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1. Kuendgen A, Schmid M, Schlenk R, Knipp S, Hildebrandt B, Steidl C, Germing U, Haas R, Dohner H, Gattermann N: The histone deacetylase (HDAC) inhibitor valproic acid as monotherapy or in combination with all-trans retinoic acid in patients with acute myeloid leukemia. Cancer; 2006 Jan 1;106(1):112-9
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  • [Title] The histone deacetylase (HDAC) inhibitor valproic acid as monotherapy or in combination with all-trans retinoic acid in patients with acute myeloid leukemia.
  • BACKGROUND: Valproic acid (VPA) inhibits histone deacetylase activity and, synergizing with all-trans retinoic acid (ATRA), achieves differentiation induction of myeloid blast cells in vitro.
  • METHODS: We used VPA in 58 patients with acute myeloid leukemia (AML) who were too old and/or medically unfit to receive intensive chemotherapy (32 AML secondary to myelodysplastic syndrome [MDS], 22 de novo AML, 4 AML secondary to myeloproliferative syndrome).
  • RESULTS: The response rate was only 5% according to International Working Group (IWG) criteria for AML but was 16% when IWG response criteria for MDS were used, which capture hematologic improvement and stabilization of the disease.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Histone Deacetylase Inhibitors. Leukemia, Myeloid / drug therapy. Tretinoin / therapeutic use. Valproic Acid / therapeutic use
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Male. Middle Aged. Treatment Outcome


2. Juliusson G, Billström R, Gruber A, Hellström-Lindberg E, Höglunds M, Karlsson K, Stockelberg D, Wahlin A, Aström M, Arnesson C, Brunell-Abrahamsson U, Carstensen J, Fredriksson E, Holmberg E, Nordenskjöld K, Wiklund F, Swedish Adult Acute Leukemia Registry Group: Attitude towards remission induction for elderly patients with acute myeloid leukemia influences survival. Leukemia; 2006 Jan;20(1):42-7
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  • [Title] Attitude towards remission induction for elderly patients with acute myeloid leukemia influences survival.
  • Combination chemotherapy may induce remission from acute myeloid leukemia (AML), but validated criteria for treatment of elderly are lacking.
  • The remission intention (RI) rate for elderly patients, as reported to the Swedish Leukemia Registry, was known to be different when comparing the six health care regions, but the consequences of different management are unknown.
  • The Leukemia Registry, containing 1672 AML patients diagnosed between 1997 and 2001, with 98% coverage and a median follow-up of 4 years, was completed with data from the compulsory cancer and population registries.
  • Among 506 treated and untreated patients aged 70-79 years with AML (non-APL), there was a direct correlation between the RI rate in each health region (range 36-76%) and the two-year overall survival, with no censored observations (6-21%) (chi-squared for trend=11.3, P<0.001; r2=0.86, P<0.02, nonparametric).
  • Differences could not be explained by demographics, and was found in both de novo and secondary leukemias.
  • Survival of 70-79-year-old AML patients is better in regions where more elderly patients are judged eligible for remission induction.
  • [MeSH-major] Attitude of Health Personnel. Leukemia, Myeloid / drug therapy. Patient Selection
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Distribution. Age Factors. Aged. Aged, 80 and over. Follow-Up Studies. Humans. Middle Aged. Registries. Remission Induction. Survival Rate. Sweden / epidemiology. Treatment Outcome


3. Nakamae H, Himuro K, Hagihara K, Terada Y, Sakamoto E, Takeoka Y, Nakane T, Nakamae M, Ohta K, Yamane T, Shimada H, Miki T, Hino M: [Chronic GVHD with polymyositis after non-myeloablative stem cell transplantation]. Rinsho Ketsueki; 2005 Nov;46(11):1213-7
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  • [Title] [Chronic GVHD with polymyositis after non-myeloablative stem cell transplantation].
  • He was diagnosed with further hematological examination as having acute myeloid leukemia with multilineage dysplasia following secondary myelodysplastic syndrome.

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  • (PMID = 16440806.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 9PHQ9Y1OLM / Prednisolone
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4. Junghanss C, Waak M, Knopp A, Kleine HD, Kundt G, Leithäuser M, Hilgendorf I, Wolff D, Casper J, Freund M: Multivariate analyses of prognostic factors in acute myeloid leukemia: relevance of cytogenetic abnormalities and CD34 expression. Neoplasma; 2005;52(5):402-10
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  • [Title] Multivariate analyses of prognostic factors in acute myeloid leukemia: relevance of cytogenetic abnormalities and CD34 expression.
  • Identification of additional prognostic factors besides karyotype is important for the improvement of the risk adapted treatment strategies in acute myeloid leukemia (AML).
  • The aim of this study was to investigate whether other factors besides karyotype could be used as a prognostic tool in newly diagnosed AML.
  • Biological and disease related established and potential prognostic factors were retrospectively analysed in 124 consecutive AML patients treated between 1993 and 2002 at the University hospital Rostock (Germany).
  • In patients that received potential curative therapies LDH >or=2000 U/l, WBC >50 GPT/l, CD34 surface expression on the AML blasts, secondary AML, unfavorable karyotype and no allogeneic HSCT at some point of treatment course were associated with unfavorable prognosis.
  • However, in the multivariate risk factor analyses only unfavorable karyotype (p=0.012), CD34 positivity of AML blasts (p=0.046), no allogeneic HSCT (p=0.008) and first diagnosis after 1997 (p=0.025) were independent unfavourable prognostic factors.
  • In conclusion, karyotype and CD34 expression are independent prognostic markers in newly diagnosed AML.
  • Furthermore, receiving an allogeneic HSCT at some point of the treatment course seems to be of benefit for AML patients.
  • [MeSH-major] Antigens, CD34 / metabolism. Biomarkers, Tumor / analysis. Chromosome Aberrations. Leukemia, Myeloid / genetics. Leukemia, Myeloid / mortality
  • [MeSH-minor] Acute Disease / therapy. Adult. Age Factors. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Flow Cytometry. Hematopoietic Stem Cell Transplantation. Humans. Karyotyping. Middle Aged. Multivariate Analysis. Palliative Care. Prognosis. Remission Induction. Retrospective Studies. Risk Factors. Survival Analysis. Treatment Outcome

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  • (PMID = 16151585.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers, Tumor
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5. Dimou J, Jithoo R, Tsui A, Morokoff AP: Spinal cord compression as the initial presentation of acute biphenotypic leukaemia. J Clin Neurosci; 2009 Dec;16(12):1696-8
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  • [Title] Spinal cord compression as the initial presentation of acute biphenotypic leukaemia.
  • Acute biphenotypic leukaemia (BAL) is an uncommon haematological malignancy with features of myeloid and lymphoid origin and poor overall prognosis.
  • We report a 68-year-old man who presented with rapidly progressive upper thoracic spinal cord compression secondary to an extradural lesion.
  • Histopathology confirmed the diagnosis of acute biphenotypic (B/myeloid) leukaemia.
  • While central nervous system involvement with acute leukaemia is well recognised, this is the first reported patient with spinal cord compression secondary to this leukaemia subtype.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / etiology. Spinal Cord Compression / complications

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  • (PMID = 19815414.001).
  • [ISSN] 1532-2653
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antigens, CD79; EC 1.11.1.7 / Peroxidase
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6. Burnett AK, Milligan D, Goldstone A, Prentice A, McMullin MF, Dennis M, Sellwood E, Pallis M, Russell N, Hills RK, Wheatley K, United Kingdom National Cancer Research Institute Haematological Oncology Study Group: The impact of dose escalation and resistance modulation in older patients with acute myeloid leukaemia and high risk myelodysplastic syndrome: the results of the LRF AML14 trial. Br J Haematol; 2009 May;145(3):318-32
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  • [Title] The impact of dose escalation and resistance modulation in older patients with acute myeloid leukaemia and high risk myelodysplastic syndrome: the results of the LRF AML14 trial.
  • The acute myeloid leukaemia (AML)14 trial addressed four therapeutic questions in patients predominantly aged over 60 years with AML and High Risk Myelodysplastic Syndrome: (i) Daunorubicin 50 mg/m(2) vs. 35 mg/m(2);.
  • Multivariable analysis identified cytogenetics, presenting white blood count, age and secondary disease as the main predictors of outcome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy

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  • [CommentIn] Br J Haematol. 2009 May;145(3):333 [19222475.001]
  • (PMID = 19291085.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300133
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclosporins; 04079A1RDZ / Cytarabine; Q7ZP55KF3X / valspodar; ZS7284E0ZP / Daunorubicin
  • [Investigator] Culligan DJ; Tighe J; Craig J; Marcus RE; Cuthbert AC; Cuthbert RJ; Ryan MF; Deeble TJ; Galvani DW; Berney SI; Harvey D; Virchis A; Cuthbert RJ; Jones F; Kettle P; McMullin MF; Morris TC; Fegan C; Johnson RJ; Milligan DW; Pratt GE; Gelly K; Tucker J; Newton LJ; Parapia LA; Williams AT; Bird JM; Evely R; Hows JM; Marks D; Scott GL; Standen GR; Blundell E; Chown S; Dalton RG; Lush R; Ropner J; Collin R; Stewart R; Wodzinski M; Cavet J; Chopra R; Dennis M; Beard J; Clough JV; Rhodes E; Erskine JG; Mccoll M; Micallef-Eynaud PD; Mckernan A; Mitchell DC; Copplestone A; Hamon M; Nokes TJ; Prentice A; Rule S; Chapple MR; Speed K; Paul B; Moosa AH; Dang RK; Abrahamson G; Hedge UM; Philpott N; Gover PA; Grace RJ; Birch AD; Narayanan M; Edwards DR; Gozzard DI; Hoyle C; Mcquaker G; Parker AN; Chown S; Lush R; Hamilton MS; Schey SA; Rahemtulla A; Bynoe AG; Harrison J; Robinson LG; Kaczmarski R; Hoggarth C; Rege K; Houghton JB; Braithwaite JE; Carter C; Ali S; Patil K; Shields ML; Ademokun JA; Chalmers I; Jeha T; Sadullah S; Pocock CF; Kelsey H; Lyttleton M; Wilson-Morkeh I; Akhtar N; Grant I; Mufti G; Pagliuca A; Rowley MR; Sykes H; Child JA; Morgan GJ; Norfolk DR; Smith GM; Chapman CS; Hunter AE; Kennedy B; Snowden JA; Heppleston A; Prangnell DR; Williams C; Sekhar M; Burthem J; Liu Yin JA; Lucas GS; Galvin GP; Jacob A; Aldouri M; White DM; Cook G; Murphy JA; Singer I; Watson WH; Ardeshna K; Basu S; Jacob A; Bowen DT; Cachia PG; Meiklejohn D; Aston L; Milne A; Luckit J; Chasty RC; Chipping PM; Ibbotson RM; Schofield KP; Haines ME; Allard S; Corbett T; Panoskaltsis N; Reid CD; Byrne JL; Haynes AP; Jones PA; Russell NH; Brownell A; Lewis D; Gale RF; Gillett D; Taylor CG; Sivakumaran M; Sobolewski S; Tringham V; Galvin MC; Hillmen P; Wright D; Bell AJ; Jack F; Cranfield T; Dignum H; Ganczakowski M; Coates P; Keidan AJ; Murray JA; Bowcock SJ; Rassam S; Ward S; Forsyth P; Lush C; Murray W; Barker HF; Taylor PC; Brito-Babapulle F; Grech H; Morgenstern G; Hamblin TJ; Killick S; Oscier DG; Joyner MV; Lee R; Pocock M; Rudin C; Ethell M; Kottaridis P; Mehta A; Potter M; Jackson HA; Rees DC; Reilly JT; Snowden J; Winfield DA; Dearden CE; Ethell M; Douglas I; Jones F; McMullin MF; Bareford D; Harrison P; Neilson J; Richardson SG; Cullis JO; Parry HF; Bareford D; Wright JG; Handa S; Hasan Y; Stableforth PJ; Ezekwesili R; Jalihal S; Al-Ismail S; Duncombe A; Orchard K; Richardson D; Smith A; Eden A; Mills MJ; Manson LM; Morrison AE; Dearden CE; Scully M; Behrens J; Clarke M; Rice K; Barnard DL; Johnson R; Mcverry BA; Abdalla SH; Bevan PC; Janes S; Stross P; Carr R; Amos A; Revell P; Leach MT; Watson A; Saied K; Shafeek S; Vosylius P; Blesing NE; Gray AG; Green ES; De Lord CF; Lakhani AK; Vadher B; Grey M; Jip J; Clark RE; Booth F; Roberts P; Rymes N; Smith S; Turner D; Ardeshna K; Devereux S; Goldstone AH; Khwaja A; Linch DC; Nathwani A; Patterson KG; Porter JB; Yong K; Dasgupta R; Olujohungbe A; Sadik W; Woodcock BE; Tillyer ML; Backstrom B; Markevarn B; Sundstrom G; Wahlin A; Burnett AK; Kell J; Poynton C; Rowntree C; Whittaker JA; Bourantas KL; Rogers S; Sharp RA; Tansey P; Jackson N; Strevens MJ; Sadik W; Basu S; Mills J; Rose PE; Dearden CE; Hughes RG; Sekhar M; Davies JM; Ganly P; Johnson PR; Roddie PH; Fitzsimons EJ; Lucie NJ; Soutar R; Anderson CC; DeSilva C; Satchi G; Tappin JA; Gale RF; Allan TL; Stockley R; O'Driscoll AM; Rist CL; Aitchison R; Kelly S; Pattinson J; Bond LR; Howard MR; Gilleece M; Parry H; Seale J
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7. Li ZY, Liu DP, Liang CC: New insight into the molecular mechanisms of MLL-associated leukemia. Leukemia; 2005 Feb;19(2):183-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New insight into the molecular mechanisms of MLL-associated leukemia.
  • Rearrangements of the MLL gene (ALL1, HRX, and Hrtx) located at chromosome band 11q23 are commonly involved in adult and pediatric cases of primary acute leukemias and also found in cases of therapy-related secondary leukemias.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Mutation. Myeloid-Lymphoid Leukemia Protein. Zinc Fingers / genetics

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  • (PMID = 15618964.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 89
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8. Ooi J: The efficacy of unrelated cord blood transplantation for adult myelodysplastic syndrome. Leuk Lymphoma; 2006 Apr;47(4):599-602
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  • Diagnosis at transplantation included refractory anemia (RA) (n = 3), refractory anemia with excess blasts (RAEB) (n = 2), RAEB-t (n = 2), and MDS-related secondary acute myeloid leukemia (AML) (n = 15).
  • Twenty one patients had myeloid reconstitution and the median time to more than 0.5 x 10(9)/l absolute neutrophil count was 22.5 days.
  • Acute GVHD above grade II occurred in seven of 21 evaluable patients and chronic GVHD in 16 of 19 evaluable patients.


9. Girod A, Breton P: [Two cases of malignant tumors of the face after hematopoietic stem cell transplantation]. Rev Stomatol Chir Maxillofac; 2005 Apr;106(2):107-10
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  • OBSERVATION: Two patients underwent HSCT for acute leukemia.
  • DISCUSSION: Several factors are involved in the development of secondary malignant tumors after HSCT.
  • Squamous cell carcinoma of the oral cavity after HSCT presents the same clinical, histological and prognostic features as in the non-grafted patient.
  • [MeSH-major] Carcinoma, Mucoepidermoid / etiology. Carcinoma, Squamous Cell / etiology. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid, Acute / therapy. Parotid Neoplasms / etiology. Tongue Neoplasms / etiology
  • [MeSH-minor] Adult. Female. Graft vs Host Disease / etiology. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 15924098.001).
  • [ISSN] 0035-1768
  • [Journal-full-title] Revue de stomatologie et de chirurgie maxillo-faciale
  • [ISO-abbreviation] Rev Stomatol Chir Maxillofac
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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10. Ko KH, Hsu HH, Kao WY, Chang CF, Cheng MF, Huang GS: An unusual radiologic pattern of cryptogenic organizing pneumonia: diffuse pulmonary nodules in a leukemia patient. Korean J Radiol; 2009 Jan-Feb;10(1):93-6
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  • [Title] An unusual radiologic pattern of cryptogenic organizing pneumonia: diffuse pulmonary nodules in a leukemia patient.
  • We describe a case of COP in 49-year-old woman with acute myeloid leukemia who developed diffuse pulmonary nodules during the second course of induction chemotherapy.
  • [MeSH-major] Cryptogenic Organizing Pneumonia / radiography. Leukemia, Myeloid, Acute / complications. Lung / radiography. Multiple Pulmonary Nodules / radiography
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Lung Neoplasms / radiography. Lung Neoplasms / secondary. Middle Aged

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  • [Cites] Eur Radiol. 2002 Jun;12(6):1512-22 [12042962.001]
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  • (PMID = 19182510.001).
  • [ISSN] 1229-6929
  • [Journal-full-title] Korean journal of radiology
  • [ISO-abbreviation] Korean J Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2647170
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11. Roufosse F, Goldman M, Cogan E: Hypereosinophilic syndrome: lymphoproliferative and myeloproliferative variants. Semin Respir Crit Care Med; 2006 Apr;27(2):158-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent research in cellular and molecular biology has led to the characterization of distinct underlying hematological disorders, primitively involving cells of the myeloid or lymphoid lineage.
  • Indeed, imatinib mesylate has become first-line therapy for patients in whom the FIP1L1-PDGFRalpha fusion gene is detected, whereas corticosteroids remain the mainstay for management of patients in whom hypereosinophilia is secondary to the overproduction of interleukin 5 by abnormal T-cells.
  • As far as prognosis of these disease variants is concerned, hypereosinophilic syndrome patients with the FIP1L1-PDGFRalpha fusion gene may develop acute myelogenous (eosinophilic) leukemia, whereas those with clonal interleukin-5-producing T-cells have an increased risk of developing T-cell lymphoma.

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  • (PMID = 16612767.001).
  • [ISSN] 1069-3424
  • [Journal-full-title] Seminars in respiratory and critical care medicine
  • [ISO-abbreviation] Semin Respir Crit Care Med
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / CD52 antigen; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Glucocorticoids; 0 / Glycoproteins; 0 / Immunologic Factors; 0 / Interleukin-5; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 70
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12. Pagano L, Pulsoni A, Vignetti M, Tosti ME, Falcucci P, Fazi P, Fianchi L, Levis A, Bosi A, Angelucci E, Bregni M, Gabbas A, Peta A, Coser P, Ricciuti F, Morselli M, Caira M, Foà R, Amadori S, Mandelli F, Leone G, GIMEMA: Secondary acute myeloid leukaemia: results of conventional treatments. Experience of GIMEMA trials. Ann Oncol; 2005 Feb;16(2):228-33
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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 leukaemia: results of conventional treatments. Experience of GIMEMA trials.
  • BACKGROUND: The aim of the study was to evaluate the outcome of acute myeloid leukaemia (AML) in patients with a previous malignancy (sAML) treated with chemo- and/or radiotherapy, enrolled in conventional trials.
  • PATIENTS AND METHODS: In a multicentre setting, a prospective non-concurrent analysis was performed on 2513 new AML patients, aged 12-78 years, consecutively enrolled in EORTC-GIMEMA trials between 1987 and 2001.
  • Thirty-eight patients with sAML were identified and compared with a group of 114 de novo AML patients matched according to age, French-American-British criteria, white blood cell count at diagnosis, trial and time of diagnosis of AML.
  • RESULTS: Comparing the complete remission (CR) rate between 38 sAML patients and 114 de novo AML patients, selected according to the previously reported criteria, we observed no difference in the CR rates [25/38 (66%) versus 66/114 (58%); Pearson chi(2) 0.7393, P=0.390] as well as no differences while comparing the DFS and the OS between the two groups.
  • Similar to de novo AML patients, sAML patients show good response to treatment and the possibility of cure.

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  • (PMID = 15668275.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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13. Kim SJ, Park TS, Lee ST, Song J, Suh B, Kim SH, Jang SJ, Lee CH, Choi JR: Therapy-related myelodysplastic syndrome/acute myeloid leukemia after treatment with temozolomide in a patient with glioblastoma multiforme. Ann Clin Lab Sci; 2009;39(4):392-8
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  • [Title] Therapy-related myelodysplastic syndrome/acute myeloid leukemia after treatment with temozolomide in a patient with glioblastoma multiforme.
  • Therapy-related myelodysplastic syndrome and acute leukemia after treatment with temozolomide have rarely been described in the literature.
  • The cases included anaplastic astrocytoma (4 cases), anaplastic oligodendroglioma (2 cases), low grade astrocytoma (2 cases), low grade oligodendroglioma (1 case), and one case of secondary Philadelphia-positive acute lymphoblastic leukemia in a patient with glioblastoma multiforme.
  • Here we report a novel case of therapy-related myelodysplastic syndrome/acute myeloid leukemia associated with der(1;7)(q10;p10) in a glioblastoma multiforme patient treated with temozolomide.
  • In past reports, karyotypes in cases of therapy-related myelodysplastic syndrome/acute myeloid leukemia mostly demonstrated abnormalities in chromosomes 5 and 7.
  • However, we report a case of temozolomide-related myelodysplastic syndrome/acute myeloid leukemia with der(1;7)(q10;p10), possibly the first reported case, to the authors' knowledge.
  • [MeSH-major] Dacarbazine / analogs & derivatives. Glioblastoma / drug therapy. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced


14. Reiter A, Walz C, Watmore A, Schoch C, Blau I, Schlegelberger B, Berger U, Telford N, Aruliah S, Yin JA, Vanstraelen D, Barker HF, Taylor PC, O'Driscoll A, Benedetti F, Rudolph C, Kolb HJ, Hochhaus A, Hehlmann R, Chase A, Cross NC: The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2. Cancer Res; 2005 Apr 1;65(7):2662-7
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  • [Title] The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2.
  • We have identified a t(8;9)(p21-23;p23-24) in seven male patients (mean age 50, range 32-74) with diverse hematologic malignancies and clinical outcomes: atypical chronic myeloid leukemia/chronic eosinophilic leukemia (n = 5), secondary acute myeloid leukemia (n = 1), and pre-B-cell acute lymphoblastic leukemia (n = 1).
  • [MeSH-major] Cell Cycle Proteins / genetics. Chromosomes, Human, Pair 8 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Aged. Amino Acid Sequence. Autoantigens. Base Sequence. Humans. Janus Kinase 2. Male. Middle Aged. Molecular Sequence Data. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15805263.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantigens; 0 / Cell Cycle Proteins; 0 / Oncogene Proteins, Fusion; 0 / PCM1 protein, human; 0 / PCM1-JAK2 fusion protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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15. Liu YQ, Qiu HX, Li JY, Xu W, Xu J, Lü X, Wu HX: [Secondary acute myeloid leukemia complicated after treatment of non-Hodgkin's lymphoma]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Jun;17(3):756-9
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  • [Title] [Secondary acute myeloid leukemia complicated after treatment of non-Hodgkin's lymphoma].
  • The aim of this study was to investigate the mechanism, susceptibility, (18)F-FDG positron emission computerized tomography ((18)F-FDG PET/CT) features and the treatment of therapy-related acute myeloid leukemia.
  • One patient with NHL was affected with t-MDS after treatment and then progressed to t-AML.
  • The interval time from the chemotherapy of NHL to the occurrence of t-MDS was 105 months and t-MDS progressed to AML-M(2) in 2 months.
  • Karyotype analysis results of t-MDS and t-AML were normal. (18)F-FDG PET indicated that the FDG uptake in the bone raised diffusely.
  • In conclusion, the occurrence of t-AML/MDS may be associated with the application of the cytotoxic chemotherapeutics. (18)F-FDG PET may be an indicator predicting the transformation of t-MDS to t-AML.


16. Vaculová A, Hofmanová J, Zatloukalová J, Kozubík A: Differences in TRAIL-induced changes of Mcl-1 expression among distinct human colon epithelial cell lines. Exp Cell Res; 2009 Nov 15;315(19):3259-66
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  • We examined the changes of anti-apoptotic Mcl-1 protein level following TRAIL treatment of human cell lines representing different stages of colon carcinogenesis-adenocarcinoma (HT-29, HCT116) or secondary metastasis (SW620), together with cell line derived from human fetal colon (FHC).
  • We demonstrated an immediate impact of Mcl-1 protein level manipulations on the course of early acute apoptotic response of colon adenocarcinoma cells to TRAIL.
  • [MeSH-minor] Cell Line, Tumor. Cell Survival. Epithelial Cells / metabolism. Gene Expression Regulation. Humans. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Metastasis / pathology

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  • (PMID = 19782681.001).
  • [ISSN] 1090-2422
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / TNF-Related Apoptosis-Inducing Ligand
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17. Zuna J, Burjanivova T, Mejstrikova E, Zemanova Z, Muzikova K, Meyer C, Horsley SW, Kearney L, Colman S, Ptoszkova H, Marschalek R, Hrusak O, Stary J, Greaves M, Trka J: Covert preleukemia driven by MLL gene fusion. Genes Chromosomes Cancer; 2009 Jan;48(1):98-107
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  • Acute leukemia is considered to be a two- or multiple-step process.
  • We demonstrate here a striking sequence of events, which include a covert, protracted preleukemic phase characterized by a dominant MLL/FOXO3A clone with intact myeloid differentiation and the subsequent acquisition of a secondary genetic abnormality, leading to overt lymphoblastic leukemia.
  • Backtracking of the secondary acute lymphoblastic leukemia (sALL) with the MLL rearrangement showed no blasts in the bone marrow (BM) during the protracted preleukemic phase.
  • However, at the same time (more than 1 year before the sALL diagnosis) the MLL/FOXO3A was present in up to 90% of BM cells including myeloid lineage, suggesting that the fusion arose in a multipotent progenitor.
  • These data provide insight into the dynamics of leukemogenesis in secondary leukemia with MLL rearrangement.
  • [MeSH-major] Gene Fusion. Leukemia, Promyelocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Preleukemia / genetics
  • [MeSH-minor] Adolescent. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Chromosomes, Human, Pair 19 / genetics. Cytogenetic Analysis. Female. Forkhead Transcription Factors / genetics. Forkhead Transcription Factors / metabolism. Gene Expression Regulation, Leukemic. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Myeloid Cells / metabolism. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. Polymorphism, Single Nucleotide

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  • (PMID = 18932267.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / FOXO3 protein, human; 0 / Forkhead Transcription Factors; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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18. Larson RA, Le Beau MM: Therapy-related myeloid leukaemia: a model for leukemogenesis in humans. Chem Biol Interact; 2005 May 30;153-154:187-95
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  • [Title] Therapy-related myeloid leukaemia: a model for leukemogenesis in humans.
  • Therapy-related myeloid leukemia (t-AML) is a distinctive clinical syndrome occurring after exposure to chemotherapy (CT) or radiotherapy (RT).
  • Since 1972, 141 males and 165 females with a median age of 51 years (range: 3-83 years) at primary diagnosis and 58 years (range: 6-86 years) at secondary diagnosis were analyzed.
  • At diagnosis of t-AML, 282 (92%) had clonal abnormalities involving chromosome 5 (n=63), chromosome 7 (n=85), both chromosomes 5 and 7 (n=66), recurring balanced rearrangements (n=31), or other clonal abnormalities (n=39); 24 had a normal karyotype.
  • Seventeen patients had developed t-AML after autologous stem cell transplantation, but no unique pattern of cytogenetic abnormalities was observed.
  • Patients presenting with acute leukemia were more likely to have a balanced rearrangement than those presenting with myelodysplasia (28% versus 4%, p<0.0001).
  • Median survival after diagnosis of t-AML was 8 months; survival at 5 years was less than 10%.
  • To gain insights into the molecular basis of this disease, we performed gene expression profiling of CD34+ hematopoietic progenitor cells from t-AML patients.
  • We found distinct subtypes of t-AML that have characteristic gene expression patterns.
  • A second subgroup of t-AML is characterized by down-regulation of transcription factors involved in early hematopoiesis (TAL1, GATA1, and EKLF) and overexpression of proteins involved in signaling pathways in myeloid cells (FLT3) and cell survival (BCL2).
  • Establishing the molecular pathways involved in t-AML may facilitate the identification of selectively expressed genes that can be exploited for the development of targeted therapies.
  • [MeSH-major] Chromosomes, Human, Pair 5. Chromosomes, Human, Pair 7. Leukemia, Myeloid / genetics. Neoplasms, Second Primary / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD34 / genetics. Child. Child, Preschool. Chromosome Aberrations. Female. Gene Expression Profiling. Hematopoietic Stem Cell Transplantation. Hematopoietic Stem Cells. Humans. Male. Middle Aged. Neoplasms / drug therapy. Neoplasms / radiotherapy

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  • (PMID = 15935816.001).
  • [ISSN] 0009-2797
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA14599; United States / NCI NIH HHS / CA / CA40046
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antigens, CD34
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19. Morerio C, Acquila M, Rapella A, Tassano E, Rosanda C, Panarello C: Inversion (11)(p15q22) with NUP98-DDX10 fusion gene in pediatric acute myeloid leukemia. Cancer Genet Cytogenet; 2006 Dec;171(2):122-5
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  • [Title] Inversion (11)(p15q22) with NUP98-DDX10 fusion gene in pediatric acute myeloid leukemia.
  • The inv(11)(p15q22), a rare but recurrent chromosome abnormality that creates a NUP98-DDX10 fusion gene, is associated with de novo or secondary myeloid malignancies.
  • We report a case of acute monocytic leukemia presenting this rearrangement, studied using fluorescence in situ hybridization (FISH) and reverse transcriptase-PCR (RT-PCR).
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 11 / genetics. DEAD-box RNA Helicases / genetics. Gene Fusion. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / genetics

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  • (PMID = 17116492.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AB040537/ AB040538
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; EC 3.6.1.- / DDX10 protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases
  • [Number-of-references] 12
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20. 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.


21. Chau M, Christensen JL, Ajami AM, Capizzi RL: Amonafide, a topoisomerase II inhibitor, is unaffected by P-glycoprotein-mediated efflux. Leuk Res; 2008 Mar;32(3):465-73
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  • Over-expression of P-glycoprotein (Pgp+) has been related to resistance to classical Topo II inhibitors used in the treatment of AML and is common in patients with poor-prognosis, such as those with secondary AML (sAML).
  • Since clinical trials with amonafide, a unique ATP-independent Topo II inhibitor, in combination with cytarabine, have shown significant efficacy for remission induction in patients with sAML, we compared the cytotoxic effect of amonafide (amonafide l-malate, Xanafide) to the classical Topo II inhibitors (daunorubicin, doxorubicin, idarubicin, etoposide, and mitoxantrone) in K562 leukemia cells and in the MDR subline, K562/DOX.
  • Pgp expression was found to be approximately 6.5-fold greater in K562/DOX and causes the rapid efflux of these drugs from the leukemia cell.
  • A similar result was also observed in murine P388 and P388/ADR leukemia cells.
  • These observations suggest that amonafide is a promising therapeutic candidate directed toward bypassing this common mechanism of drug resistance encountered in the treatment of patients with AML, and possibly in other resistant hematological malignancies as well.

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  • (PMID = 17826829.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Imides; 0 / Isoquinolines; 0 / Naphthalimides; 0 / P-Glycoprotein; 0 / Topoisomerase II Inhibitors; 1Q8D39N37L / amonafide
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22. Cheung AM, Chow HC, Kwong YL, Liang R, Leung AY: FLT3/internal tandem duplication subclones in acute myeloid leukemia differ in their engraftment potential in NOD/SCID mice. Leuk Res; 2010 Jan;34(1):119-22
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  • [Title] FLT3/internal tandem duplication subclones in acute myeloid leukemia differ in their engraftment potential in NOD/SCID mice.
  • In this study, we tested if FLT3/internal tandem duplication (ITD) in acute myeloid leukemia (AML) might occur at different hierarchical stages during leukemogenesis.
  • In 56 AML cases, 10 showed FLT3/ITD (single ITD=5; multiple ITD=5).
  • Two patients carried single FLT3/ITD subclones, which were maintained during primary and secondary transplantations.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid, Acute / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • [Copyright] 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19683812.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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23. 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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24. Le H, Singh S, Shih SJ, Du N, Schnyder S, Loredo GA, Bien C, Michaelis L, Toor A, Diaz MO, Vaughan AT: Rearrangements of the MLL gene are influenced by DNA secondary structure, potentially mediated by topoisomerase II binding. Genes Chromosomes Cancer; 2009 Sep;48(9):806-15
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  • [Title] Rearrangements of the MLL gene are influenced by DNA secondary structure, potentially mediated by topoisomerase II binding.
  • The location of MLL translocation breakpoints within therapy-related acute myeloid leukemia linked to drugs targeting Topoisomerase II and infant acute leukemia (IAL) are biased toward the intron 11-exon 12 region of MLL, although lacking a comprehensive explanation.
  • We propose a model whereby Topoisomerase II facilitates the organization of nuclease-sensitive secondary structures, stabilized by palindrome association, which are prone to rearrangement.

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  • (PMID = 19530238.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA105049-01A20001; United States / NCI NIH HHS / CA / P01 CA105049; United States / NCI NIH HHS / CA / CA105049; United States / NCI NIH HHS / CA / P01 CA105049-01A20001
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Topoisomerase II Inhibitors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 9007-49-2 / DNA; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 5.99.1.3 / DNA Topoisomerases, Type II
  • [Other-IDs] NLM/ NIHMS125607; NLM/ PMC2764312
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25. Serefhanoglu S, Goker H, Aksu S, Buyukasik Y, Sayinalp N, Haznedaroglu IC, Ozcebe OI: Spinal myeloid sarcoma in two non-leukemic patients. Intern Med; 2010;49(22):2493-7
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  • [Title] Spinal myeloid sarcoma in two non-leukemic patients.
  • Myeloid sarcoma, formerly termed granulocytic sarcoma or chloroma, consists of neoplastic granulocytic precursors and myeloblasts.
  • Isolated chloromas (granulocytic sarcomas) are rare tumors.
  • Spinal complications of chloromas, such as cord compression secondary to epidural tumor or cauda equine syndrome have been described but are rare.
  • We herein report two cases with spinal granulocytic sarcomas in non-leukemic patients.
  • The case of a previously healthy 22-year-old man diagnosed with multiple spinal granulocytic sarcomas with no evidence of bone marrow or other hematological involvement is described.
  • And, a 43-year-old woman diagnosed cervical spinal granulocytic sarcoma with no evidence of bone marrow or other hematological involvement is described.
  • The histopathological examination was consistent with granulocytic sarcoma.
  • Granulocytic sarcoma should be considered in the differential diagnosis of an epidural mass in patients with or without acute leukemia, because early diagnosis followed by appropriate combined chemotherapy and radiation may obviate surgical intervention and eventually prevent leukemic transformation.
  • [MeSH-major] Sarcoma, Myeloid. Spinal Neoplasms

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  • (PMID = 21088356.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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26. 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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27. Fadilah SA, Raja-Zahratul-Azma RS, Leong CF: Extensive myelofibrosis responsive to treatment for acute erythroblastic leukaemia. Malays J Pathol; 2006 Jun;28(1):55-8
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  • [Title] Extensive myelofibrosis responsive to treatment for acute erythroblastic leukaemia.
  • Intense myelofibrosis is rarely associated with de novo acute myeloid leukaemia (AML) except in acute megakaryoblastic leukaemia (AML-M7) where there is diffuse marrow fibrosis as a consequence of proliferation of neoplastic myeloid cells.
  • AML associated with significant myelofibrosis developing both de novo or secondary to primary (idiopathic) myelofibrosis is characterised by a fulminant course and extremely poor prognosis, primarily due to treatment-resistant disease.
  • The prognostic value of degree of marrow fibrosis in de novo AML has been poorly investigated.
  • We describe a case of extensive myelofibrosis associated with acute erythroblastic leukaemia (AML-M6) that responded to induction therapy of the leukaemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Erythroblastic, Acute / complications. Leukemia, Erythroblastic, Acute / drug therapy. Primary Myelofibrosis / complications. Primary Myelofibrosis / drug therapy
  • [MeSH-minor] Adult. Cytarabine / therapeutic use. Daunorubicin / therapeutic use. Female. Humans. Leukemia, Promyelocytic, Acute / complications. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / pathology

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  • (PMID = 17694960.001).
  • [ISSN] 0126-8635
  • [Journal-full-title] The Malaysian journal of pathology
  • [ISO-abbreviation] Malays J Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Malaysia
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
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28. Wang SA, Pozdnyakova O, Jorgensen JL, Medeiros LJ, Stachurski D, Anderson M, Raza A, Woda BA: Detection of paroxysmal nocturnal hemoglobinuria clones in patients with myelodysplastic syndromes and related bone marrow diseases, with emphasis on diagnostic pitfalls and caveats. Haematologica; 2009 Jan;94(1):29-37
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  • DESIGN AND METHODS: By using multiparameter flow cytometry immunophenotypic analysis with antibodies specific for four glycosylphosphatidylinositol-anchored proteins (CD55, CD59, CD16, CD66b) and performing an aerolysin lysis confirmatory test in representative cases, we assessed the paroxysmal nocturnal hemoglobinuria-phenotype granulocytes in 110 patients with myelodysplastic syndrome, 15 with myelodysplastic/myeloproliferative disease, 5 with idiopathic myelofibrosis and 6 with acute myeloid leukemia.
  • Altered glycosylphosphatidylinositol-anchored protein expression secondary to granulocytic hypogranulation, immaturity, and/or immunophenotypic abnormalities was present in a substantial number of cases and diagnostically challenging.


29. Jabbour E, Cortes J, Kantarjian H, Giralt S, Andersson BS, Giles F, Shpall E, Kebriaei P, Champlin R, de Lima M: Novel tyrosine kinase inhibitor therapy before allogeneic stem cell transplantation in patients with chronic myeloid leukemia: no evidence for increased transplant-related toxicity. Cancer; 2007 Jul 15;110(2):340-4
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  • [Title] Novel tyrosine kinase inhibitor therapy before allogeneic stem cell transplantation in patients with chronic myeloid leukemia: no evidence for increased transplant-related toxicity.
  • BACKGROUND: Patients undergoing allogeneic hematopoietic stem cell transplantation (HSCT) for chronic myeloid leukemia (CML) are increasingly likely to have received a novel tyrosine kinase inhibitor (NTKI) after failing imatinib mesylate.
  • One patient developed secondary graft failure after 6 months from the first HSCT that required a second HSCT.
  • Acute and chronic graft-versus-host disease (GVHD) was observed in 7 and 6 patients, respectively.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. Thiazoles / therapeutic use


30. Hashmi KU, Khan B, Ahmed P, Raza S, Hussain I, Mahmood A, Iqbal H, Malik HS, Anwar M: FLAG-IDA in the treatment of refractory/relapsed acute leukaemias: single centre study. J Pak Med Assoc; 2005 Jun;55(6):234-8
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  • [Title] FLAG-IDA in the treatment of refractory/relapsed acute leukaemias: single centre study.
  • OBJECTIVE: To evaluate the efficacy and toxicity profile of the combination of fludarabine, high dose cytarabine, idarubicin, and granulocyte colony stimulating factor in refractory relapsed cases of acute leukaemia, a study is being conducted at Armed Forces Bone Marrow Transplant Centre (AFBMTC) Rawalpindi since January 2003.
  • METHODS: Twelve Patients with refractory/relapsed (Ref/Rel) acute leukaemia (AL) were treated with fludarabine 30 mg/m2 and cytosine arabinoside (AraC) Arac 2 g/m2 for 5 days, idarubicin 10 mg/m2 for 3 days, and granulocyte colony stimulating factor G-CSF 5 micro g/kg from day 0 till neutrophil recovery (ANC > 1.0 x 10(9)/1).
  • RESULTS: Patients included were refractory acute lymphoblastic leukaemia (ALL) (n=2), relapsed ALL (n = 3), refractory acute myeloid leukaemia (AML) (n = 3), secondary AML (n=2) relapsed AML (n = 1) and acute undifferentiated leukaemia (AUL) (n = 1).
  • CONCLUSION: In our experience, FLAG-IDA is well tolerated and effective regimen in relapsed/refractory acute leukaemias.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antibiotics, Antineoplastic / therapeutic use. Antimetabolites, Antineoplastic / therapeutic use. Child. Cytarabine / therapeutic use. Female. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Idarubicin / therapeutic use. Male. Middle Aged. Recurrence

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  • (PMID = 16045091.001).
  • [ISSN] 0030-9982
  • [Journal-full-title] JPMA. The Journal of the Pakistan Medical Association
  • [ISO-abbreviation] J Pak Med Assoc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; ZRP63D75JW / Idarubicin
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31. Hijiya N, Hudson MM, Lensing S, Zacher M, Onciu M, Behm FG, Razzouk BI, Ribeiro RC, Rubnitz JE, Sandlund JT, Rivera GK, Evans WE, Relling MV, Pui CH: Cumulative incidence of secondary neoplasms as a first event after childhood acute lymphoblastic leukemia. JAMA; 2007 Mar 21;297(11):1207-15
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  • [Title] Cumulative incidence of secondary neoplasms as a first event after childhood acute lymphoblastic leukemia.
  • CONTEXT: Little is known about the incidence of secondary neoplasms after 15 to 20 years in children and adolescents who were treated for acute lymphoblastic leukemia.
  • OBJECTIVES: To investigate the cumulative incidence of secondary neoplasms in pediatric patients treated for acute lymphoblastic leukemia over 30 years and to characterize late-occurring tumors.
  • DESIGN, SETTING, AND PATIENTS: Retrospective study of 2169 patients with acute lymphoblastic leukemia treated between 1962 and 1998 at St Jude Children's Research Hospital, Memphis, Tenn, who achieved complete remission and had a median follow-up time of 18.7 years (range, 2.4-41.3 years).
  • MAIN OUTCOME MEASURES: Cumulative incidences of secondary neoplasms in first remission and standard incidence ratios of observed rates compared with rates of cancer development in the general US population.
  • RESULTS: Secondary neoplasms developed as the first event in 123 patients and comprised 46 myeloid malignancies, 3 lymphomas, 14 basal cell carcinomas, 16 other carcinomas, 6 sarcomas, 16 meningiomas, and 22 other brain tumors.
  • The cumulative incidence of secondary neoplasm was 4.17% (SE, 0.46%) at 15 years and increased substantially after 20 years, reaching 10.85% (SE, 1.27%) at 30 years.
  • The cumulative incidence of each tumor type at 30 years was 2.19% (SE, 0.32%) for myeloid malignancy, 0.17% (SE, 0.10%) for lymphoma, 3.00% (SE, 0.59%) for brain tumor, 4.91% (SE, 1.04%) for carcinoma, and 0.57% (SE, 0.37%) for sarcoma.
  • CONCLUSIONS: The cumulative incidence of secondary neoplasms increases steadily over 30 years after treatment of acute lymphoblastic leukemia.
  • Although the majority of the late-occurring secondary neoplasms are low-grade tumors, the increase in incidence of more aggressive malignant neoplasms is significantly higher than expected in the general population.
  • These results suggest that lifelong follow-up of acute lymphoblastic leukemia survivors is needed to ascertain the full impact of treatment and other leukemia-related factors on secondary neoplasm development.

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  • (PMID = 17374815.001).
  • [ISSN] 1538-3598
  • [Journal-full-title] JAMA
  • [ISO-abbreviation] JAMA
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-36401; United States / NCI NIH HHS / CA / CA-51001; United States / NCI NIH HHS / CA / CA-60419; United States / NCI NIH HHS / CA / CA-71907; United States / NCI NIH HHS / CA / CA-78224; United States / NIGMS NIH HHS / GM / GM-61393
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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32. Marcucci G, Mrózek K, Ruppert AS, Maharry K, Kolitz JE, Moore JO, Mayer RJ, Pettenati MJ, Powell BL, Edwards CG, Sterling LJ, Vardiman JW, Schiffer CA, Carroll AJ, Larson RA, Bloomfield CD: Prognostic factors and outcome of core binding factor acute myeloid leukemia patients with t(8;21) differ from those of patients with inv(16): a Cancer and Leukemia Group B study. J Clin Oncol; 2005 Aug 20;23(24):5705-17
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  • [Title] Prognostic factors and outcome of core binding factor acute myeloid leukemia patients with t(8;21) differ from those of patients with inv(16): a Cancer and Leukemia Group B study.
  • PURPOSE: Because both t(8;21) and inv(16) disrupt core binding factor (CBF) in acute myeloid leukemia (AML) and confer relatively favorable prognoses, these cytogenetic groups are often treated similarly.
  • PATIENTS AND METHODS: We analyzed 144 consecutive adults with t(8;21) and 168 with inv(16) treated on Cancer and Leukemia Group B front-line studies.
  • RESULTS: With a median follow-up of 6.4 years, for CBF AML as a whole, the CR rate was 88%, 5-year OS was 50% and CIR was 53%.
  • Unexpectedly, race was an important predictor for t(8;21) AML, in that nonwhites failed induction more often (odds ratio = 5.7; P = .006) and had shorter OS than whites when certain secondary cytogenetic abnormalities were present.
  • For inv(16) AML, secondary cytogenetic abnormalities (especially +22) and male sex predicted better outcome.
  • CONCLUSION: When the prognostic impact of race, secondary cytogenetic abnormalities, sex, and response to salvage treatment is considered, t(8;21) and inv(16) AMLs seem to be distinct clinical entities and should be stratified and reported separately.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Aged. Aziridines / administration & dosage. Benzoquinones / administration & dosage. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Etoposide / administration & dosage. Female. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Prognosis. Proportional Hazards Models. Prospective Studies. Remission Induction. Statistics, Nonparametric. Survival Analysis

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  • (PMID = 16110030.001).
  • [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 / CA101140; United States / NCI NIH HHS / CA / CA31946; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / K08-CA90469; United States / NCI NIH HHS / CA / P30-CA16058
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aziridines; 0 / Benzoquinones; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; FQL5EUP13W / diaziquone; ZS7284E0ZP / Daunorubicin
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33. Kindler T, Lipka DB, Fischer T: FLT3 as a therapeutic target in AML: still challenging after all these years. Blood; 2010 Dec 9;116(24):5089-102
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  • [Title] FLT3 as a therapeutic target in AML: still challenging after all these years.
  • Mutations within the FMS-like tyrosine kinase 3 (FLT3) gene on chromosome 13q12 have been detected in up to 35% of acute myeloid leukemia (AML) patients and represent one of the most frequently identified genetic alterations in AML.
  • Over the last years, FLT3 has emerged as a promising molecular target in therapy of AML.
  • Here, we review results of clinical trials and of correlative laboratory studies using small molecule FLT3 tyrosine kinase inhibitors (TKIs) in AML patients.
  • We also review mechanisms of primary and secondary drug resistance to FLT3-TKI, and from the data currently available we summarize lessons learned from FLT3-TKI monotherapy.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors

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  • (PMID = 20705759.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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34. Matkowskyj KA, Wiseman WR, Robin JC, Norvell JP, Puthumana J, Nelson B, Peterson L, McGarry TJ, Tourtellotte WG: Therapy-related myelodysplastic syndrome presenting as fulminant heart failure secondary to myeloid sarcoma. J Hematop; 2010;3(1):41-6
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  • [Title] Therapy-related myelodysplastic syndrome presenting as fulminant heart failure secondary to myeloid sarcoma.
  • Rapidly progressive heart failure is commonly caused by an extensive myocardial infarction, a mechanical complication of infarction, myocarditis, or acute valvular insufficiency.
  • We present an unusual case that was caused by a diffuse infiltration of the myocardium with leukemic cells (myeloid sarcoma).
  • At autopsy, the heart was massively infiltrated with myeloblasts and other immature myeloid cells.
  • There was no evidence of acute leukemia in the bone marrow or peripheral blood.
  • The recognition of this entity is becoming increasingly important as the incidence of cardiac myeloid sarcoma may be on the rise as the number of patients receiving chemotherapy increases.

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  • (PMID = 21544187.001).
  • [ISSN] 1865-5785
  • [Journal-full-title] Journal of hematopathology
  • [ISO-abbreviation] J Hematop
  • [Language] eng
  • [Grant] United States / NIH HHS / OD / K26 OD010945
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2883902
  • [Keywords] NOTNLM ; Leukemia cordis / Myeloid sarcoma / Rapidly progressive heart failure / Therapy-related myelodysplastic syndrome
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35. Takei N, Suzukawa K, Mukai HY, Itoh T, Okoshi Y, Yoda Y, Nagasawa T: Therapy-related acute myeloid leukemia 6 years after clonal detection of inv(11)(q21q23) and MLL gene rearrangement. Int J Hematol; 2006 Apr;83(3):247-51
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  • [Title] Therapy-related acute myeloid leukemia 6 years after clonal detection of inv(11)(q21q23) and MLL gene rearrangement.
  • Results of recent studies with animal models suggest that expression of MLL fusion proteins promotes acute leukemogenesis.
  • However, the most potent MLL fusion proteins are not sufficient for the development of acute myeloid leukemia (AML).
  • The clinical data on the pathogenesis of this type of leukemia are limited.
  • We analyzed the case of a patient with therapy-related AML with MLL rearrangement.
  • The patient initially developed AML with t(8;21).
  • After 6-year persistence of a clone with the inversion 11 karyotype in the bone marrow, secondary AML developed.
  • One was that MLL rearrangement was not sufficient for the development of leukemia.
  • [MeSH-major] Chromosome Inversion / genetics. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics
  • [MeSH-minor] Antigens, CD13 / biosynthesis. Antigens, CD34 / biosynthesis. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Female. Humans. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 16720556.001).
  • [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] Japan
  • [Chemical-registry-number] 0 / Antigens, CD34; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.4.11.2 / Antigens, CD13
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36. Ferrara F, D'Arco AM, De Simone M, Mele G, Califano C, Pocali B, Danise P, Palmieri S: Fludarabine and cytarabine as continuous sequential infusion for elderly patients with acute myeloid leukemia. Haematologica; 2005 Jun;90(6):776-84
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  • [Title] Fludarabine and cytarabine as continuous sequential infusion for elderly patients with acute myeloid leukemia.
  • BACKGROUND AND OBJECTIVES: A phase II study was conducted to investigate the effects of a therapeutic program based on the combination of fludarabine and cytarabine (ARA-C) administered as a sequential continuous infusion in untreated elderly patients with acute myeloid leukemia (AML).
  • DESIGN AND METHODS: Sixty-three patients with non-M3 AML, median age 69 years (range 61-81), were accrued.
  • Twenty-four patients (38%) had AML secondary to myelodysplastic syndrome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Vidarabine / analogs & derivatives

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  • (PMID = 15951290.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD34; 04079A1RDZ / Cytarabine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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37. Sumi M, Shimizu I, Sato K, Ueki T, Akahane D, Ueno M, Ichikawa N, Nakao S, Kobayashi H: Graft failure in cord blood transplantation successfully treated with short-term reduced-intensity conditioning regimen and second allogeneic transplantation. Int J Hematol; 2010 Dec;92(5):744-50
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  • In 36 adult patients undergoing CBT at our hospital between July 2003 and December 2009, six patients developed GF (primary, n = 5; secondary, n = 1).
  • Three patients had acute myeloid leukemia, one had acute lymphoblastic leukemia, one had chronic myeloid leukemia, and one had aplastic anemia.
  • Secondary GF was diagnosed on day 567.
  • In the patient with secondary GF, the elapsed time was 35 days.

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  • (PMID = 21052879.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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38. Krishnan B, Morgan GJ: Non-Hodgkin lymphoma secondary to cancer chemotherapy. Cancer Epidemiol Biomarkers Prev; 2007 Mar;16(3):377-80
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  • [Title] Non-Hodgkin lymphoma secondary to cancer chemotherapy.
  • Therapy-related acute myeloid leukemia has been frequently documented in these patient cohorts, and its biology well studied.
  • Recognition of secondary non-Hodgkin lymphoma as a cause of significant morbidity and mortality in these patients is equally important.
  • The patterns of incidence and latency of secondary lymphomas is distinct from that of myeloid malignancies and other solid cancers.
  • Risk of secondary lymphomas increases after the first 5 years of completion of chemotherapy or radiotherapy and persists for more than three decades.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Lymphoma, Non-Hodgkin / chemically induced. Neoplasms / drug therapy. Neoplasms, Second Primary / chemically induced

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  • (PMID = 17372233.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 24
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39. Cornely OA, Maertens J, Winston DJ, Perfect J, Ullmann AJ, Walsh TJ, Helfgott D, Holowiecki J, Stockelberg D, Goh YT, Petrini M, Hardalo C, Suresh R, Angulo-Gonzalez D: Posaconazole vs. fluconazole or itraconazole prophylaxis in patients with neutropenia. N Engl J Med; 2007 Jan 25;356(4):348-59
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  • BACKGROUND: Patients with neutropenia resulting from chemotherapy for acute myelogenous leukemia or the myelodysplastic syndrome are at high risk for difficult-to-treat and often fatal invasive fungal infections.
  • We compared the incidence of proven or probable invasive fungal infections during treatment (the primary end point) between the posaconazole and fluconazole or itraconazole groups; death from any cause and time to death were secondary end points.
  • CONCLUSIONS: In patients undergoing chemotherapy for acute myelogenous leukemia or the myelodysplastic syndrome, posaconazole prevented invasive fungal infections more effectively than did either fluconazole or itraconazole and improved overall survival.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents / adverse effects. Female. Humans. Kaplan-Meier Estimate. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / mortality. Male. Middle Aged. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / mortality. Single-Blind Method. Treatment Outcome


40. Pidala J, Kim J, Anasetti C, Kharfan-Dabaja MA, Nishihori T, Field T, Perkins J, Perez L, Fernandez HF: Pharmacokinetic targeting of intravenous busulfan reduces conditioning regimen related toxicity following allogeneic hematopoietic cell transplantation for acute myelogenous leukemia. J Hematol Oncol; 2010;3:36
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  • [Title] Pharmacokinetic targeting of intravenous busulfan reduces conditioning regimen related toxicity following allogeneic hematopoietic cell transplantation for acute myelogenous leukemia.
  • Optimal conditioning therapy for hematopoietic cell transplantation (HCT) in acute myelogenous leukemia (AML) remains undefined.
  • We retrospectively compared outcomes of a consecutive series of 51 AML patients treated with oral busulfan (1 mg/kg every 6 hours for 4 days) and cyclophosphamide (60 mg/kg IV × 2 days) - (Bu/Cy) with 100 consecutive AML patients treated with pharmacokinetic targeted IV busulfan (AUC < 6000 μM/L*min per day × 4 days) and fludarabine (40 mg/m2 × 4 days) - (t-IV Bu/Flu).
  • The Bu/Cy and t-IV Bu/Flu groups significantly differed according to donor relation, stem cell source, aGVHD prophylaxis, remission status, primary vs. secondary disease, median age, and % blasts prior to HCT (p < 0.01 for each).
  • However, multivariable analysis did not demonstrate significant differences in overall survival (p = 0.78) or non-relapse mortality (p = 0.6) according to conditioning regimen delivered.
  • [MeSH-major] Busulfan / pharmacokinetics. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Transplantation Conditioning

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  • (PMID = 20925957.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ PMC2958877
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41. Battaglini CL, Hackney AC, Garcia R, Groff D, Evans E, Shea T: The effects of an exercise program in leukemia patients. Integr Cancer Ther; 2009 Jun;8(2):130-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effects of an exercise program in leukemia patients.
  • PURPOSE: To examine the feasibility of administering an in-hospital exercise program to acute leukemia patients undergoing chemotherapy.
  • A secondary purpose explored the impact of exercise on selected physiological, psychological, and inflammatory markers.
  • METHODS: Ten patients, aged 18 to 50 years, diagnosed with acute leukemia or newly relapsed were assessed for body weight, height, body composition (skinfolds), cardiorespiratory endurance (total minutes on bicycle ergometer at 60% heart rate reserve), dynamic muscular endurance (Rocky Mountain Cancer Rehabilitation Institute protocol), fatigue (Revised Piper Fatigue Scale), depression (Center for Epidemiologic Studies Depression scale, National Institute of Mental Health questionnaire), and quality of life (Functional Assessment of Cancer Therapy-General) at baseline (within 3 days of diagnosis) and at the end of induction phase of treatment.
  • CONCLUSION: Administration of exercise to acute leukemia patients undergoing treatment is feasible.
  • [MeSH-major] Exercise Therapy / methods. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 19679621.001).
  • [ISSN] 1534-7354
  • [Journal-full-title] Integrative cancer therapies
  • [ISO-abbreviation] Integr Cancer Ther
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines
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42. Huang Q, Wu Y, Snyder DS, Chang KL, Slovak ML, Gaal KK, Palmer JM, Weiss LM: Clinical and pathologic analysis of 16 cases of relapsed chronic myeloid leukemia after stem cell transplantation. Am J Clin Pathol; 2007 Oct;128(4):565-70
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  • [Title] Clinical and pathologic analysis of 16 cases of relapsed chronic myeloid leukemia after stem cell transplantation.
  • Chronic myeloid leukemia (CML) is a myeloproliferative disease that originates in an abnormal pluripotent bone marrow stem cell and is characteristically associated with the Philadelphia chromosome and/or the bcr/abl fusion gene.
  • The frequency of acute leukemic transformation at time of relapse was largely associated with pre-HCT disease status and acquired secondary cytogenetic abnormalities.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Neoplasm Recurrence, Local / pathology


43. Bellos F, Mahlknecht U: Valproic acid and all-trans retinoic acid: meta-analysis of a palliative treatment regimen in AML and MDS patients. Onkologie; 2008 Nov;31(11):629-33
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  • [Title] Valproic acid and all-trans retinoic acid: meta-analysis of a palliative treatment regimen in AML and MDS patients.
  • Currently, no standard treatment is available for elderly patients with de novo/secondary acute myeloid leukemia (AML) who are not eligible for intensive chemotherapy.
  • We treated 21 patients with de novo/secondary AML and 1 patient with myelodysplastic syndrome with ATRA (45 mg/m(2)/day in 2 doses, 14 days, q29 days) and VPA (150 mg/day 1 week, then 300 mg/day, continuously).
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / epidemiology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / epidemiology. Palliative Care / statistics & numerical data. Tretinoin / administration & dosage. Valproic Acid / administration & dosage


44. 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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45. 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


46. Teo WY, Chan MY, Lam CM, Chong CY: Skin manifestation of Stenotrophomonas maltophilia infection--a case report and review article. Ann Acad Med Singapore; 2006 Dec;35(12):897-900
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  • MATERIALS AND METHODS: We present a case of an 8-year-old girl with acute myeloid leukaemia who developed metastatic skin lesions secondary to Stenotrophomonas maltophilia bacteraemia.
  • [MeSH-major] Gram-Negative Bacterial Infections / complications. Leukemia, Myeloid / epidemiology. Skin Diseases, Bacterial / epidemiology. Stenotrophomonas maltophilia
  • [MeSH-minor] Acute Disease. Anti-Infective Agents / therapeutic use. Bacteremia / epidemiology. Bacteremia / microbiology. Cellulitis / epidemiology. Cellulitis / microbiology. Child. Comorbidity. Female. Humans. Neutropenia / epidemiology. Prognosis. Trimethoprim, Sulfamethoxazole Drug Combination / therapeutic use

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  • (PMID = 17219003.001).
  • [ISSN] 0304-4602
  • [Journal-full-title] Annals of the Academy of Medicine, Singapore
  • [ISO-abbreviation] Ann. Acad. Med. Singap.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 8064-90-2 / Trimethoprim, Sulfamethoxazole Drug Combination
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47. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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48. Cho BS, Kim HJ, Eom KS, Lee JW, Min WS, Kim CC: A case report of the second de novo acute myeloid leukemia (AML) following allogeneic stem cell transplantation in a patient with the first AML. Korean J Intern Med; 2010 Mar;25(1):110-3
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  • [Title] A case report of the second de novo acute myeloid leukemia (AML) following allogeneic stem cell transplantation in a patient with the first AML.
  • Secondary leukemia occurring after hematopoietic stem cell transplantation (HSCT) for acute myeloid leukemia (AML) is rare.
  • Secondary AML usually follows autologous and not allogeneic transplants.
  • When a new leukemia develops in a patient successfully treated with an allogeneic HSCT, the possibility of a de novo or secondary leukemia from either the donor or recipient should be considered.
  • We present a case initially diagnosed as de novo AML without a cytogenetic abnormality.
  • However, more than six years later, AML developed again and was associated with new complex cytogenetic abnormalities.
  • Considering the allogeneic setting, the newly developed cytogenetic abnormalities, a relatively long latent period, and the good clinical course after the second allogeneic HSCT, this case might represent a second de novo AML following successful treatment of the first AML.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / therapy. Neoplasms, Second Primary / etiology


49. 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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50. Joslin JM, Fernald AA, Tennant TR, Davis EM, Kogan SC, Anastasi J, Crispino JD, Le Beau MM: Haploinsufficiency of EGR1, a candidate gene in the del(5q), leads to the development of myeloid disorders. Blood; 2007 Jul 15;110(2):719-26
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  • [Title] Haploinsufficiency of EGR1, a candidate gene in the del(5q), leads to the development of myeloid disorders.
  • Loss of a whole chromosome 5 or a deletion of the long arm, del(5q), is a recurring abnormality in myelodysplastic syndromes (MDSs) and acute myeloid leukemia (AML).
  • To identify a leukemia-related gene on chromosome 5, we previously delineated a 970-kb segment of 5q31 that is deleted in all patients examined, and prepared a transcript map of this region.
  • To test the hypothesis that loss of function of Egr1 is an initiating event in the pathogenesis of AML/MDS, Egr1-deficient mice were treated with a potent DNA alkylating agent, N-ethyl-nitrosourea (ENU), to induce secondary cooperating mutations.
  • Our data suggest that haploinsufficiency for Egr1 plays a role in murine leukemogenesis, and in the development of AML/MDS characterized by abnormalities of chromosome 5.

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  • (PMID = 17420284.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / CA84221; United States / NCI NIH HHS / CA / R01 CA101774; United States / NCI NIH HHS / CA / R01 CA101774-06; United States / NCI NIH HHS / CA / CA101774-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EGR1 protein, human; 0 / Early Growth Response Protein 1; 0 / Egr1 protein, mouse
  • [Other-IDs] NLM/ PMC1924479
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51. 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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52. Azarova AM, Lyu YL, Lin CP, Tsai YC, Lau JY, Wang JC, Liu LF: Roles of DNA topoisomerase II isozymes in chemotherapy and secondary malignancies. Proc Natl Acad Sci U S A; 2007 Jun 26;104(26):11014-9
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  • [Title] Roles of DNA topoisomerase II isozymes in chemotherapy and secondary malignancies.
  • However, Top2-based chemotherapy has been associated with higher incidences of secondary malignancies, notably the development of acute myeloid leukemia in VP-16-treated patients.
  • These results point to the importance of developing Top2alpha-specific anticancer drugs for effective chemotherapy without the development of treatment-related secondary malignancies.

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  • (PMID = 17578914.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM024544; United States / NCI NIH HHS / CA / CA102463; United States / NCI NIH HHS / CA / R01 CA102463; United States / NIGMS NIH HHS / GM / R37 GM024544; United States / NIGMS NIH HHS / GM / GM24544
  • [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 / Antineoplastic Agents; 0 / Isoenzymes; 0 / Protease Inhibitors; 0 / Topoisomerase II Inhibitors; 6PLQ3CP4P3 / Etoposide; EC 5.99.1.3 / DNA Topoisomerases, Type II
  • [Other-IDs] NLM/ PMC1904155
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53. Krivtsov AV, Twomey D, Feng Z, Stubbs MC, Wang Y, Faber J, Levine JE, Wang J, Hahn WC, Gilliland DG, Golub TR, Armstrong SA: Transformation from committed progenitor to leukaemia stem cell initiated by MLL-AF9. Nature; 2006 Aug 17;442(7104):818-22
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  • The LSC were capable of transferring leukaemia to secondary recipient mice when only four cells were transferred, and possessed an immunophenotype and global gene expression profile very similar to that of normal granulocyte macrophage progenitors.
  • [MeSH-major] Cell Transformation, Neoplastic. Leukemia / metabolism. Leukemia / pathology. Myeloid-Lymphoid Leukemia Protein / metabolism. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. Oncogene Proteins, Fusion / metabolism
  • [MeSH-minor] Animals. Cell Differentiation. Cell Division. Cell Line. Cell Lineage. Granulocytes / cytology. Granulocytes / pathology. Humans. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / metabolism. Leukemia, Myelomonocytic, Acute / pathology. Macrophages / cytology. Macrophages / pathology. Mice. Neoplasm Transplantation. Survival Rate


54. Shono Y, Toubai T, Ota S, Ibata M, Mashiko S, Hirate D, Miura Y, Umehara S, Toyoshima N, Tanaka J, Asaka M, Imamura M: Abnormal expansion of naïve B lymphocytes after unrelated cord blood transplantation--a case report. Clin Lab Haematol; 2006 Oct;28(5):351-4
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  • A 33-year-old woman underwent unrelated cord blood transplantation (U-CBT) for myelodysplastic syndrome (MDS)-related secondary AML.
  • [MeSH-minor] Adult. Female. Humans. Immunophenotyping / methods. Leukemia, Myeloid, Acute / therapy. Lymphocyte Activation / immunology. Myelodysplastic Syndromes / therapy. Transplantation, Homologous


55. Ghoshal K, Bai S: DNA methyltransferases as targets for cancer therapy. Drugs Today (Barc); 2007 Jun;43(6):395-422
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  • Clinical trials have shown that both drugs have therapeutic potential against leukemia such as MDS, acute myeloid leukemia, chronic myelogenous leukemia and chronic myelomonocytic leukemia.
  • The major hindrance of their usage as anticancer agents is their instability in vivo as well as the toxicity secondary to their excessive incorporation into DNA, which causes cell cycle arrest.
  • [MeSH-minor] Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Azacitidine / therapeutic use. Epigenesis, Genetic. Female. Gene Expression Regulation. Gene Silencing. Hematologic Neoplasms / drug therapy. Hematologic Neoplasms / metabolism. Humans. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Male. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / metabolism. Transcriptional Activation

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  • (PMID = 17612710.001).
  • [ISSN] 1699-3993
  • [Journal-full-title] Drugs of today (Barcelona, Spain : 1998)
  • [ISO-abbreviation] Drugs Today
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA086978; United States / NCI NIH HHS / CA / CA86978
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 776B62CQ27 / decitabine; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; M801H13NRU / Azacitidine
  • [Number-of-references] 252
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56. Clark WB, Strickland SA, Barrett AJ, Savani BN: Extramedullary relapses after allogeneic stem cell transplantation for acute myeloid leukemia and myelodysplastic syndrome. Haematologica; 2010 Jun;95(6):860-3
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  • [Title] Extramedullary relapses after allogeneic stem cell transplantation for acute myeloid leukemia and myelodysplastic syndrome.
  • [MeSH-major] Leukemia, Myeloid, Acute / surgery. Myelodysplastic Syndromes / surgery. Stem Cell Transplantation / adverse effects
  • [MeSH-minor] Animals. Humans. Postoperative Complications / prevention & control. Postoperative Complications / surgery. Secondary Prevention. Transplantation, Homologous


57. Otsuka Y, Konishi T, Nara S, Furushima K, Nakajima K, Shimada H: Secondary myelodysplastic syndrome after small cell lung cancer and esophageal cancer. J Gastroenterol Hepatol; 2005 Sep;20(9):1318-21
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  • [Title] Secondary myelodysplastic syndrome after small cell lung cancer and esophageal cancer.
  • Esophagectomy accompanying postoperative chemotherapy was applied, but he died of secondary myelodysplastic syndrome with its acute myeloblastic transformation.
  • In post-therapeutic follow up of patients with such past therapeutic histories, we should be cautious about secondary malignancies even if primary malignant disease was evaluated as complete remission in long past history.
  • [MeSH-minor] Carcinoma, Small Cell / therapy. Esophagectomy. Fatal Outcome. Humans. Leukemia, Myeloid, Acute / etiology. Lung Neoplasms / therapy. Male. Middle Aged. Neoplasms, Second Primary / therapy. Treatment Outcome


58. Attili SV, Dadhich HK, Jacob LA, Anupama G, Bapsy PP, Devi L, Sundereshan TS, Babu GK, Loknath D: A retrospective study of clinico-hematological and cytogenetic profile of erythroleukemia from South India. Turk J Haematol; 2006 Sep 5;23(3):158-63
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  • Case records of all patients with acute myeloid leukemia seen in the Department of Medical Oncology at Kidwai Memorial Institute of Oncology, Bangalore, between January 1997 and December 2004 were reviewed.
  • A total of 326 AML patient were diagnosed of whom 14 patients had AML M6.
  • Contribution of EL to all forms of AML was 4.3%.
  • As a conclusion relative low incidence of secondary EL, more frequent normal karyotype, and relatively younger age observed in our series makes the picture of EL in our subcontinent different from that in other series reported thus far.

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  • (PMID = 27265484.001).
  • [ISSN] 1300-7777
  • [Journal-full-title] Turkish journal of haematology : official journal of Turkish Society of Haematology
  • [ISO-abbreviation] Turk J Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
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59. Abdullah S, Diezi M, Sung L, Dupuis LL, Geary D, Abla O: Sevelamer hydrochloride: a novel treatment of hyperphosphatemia associated with tumor lysis syndrome in children. Pediatr Blood Cancer; 2008 Jul;51(1):59-61
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  • OBJECTIVES: To describe the safety of sevelamer in children with hyperphosphatemia secondary to tumor lysis syndrome and the serum phosphate concentrations observed following its administration.
  • PROCEDURE: A retrospective chart review of all children with leukemia/lymphoma diagnosed between November 2002 and April 2004 who received sevelamer during their initial admission was conducted.
  • Nine children had acute lymphoblastic leukemia, one had acute myeloid leukemia and 3 had non-Hodgkin's lymphoma.

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18240167.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium Phosphates; 0 / Chelating Agents; 0 / Phosphates; 0 / Polyamines; 97Z1WI3NDX / calcium phosphate; 9YCX42I8IU / Sevelamer
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60. Usuki K, Nakasone H, Taoka K, Kida M, Iki S, Urabe A: [Transient chromosomal abnormalities following autologous peripheral blood stem cell transplantation for acute myelogenous leukemia]. Rinsho Ketsueki; 2007 Aug;48(8):618-23
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  • [Title] [Transient chromosomal abnormalities following autologous peripheral blood stem cell transplantation for acute myelogenous leukemia].
  • Twenty-three patients with acute myelogenous leukemia (AML) have received autologous hematopoietic stem cell transplantation (autoHSCT) in our institute from 1997 to 2005.
  • In these 4 patients with AML1/MTG8 or CBFbeta/MYH11 AML, RT-PCR findings using bone marrow cells were all negative when a cytogenetic abnormality was detected.
  • We present our finding together with a review of the literature on post-autoHSCT cytogenetic abnormalities not related to relapse or secondary leukemia/myelodysplastic syndrome.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / therapy. Peripheral Blood Stem Cell Transplantation / adverse effects


61. Leleu X, Tamburini J, Roccaro A, Morel P, Soumerai J, Lévy V, Wemeau M, Balkaran S, Poulain S, Hunter ZR, Ghobrial IM, Treon SP, Leblond V: Balancing risk versus benefit in the treatment of Waldenström's Macroglobulinemia patients with nucleoside analogue-based therapy. Clin Lymphoma Myeloma; 2009 Mar;9(1):71-3
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  • There are sporadic reports on increased incidence of transformation to high grade non-Hodgkin lymphoma (transformation to NHL) and development of therapy related-myelodysplasia/acute leukemia (t-MDS/AML) among WM patients treated with NA.
  • The incidences of transformation to NHL and t-MDS/AML ranged from 4.7% to 8%, and from 1.4% to 8.9%, respectively, and demonstrated an increased incidence of these late events among WM patients treated with NA.
  • The effect of these secondary malignancies needs to be better evaluated in prospective studies, especially in young patients.
  • [MeSH-minor] Disease Progression. Humans. Leukemia, Myeloid, Acute / pathology. Lymphoma, Non-Hodgkin / pathology

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  • (PMID = 19362978.001).
  • [ISSN] 1557-9190
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nucleosides
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62. Zhu GH, Shi HW: [Granulocytic sarcoma secondary to acute lymphoblastic leukemia in a boy]. Zhonghua Er Ke Za Zhi; 2005 Mar;43(3):238
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  • [Title] [Granulocytic sarcoma secondary to acute lymphoblastic leukemia in a boy].
  • [MeSH-major] Neoplasms, Second Primary / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Sarcoma, Myeloid / etiology

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  • (PMID = 15833214.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
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63. Rudd E, Göransdotter Ericson K, Zheng C, Uysal Z, Ozkan A, Gürgey A, Fadeel B, Nordenskjöld M, Henter JI: Spectrum and clinical implications of syntaxin 11 gene mutations in familial haemophagocytic lymphohistiocytosis: association with disease-free remissions and haematopoietic malignancies. J Med Genet; 2006 Apr;43(4):e14
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  • Two of the six patients harbouring STX11 gene defects developed myelodysplastic syndrome (MDS) or acute myelogenous leukaemia (AML).
  • These results suggest that STX11 gene mutations may be associated with secondary malignancies (MDS/AML), and that there is segregation of specific clinical features in FHL patients with an underlying genotype.
  • [MeSH-major] Leukemia, Myeloid / genetics. Lymphohistiocytosis, Hemophagocytic / diagnosis. Lymphohistiocytosis, Hemophagocytic / genetics. Mutation. Myelodysplastic Syndromes / genetics. Qa-SNARE Proteins / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged, 80 and over. Child. Child, Preschool. DNA Mutational Analysis. Female. Genotype. Humans. Infant. Male. Pedigree. Phenotype. Psychomotor Disorders / complications. Psychomotor Disorders / genetics. Remission, Spontaneous


64. Celkan T, Berrak S, Kazanci E, Ozyürek E, Unal S, Uçar C, Yilmaz S, Gürgey A: Malignancy-associated hemophagocytic lymphohistiocytosis in pediatric cases: a multicenter study from Turkey. Turk J Pediatr; 2009 May-Jun;51(3):207-13
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  • This study evaluates the clinical and laboratory data of children with secondary hemophagocytic lymphohistiocytosis (sHLH) related to malignancy.
  • Twenty cases (18 ALL and 2 AML) with acute leukemia (10 girls/10 boys, median age: 8 years [3-14 years]) were found to have sHLH.
  • Five patients with acute leukemia had HLH at the time of diagnosis (Group 1a), and 15 patients with acute leukemia were diagnosed as having sHLH during therapy (Group 1b), namely reactive sHLH associated with the chemotherapy.
  • Nine patients, including two cases each of rhabdomyosarcoma, neuroblastoma, Hodgkin disease, and non-Hodgkin lymphoma (NHL) and one case with Langerhans cell histiocytosis, were diagnosed as having concomitant hemophagocytosis at the initial evaluation of the tumor (Group 2).
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Lymphohistiocytosis, Hemophagocytic / diagnosis. Lymphohistiocytosis, Hemophagocytic / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications


65. Carneiro BA, Kaminer L, Eldibany M, Sreekantaiah C, Kaul K, Locker GY: Oxaliplatin-related acute myelogenous leukemia. Oncologist; 2006 Mar;11(3):261-2
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  • [Title] Oxaliplatin-related acute myelogenous leukemia.
  • Bone marrow biopsy was consistent with therapy-related acute myelogenous leukemia.
  • It is likely that the leukemia was related to the oxaliplatin administration.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid, Acute / chemically induced
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Bevacizumab. Cecal Neoplasms / drug therapy. Cecal Neoplasms / pathology. Chromosome Deletion. Female. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Humans. Leucovorin / administration & dosage. Leucovorin / adverse effects. Middle Aged. Omentum / pathology. Organoplatinum Compounds / administration & dosage. Organoplatinum Compounds / adverse effects. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / secondary. Peritoneal Neoplasms / drug therapy. Peritoneal Neoplasms / secondary. Sigmoid Neoplasms / drug therapy. Sigmoid Neoplasms / secondary. Trisomy

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  • (PMID = 16549810.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Organoplatinum Compounds; 2S9ZZM9Q9V / Bevacizumab; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; Folfox protocol
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66. Ferrés G M, Bidart H T, Zubieta A M: [Importance of images and etiological diagnosis of central nervous system involvement in immunocompromised patient]. Rev Chilena Infectol; 2010 Dec;27(6):541-3
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  • We report a 16 years old boy with diagnosis of Acute Myeloid Leukemia with severe immune suppression secondary to his primary disease and to leukemia's treatment.
  • Brain biopsy should be discussed when all the non invasive attempts for etiology identification have failed.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Immunocompromised Host. Leukemia, Myeloid, Acute / immunology. Neuroaspergillosis / etiology

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  • (PMID = 21279293.001).
  • [ISSN] 0716-1018
  • [Journal-full-title] Revista chilena de infectología : órgano oficial de la Sociedad Chilena de Infectología
  • [ISO-abbreviation] Rev Chilena Infectol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Chile
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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67. Falini B, Mecucci C, Tiacci E, Alcalay M, Rosati R, Pasqualucci L, La Starza R, Diverio D, Colombo E, Santucci A, Bigerna B, Pacini R, Pucciarini A, Liso A, Vignetti M, Fazi P, Meani N, Pettirossi V, Saglio G, Mandelli F, Lo-Coco F, Pelicci PG, Martelli MF, GIMEMA Acute Leukemia Working Party: Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotype. N Engl J Med; 2005 Jan 20;352(3):254-66
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  • [Title] Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotype.
  • METHODS: We used immunohistochemical methods to study the subcellular localization of NPM in bone marrow-biopsy specimens from 591 patients with primary acute myelogenous leukemia (AML).
  • RESULTS: Cytoplasmic NPM was detected in 208 (35.2 percent) of the 591 specimens from patients with primary AML but not in 135 secondary AML specimens or in 980 hematopoietic or extrahematopoietic neoplasms other than AML.
  • There was a high frequency of FLT3 internal tandem duplications and absence of CD34 and CD133 in AML specimens with a normal karyotype and cytoplasmic dislocation of NPM, but not in those in which the protein was restricted to the nucleus.
  • AML specimens with cytoplasmic NPM carried mutations of the NPM gene that were predicted to alter the protein at its C-terminal; this mutant gene caused cytoplasmic localization of NPM in transfected cells.
  • CONCLUSIONS: Cytoplasmic NPM is a characteristic feature of a large subgroup of patients with AML who have a normal karyotype, NPM gene mutations, and responsiveness to induction chemotherapy.
  • [MeSH-major] Bone Marrow / pathology. Cytoplasm / chemistry. Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics


68. Vehreschild JJ, Böhme A, Buchheidt D, Arenz D, Harnischmacher U, Heussel CP, Ullmann AJ, Mousset S, Hummel M, Frommolt P, Wassmer G, Drzisga I, Cornely OA: A double-blind trial on prophylactic voriconazole (VRC) or placebo during induction chemotherapy for acute myelogenous leukaemia (AML). J Infect; 2007 Nov;55(5):445-9
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  • [Title] A double-blind trial on prophylactic voriconazole (VRC) or placebo during induction chemotherapy for acute myelogenous leukaemia (AML).
  • We conducted a trial to analyze the efficacy and safety of voriconazole in the prevention of lung infiltrates during induction chemotherapy for acute myelogenous leukaemia (AML).
  • METHODS: This was a prospective, randomised, double-blind, placebo-controlled phase III trial in AML patients undergoing remission induction chemotherapy.
  • Secondary objectives were incidence of infections, length of stay in hospital, time to antifungal treatment, time to first fever, and drug safety.
  • CONCLUSION: In AML patients undergoing induction chemotherapy, prophylactic oral voriconazole 200 mg twice daily resulted in trends towards reduced incidences of lung infiltrates and hepatosplenic candidiasis.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Lung Diseases, Fungal / prevention & control. Mycoses / prevention & control. Pyrimidines / adverse effects. Pyrimidines / therapeutic use. Triazoles / adverse effects. Triazoles / therapeutic use

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  • (PMID = 17822770.001).
  • [ISSN] 1532-2742
  • [Journal-full-title] The Journal of infection
  • [ISO-abbreviation] J. Infect.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Placebos; 0 / Pyrimidines; 0 / Triazoles; JFU09I87TR / Voriconazole
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69. 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


70. Cutts BA, Sjogren AK, Andersson KM, Wahlstrom AM, Karlsson C, Swolin B, Bergo MO: Nf1 deficiency cooperates with oncogenic K-RAS to induce acute myeloid leukemia in mice. Blood; 2009 Oct 22;114(17):3629-32
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  • [Title] Nf1 deficiency cooperates with oncogenic K-RAS to induce acute myeloid leukemia in mice.
  • Hyperactive RAS signaling is caused by mutations in RAS genes or a deficiency of the neurofibromatosis gene (NF1) and is common in myeloid malignancies.
  • In mice, expression of oncogenic K-RAS or inactivation of Nf1 in hematopoietic cells results in myeloproliferative disorders (MPDs) that do not progress to acute myeloid leukemia (AML).
  • Here, we show that the simultaneous inactivation of Nf1 and expression of K-RAS(G12D) in mouse hematopoietic cells results in AML that was fatal in primary mice within 4 weeks and transplantable to sublethally irradiated secondary recipients.
  • [MeSH-major] Genes, Neurofibromatosis 1 / physiology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Neurofibromin 1 / deficiency. Proto-Oncogene Proteins p21(ras) / physiology

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  • (PMID = 19710506.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / Neurofibromin 1; 0 / RNA, Messenger; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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71. Ojeda-Uribe M, Herbrecht R, Kiefer MH, Schultz P, Chain J, Chenard MP, Servant JM, Debry C: Lessons from a case of oromandibular mucormycosis treated with surgery and a combination of amphotericin B lipid formulation plus caspofungin. Acta Haematol; 2010;124(2):98-102
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  • A rare case of oromandibular Rhizopus oryzae infection is described in a 55-year-old woman with acute myeloid leukaemia and decompensated diabetes mellitus.
  • Eight weeks of combined antifungal therapy were followed by secondary prophylaxis with amphotericin B lipid formulation during consolidation chemotherapy after achieving complete response of both leukaemia and mucormycosis.
  • [MeSH-major] Amphotericin B / administration & dosage. Echinocandins / administration & dosage. Leukemia, Myeloid, Acute / complications. Mucormycosis / drug therapy. Mucormycosis / surgery

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  • [Copyright] Copyright © 2010 S. Karger AG, Basel.
  • (PMID = 20689269.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Echinocandins; 7XU7A7DROE / Amphotericin B; F0XDI6ZL63 / caspofungin
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72. Subramanyam D, Belair CD, Barry-Holson KQ, Lin H, Kogan SC, Passegué E, Blelloch R: PML-RAR{alpha} and Dnmt3a1 cooperate in vivo to promote acute promyelocytic leukemia. Cancer Res; 2010 Nov 1;70(21):8792-801
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  • [Title] PML-RAR{alpha} and Dnmt3a1 cooperate in vivo to promote acute promyelocytic leukemia.
  • The PML-RARα oncogene is the central effector of acute promyelocytic leukemia (APL).
  • Here, we show that increased expression of Dnmt3a1 cooperates with PML-RARα in vivo to promote early lethality secondary to myeloid expansion and dysfunction in primary mice.

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  • [Copyright] ©2010 AACR.
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  • (PMID = 20861188.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / K08 NS048118; United States / NCI NIH HHS / CA / R01 CA095274; United States / NINDS NIH HHS / NS / R01 NS057221; United States / NINDS NIH HHS / NS / K08 NS48118
  • [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 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA methyltransferase 3A
  • [Other-IDs] NLM/ NIHMS256798; NLM/ PMC3021794
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73. Matsouka P, Pagoni M, Zikos P, Giannakoulas N, Apostolidis I, Asprogeraka T, Arvanitopoulou E, Spanoudakis E, Kotsianidis I, Tsatalas K, Papaioannou M, Marinakis T, Skandali A, Viniou N, Yataganas X, Bakiri M: Addition of cyclosporin-A to chemotherapy in secondary (post-MDS) AML in the elderly. A multicenter randomized trial of the Leukemia Working Group of the Hellenic Society of Hematology. Ann Hematol; 2006 Apr;85(4):250-6
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  • [Title] Addition of cyclosporin-A to chemotherapy in secondary (post-MDS) AML in the elderly. A multicenter randomized trial of the Leukemia Working Group of the Hellenic Society of Hematology.
  • In elderly patients with secondary leukemia, poor therapeutic response and low overall survival have been attributed mainly to age and to the primary resistance of leukemic cells to chemotherapy.
  • We conducted an open, randomized multicenter clinical trial involving patients more than 60 years old with secondary leukemia preceded by a myelodysplastic syndrome.
  • Leukemia-free survival was more favorable in patients who received cyclosporin-A, 12 vs 7 months for groups B and A, respectively (p=0.03).
  • Modulation of drug resistance by CsA in elderly people suffering from secondary acute leukemia may improve the outcome of chemotherapy without increasing drug toxicity and treatment-related mortality.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclosporine / administration & dosage. Leukemia, Myeloid / drug therapy. Neoplasms, Second Primary / drug therapy
  • [MeSH-minor] Acute Disease. Administration, Oral. Aged. Aged, 80 and over. Cytarabine / administration & dosage. Cytarabine / therapeutic use. Data Interpretation, Statistical. Disease-Free Survival. Etoposide / administration & dosage. Etoposide / therapeutic use. Female. Follow-Up Studies. Greece. Humans. Idarubicin / administration & dosage. Idarubicin / therapeutic use. Infusions, Intravenous. Male. Middle Aged. Remission Induction. Societies, Medical. Survival Analysis. Treatment Outcome

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  • (PMID = 16416114.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 83HN0GTJ6D / Cyclosporine; ZRP63D75JW / Idarubicin
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74. Roboz GJ, Ritchie EK, Curcio T, Provenzano J, Carlin R, Samuel M, Wittenberg B, Mazumdar M, Christos PJ, Mathew S, Allen-Bard S, Feldman EJ: Arsenic trioxide and low-dose cytarabine in older patients with untreated acute myeloid leukemia, excluding acute promyelocytic leukemia. Cancer; 2008 Nov 1;113(9):2504-11
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  • [Title] Arsenic trioxide and low-dose cytarabine in older patients with untreated acute myeloid leukemia, excluding acute promyelocytic leukemia.
  • BACKGROUND: Acute myeloid leukemia (AML) carries a dismal prognosis in older patients.
  • In this study, the authors evaluated the safety and efficacy of arsenic trioxide combined with low-dose cytarabine in untreated patients aged >or=60 years with AML.
  • Of 64 patients who had pathologically confirmed AML, excluding patients with acute promyelocytic leukemia and using World Health Organization criteria, the median age was 71 years, 10 patients (16%) had treatment-related AML, 40 patients (63%) had an antecedent myelodysplastic syndrome or myeloproliferative disorder, and 35 patients (55%) had unfavorable cytogenetics.
  • RESULTS: Complete remission was achieved in 21 of 61 patients (34%), including 15 of 50 patients (30%) who had secondary or treatment-related AML, 10 of 33 patients (30%) who had unfavorable cytogenetics, and 6 of 34 patients (18%) who had a poor baseline performance status.
  • CONCLUSIONS: The addition of arsenic trioxide to low-dose cytarabine appeared to improve responses in elderly patients who had AML compared with either agent alone, and a randomized trial of the combination versus single-agent low-dose cytarabine is ongoing.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Arsenicals / administration & dosage. Cytarabine / administration & dosage. Female. Humans. Leukemia, Promyelocytic, Acute. Male. Middle Aged. Oxides / administration & dosage. Prognosis. Remission Induction. Survival Rate


75. Im M, Lee JK, Lee DY, Hong YJ, Hong SI, Kang HJ, Chang YH: [Near-tetraploidy acute myeloid leukemia with RUNX1-RUNX1T1 rearrangement due to cryptic t(8;21)]. Korean J Lab Med; 2009 Dec;29(6):510-4
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  • [Title] [Near-tetraploidy acute myeloid leukemia with RUNX1-RUNX1T1 rearrangement due to cryptic t(8;21)].
  • Tetraploidy or near-tetraploidy is a rare cytogenetic abnormality found in AML, and is divided into primary and secondary forms.
  • The secondary tetraploidy or near-tetraploidy found in AML is known to be specifically associated with t(8;21).
  • This is the first case report of tetraploidy or near-tetraploidy AML with cryptic RUNX1/RUNX1T1 in Korea.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Polyploidy. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 20046081.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
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76. Havelange V, Antoine-Poirel H, Saussoy P, Van Den Neste E, Ferrant A: Donor cell leukemia developing after hematopoietic stem cell transplantation for multiple myeloma. Acta Clin Belg; 2006 Mar-Apr;61(2):82-6
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  • [Title] Donor cell leukemia developing after hematopoietic stem cell transplantation for multiple myeloma.
  • The development of secondary leukemia in donor cells after allogeneic stem cell transplantation is a rare event.
  • We describe the occurrence of acute myeloid leukemia in donor cells 4 years after a stem cell transplantation for multiple myeloma.
  • The multiple myeloma was relapsing at the time of the onset of acute myeloid leukemia.
  • Secondary leukemia in donor cells after transplantation for multiple myeloma has not yet been reported.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / etiology. Living Donors. Multiple Myeloma / therapy


77. Mimura N, Tsujimura H, Ise M, Sakai C, Takagi T, Nagata M, Kumagai K: Therapy-related leukemia following chemoradiotherapy for esophageal cancer. Eur J Haematol; 2010 Oct;85(4):353-7
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  • [Title] Therapy-related leukemia following chemoradiotherapy for esophageal cancer.
  • Although a sufficiently long-time survival has resulted in the increase of several treatment-related late toxicities, little is still known about the incidence of secondary malignancies.
  • Four patients developed leukemia after 19-48 months of follow-up.
  • Two patients were diagnosed with overt leukemia from myelodysplastic syndrome presenting a complex karyotype, including the deletion of chromosome 5 or 7.
  • Other patients developed acute myeloid leukemia with t(9;22)(q34;q11) and Burkitt leukemia with t(8;14)(q24;q32).
  • All patients eventually succumbed to leukemia.
  • Platinum and fluorouracil have shown relatively lower risks for secondary malignancies in comparison with alkylating agents and topoisomerase II inhibitors.
  • Especially, nedaplatin has never been described to introduce secondary neoplasms.
  • Our report supports the idea that the concurrent administration of radiotherapy with these agents affects the risk of leukemia.
  • Interestingly, rare balanced chromosomal abnormalities were observed in the present cases, thus providing new insights into the leukemogenesis of therapy-related leukemia.
  • [MeSH-major] Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / radiotherapy. Leukemia, Myeloid, Acute. Myelodysplastic Syndromes. Neoplasms, Second Primary


78. Zwerdling T, Krailo M, Monteleone P, Byrd R, Sato J, Dunaway R, Seibel N, Chen Z, Strain J, Reaman G, Children's Oncology Group: Phase II investigation of docetaxel in pediatric patients with recurrent solid tumors: a report from the Children's Oncology Group. Cancer; 2006 Apr 15;106(8):1821-8
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  • One patient each had acute myeloid leukemia, acute lymphoid leukemia, and high-grade glioma reported as secondary malignancies.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Glioma / drug therapy. Glioma / secondary. Neoplasm Recurrence, Local / drug therapy. Sarcoma / drug therapy. Sarcoma / secondary. Taxoids / therapeutic use

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  • [Copyright] 2006 American Cancer Society
  • (PMID = 16532433.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel
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79. Sabnis AJ, Cheung LS, Dail M, Kang HC, Santaguida M, Hermiston ML, Passegué E, Shannon K, Braun BS: Oncogenic Kras initiates leukemia in hematopoietic stem cells. PLoS Biol; 2009 Mar 17;7(3):e59
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  • [Title] Oncogenic Kras initiates leukemia in hematopoietic stem cells.
  • MPD could be initiated by Kras(G12D) expression in a highly restricted population enriched for hematopoietic stem cells (HSCs), but not in common myeloid progenitors.
  • Transplanted Kras(G12D) HSCs efficiently initiated acute T-lineage leukemia/lymphoma, which was associated with secondary Notch1 mutations in thymocytes.
  • [MeSH-major] Hematopoietic Stem Cells / pathology. Leukemia, Experimental / pathology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Proto-Oncogene Proteins p21(ras) / metabolism

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  • (PMID = 19296721.001).
  • [ISSN] 1545-7885
  • [Journal-full-title] PLoS biology
  • [ISO-abbreviation] PLoS Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / R37 CA72614; United States / NCI NIH HHS / CA / R37 CA072614; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / K08 CA103868; United States / NCI NIH HHS / CA / U01 CA84221
  • [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 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ PMC2656550
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80. Longway M, Matthews CA: Resumption of ovarian function 20 years after chemotherapy-induced ovarian failure: a case report. Fertil Steril; 2009 Jul;92(1):392.e17-8
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  • RESULT(S): Confirmation that ovarian function returned in a women who presented with cyclic vaginal bleeding after a 20-year history of amenorrhea secondary to chemotherapy-induced ovarian failure.
  • [MeSH-minor] Adult. Estradiol / blood. Female. Follicle Stimulating Hormone / blood. Humans. Leukemia, Myeloid, Acute / drug therapy. Menarche. Reference Values

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  • (PMID = 19403127.001).
  • [ISSN] 1556-5653
  • [Journal-full-title] Fertility and sterility
  • [ISO-abbreviation] Fertil. Steril.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 4TI98Z838E / Estradiol; 9002-68-0 / Follicle Stimulating Hormone
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81. 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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82. Erikci AA, Ozturk A, Tekgunduz E, Sayan O: Acute myeloid leukemia complicating multiple myeloma: a case successfully treated with etoposide, thioguanine, and cytarabine. Clin Lymphoma Myeloma; 2009 Aug;9(4):E14-5
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  • [Title] Acute myeloid leukemia complicating multiple myeloma: a case successfully treated with etoposide, thioguanine, and cytarabine.
  • BACKGROUND: The association of acute leukemia and multiple myeloma (MM) has been usually described not only as a complication of chemotherapy but also in the absence of chemotherapy or together at the time of diagnosis.
  • Such leukemias are typically acute myeloid leukemia (AML).
  • CASE REPORT: We report a case of a 68-year-old female who developed AML 2 years after the diagnosis of light chain (kappa) myeloma.
  • This therapy might be a safe alternative in secondary leukemia especially for elderly patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / therapeutic use. Etoposide / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Multiple Myeloma / drug therapy. Thioguanine / therapeutic use


83. Dicker F, Haferlach C, Sundermann J, Wendland N, Weiss T, Kern W, Haferlach T, Schnittger S: Mutation analysis for RUNX1, MLL-PTD, FLT3-ITD, NPM1 and NRAS in 269 patients with MDS or secondary AML. Leukemia; 2010 Aug;24(8):1528-32
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  • [Title] Mutation analysis for RUNX1, MLL-PTD, FLT3-ITD, NPM1 and NRAS in 269 patients with MDS or secondary AML.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Genes, ras. Leukemia, Myeloid, Acute / genetics. Mutation. Myelodysplastic Syndromes / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 20520634.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Nuclear Proteins; 0 / RUNX1 protein, human; 117896-08-9 / nucleophosmin; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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84. Schroeder T, Czibere A, Zohren F, Aivado M, Gattermann N, Germing U, Haas R: Meningioma 1 gene is differentially expressed in CD34 positive cells from bone marrow of patients with myelodysplastic syndromes with the highest expression in refractory anemia with excess of blasts and secondary acute myeloid leukemia. Leuk Lymphoma; 2009 Jun;50(6):1043-6
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  • [Title] Meningioma 1 gene is differentially expressed in CD34 positive cells from bone marrow of patients with myelodysplastic syndromes with the highest expression in refractory anemia with excess of blasts and secondary acute myeloid leukemia.
  • [MeSH-major] Anemia / genetics. Antigens, CD34 / blood. Bone Marrow Cells / metabolism. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Disease Progression. Female. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Humans. Male. Middle Aged. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction


85. Bayona C, Lassaletta A, Pérez A, Sevilla J, Albi G, Villa JR, Madero L: [Fatal hemoptysis secondary to invasive pulmonary aspergillosis in a girl with acute myeloblastic leukemia]. An Pediatr (Barc); 2007 Sep;67(3):278-9
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  • [Title] [Fatal hemoptysis secondary to invasive pulmonary aspergillosis in a girl with acute myeloblastic leukemia].
  • [MeSH-major] Aspergillosis / complications. Hemoptysis / etiology. Leukemia, Myeloid, Acute / complications. Lung Diseases, Fungal / complications

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  • (PMID = 17785168.001).
  • [ISSN] 1695-4033
  • [Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)
  • [ISO-abbreviation] An Pediatr (Barc)
  • [Language] spa
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Spain
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86. Dang L, Jin S, Su SM: IDH mutations in glioma and acute myeloid leukemia. Trends Mol Med; 2010 Sep;16(9):387-97
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  • [Title] IDH mutations in glioma and acute myeloid leukemia.
  • Subsequent studies have confirmed recurrent IDH1 and IDH2 mutations in up to 70% of low-grade glioma and secondary GBM, as well as in 10% of acute myeloid leukemia (AML) cases.
  • This review surveys the prevalence of IDH mutations in cancer and explores current mechanistic understanding of IDH mutations with implications for diagnostic and therapeutic development for the treatment of gliomas and AML.
  • [MeSH-major] Brain Neoplasms / enzymology. Glioma / enzymology. Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / enzymology. Mutation


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


88. Creutzig U, Zimmermann M, Ritter J, Reinhardt D, Hermann J, Henze G, Jürgens H, Kabisch H, Reiter A, Riehm H, Gadner H, Schellong G: Treatment strategies and long-term results in paediatric patients treated in four consecutive AML-BFM trials. Leukemia; 2005 Dec;19(12):2030-42
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  • [Title] Treatment strategies and long-term results in paediatric patients treated in four consecutive AML-BFM trials.
  • A total of 1111 children with acute myeloblastic leukaemia (AML) were treated in four consecutive Berlin-Frankfurt-Münster (BFM) studies from 1978 to 1998.
  • The first cooperative trial AML-BFM 78 established intensive chemotherapy with seven drugs, CNS irradiation and 2-year maintenance, achieving a long-term survival (overall survival (OS)) of 40%.
  • Induction intensification in AML-BFM 83 resulted in significant improvement of disease-free survival (DFS).
  • In AML-BFM 87, the benefit of CNS irradiation in preventing CNS/systemic relapses was demonstrated.
  • In AML-BFM 93, the introduction of idarubicin during first induction followed by intensification with HAM increased the 5-year EFS, DFS and OS to 50+/-2, 61+/-3 and 57+/-2%, respectively.
  • The AML-BFM studies performed in three European countries with >70 cooperating centres have significantly improved the outcome in AML children; nevertheless, increasing experience with these intensive treatment regimens is of fundamental importance to reduce fatal complications.
  • [MeSH-major] Antineoplastic Protocols / standards. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Cranial Irradiation. Dose-Response Relationship, Drug. Female. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Hemorrhage / etiology. Humans. Infant. Infant, Newborn. Male. Remission Induction / methods. Risk Assessment. Secondary Prevention. Treatment Outcome

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  • (PMID = 16304570.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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89. 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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90. Sun Q, So CC, Yip SF, Wan TS, Ma SK, Chan LC: Functional alterations of Lin-CD34+CD38+ cells in chronic myelomonocytic leukemia and on progression to acute leukemia. Leuk Res; 2008 Sep;32(9):1374-81
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  • [Title] Functional alterations of Lin-CD34+CD38+ cells in chronic myelomonocytic leukemia and on progression to acute leukemia.
  • The functional behavior of hematopoietic stem cell (HSC) and progenitors in chronic myelomonocytic leukemia (CMML) and on disease progression is little known.
  • We performed cell proliferation, apoptosis, hematopoietic colony forming/replating and differentiation potential studies in the purified subpopulations of Lin(-)CD34(+)CD38(-) and Lin(-)CD34(+)CD38(+) cells from 16 CMML with 6 cases after acute myeloid leukemia transformation (AML-t).
  • We observed an expansion of the hematopoietic progenitor pool (Lin(-)CD34(+) cells) in AML-t comprising mainly Lin(-)CD34(+)CD38(+) cells.
  • The Lin(-)CD34(+)CD38(+) cells in AML-t displayed high proliferative activity, resistance to apoptosis, enhanced myeloid colony formation/replating ability and a complete dendritic cell (DC) differentiation block.
  • Our findings suggest Lin(-)CD34(+)CD38(+) cells instead of Lin(-)CD34(+)CD38(-) cells could be the target(s) of secondary genetic lesions underpinning progression from CMML to AML, which have implications for the further study of the biology of leukemic transformation and the design of new strategies for the effective treatment of CMML.
  • [MeSH-major] Antigens, CD34 / metabolism. Antigens, CD38 / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myelomonocytic, Chronic / metabolism. Membrane Glycoproteins / metabolism


91. Cilloni D, Messa E, Messa F, Carturan S, Defilippi I, Arruga F, Rosso V, Catalano R, Bracco E, Nicoli P, Saglio G: Genetic abnormalities as targets for molecular therapies in myelodysplastic syndromes. Ann N Y Acad Sci; 2006 Nov;1089:411-23
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  • Recent advances in molecular genetics have increased knowledge regarding the mechanisms leading to myelodysplastic syndrome (MDS), secondary acute myeloid leukemia (AML), and therapy-induced MDS.
  • Many genetic defects underlying MDS and AML have been identified thereby allowing the development of new molecular-targeted therapies.
  • These agents have been tested in patients with solid tumors and hematologic malignancies such as AML and MDS.

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  • (PMID = 17261784.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / MECOM protein, human; 0 / Transcription Factors; 0 / WT1 Proteins; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Number-of-references] 76
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92. La Starza R, Aventin A, Matteucci C, Crescenzi B, Romoli S, Testoni N, Pierini V, Ciolli S, Sambani C, Locasciulli A, Di Bona E, Lafage-Pochitaloff M, Martelli MF, Marynen P, Mecucci C: Genomic gain at 6p21: a new cryptic molecular rearrangement in secondary myelodysplastic syndrome and acute myeloid leukemia. Leukemia; 2006 Jun;20(6):958-64
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  • [Title] Genomic gain at 6p21: a new cryptic molecular rearrangement in secondary myelodysplastic syndrome and acute myeloid leukemia.
  • Fluorescence in situ hybridization and comparative genomic hybridization characterized 6p rearrangements in eight primary and in 10 secondary myeloid disorders (including one patient with Fanconi anemia) and found different molecular lesions in each group.
  • In the 10 patients with secondary acute myeloid leukemia/myelodysplastic syndrome (AML/MDS), the short arm of chromosome 6 was involved in unbalanced translocations in 7.
  • Consequently, in secondary AML/MDS, we hypothesize that 6p gains are major pathogenetic events arising from acquired and/or congenital genomic instability.
  • [MeSH-major] Chromosomes, Human, Pair 6 / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Neoplasms, Second Primary / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Cytogenetic Analysis. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Sensitivity and Specificity


93. Doki N, Hoshino T, Irisawa H, Sakura T, Miyawaki S: [Acute myeloid leukemia complicated with pulmonary alveolar proteinosis at presentation]. Rinsho Ketsueki; 2005 Jul;46(7):522-6
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  • [Title] [Acute myeloid leukemia complicated with pulmonary alveolar proteinosis at presentation].
  • Following the results obtained from a bone marrow aspiration, he was diagnosed as having acute myeloid leukemia (AML).
  • As a result of the autopsy findings, a diagnosis of secondary pulmonary alveolar proteinosis (PAP) associated with AML was made.
  • Among the reported cases of PAP in hematological malignancy, there has not been one case detected at the time AML was diagnosed.
  • If there is evidence of an unknown cause of lung infiltration when AML is diagnosed, attention should be paid to the possibility of the presence of PAP.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Pulmonary Alveolar Proteinosis / etiology

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  • (PMID = 16440746.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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94. Laurenti L, Tarnani M, Chiusolo P, La Torre G, Garzia M, Zollino M, Zini G, Balducci M, Leone G, Sica S: Low incidence of secondary neoplasia after autotransplantation for lymphoproliferative disease: the role of pre-transplant therapy. Clin Transplant; 2008 Mar-Apr;22(2):191-9
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  • [Title] Low incidence of secondary neoplasia after autotransplantation for lymphoproliferative disease: the role of pre-transplant therapy.
  • To asses the real contribution of pre-transplantation treatment in the incidence of secondary neoplasia after autologous transplant for lymphoproliferative disorders, we used stringent inclusion/exclusion criteria.
  • Three patients developed secondary myelodysplastic syndrome/acute myeloid leukemia (sMDS/AML) and three patients developed solid neoplasia.
  • By univariate analysis diagnosis chronic lymphocytic leukemia and use of fludarabine and monoclonal antibodies were the only variables significantly associated with the development of sMDS/AML.
  • By multivariate analysis, the variables associated with sMDS/AML were the use of fludarabine and disease status at PBSCT.
  • By univariate analysis, we found that radiotherapy and the use of monoclonal antibodies were significantly associated with the development of secondary solid neoplasia.
  • We report the lowest incidence of sMDS/AML after autologous stem-cell transplantation for lymphoproliferative malignancies.
  • Major reasons could be ascribed to the stringent inclusion/exclusion criteria used to establish the real incidence of sMDS/AML because of chemo-radiotherapy used before transplant procedure.
  • The low incidence of secondary solid tumors could be caused by the absence of total body irradiation as part of the conditioning regimen or the short follow-up.
  • [MeSH-minor] Adolescent. Adult. Female. Humans. Incidence. Italy / epidemiology. Kaplan-Meier Estimate. Leukemia, Myeloid, Acute / complications. Male. Middle Aged. Myelodysplastic Syndromes / complications. Proportional Hazards Models. Retrospective Studies. Transplantation, Autologous / adverse effects

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  • (PMID = 18339139.001).
  • [ISSN] 1399-0012
  • [Journal-full-title] Clinical transplantation
  • [ISO-abbreviation] Clin Transplant
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
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95. Haferlach C, Mecucci C, Schnittger S, Kohlmann A, Mancini M, Cuneo A, Testoni N, Rege-Cambrin G, Santucci A, Vignetti M, Fazi P, Martelli MP, Haferlach T, Falini B: AML with mutated NPM1 carrying a normal or aberrant karyotype show overlapping biologic, pathologic, immunophenotypic, and prognostic features. Blood; 2009 Oct 1;114(14):3024-32
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  • [Title] AML with mutated NPM1 carrying a normal or aberrant karyotype show overlapping biologic, pathologic, immunophenotypic, and prognostic features.
  • Acute myeloid leukemia (AML) with mutated NPM1 usually carries normal karyotype (NK), but it may harbor chromosomal aberrations whose significance remains unclear.
  • We addressed this question in 631 AML patients with mutated/cytoplasmic NPM1.
  • Chromosome aberrations in NPM1-mutated AML were similar to, but occurred less frequently than additional chromosome changes found in other AML with recurrent cytogenetic abnormalities according to WHO classification.
  • Four of the 31 NPM1-mutated AML patients karyotyped at different time points had NK at diagnosis but AK at relapse: del(9q) (n = 2), t(2;11) (n = 1), inv(12) (n = 1).
  • NPM1-mutated AML with NK or AK showed overlapping morphologic, immunophenotypic (CD34 negativity), and gene expression profile (down-regulation of CD34 and up-regulation of HOX genes).
  • No difference in survival was observed among NPM1-mutated AML patients independently of whether they carried a NK or an AK, the NPM1-mutated/FLT3-ITD negative cases showing the better prognosis.
  • Findings in our patients point to chromosomal aberrations as secondary events, reinforce the concept that NPM1 mutation is a founder genetic lesion, and indicate that NPM1-mutated AML should be clinically handled as one entity, irrespective of the karyotype.
  • [MeSH-major] Antigens, CD34 / metabolism. Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / immunology. Mutation / genetics. Nuclear Proteins / genetics

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  • [CommentIn] Blood. 2009 Nov 12;114(20):4601-2; author reply 4602-3 [19965707.001]
  • (PMID = 19429869.001).
  • [ISSN] 1528-0020
  • [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 / Antigens, CD34; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / RNA, Messenger; 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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96. 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


97. Cook G, Clark RE, Crawley C, Mackinnon S, Russell N, Thomson K, Pearce RM, Towlson K, Marks DI: The outcome of sibling and unrelated donor allogeneic stem cell transplantation in adult patients with acute myeloid leukemia in first remission who were initially refractory to first induction chemotherapy. Biol Blood Marrow Transplant; 2006 Mar;12(3):293-300
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  • [Title] The outcome of sibling and unrelated donor allogeneic stem cell transplantation in adult patients with acute myeloid leukemia in first remission who were initially refractory to first induction chemotherapy.
  • The optimal management of patients with initially refractory acute myeloid leukemia is unknown.
  • We analyzed the outcomes of 68 adult patients (median age, 37 years) with acute myeloid leukemia in first complete remission with initially refractory disease who were treated with matched sibling (n=44) or unrelated donor (n=22) stem cell transplantation or who received transplants from other donors (n=2).
  • Grades II to IV and III/IV acute graft-versus-host disease (GVHD) were seen in 34% and 14% of patients, respectively.
  • Approximately one third of patients survived 4 years after allogeneic stem cell transplantation for initially refractory acute myeloid leukemia in first complete remission: relapse and treatment-related mortality were the major causes of treatment failure.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Living Donors. Stem Cell Transplantation. Transplantation Conditioning
  • [MeSH-minor] Adolescent. Adult. Chronic Disease. Cyclophosphamide / administration & dosage. Disease-Free Survival. Female. Graft vs Host Disease / etiology. Graft vs Host Disease / mortality. Graft vs Host Disease / prevention & control. Humans. Male. Middle Aged. Myeloablative Agonists / administration & dosage. Remission Induction / methods. Retrospective Studies. Secondary Prevention. Survival Rate. Time Factors. Transplantation, Homologous. Treatment Failure. Whole-Body Irradiation / methods. Whole-Body Irradiation / mortality


98. Lin P, Chen L, Luthra R, Konoplev SN, Wang X, Medeiros LJ: Acute myeloid leukemia harboring t(8;21)(q22;q22): a heterogeneous disease with poor outcome in a subset of patients unrelated to secondary cytogenetic aberrations. Mod Pathol; 2008 Aug;21(8):1029-36
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  • [Title] Acute myeloid leukemia harboring t(8;21)(q22;q22): a heterogeneous disease with poor outcome in a subset of patients unrelated to secondary cytogenetic aberrations.
  • Acute myeloid leukemia with t(8;21)(q22;q22) is a distinct type of leukemia considered to have a favorable prognosis.
  • We studied 56 patients with acute myeloid leukemia associated with t(8;21) and correlated clinicopathologic, cytogenetic and molecular findings with outcome to identify markers of prognosis.
  • The 5-year overall survival rate of patients with mutated leukemia was 20%.
  • We conclude that acute myeloid leukemia associated with t(8;21) is a heterogeneous disease with poor survival in a subset of patients unrelated to common secondary cytogenetic aberrations.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 18536654.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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99. Poiraud C, Gagey-Caron V, Barbarot S, Durant C, Ayari S, Stalder JF: [Cutaneous, mucosal and systemic pyoderma gangrenosum]. Ann Dermatol Venereol; 2010 Mar;137(3):212-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The patient presented secondary worsening of his acute myeloid leukaemia type-IV requiring bone marrow rescue.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Mouth Mucosa / pathology. Pyoderma Gangrenosum / pathology

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  • [Copyright] Copyright 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20227565.001).
  • [ISSN] 0151-9638
  • [Journal-full-title] Annales de dermatologie et de vénéréologie
  • [ISO-abbreviation] Ann Dermatol Venereol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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100. Yin CC, Cortes J, Barkoh B, Hayes K, Kantarjian H, Jones D: t(3;21)(q26;q22) in myeloid leukemia: an aggressive syndrome of blast transformation associated with hydroxyurea or antimetabolite therapy. Cancer; 2006 Apr 15;106(8):1730-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] t(3;21)(q26;q22) in myeloid leukemia: an aggressive syndrome of blast transformation associated with hydroxyurea or antimetabolite therapy.
  • BACKGROUND: The t(3;21)(q26;q22) translocation is associated with myeloid leukemias and results in a chimeric oncoprotein containing AML1/RUNX1 variably fused to EAP, MDS1, and/or EVI1.
  • RESULTS: In all 16 patients with chronic myeloproliferative disorders, including 14 with chronic myelogenous leukemia (CML), the occurrence of t(3;21) heralded myeloid blast transformation.
  • Among 10 cases of t(3;21)-associated acute myeloid leukemia, 8 were secondary tumors after chemotherapy for other neoplasms that had been treated with regimens including fludarabine and 5-fluorouracil in 3 patients each and etoposide in 2 patients.
  • The immunophenotype of the blasts in all 22 tested cases was similar, with uniform expression of myeloid markers and CD34 and variable expression of CD7 and CD9, but minimal morphological myeloid maturation.
  • Among patients with acute myeloid leukemia/myelodysplastic syndrome, 7 died of disease (at a median of 2 mos) and 2 had persistent leukemia with short follow-up.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Antineoplastic Agents / adverse effects. Chromosomes, Human, Pair 21 / drug effects. Chromosomes, Human, Pair 3 / drug effects. Hydroxyurea / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / genetics. Lymphocyte Activation / drug effects. Myeloproliferative Disorders / drug therapy. Oncogene Proteins, Fusion / analysis. Translocation, Genetic / drug effects

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  • [Copyright] 2006 American Cancer Society
  • (PMID = 16532439.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672
  • [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 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 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; X6Q56QN5QC / Hydroxyurea
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