, Neubauer A, Ruthardt M, Ottmann OG: Clinical trial of valproic acid and all-trans retinoic acid in patients with poor-risk acute myeloid leukemia. Cancer; 2005 Dec 15;104(12):2717-25
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  • [Title] Clinical trial of valproic acid and all-trans retinoic acid in patients with poor-risk acute myeloid leukemia.
  • BACKGROUND: Valproic acid (VPA), a histone deacetylase (HDAC) inhibitor, induced in vitro differentiation of primary acute myeloid leukemia (AML) blasts, an effect enhanced by all-trans retinoic acid (ATRA).
  • Herein, the authors have described results of a clinical trial with VPA plus ATRA in 26 patients with poor-risk AML.
  • No patient achieved complete remission, one with de novo AML had a minor response, and two patients with secondary AML arising from myeloproliferative disorder (MPD) achieved a partial remission and clearance of PB blasts, respectively.
  • The latter responses were accompanied by profound granulocytosis and erythrocytosis in both patients, reminiscent of the response pattern known from ATRA treatment of acute promyelocytic leukemia.
  • CONCLUSIONS: Treatment with VPA/ATRA results in transient disease control in a subset of patients with AML that has evolved from a myeloproliferative disorder but not in patients with a primary or MDS-related AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / drug therapy. Tretinoin / administration & dosage. Valproic Acid / administration & dosage

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  • [Copyright] Copyright 2005 American Cancer Society.
  • (PMID = 16294345.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5688UTC01R / Tretinoin; 614OI1Z5WI / Valproic Acid
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91. Tefferi A: Novel mutations and their functional and clinical relevance in myeloproliferative neoplasms: JAK2, MPL, TET2, ASXL1, CBL, IDH and IKZF1. Leukemia; 2010 Jun;24(6):1128-38
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  • Beginning in early 2005, a number of novel mutations involving Janus kinase 2 (JAK2), Myeloproliferative Leukemia Virus (MPL), TET oncogene family member 2 (TET2), Additional Sex Combs-Like 1 (ASXL1), Casitas B-lineage lymphoma proto-oncogene (CBL), Isocitrate dehydrogenase (IDH) and IKAROS family zinc finger 1 (IKZF1) have been described in BCR-ABL1-negative MPNs.
  • The incidence of TET2, ASXL1, CBL, IDH or IKZF1 mutations in these disorders ranges from 0 to 17%; these latter mutations are more common in chronic (TET2, ASXL1, CBL) or juvenile (CBL) myelomonocytic leukemias, mastocytosis (TET2), myelodysplastic syndromes (TET2, ASXL1) and secondary acute myeloid leukemia, including blast-phase MPN (IDH, ASXL1, IKZF1).

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  • [Cites] Haematologica. 2007 Dec;92(12):1717-8 [18056003.001]
  • [Cites] Haematologica. 2008 Jan;93(1):34-40 [18166783.001]
  • [Cites] Leukemia. 2008 Jan;22(1):216 [17851549.001]
  • [Cites] N Engl J Med. 1976 Oct 21;295(17):913-6 [967201.001]
  • [Cites] Blood. 1981 Nov;58(5):916-9 [7296002.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1411-5 [15920487.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1207-9 [15860661.001]
  • [Cites] N Engl J Med. 2005 Sep 29;353(13):1416-7; author reply 1416-7 [16192494.001]
  • [Cites] Br J Haematol. 2005 Oct;131(2):166-71 [16197445.001]
  • [Cites] Br J Haematol. 2005 Nov;131(3):320-8 [16225651.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3377-9 [16081687.001]
  • [Cites] Lancet. 2005 Dec 3;366(9501):1945-53 [16325696.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):18962-7 [16365288.001]
  • [Cites] Cancer. 2006 Feb 1;106(3):631-5 [16369984.001]
  • [Cites] Blood. 2006 Mar 1;107(5):2098-100 [16293597.001]
  • [Cites] Leukemia. 2006 Jan;20(1):157-8 [16331280.001]
  • [Cites] Leukemia. 2006 Jun;20(6):971-8 [16598306.001]
  • [Cites] Gastroenterology. 2006 Jun;130(7):2031-8 [16762626.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1377-80 [16675710.001]
  • [Cites] J Cell Physiol. 2006 Oct;209(1):21-43 [16741904.001]
  • [Cites] Leukemia. 2006 Nov;20(11):2067-70 [16990759.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3472-6 [16868251.001]
  • [Cites] PLoS Med. 2006 Jul;3(7):e270 [16834459.001]
  • [Cites] Br J Haematol. 2006 Dec;135(5):683-7 [17107350.001]
  • [Cites] N Engl J Med. 2007 Feb 1;356(5):459-68 [17267906.001]
  • [Cites] Br J Haematol. 2007 Feb;136(4):678-9 [17223913.001]
  • [Cites] J Immunol. 2007 Mar 1;178(5):2623-9 [17312100.001]
  • [Cites] Br J Haematol. 2007 May;137(3):244-7 [17408465.001]
  • [Cites] Cancer. 2007 Jun 1;109(11):2279-84 [17440984.001]
  • [Cites] Blood. 2007 Jul 1;110(1):375-9 [17363731.001]
  • [Cites] Leukemia. 2007 Aug;21(8):1658-68 [17541402.001]
  • [Cites] Blood. 2007 Aug 1;110(3):840-6 [17379742.001]
  • [Cites] Blood. 2007 Aug 1;110(3):1004-12 [17446348.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1092-7 [17488875.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2074-5 [17476276.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1960-3 [17597810.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1952-9 [17625606.001]
  • [Cites] Stem Cells. 2007 Sep;25(9):2358-62 [17540852.001]
  • [Cites] Leukemia. 2007 Oct;21(10):2206-7 [17507998.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3735-43 [17709604.001]
  • [Cites] Blood. 2007 Dec 1;110(12):4030-6 [17712047.001]
  • [Cites] Leukemia. 2008 Jan;22(1):14-22 [17882280.001]
  • [Cites] Leukemia. 2008 Jan;22(1):23-30 [17882282.001]
  • [Cites] Leukemia. 2008 Jan;22(1):3-13 [17882283.001]
  • [Cites] Leukemia. 2008 Jan;22(1):87-95 [18033315.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1686-9 [17984312.001]
  • [Cites] Leukemia. 2008 Feb;22(2):450-1 [17851561.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2785-9 [18006699.001]
  • [Cites] Blood. 2008 Apr 15;111(8):3931-40 [18160670.001]
  • [Cites] Leukemia. 2008 Apr;22(4):870-3 [17914411.001]
  • [Cites] Leukemia. 2008 Sep;22(9):1790-2 [18354492.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1807-12 [18772396.001]
  • [Cites] Haematologica. 2008 Oct;93(10):1595-7 [18698078.001]
  • [Cites] Leukemia. 2008 Oct;22(10):1813-7 [18754026.001]
  • [Cites] Leukemia. 2008 Oct;22(10):1841-8 [18754034.001]
  • [Cites] Leukemia. 2008 Oct;22(10):1828-40 [18769448.001]
  • [Cites] Trends Cell Biol. 2008 Nov;18(11):545-51 [18848449.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Nov 4;105(44):17050-4 [18957548.001]
  • [Cites] Acta Neuropathol. 2008 Dec;116(6):597-602 [18985363.001]
  • [Cites] Leukemia. 2009 Jan;23(1):144-52 [18843287.001]
  • [Cites] Hum Mutat. 2009 Jan;30(1):7-11 [19117336.001]
  • [Cites] N Engl J Med. 2009 Feb 19;360(8):765-73 [19228619.001]
  • [Cites] Leuk Lymphoma. 2009 Feb;50(2):247-53 [19235016.001]
  • [Cites] Blood. 2009 Feb 26;113(9):2022-7 [19047681.001]
  • [Cites] Br J Haematol. 2009 Mar;144(6):904-8 [19170680.001]
  • [Cites] Leukemia. 2009 Mar;23(3):610-4 [18818701.001]
  • [Cites] J Cell Mol Med. 2009 Feb;13(2):215-37 [19175693.001]
  • [Cites] Immunol Rev. 2009 Mar;228(1):273-87 [19290934.001]
  • [Cites] Blood. 2009 Mar 26;113(13):2895-901 [18988864.001]
  • [Cites] Nat Genet. 2009 Apr;41(4):446-9 [19287382.001]
  • [Cites] Nat Genet. 2009 Apr;41(4):450-4 [19287385.001]
  • [Cites] Blood. 1978 Feb;51(2):189-94 [620081.001]
  • [Cites] Clin Cancer Res. 2009 Apr 1;15(7):2238-47 [19276253.001]
  • [Cites] Science. 2009 Apr 10;324(5924):261-5 [19359588.001]
  • [Cites] Eur J Haematol. 2009 May;82(5):329-38 [19141119.001]
  • [Cites] Leukemia. 2009 May;23(5):1008-9 [19151782.001]
  • [Cites] Leukemia. 2009 May;23(5):852-5 [19194467.001]
  • [Cites] Leukemia. 2009 May;23(5):900-4 [19262599.001]
  • [Cites] Leukemia. 2009 May;23(5):905-11 [19262601.001]
  • [Cites] Leukemia. 2009 May;23(5):834-44 [19295544.001]
  • [Cites] Science. 2009 May 15;324(5929):930-5 [19372391.001]
  • [Cites] N Engl J Med. 2009 May 28;360(22):2289-301 [19474426.001]
  • [Cites] Int J Cancer. 2009 Jul 15;125(2):353-5 [19378339.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6182-92 [19387008.001]
  • [Cites] Blood. 2009 Jun 18;113(25):6403-10 [19372255.001]
  • [Cites] Nat Genet. 2009 Jul;41(7):838-42 [19483684.001]
  • [Cites] Blood. 2009 Jul 2;114(1):144-7 [19420352.001]
  • [Cites] Leukemia. 2009 Jul;23(7):1343-5 [19295549.001]
  • [Cites] Br J Haematol. 2009 Jun;145(6):788-800 [19388938.001]
  • [Cites] Blood. 2009 Jul 30;114(5):937-51 [19357394.001]
  • [Cites] Leukemia. 2009 Aug;23(8):1441-5 [19295546.001]
  • [Cites] Nature. 2009 Aug 13;460(7257):904-8 [19620960.001]
  • [Cites] J Clin Oncol. 2009 Aug 20;27(24):4002-6 [19528370.001]
  • [Cites] Blood. 2009 Aug 20;114(8):1477-83 [19549988.001]
  • [Cites] Blood. 2009 Aug 27;114(9):1859-63 [19571318.001]
  • [Cites] J Clin Oncol. 2009 Sep 1;27(25):4150-4 [19636000.001]
  • [Cites] Acta Neuropathol. 2009 Oct;118(4):469-74 [19554337.001]
  • [Cites] N Engl J Med. 2009 Sep 10;361(11):1058-66 [19657110.001]
  • [Cites] N Engl J Med. 2009 Sep 10;361(11):1117; author reply 1117-8 [19741235.001]
  • [Cites] Leukemia. 2003 Mar;17(3):637-41 [12646957.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Jun;37(2):214-9 [12696071.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 3;101(31):11444-7 [15269348.001]
  • [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] J Clin Oncol. 2009 Dec 20;27(36):6109-16 [19901108.001]
  • [Cites] Am J Hematol. 2010 Jan;85(1):81-3 [19957346.001]
  • [Cites] J Biol Chem. 2010 Jan 1;285(1):18-29 [19880879.001]
  • [Cites] Blood. 2010 Jan 7;115(1):38-46 [19861679.001]
  • [Cites] Haematologica. 2010 Jan;95(1):65-70 [19713221.001]
  • [Cites] Leukemia. 2010 Jan;24(1):201-3 [19710701.001]
  • [Cites] Leukemia. 2010 Jan;24(1):110-4 [19847198.001]
  • [Cites] Leukemia. 2010 Jan;24(1):105-9 [19847199.001]
  • [Cites] Cancer Res. 2010 Jan 15;70(2):447-52 [20068184.001]
  • [Cites] N Engl J Med. 2010 Jan 28;362(4):369-70 [20107228.001]
  • [Cites] Blood. 2010 Jan 28;115(4):778-82 [19965680.001]
  • [Cites] Blood. 2010 Feb 4;115(5):1037-48 [19996410.001]
  • [Cites] Leukemia. 2010 Feb;24(2):469-73 [19865112.001]
  • [Cites] Blood. 2010 Feb 11;115(6):1254-63 [19880496.001]
  • [Cites] J Biol Chem. 2010 Feb 19;285(8):5296-307 [20028972.001]
  • [Cites] J Exp Med. 2010 Feb 15;207(2):339-44 [20142433.001]
  • [Cites] Hum Mutat. 2010 Mar;31(3):E1186-99 [20077503.001]
  • [Cites] J Clin Endocrinol Metab. 2010 Mar;95(3):1274-8 [19915015.001]
  • [Cites] Haematologica. 2010 Mar;95(3):518-9 [19903679.001]
  • [Cites] Blood. 2010 Mar 11;115(10):1969-75 [20008299.001]
  • [Cites] Blood. 2010 Mar 11;115(10):2003-7 [20061559.001]
  • [Cites] Cancer Cell. 2010 Mar 16;17(3):225-34 [20171147.001]
  • [Cites] Acta Neuropathol. 2010 Apr;119(4):487-94 [20127344.001]
  • [Cites] Hum Mol Genet. 2010 Apr 15;19(8):1507-14 [20093295.001]
  • [Cites] Blood. 2010 Apr 8;115(14):2891-900 [20008300.001]
  • [Cites] Leukemia. 2010 Apr;24(4):859-60 [20111067.001]
  • [Cites] Blood. 2010 Apr 29;115(17):3589-97 [20197548.001]
  • [Cites] Leukemia. 2010 May;24(5):1069-73 [20182460.001]
  • [Cites] Leukemia. 2010 Jun;24(6):1146-51 [20410924.001]
  • [Cites] Leukemia. 2008 Apr;22(4):740-7 [18079739.001]
  • [Cites] Leukemia. 2008 Apr;22(4):756-61 [18216871.001]
  • [Cites] Nature. 2008 May 1;453(7191):110-4 [18408710.001]
  • [Cites] Leuk Lymphoma. 2008 May;49(5):847-9 [18464105.001]
  • [Cites] Leukemia. 2008 May;22(5):1059-62 [17972958.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1295-8 [18059483.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1289 [18079740.001]
  • [Cites] Blood. 2008 Jul 1;112(1):141-9 [18451306.001]
  • [Cites] Leukemia. 2008 Jul;22(7):1472-4 [18239619.001]
  • [Cites] Leukemia. 2008 Jul;22(7):1299-307 [18496562.001]
  • [Cites] Blood. 2008 Aug 1;112(3):844-7 [18519816.001]
  • [Cites] Blood. 2008 Aug 15;112(4):1402-12 [18515659.001]
  • [Cites] Leukemia. 2008 Aug;22(8):1557-66 [18528423.001]
  • [Cites] Blood. 2008 Sep 15;112(6):2199-204 [18451307.001]
  • [Cites] Blood. 2008 Sep 15;112(6):2429-38 [18612101.001]
  • [Cites] Int J Cancer. 2009 Nov 15;125(10):2485-6 [19530255.001]
  • [Cites] Blood. 2009 Oct 1;114(14):3018-23 [19541820.001]
  • [Cites] Clin Cancer Res. 2009 Oct 1;15(19):6002-7 [19755387.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Sep 29;106(39):16616-21 [19805346.001]
  • [Cites] Nature. 2009 Oct 8;461(7265):819-22 [19783980.001]
  • [Cites] Blood. 2009 Oct 8;114(15):3285-91 [19666869.001]
  • [Cites] Leukemia. 2009 Oct;23(10):1924-6 [19440215.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2009 Nov;297(5):H1545-56 [19717737.001]
  • [Cites] N Engl J Med. 2009 Nov 5;361(19):1872-85 [19890130.001]
  • [Cites] Blood. 2009 Nov 5;114(19):4197-208 [19734451.001]
  • [Cites] Leukemia. 2009 Nov;23(11):2183-6 [19609284.001]
  • [Cites] J Clin Oncol. 2009 Dec 1;27(34):5743-50 [19805672.001]
  • [Cites] Haematologica. 2009 Dec;94(12):1676-81 [19797729.001]
  • [Cites] J Clin Oncol. 2009 Dec 10;27(35):5874-80 [19901110.001]
  • [Cites] Nature. 2009 Dec 10;462(7274):739-44 [19935646.001]
  • (PMID = 20428194.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ASXL1 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / IKZF1 protein, human; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Thrombopoietin; 0 / Repressor Proteins; 0 / TET2 protein, human; 143641-95-6 / MPL protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Number-of-references] 171
  • [Other-IDs] NLM/ PMC3035972
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92. Roboz GJ, Giles FJ, List AF, Cortes JE, Carlin R, Kowalski M, Bilic S, Masson E, Rosamilia M, Schuster MW, Laurent D, Feldman EJ: Phase 1 study of PTK787/ZK 222584, a small molecule tyrosine kinase receptor inhibitor, for the treatment of acute myeloid leukemia and myelodysplastic syndrome. Leukemia; 2006 Jun;20(6):952-7
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  • [Title] Phase 1 study of PTK787/ZK 222584, a small molecule tyrosine kinase receptor inhibitor, for the treatment of acute myeloid leukemia and myelodysplastic syndrome.
  • The objective of this Phase I study was to evaluate the safety, tolerability, biologic activity and pharmacologic profile of PTK/ZK administered orally, twice daily, on a continuous dosing schedule in patients with primary refractory or relapsed acute myeloid leukemia (AML), secondary AML, poor-prognosis de novo AML or advanced myelodysplastic syndrome (MDS).
  • Acute myeloid leukemia patients for whom PTK/ZK monotherapy was ineffective could receive PTK/ZK combined with standard induction chemotherapy.
  • Complete remission was observed in five of 17 AML patients treated with PTK/ZK combined with chemotherapy.
  • The drug is generally well tolerated and can be given in combination with chemotherapy for patients with MDS and AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. Phthalazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyridines / therapeutic use
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Cell Proliferation / drug effects. Cohort Studies. Dose-Response Relationship, Drug. Drug Therapy, Combination. Female. Humans. Male. Middle Aged. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Treatment Outcome. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors


93. Rodriguez CP, Baz R, Jawde RA, Rybicki LA, Kalaycio ME, Advani A, Sobecks R, Sekeres MA: Impact of socioeconomic status and distance from treatment center on survival in patients receiving remission induction therapy for newly diagnosed acute myeloid leukemia. Leuk Res; 2008 Mar;32(3):413-20
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  • [Title] Impact of socioeconomic status and distance from treatment center on survival in patients receiving remission induction therapy for newly diagnosed acute myeloid leukemia.
  • BACKGROUND: While socioeconomic status (SES) and the distance patients travel to a treatment center (DTC) impact survival of certain solid tumors, little is known of their influence in acute myeloid leukemia (AML).
  • METHODS: We retrospectively reviewed patients receiving remission induction therapy for AML at the Cleveland Clinic between January 1997 and December 2005.
  • Known prognostic factors (age, WBC count at diagnosis, cytogenetics, AML etiology) were collected and controlled for in Cox proportional hazards analysis.
  • RESULTS: Induction chemotherapy was administered to 281 patients; 91% were Caucasian (C), 8% were African American (AA), and 1% were neither (non-AA non-C).
  • In multivariable analyses, age >or=60 years, unfavorable cytogenetics, initial WBC count and secondary AML significantly influenced survival (p<0.001, p<0.001, p=0.035, and p=0.010, respectively).
  • OS was similar for AAs and non-AA non-Cs compared to Cs (HR=1.12, 95% CI=.61-2.07, p=.71, and HR=0.87, CI=0.21-3.62, p=.84, respectively).
  • CONCLUSION: Unlike with many solid tumors, SES and DTC are not predictive of outcome in AML patients.
  • [MeSH-major] Leukemia, Myeloid, Acute / psychology. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 17727945.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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94. Marcucci G, Stock W, Dai G, Klisovic RB, Liu S, Klisovic MI, Blum W, Kefauver C, Sher DA, Green M, Moran M, Maharry K, Novick S, Bloomfield CD, Zwiebel JA, Larson RA, Grever MR, Chan KK, Byrd JC: Phase I study of oblimersen sodium, an antisense to Bcl-2, in untreated older patients with acute myeloid leukemia: pharmacokinetics, pharmacodynamics, and clinical activity. J Clin Oncol; 2005 May 20;23(15):3404-11
Hazardous Substances Data Bank. DAUNORUBICIN .

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  • [Title] Phase I study of oblimersen sodium, an antisense to Bcl-2, in untreated older patients with acute myeloid leukemia: pharmacokinetics, pharmacodynamics, and clinical activity.
  • PURPOSES: Pharmacologic downregulation of Bcl-2, an antiapoptotic protein overexpressed in cancer, might increase chemosensitivity in acute myeloid leukemia (AML).
  • Herein, we investigated the feasibility of this approach in untreated elderly AML patients by administering oblimersen sodium (G3139), an 18-mer phosphorothioate antisense to Bcl-2, during induction and consolidation treatments.
  • PATIENTS AND METHODS: Untreated patients with primary or secondary AML (stratified to cohort 1 or 2, respectively) who were > or = 60 years received induction with G3139, cytarabine, and daunorubicin at one of two different dose levels (45 and 60 mg/m2) and, on achievement of complete remission (CR), consolidation with G3139 and high-dose cytarabine.
  • [MeSH-major] Daunorubicin / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Proto-Oncogene Proteins c-bcl-2 / drug effects. Remission Induction. Thionucleotides / administration & dosage. Thionucleotides / pharmacokinetics

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  • (PMID = 15824414.001).
  • [ISSN] 0732-183X
  • [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 / K08-CA90469; United States / NCI NIH HHS / CA / P30-CA16058; United States / NCI NIH HHS / CA / R01-CA102031; United States / NCI NIH HHS / CA / R21-CA 094552; United States / NCI NIH HHS / CA / U01-CA76576
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Comparative Study; 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 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Thionucleotides; 85J5ZP6YSL / oblimersen; ZS7284E0ZP / Daunorubicin
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95. Vitolo U, Liberati AM, Cabras MG, Federico M, Angelucci E, Baldini L, Boccomini C, Brugiatelli M, Calvi R, Ciccone G, Genua A, Deliliers GL, Levis A, Parvis G, Pavone E, Salvi F, Sborgia M, Gallo E, Intergruppo Italiano Linfomi: High dose sequential chemotherapy with autologous transplantation versus dose-dense chemotherapy MegaCEOP as first line treatment in poor-prognosis diffuse large cell lymphoma: an "Intergruppo Italiano Linfomi" randomized trial. Haematologica; 2005 Jun;90(6):793-801
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  • Two cases of secondary acute myeloid leukemia were observed after treatment in group A.

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  • (PMID = 15951292.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 3Z8479ZZ5X / Epirubicin; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; Q41OR9510P / Melphalan; VB0R961HZT / Prednisone
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96. Makishima H, Cazzolli H, Szpurka H, Dunbar A, Tiu R, Huh J, Muramatsu H, O'Keefe C, Hsi E, Paquette RL, Kojima S, List AF, Sekeres MA, McDevitt MA, Maciejewski JP: Mutations of e3 ubiquitin ligase cbl family members constitute a novel common pathogenic lesion in myeloid malignancies. J Clin Oncol; 2009 Dec 20;27(36):6109-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutations of e3 ubiquitin ligase cbl family members constitute a novel common pathogenic lesion in myeloid malignancies.
  • PURPOSE: Acquired somatic uniparental disomy (UPD) is commonly observed in myelodysplastic syndromes (MDS), myelodysplastic/myeloproliferative neoplasms (MDS/MPN), or secondary acute myelogenous leukemia (sAML) and may point toward genes harboring mutations.
  • METHODS: We applied high-density SNP-A karyotyping to identify loss of heterozygosity of 11q in 442 patients with MDS, MDS/MPN, MPN, sAML evolved from these conditions, and primary AML.
  • RESULTS: We identified c-Cbl mutations in 5% and 9% of patients with chronic myelomonocytic leukemia (CMML) and sAML, and also in CML blast crisis and juvenile myelomonocytic leukemia (JMML).
  • CONCLUSION: Mutations in the Cbl family RING finger domain or linker sequence constitute important pathogenic lesions associated with not only preleukemic CMML, JMML, and other MPN, but also progression to AML, suggesting that impairment of degradation of activated tyrosine kinases constitutes an important cancer mechanism.

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  • [Cites] Leukemia. 2009 Mar;23(3):610-4 [18818701.001]
  • [Cites] Haematologica. 2008 Oct;93(10):1595-7 [18698078.001]
  • [Cites] Nat Genet. 2004 Sep;36(9):949-51 [15286789.001]
  • [Cites] Oncogene. 1991 Apr;6(4):653-7 [2030914.001]
  • [Cites] Mol Cell Biol. 1998 Aug;18(8):4872-82 [9671496.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [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] Nat Rev Mol Cell Biol. 2005 Dec;6(12):907-18 [16227975.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1242-3 [16434499.001]
  • [Cites] PLoS Genet. 2005 Dec;1(6):e49 [16444292.001]
  • [Cites] Blood. 2006 Mar 1;107(5):1791-9 [16254134.001]
  • [Cites] J Cell Physiol. 2006 Oct;209(1):21-43 [16741904.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2173-81 [16741247.001]
  • [Cites] PLoS Med. 2006 Jul;3(7):e270 [16834459.001]
  • [Cites] Am J Surg Pathol. 2007 Feb;31(2):233-9 [17255768.001]
  • [Cites] Blood. 2007 Aug 1;110(3):1004-12 [17446348.001]
  • [Cites] Blood. 2007 Aug 1;110(3):1022-4 [17475912.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2058-61 [17525728.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3365-73 [17634407.001]
  • [Cites] PLoS One. 2007;2(11):e1225 [18030353.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1534-42 [17954704.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]
  • [Cites] Blood. 2008 Aug 15;112(4):965-74 [18505780.001]
  • [Cites] Semin Oncol. 2008 Aug;35(4):365-77 [18692687.001]
  • [Cites] Leukemia. 2008 Aug;22(8):1539-41 [18528419.001]
  • [Cites] Cancer Res. 2008 Dec 15;68(24):10349-57 [19074904.001]
  • [Cites] Blood. 2008 Sep 1;112(5):2017-9 [18566322.001]
  • [Cites] Curr Opin Hematol. 2001 Jul;8(4):189-91 [11561153.001]
  • (PMID = 19901108.001).
  • [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 / NHLBI NIH HHS / HL / K24 HL077522; United States / NHLBI NIH HHS / HL / R01 HL082983; United States / NCRR NIH HHS / RR / U54 RR019391; United States / NHLBI NIH HHS / HL / K24 HL-077522; United States / NHLBI NIH HHS / HL / R01HL-082983; United States / NCRR NIH HHS / RR / S10 RR019391
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Other-IDs] NLM/ PMC3040009
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97. Tangen JM, Fløisand Y, Foss-Abrahamsen J, Haukås E, Naess IA, Skjelbakken T: [Survival in adults with acute myelogenous leukemia]. Tidsskr Nor Laegeforen; 2008 May 15;128(10):1164-7
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  • [Title] [Survival in adults with acute myelogenous leukemia].
  • BACKGROUND: Acute myelogenous leukemia is the most common type of acute leukemia in adults.
  • MATERIAL AND METHODS: Survival data were retrieved from the Norwegian Registry for Acute Leukemias and Lymphoblastic Lymphomas for patients with acute myelogenous leukemia (aged from 16 to 60 years) who were registered in the period 1.1.2000-31.12.2005.
  • Patients with secondary acute myelogenous leukemia were classified as high-risk.
  • RESULTS AND INTERPRETATION: 4-year survival was 94.5% in acute promyelocytic leukemia, 77.7% in other low-risk acute myelogenous leukemia, 39.0% in standard risk patients and 29.1% in high-risk patients.
  • The increase is most probably due to an intensification of chemotherapy after remission and to the implementation of all-trans-retinoic acid in the treatment of promyelocytic leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality
  • [MeSH-minor] Adolescent. Adult. Age Factors. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Female. Humans. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / mortality. Male. Middle Aged. Neoplasm Recurrence, Local / mortality. Norway / epidemiology. Risk Factors. Survival Rate

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  • [CommentIn] Tidsskr Nor Laegeforen. 2008 Aug 14;128(15):1681-2; author reply 1682 [18704137.001]
  • (PMID = 18480864.001).
  • [ISSN] 0807-7096
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Norway
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98. Viola A, Falco C, D'Elia R, D'Amico MR, Vicari L, Tambaro FP, Correale P, Laudati D, Palmieri S, Ferrara F: An antecedent diagnosis of refractory anemia with excess blasts has no influence on mobilization of peripheral blood stem cells and hematopoietic recovery after autologous stem cell transplantation in acute myeloid leukemia. Eur J Haematol; 2007 Jan;78(1):41-7
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  • [Title] An antecedent diagnosis of refractory anemia with excess blasts has no influence on mobilization of peripheral blood stem cells and hematopoietic recovery after autologous stem cell transplantation in acute myeloid leukemia.
  • Several studies have reported data on factors influencing mobilization of peripheral blood stem cells (PBSC) in non-myeloid malignancies.
  • On the contrary, data from patients with acute myeloid leukemia (AML) are very limited, in particular, as the impact of an antecedent diagnosis of refractory anemia with excess blasts (RAEB) on mobilization of PBSCs as well as hematopoietic recovery after autologous stem cell transplantation (ASCT) is concerned.
  • We retrospectively analyzed a cohort of 150 consecutive AML patients in first complete remission in order to make a comparison between patients with de novo AML and secondary AML (s-AML) in terms of CD34 positive (CD34+) cells mobilization and number of leukapheresis needed to collect at least one single stem cell graft.
  • The successful mobilization rate (>2 x 10(6) CD34+ cells/kg) was comparable between de novo AML patients (87%) and those with s-AML (76%), P:0.21.
  • An antecedent diagnosis of RAEB has no impact on mobilization and collection of PBSCs in AML as well as on hematopoietic recovery after ASCT.
  • [MeSH-major] Anemia, Refractory, with Excess of Blasts / diagnosis. Hematopoiesis. Hematopoietic Stem Cell Mobilization. Leukemia, Myeloid / therapy. Peripheral Blood Stem Cell Transplantation
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Disease-Free Survival. Female. Humans. Male. Middle Aged. Transplantation, Autologous. Treatment Outcome

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  • (PMID = 17042770.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
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99. Borchmann P, Behringer K, Josting A, Rueffer JU, Schnell R, Diehl V, Engert A, Kvasnicka HM, Thiele J: [Secondary malignancies after successful primary treatment of malignant Hodgkin's lymphoma]. Pathologe; 2006 Feb;27(1):47-52
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  • [Title] [Secondary malignancies after successful primary treatment of malignant Hodgkin's lymphoma].
  • These regimens are aggressive, including radiotherapy and chemotherapy leading to the possibility of secondary malignancies.
  • In 127 patients a secondary solid tumor was diagnosed (cumulative risk 2%, median follow-up 72 months), with bronchial carcinomas (23.6%) and colorectal adenocarcinomas (20.5%) being the most frequent neoplasms.
  • Secondary acute myeloid leukemia was found in 36 patients, another ten developed myeloid dysplasia (cumulative risk 1%, median follow-up 55 months).
  • A total of 52 patients revealed a non-Hodgkin's lymphoma (NHL; cumulative risk 0.9%, median follow-up 46 months).
  • The overall incidence of secondary malignancies was 3.9% in patients who had been treated successfully for their HL with radio- and/or chemotherapy.A secondary NHL can be particularly difficult to be distinguished from the preceding HL.
  • [MeSH-minor] Cohort Studies. Humans. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / pathology. Neoplasm Staging. Retrospective Studies

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  • (PMID = 16369761.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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100. Jekarl DW, Kim M, Lim J, Kim Y, Han K, Lee AW, Kim HJ, Min WS: CD56 antigen expression and hemophagocytosis of leukemic cells in acute myeloid leukemia with t(16;21)(p11;q22). Int J Hematol; 2010 Sep;92(2):306-13
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  • [Title] CD56 antigen expression and hemophagocytosis of leukemic cells in acute myeloid leukemia with t(16;21)(p11;q22).
  • The translocation t(16;21)(p11;q22) is rare, occurs with an incidence of 1%, in acute myeloid leukemia (AML), forming TLS/FUS-ERG fusion transcript, and it is known to cause the hemophagocytosis and vacuolation of leukemic cells.
  • As previously reported cases numbered less than 60, we aimed to identify the clinical and genetic aspects of AML with t(16;21).
  • Among 1,277 patients diagnosed with de novo and secondary AML, 12 AML patients with t(16;21) were retrospectively evaluated (0.94%, 12/1,277).
  • AML with t(16;21) expressed CD56 with a median value of 45% (7.8-87%), and the rate of hemophagocytosis plus vacuolation of leukemic cells was 2.9% (2.0-9.0%).
  • AML with t(16;21) expressed CD13, CD33, CD34, CD117, CD56, HLA-DR, and cytoplasmic myeloperoxidase.
  • RUNX1, which regulates a gene for hematopoiesis, is frequently mutated in AML and, in this study, one out of three patients showed the mutation R174Q in RUNX1.
  • AML with t(16;21) showed a very low rate of complete remission after induction chemotherapy (8.3%), and high relapse (75%) and mortality (75%) rates.
  • AML with t(16;21) exhibited a distinct morphology with frequent CD56 expression and a poor prognosis.
  • [MeSH-major] Antigens, CD56 / analysis. Cytophagocytosis. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Translocation, Genetic

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
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  • (PMID = 20694842.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56
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