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1. Zhang WW, Habeebu S, Sheehan AM, Naeem R, Hernandez VS, Dreyer ZE, López-Terrada D: Molecular monitoring of 8p11 myeloproliferative syndrome in an infant. J Pediatr Hematol Oncol; 2009 Nov;31(11):879-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Typical pathologic findings include myeloid hyperplasia, lymphadenopathy, precursor T-lymphoblastic lymphoma, and eosinophilia.
  • The disease is usually associated with an aggressive course and progression to acute myeloid leukemia is frequent.

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  • (PMID = 19829149.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 0 / ZMYM2 protein, human; EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1
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2. Epling-Burnette PK, Bai F, Painter JS, Rollison DE, Salih HR, Krusch M, Zou J, Ku E, Zhong B, Boulware D, Moscinski L, Wei S, Djeu JY, List AF: Reduced natural killer (NK) function associated with high-risk myelodysplastic syndrome (MDS) and reduced expression of activating NK receptors. Blood; 2007 Jun 1;109(11):4816-24
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  • Myelodysplastic syndromes (MDS) are characterized by ineffective hematopoiesis with potential for progression to acute myeloid leukemia (AML).
  • Collectively, these findings suggest that impairment of NK cytolytic function derives in part from reduced activating NK receptors such as NKG2D in association with disease progression.
  • Evasion of NK immunosurveillance may have importance for MDS disease progression.

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  • (PMID = 17341666.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 112112-01; United States / NCI NIH HHS / CA / R01 CA112112; United States / NIAID NIH HHS / AI / AI 056213; United States / NCI NIH HHS / CA / CA 098080; United States / NCI NIH HHS / CA / R01 CA098080; United States / NIAID NIH HHS / AI / R01 AI056213
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34
  • [Other-IDs] NLM/ PMC1885518
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3. Kim HG, Kojima K, Swindle CS, Cotta CV, Huo Y, Reddy V, Klug CA: FLT3-ITD cooperates with inv(16) to promote progression to acute myeloid leukemia. Blood; 2008 Feb 01;111(3):1567-74
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  • [Title] FLT3-ITD cooperates with inv(16) to promote progression to acute myeloid leukemia.
  • The inversion of chromosome 16 in the inv(16)(p13q22) is one of the most frequent cytogenetic abnormalities observed in acute myeloid leukemia (AML).
  • Compared with animals transplanted with only CBFbeta-SMMHC-expressing cells, FLT3-ITD further restricted early myeloid differentiation and promoted peripheralization of primitive myeloblasts as early as 2.5 weeks after transplantation.
  • FLT3-ITD also accelerated disease progression in all CBFbeta-SMMHC/FLT3-ITD-reconstituted animals, which died of a highly aggressive and transplantable AML within 3 to 5 months.
  • [MeSH-major] Chromosome Inversion / genetics. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. Oncogene Proteins, Fusion / metabolism. fms-Like Tyrosine Kinase 3 / metabolism
  • [MeSH-minor] Animals. Core Binding Factor beta Subunit / genetics. Core Binding Factor beta Subunit / metabolism. Disease Progression. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Lymphopoiesis. Mice. Mutation / genetics. Myelopoiesis. Smooth Muscle Myosins / genetics. Smooth Muscle Myosins / metabolism. Survival Rate

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  • (PMID = 17967943.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K01 DK067186; United States / NCI NIH HHS / CA / R01 CA096798; United States / NIAID NIH HHS / AI / T32 AI007051; United States / NCI NIH HHS / CA / R01CA96798
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor beta Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.1.- / Smooth Muscle Myosins
  • [Other-IDs] NLM/ PMC2214774
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4. Buccisano F, Maurillo L, Tamburini A, Del Poeta G, Del Principe MI, Ammatuna E, Consalvo MI, Campagna S, Ottaviani L, Sarlo C, Renzi D, Faccia S, Fraboni D, Lo Coco F, Amadori S, Venditti A: Evaluation of the prognostic relevance of L-selectin and ICAM1 expression in myelodysplastic syndromes. Eur J Haematol; 2008 Feb;80(2):107-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: An aberrant pattern of expression of L-selectin and intercellular adhesion molecule 1 (ICAM1) may characterise CD34+ blast cells in myelodysplastic syndromes (MDS) and secondary acute myeloid leukaemia (sAML).
  • RESULTS: The ratio of L-selectin/ICAM1 expression was identified as a parameter correlated with the percentage of BM blast infiltration and the time to leukaemic progression among MDS patients.
  • Furthermore, MDS patients with a baseline ratio <1 had a higher leukaemic progression rate (41% vs. 19%, P = 0.008); the actuarial risk of disease progression for this subgroup of MDS patients was also higher (64% vs. 11% at 2 yr, P = 0.002).
  • (ii) the ratio of their expression has a prognostic role; and (iii) a ratio <1 significantly predicts progression to overt leukaemia in MDS patients.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Bone Marrow / metabolism. Disease Progression. Female. Humans. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / metabolism. Male. Middle Aged. Prognosis. Time Factors


5. Kobayashi H, Matsuyama T, Ueda M, Suzuki T, Ozaki K, Mori M, Nagai T, Muroi K, Ozawa K: Predictive factors of response and survival following chemotherapy treatment in acute myeloid leukemia progression from myelodysplastic syndrome. Intern Med; 2009;48(18):1629-33
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  • [Title] Predictive factors of response and survival following chemotherapy treatment in acute myeloid leukemia progression from myelodysplastic syndrome.
  • OBJECTIVE: The progression of myelodysplastic syndrome to acute myeloid leukemia (MDS/AML) is generally incurable and its prognosis is extremely poor.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


6. Müller-Berndorff H, Haas PS, Kunzmann R, Schulte-Mönting J, Lübbert M: Comparison of five prognostic scoring systems, the French-American-British (FAB) and World Health Organization (WHO) classifications in patients with myelodysplastic syndromes: Results of a single-center analysis. Ann Hematol; 2006 Aug;85(8):502-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We retrospectively studied 89 consecutive patients diagnosed with primary myelodysplastic syndrome (MDS) over a period of 10 years to (1) identify prognostic factors for overall survival (OS) and leukemia-free survival (LFS);.
  • Median OS was 3 years; 67 patients (75%) have died, and 28 (31%) had progression to acute myeloid leukemia (AML).


7. Follo MY, Mongiorgi S, Finelli C, Clissa C, Ramazzotti G, Fiume R, Faenza I, Manzoli L, Martelli AM, Cocco L: Nuclear inositide signaling in myelodysplastic syndromes. J Cell Biochem; 2010 Apr 15;109(6):1065-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Although distinct morphologic subgroups exist, the natural history of MDS is progression to acute myeloid leukemia (AML).
  • Inositides are key cellular second messengers with well-established roles in signal transduction pathways, and nuclear metabolism elicited by phosphoinositide-specific phospholipase C (PI-PLC) beta1 and Akt plays an important role in the control of the balance between cell cycle progression and apoptosis in both normal and pathologic conditions.
  • [MeSH-minor] Animals. Humans. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. Phosphatidylinositols / metabolism. Phospholipase C beta / metabolism. Proto-Oncogene Proteins c-akt / metabolism


8. Montoto S, Canals C, Rohatiner AZ, Taghipour G, Sureda A, Schmitz N, Gisselbrecht C, Fouillard L, Milpied N, Haioun C, Slavin S, Conde E, Fruchart C, Ferrant A, Leblond V, Tilly H, Lister TA, Goldstone AH, EBMT Lymphoma Working Party: Long-term follow-up of high-dose treatment with autologous haematopoietic progenitor cell support in 693 patients with follicular lymphoma: an EBMT registry study. Leukemia; 2007 Nov;21(11):2324-31
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  • A total of 375 patients (54%) developed recurrent lymphoma, 10-year progression-free survival (PFS) being 31%.
  • Thirty-nine patients developed secondary myelodysplastic syndrome/acute myeloid leukaemia (MDS/AML), in 34 cases having received TBI as the conditioning regimen.


9. Cocco L, Manzoli L, Palka G, Martelli AM: Nuclear phospholipase C beta1, regulation of the cell cycle and progression of acute myeloid leukemia. Adv Enzyme Regul; 2005;45:126-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nuclear phospholipase C beta1, regulation of the cell cycle and progression of acute myeloid leukemia.
  • PLC beta1 is a well-known example, given that it has been shown that only the enzyme located in the nucleus targets the cyclin D3/cdk4 complex, playing, in turn, a key role in the control of normal progression through the G1 phase of the cell cycle.
  • Moreover, non-specific alterations in chromosome 20 have been found in patients affected by MDS and acute myeloid leukemia AML.
  • The availability of a highly specific probe gave an opportunity to perform in patients affected with MDS/AML, associated with normal karyotype, painting and FISH analysis aimed to check the PLC beta1 gene, given that this signaling molecule is a key player in the control of some checkpoints of the normal progression through the cell cycle.
  • The reported data strengthen the contention of a key role played by PLC beta1 in the nucleus, suggest a possible involvement of PLC beta1 in the progression of MDS to AML and pave the way for a larger investigation aimed at identifying a possible high risk group among MDS patients with a normal karyotype.
  • [MeSH-major] Cell Cycle / physiology. Cell Nucleus / enzymology. Isoenzymes / physiology. Leukemia, Myeloid / pathology. Myelodysplastic Syndromes / pathology. Type C Phospholipases / physiology
  • [MeSH-minor] Acute Disease. Gene Deletion. Humans. Phospholipase C beta. Signal Transduction / physiology


10. Ullah K, Ahmed P, Raza S, Satti TM, Chaudhry QU, Akhtar F, Kamal MK, Akhtar FM, Khan B: Management of acute myeloid leukaemia--5 years experience at Armed Forces Bone Marrow Transplant Centre, Rawalpindi. J Pak Med Assoc; 2007 Sep;57(9):434-9
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  • [Title] Management of acute myeloid leukaemia--5 years experience at Armed Forces Bone Marrow Transplant Centre, Rawalpindi.
  • METHODS: A retrospective study on acute myeloid leukaemia (AML) patients was carried out at Armed Forces Bone Marrow Transplant Centre Rawalpindi Pakistan between July 2001 and June 2006.
  • These 46 patients were categorized into two groups on the basis of type of leukaemia and chemotherapy given.
  • [MeSH-major] Anthracyclines / therapeutic use. Antineoplastic Agents / therapeutic use. Cytarabine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Military Medicine. Military Personnel. Treatment Outcome. Tretinoin / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Child. Disease Progression. Female. Humans. Male. Middle Aged. Pakistan. Retrospective Studies. Time Factors


11. Roy P, Reavey E, Rayne M, Roy S, Abed El Baky M, Ishii Y, Bartholomew C: Enhanced sensitivity to hydrogen peroxide-induced apoptosis in Evi1 transformed Rat1 fibroblasts due to repression of carbonic anhydrase III. FEBS J; 2010 Jan;277(2):441-52
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  • EVI1 is a nuclear zinc finger protein essential to normal development, which participates in acute myeloid leukaemia progression and transforms Rat1 fibroblasts.

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  • (PMID = 20015077.001).
  • [ISSN] 1742-4658
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / Evi1 protein, mouse; 0 / RNA, Small Interfering; 0 / Recombinant Proteins; 0 / Transcription Factors; BBX060AN9V / Hydrogen Peroxide; EC 3.4.22.- / Casp3 protein, rat; EC 3.4.22.- / Caspase 3; EC 4.2.1.- / Carbonic Anhydrase III; P88XT4IS4D / Paclitaxel
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12. Coppo P, Flamant S, De Mas V, Jarrier P, Guillier M, Bonnet ML, Lacout C, Guilhot F, Vainchenker W, Turhan AG: BCR-ABL activates STAT3 via JAK and MEK pathways in human cells. Br J Haematol; 2006 Jul;134(2):171-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Chronic myeloid leukaemia (CML) is characterised by a progression from a chronic towards an acute phase.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Protein-Tyrosine Kinases / physiology. STAT3 Transcription Factor / metabolism

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  • (PMID = 16846476.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / STAT3 Transcription Factor; EC 2.7.010.2 / JAK1 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.11.25 / MAP Kinase Kinase Kinases
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13. Jabbour E, Giles FJ: New agents in myelodysplastic syndromes. Curr Hematol Malig Rep; 2006 Mar;1(1):25-33
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  • Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal hematopoietic disorders characterized by ineffective hematopoiesis resulting in peripheral cytopenia and by increased progression to acute myeloid leukemia (AML).
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Blood Transfusion. Clinical Trials as Topic. Combined Modality Therapy. Disease Progression. Drug Design. Enzyme Inhibitors / therapeutic use. Erythropoietin / therapeutic use. Granulocyte Colony-Stimulating Factor / therapeutic use. Hematopoietic Stem Cell Transplantation. Humans. Multicenter Studies as Topic. Prognosis. Risk. Tretinoin / therapeutic use


14. Lee JH, Kwon KA, Lee S, Oh SY, Kim SH, Kwon HC, Han JY, Song MK, Chung JS, Lee HS, Kim YS, Lee SM, Joo YD, Kim HJ: Incidence and clinical characteristics of clonal cytogenetic abnormalities of acquired aplastic anemia in adults. Korean J Hematol; 2010 Dec;45(4):242-6
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  • In Group 2, 2 patients later developed CA without progression to acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS); the other 2 patients later progressed to AML.

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  • (PMID = 21253425.001).
  • [ISSN] 2092-9129
  • [Journal-full-title] The Korean journal of hematology
  • [ISO-abbreviation] Korean J Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC3023049
  • [Keywords] NOTNLM ; Aplastic anemia / Cytogenetic abnormality
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15. Trikalinos NA, Soupir CP, Dey BR: Lineage switch of acute lymphocyctic leukaemia with t(4;11)(q21;q23) into acute myeloid leukaemia in an adult patient after allogeneic stem cell transplantation. Br J Haematol; 2009 Apr;145(2):262-4
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  • [Title] Lineage switch of acute lymphocyctic leukaemia with t(4;11)(q21;q23) into acute myeloid leukaemia in an adult patient after allogeneic stem cell transplantation.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 4. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Disease Progression. Female. Humans

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  • (PMID = 19208102.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
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16. Edlin R, Connock M, Tubeuf S, Round J, Fry-Smith A, Hyde C, Greenheld W: Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia. Health Technol Assess; 2010 May;14 Suppl 1:69-74
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  • [Title] Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia.
  • This paper presents a summary of the evidence review group (ERG) report into the clinical effectiveness and cost-effectiveness of azacitidine (aza) compared with conventional care regimes (CCR) for higher risk patients with myelodysplastic syndrome (MDS), chronic myelomonocytic leukaemia (CMML) and acute myeloid leukaemia (AML), based on the evidence submission from the manufacturer to the National Institute for Health and Clinical Excellence (NICE) as part of the single technology appraisal process.
  • The patient outcomes governing relative effectiveness and cost-effectiveness were defined as overall survival, time to progression (TTP) to AML, adverse events and health-related quality of life (HRQoL).
  • The AZA-001 study showed that, compared with CCR, those MDS patients receiving aza had prolonged median survival, had delayed progression to AML, had reduced dependence on transfusions and had a small improvement in response rate.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myelomonocytic, Chronic / drug therapy. Myelodysplastic Syndromes / drug therapy


17. Passamonti F, Cervantes F, Vannucchi AM, Morra E, Rumi E, Cazzola M, Tefferi A: Dynamic International Prognostic Scoring System (DIPSS) predicts progression to acute myeloid leukemia in primary myelofibrosis. Blood; 2010 Oct 14;116(15):2857-8
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  • [Title] Dynamic International Prognostic Scoring System (DIPSS) predicts progression to acute myeloid leukemia in primary myelofibrosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Primary Myelofibrosis / complications
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. Proportional Hazards Models. Time Factors


18. Neukirchen J, Blum S, Kuendgen A, Strupp C, Aivado M, Haas R, Aul C, Gattermann N, Germing U: Platelet counts and haemorrhagic diathesis in patients with myelodysplastic syndromes. Eur J Haematol; 2009 Nov;83(5):477-82
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  • Platelets lower than 100 000/microL were associated with significantly shortened survival (P < 0.00005), because of an increased risk of progression to acute myeloid leukaemia (AML) (30% vs. 21%) (P < 0.02) and bleeding (16% vs. 8%) (P = 0.0005).
  • [MeSH-minor] Disease-Free Survival. Female. Humans. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Male. Platelet Transfusion. Predictive Value of Tests. Registries. Retrospective Studies. Survival Rate. Thrombocytopenia / blood. Thrombocytopenia / complications. Thrombocytopenia / mortality. Thrombocytopenia / therapy


19. Hara T, Schwieger M, Kazama R, Okamoto S, Minehata K, Ziegler M, Löhler J, Stocking C: Acceleration of chronic myeloproliferation by enforced expression of Meis1 or Meis3 in Icsbp-deficient bone marrow cells. Oncogene; 2008 Jun 19;27(27):3865-9
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  • Interferon consensus sequence-binding protein (ICSBP) is a tumor suppressor, whose downregulation cooperates with BCR-ABL and NUP98-TOP1 gene products to accelerate leukemia induction in mouse models.
  • Similarly, Meis1 synergizes with HoxA9 or NUP98-HOX (but not NUP98-TOP1) fusion genes to promote the early onset of leukemia.
  • Secondary mutations, such as activation of Mn1, led to the progression to acute myeloid leukemia in a few mice.
  • These results reveal a novel collaboration between Icsbp deficiency and Meis1/Meis3 in the acceleration of chronic myeloid leukemia-like disease.
  • [MeSH-minor] Animals. Cell Division. Gene Expression Regulation. Kinetics. Leukemia, Myeloid, Acute / genetics. Mice. Mice, Knockout. Mutation

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  • (PMID = 18223676.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Interferon Regulatory Factors; 0 / Meis3 protein, mouse; 0 / Neoplasm Proteins; 0 / Transcription Factors; 0 / interferon regulatory factor-8; 0 / myeloid ecotropic viral integration site 1 protein
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20. Pabst T, Stillner E, Neuberg D, Nimer S, Willman CL, List AF, Melo JV, Tenen DG, Mueller BU: Mutations of the myeloid transcription factor CEBPA are not associated with the blast crisis of chronic myeloid leukaemia. Br J Haematol; 2006 May;133(4):400-2
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  • [Title] Mutations of the myeloid transcription factor CEBPA are not associated with the blast crisis of chronic myeloid leukaemia.
  • The transcription factor CEBPA is crucial for normal myeloid differentiation.
  • CEBPA gene mutations have been reported in patients with acute myeloid leukaemia.
  • The inevitable evolution of chronic myeloid leukaemia (CML) in chronic phase (CP) to a fatal blast crisis (BC) is assumed to result from the acquisition of additional genetic changes in the leukaemic clone.
  • Gain of CEBPA mutations might represent a key event causing the differentiation block observed in myeloid CML-BC, but not in CML-CP.
  • [MeSH-major] Blast Crisis / genetics. CCAAT-Enhancer-Binding Protein-alpha / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mutation
  • [MeSH-minor] Cell Differentiation / genetics. Cell Line, Tumor. Disease Progression. Humans

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  • (PMID = 16643447.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha
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21. Xiao L, Qiong L, Yan Z, Zheng Z, Luxi S, Li X, Ying T, Yizhi L, Quan P: Experimental and clinical characteristics in myelodysplastic syndrome patients with or without HLA-DR15 allele. Hematol Oncol; 2010 Jun;28(2):98-103
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  • We noted the following observations with regard to disease progression: None of the 46 HLA-DR15 positive patients with international prognostic scoring system (IPSS) scores <or=1 developed acute myeloid leukaemia (AML) during the follow-up period, while six of the 63 DR15-negative patients with the same IPSS score developed AML within a shorter follow-up period (p = 0.039).
  • We concluded that the presence of the HLA-DR15 allele is indicative of a genetic susceptibility to MDS and, the presence of the HLA-DR15 allele showed less association with disease progression and greater association with BM failure.
  • [MeSH-minor] Alleles. Asian Continental Ancestry Group / genetics. Bone Marrow / chemistry. Bone Marrow / pathology. CD4 Lymphocyte Count. CD4-CD8 Ratio. Disease Progression. Gene Frequency. Genetic Predisposition to Disease. HLA-DR Serological Subtypes. Humans. Interferon-gamma / analysis. Tumor Necrosis Factor-alpha / analysis

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  • [Copyright] (c) 2009 John Wiley & Sons, Ltd.
  • (PMID = 19593744.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA-DR Antigens; 0 / HLA-DR Serological Subtypes; 0 / HLA-DR15 antigen; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
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22. Capello D, Deambrogi C, Rossi D, Lischetti T, Piranda D, Cerri M, Spina V, Rasi S, Gaidano G, Lunghi M: Epigenetic inactivation of suppressors of cytokine signalling in Philadelphia-negative chronic myeloproliferative disorders. Br J Haematol; 2008 May;141(4):504-11
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  • We investigated epigenetic and genetic inactivation of SOCS3, SOCS1 and PTPN6 in 112 CMPD and 20 acute myeloid leukaemia (AML) post-CMPD.
  • [MeSH-minor] Chronic Disease. DNA Methylation. Disease Progression. Humans. Janus Kinase 2 / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Mutation. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Philadelphia Chromosome. Protein Tyrosine Phosphatase, Non-Receptor Type 6 / genetics. Protein Tyrosine Phosphatase, Non-Receptor Type 6 / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods. Signal Transduction

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  • (PMID = 18318760.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / SOCS1 protein, human; 0 / SOCS3 protein, human; 0 / Suppressor of Cytokine Signaling Proteins; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 3.1.3.48 / PTPN6 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6
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23. Keith T, Araki Y, Ohyagi M, Hasegawa M, Yamamoto K, Kurata M, Nakagawa Y, Suzuki K, Kitagawa M: Regulation of angiogenesis in the bone marrow of myelodysplastic syndromes transforming to overt leukaemia. Br J Haematol; 2007 May;137(3):206-15
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  • [Title] Regulation of angiogenesis in the bone marrow of myelodysplastic syndromes transforming to overt leukaemia.
  • To investigate the regulatory mechanisms of angiogenesis in the development of myelodysplastic syndromes (MDS) and its progression to overt leukaemia (OL), bone marrow samples from control, paired samples from MDS patients before and after transformation to OL (MDS --> OL) and de novo acute myeloid leukaemia (AML) were analysed.
  • Immunohistochemical staining showed a significant increase of bone marrow microvascular density (MVD) in MDS and de novo AML compared with controls.
  • Surprisingly, in MDS, MVD significantly decreased upon transformation to OL, which was also significantly lower than the MVD of de novo AML.
  • These findings indicate that the bone marrow microenvironment in MDS --> OL and de novo AML differs remarkably, suggesting the different efficacy of anti-angiogenic therapy between de novo AML and leukaemia secondary to MDS.
  • [MeSH-major] Bone Marrow / physiopathology. Leukemia / physiopathology. Myelodysplastic Syndromes / physiopathology. Neovascularization, Pathologic / physiopathology
  • [MeSH-minor] Aged. Angiopoietin-1 / analysis. Angiopoietin-2 / analysis. Disease Progression. Female. Fibroblast Growth Factor 2 / analysis. Hepatocyte Growth Factor / analysis. Humans. Immunohistochemistry / methods. Leukemia, Myeloid, Acute / physiopathology. Male. Microcirculation / physiopathology. Middle Aged. RNA, Messenger / analysis. Receptor, TIE-2 / analysis. Transforming Growth Factor beta / analysis. Tumor Necrosis Factor-alpha / analysis. Vascular Endothelial Growth Factor A / analysis. Vascular Endothelial Growth Factor Receptor-2 / analysis

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  • (PMID = 17408459.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiopoietin-1; 0 / Angiopoietin-2; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2; 67256-21-7 / Hepatocyte Growth Factor; EC 2.7.10.1 / Receptor, TIE-2; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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24. Ley TJ, Mardis ER, Ding L, Fulton B, McLellan MD, Chen K, Dooling D, Dunford-Shore BH, McGrath S, Hickenbotham M, Cook L, Abbott R, Larson DE, Koboldt DC, Pohl C, Smith S, Hawkins A, Abbott S, Locke D, Hillier LW, Miner T, Fulton L, Magrini V, Wylie T, Glasscock J, Conyers J, Sander N, Shi X, Osborne JR, Minx P, Gordon D, Chinwalla A, Zhao Y, Ries RE, Payton JE, Westervelt P, Tomasson MH, Watson M, Baty J, Ivanovich J, Heath S, Shannon WD, Nagarajan R, Walter MJ, Link DC, Graubert TA, DiPersio JF, Wilson RK: DNA sequencing of a cytogenetically normal acute myeloid leukaemia genome. Nature; 2008 Nov 6;456(7218):66-72
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  • [Title] DNA sequencing of a cytogenetically normal acute myeloid leukaemia genome.
  • Acute myeloid leukaemia is a highly malignant haematopoietic tumour that affects about 13,000 adults in the United States each year.
  • Here we present the results obtained from sequencing a typical acute myeloid leukaemia genome, and its matched normal counterpart obtained from the same patient's skin.
  • We discovered ten genes with acquired mutations; two were previously described mutations that are thought to contribute to tumour progression, and eight were new mutations present in virtually all tumour cells at presentation and relapse, the function of which is not yet known.


25. Issa JP: Epigenetic changes in the myelodysplastic syndrome. Hematol Oncol Clin North Am; 2010 Apr;24(2):317-30
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  • Myelodysplastic syndrome (MDS) is characterized by frequent epigenetic abnormalities, including the hypermethylation of genes that control proliferation, adhesion, and other characteristic features of this leukemia.
  • Aberrant DNA hypermethylation is associated with a poor prognosis in MDS that can be accounted for by more rapid progression to acute myeloid leukemia.

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20359628.001).
  • [ISSN] 1558-1977
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA108631-050003; United States / NCI NIH HHS / CA / P50 CA100632-06S1; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / R01 CA121104-03; United States / NCI NIH HHS / CA / CA100632-060001; United States / NCI NIH HHS / CA / R01 CA121104; United States / NCI NIH HHS / CA / CA100632-06S1; United States / NCI NIH HHS / CA / P01 CA108631; United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / P50 CA100632-060001; United States / NCI NIH HHS / CA / CA108631-050003; United States / NCI NIH HHS / CA / R01 CA098006; United States / NCI NIH HHS / CA / CA121104-03; United States / NCI NIH HHS / CA / CA098006; United States / NCI NIH HHS / CA / P50 CA100632-010001; United States / NCI NIH HHS / CA / CA121104; United States / NCI NIH HHS / CA / CA100632-010001
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 0 / Histones; 776B62CQ27 / decitabine; EC 3.5.1.98 / Histone Deacetylases; M801H13NRU / Azacitidine
  • [Number-of-references] 107
  • [Other-IDs] NLM/ NIHMS177428; NLM/ PMC2848959
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26. Jabbour EJ, Giles FJ: New agents in myelodysplastic syndromes. Curr Hematol Rep; 2005 May;4(3):191-9
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  • Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal hematopoietic disorders characterized by ineffective hematopoiesis resulting in peripheral cytopenia and by increased progression to acute myeloid leukemia (AML).

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  • (PMID = 15865871.001).
  • [ISSN] 1541-0714
  • [Journal-full-title] Current hematology reports
  • [ISO-abbreviation] Curr. Hematol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Arsenicals; 0 / Benzamides; 0 / Cytokines; 0 / Enzyme Inhibitors; 0 / Growth Substances; 0 / Immunosuppressive Agents; 0 / Oligonucleotides, Antisense; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase; M801H13NRU / Azacitidine
  • [Number-of-references] 89
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27. Loaiza-Bonilla A, Gore SD, Carraway HE: Novel approaches for myelodysplastic syndromes: beyond hypomethylating agents. Curr Opin Hematol; 2010 Mar;17(2):104-9
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  • DNA methyltransferase inhibitors are well tolerated in outpatient settings, with azacitidine prolonging survival and decreasing time to acute myeloid leukemia progression in patients with high-risk myelodysplastic syndromes.

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  • (PMID = 20178141.001).
  • [ISSN] 1531-7048
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K24 CA111717; United States / NCI NIH HHS / CA / L30 CA111124
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzoates; 0 / Enzyme Inhibitors; 0 / Hydrazines; 0 / Pyrazoles; 0 / eltrombopag; 4Z8R6ORS6L / Thalidomide; EC 2.1.1.- / Methyltransferases; F0P408N6V4 / lenalidomide
  • [Number-of-references] 48
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28. Vyas P, Roberts I: Down myeloid disorders: a paradigm for childhood preleukaemia and leukaemia and insights into normal megakaryopoiesis. Early Hum Dev; 2006 Dec;82(12):767-73
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  • [Title] Down myeloid disorders: a paradigm for childhood preleukaemia and leukaemia and insights into normal megakaryopoiesis.
  • Newborns and children with Down Syndrome are predisposed to a range of blood disorders, which include acute lymphoblastic leukaemia and acute megakaryocytic leukaemia (AMKL).
  • Over the last four years there has been considerable progress in our understanding of DS AMKL.
  • In approximately 30% of TMD patients, additional as yet unidentified (epi)genetic mutations are required for progression to AMKL.
  • Thus, DS TMD and AMKL provide a unique model of childhood leukaemia where the preleukaemic and leukaemic phases are ascertainable and separable allowing distinct steps in leukaemogenesis to be studied individually.
  • These findings also have implications for the clinical management of DS TMD and AMKL specifically and also of childhood leukaemia more generally.
  • [MeSH-major] Down Syndrome / complications. Leukemia, Megakaryoblastic, Acute / physiopathology. Megakaryocytes / physiology. Thrombopoiesis / physiology

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  • (PMID = 17064858.001).
  • [ISSN] 0378-3782
  • [Journal-full-title] Early human development
  • [ISO-abbreviation] Early Hum. Dev.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human
  • [Number-of-references] 23
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29. Jiang Y, Dunbar A, Gondek LP, Mohan S, Rataul M, O'Keefe C, Sekeres M, Saunthararajah Y, Maciejewski JP: Aberrant DNA methylation is a dominant mechanism in MDS progression to AML. Blood; 2009 Feb 5;113(6):1315-25
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  • [Title] Aberrant DNA methylation is a dominant mechanism in MDS progression to AML.
  • Myelodysplastic syndromes (MDSs) are clonal hematologic disorders that frequently represent an intermediate disease stage before progression to acute myeloid leukemia (AML).
  • In 184 patients with MDS and AML, DNA methylation microarray and high-density single nucleotide polymorphism array (SNP-A) karyotyping were used to assess the relative contributions of aberrant DNA methylation and chromosomal deletions to tumor-suppressor gene (TSG) silencing during disease progression.
  • However, the ubiquity, extent, and correlation with disease progression suggest that aberrant DNA methylation is the dominant mechanism for TSG silencing and clonal variation in MDS evolution to AML.


30. Poppe B, Yigit N, De Moerloose B, De Paepe A, Benoit Y, Speleman F: HOXA gene cluster rearrangement in a t(7;9)(p15;q34) in a child with MDS. Cancer Genet Cytogenet; 2005 Oct 1;162(1):82-4
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  • We describe the molecular characterization of a t(7;9)(p15;q34) found in a 15-month-old female patient, diagnosed with refractory anemia with excess blasts in transformation (RAEBt), in progression to acute myeloid leukemia (AML) M7.

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  • (PMID = 16157206.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 157907-48-7 / HoxA protein
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31. Brkljacic B, Cikara I, Ivanac G, Hrkac Pustahija A, Zic R, Stanec Z: Ultrasound-guided bipolar radiofrequency ablation of breast cancer in inoperable patients: a pilot study. Ultraschall Med; 2010 Apr;31(2):156-62
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  • Patients were at high-risk for general anesthesia and surgery because of severely impaired cardiac function, advanced age, or associated diseases (acute myeloid leukaemia (AML), diabetes, hypertension, depression) and/or refused surgery.
  • There were no signs of malignancy in histopathology; the patient finally died of leukemia 42 months after RFA.
  • [MeSH-minor] Aged. Aged, 80 and over. Biopsy, Needle. Cause of Death. Comorbidity. Disease Progression. Female. Follow-Up Studies. Humans. Middle Aged. Neoplasm Staging. Pilot Projects

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  • [Copyright] Georg Thieme Verlag KG Stuttgart . New York.
  • (PMID = 19941254.001).
  • [ISSN] 1438-8782
  • [Journal-full-title] Ultraschall in der Medizin (Stuttgart, Germany : 1980)
  • [ISO-abbreviation] Ultraschall Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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32. Aref S, Osman E, Mansy S, Omer N, Azmy E, Goda T, El-Sherbiny M: Prognostic relevance of circulating matrix metalloproteinase-2 in acute myeloid leukaemia patients. Hematol Oncol; 2007 Sep;25(3):121-6
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  • [Title] Prognostic relevance of circulating matrix metalloproteinase-2 in acute myeloid leukaemia patients.
  • Matrix metalloproteinases (MMPs) were postulated to have important implication in progression and invasiveness of many malignant disorders.
  • On the other hand the biological role of MMP-2 in acute myeloid leukaemia (AML) is not fully clear.
  • [MeSH-major] Leukemia, Myeloid / blood. Matrix Metalloproteinase 2 / blood. Matrix Metalloproteinase 2 / cerebrospinal fluid
  • [MeSH-minor] Acute Disease. Adult. Age Factors. Aged. Blast Crisis. Female. Hemoglobins / metabolism. Humans. Leukocyte Count. Male. Middle Aged. Platelet Count. Prognosis

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  • [Copyright] 2007 John Wiley & Sons, Ltd.
  • (PMID = 17497745.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hemoglobins; EC 3.4.24.24 / Matrix Metalloproteinase 2
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33. Hentschel N, Krusch M, Kiener PA, Kolb HJ, Salih HR, Schmetzer HM: Serum levels of sCD137 (4-1BB) ligand are prognostic factors for progression in acute myeloid leukemia but not in non-Hodgkin's lymphoma. Eur J Haematol; 2006 Aug;77(2):91-101
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  • [Title] Serum levels of sCD137 (4-1BB) ligand are prognostic factors for progression in acute myeloid leukemia but not in non-Hodgkin's lymphoma.
  • Recently, we demonstrated that low levels of soluble (s) CD137L and high levels of sCD178 correlate significantly with a long progression free survival in patients with myelodysplastic syndrome (MDS).
  • In this study, we correlated sCD137L and sCD178 levels in sera of 42 samples of patients with acute myeloid leukemia (AML) and 46 samples of patients with non-Hodgkin's lymphoma (NHL) with stages, subtypes, and the clinical course of the diseases and determined cut-off values with maximum probability for significant differentiation between cases with higher/lower probability for progress free survival.
  • Furthermore, in AML patients sCD137L levels correlate significantly with the probabilities to achieve complete remission (CR), stay in CR or with progress of the disease.
  • [MeSH-major] Biomarkers, Tumor / blood. Leukemia, Myeloid / blood. Lymphoma, Non-Hodgkin / blood. Membrane Glycoproteins / blood. Neoplasm Proteins / blood. Tumor Necrosis Factors / blood
  • [MeSH-minor] 4-1BB Ligand. Acute Disease. Adult. Aged. Aged, 80 and over. Blast Crisis / blood. Child, Preschool. Disease Progression. Disease-Free Survival. Fas Ligand Protein. Female. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / blood. Lymphoma, B-Cell / blood. Lymphoma, T-Cell / blood. Male. Middle Aged. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / blood. Prognosis. Retrospective Studies. Solubility. Survival Analysis

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  • (PMID = 16800841.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / 4-1BB Ligand; 0 / Biomarkers, Tumor; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / TNFSF9 protein, human; 0 / Tumor Necrosis Factors
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34. Rowe JM: Advances and controversies in the biology and therapy of acute leukaemia and myelodysplasia. Best Pract Res Clin Haematol; 2009 Dec;22(4):475-8
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  • [Title] Advances and controversies in the biology and therapy of acute leukaemia and myelodysplasia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Disease Progression. Humans. Survival Rate

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  • (PMID = 19959095.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Editorial
  • [Publication-country] Netherlands
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35. van Luijn MM, van den Ancker W, Chamuleau ME, Ossenkoppele GJ, van Ham SM, van de Loosdrecht AA: Impaired antigen presentation in neoplasia: basic mechanisms and implications for acute myeloid leukemia. Immunotherapy; 2010 Jan;2(1):85-97
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  • [Title] Impaired antigen presentation in neoplasia: basic mechanisms and implications for acute myeloid leukemia.
  • During onset, treatment and progression of acute myeloid leukemia (AML), inadequate immune responses against certain myeloid leukemic blasts might be associated with the occurrence of minimal residual disease and subsequent relapse.
  • In tumor cells that can express HLA class II molecules, such as myeloid leukemic blasts, abnormalities in the processing pathways of endogenous antigens could also result in impaired HLA class II-restricted tumor-associated antigen presentation to CD4(+) T helper cells.
  • More insight into impaired tumor-associated antigen presentation by myeloid leukemic blasts could explain their escape from immune recognition and might be crucial for selecting appropriate strategies to improve whole-cell or dendritic cell-based tumor vaccine efficacy in the treatment of AML patients.
  • [MeSH-major] Antigen Presentation / immunology. Leukemia, Myeloid / immunology. Neoplasm, Residual / immunology. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Acute Disease. Cancer Vaccines / immunology. Dendritic Cells / immunology. Humans. Immunotherapy / methods. Neoplasms / immunology. Neoplasms / therapy

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  • (PMID = 20635891.001).
  • [ISSN] 1750-7448
  • [Journal-full-title] Immunotherapy
  • [ISO-abbreviation] Immunotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines
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36. 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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  • [Title] Transformation from committed progenitor to leukaemia stem cell initiated by MLL-AF9.
  • Here we show that leukaemia stem cells (LSC) can maintain the global identity of the progenitor from which they arose while activating a limited stem-cell- or self-renewal-associated programme.
  • 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.
  • LSC can thus be generated from committed progenitors without widespread reprogramming of gene expression, and a leukaemia self-renewal-associated signature is activated in the process.
  • Our findings define progression from normal progenitor to cancer stem cell, and suggest that targeting a self-renewal programme expressed in an abnormal context may be possible.
  • [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


37. Martinelli G, Iacobucci I, Papayannidis C, Soverini S: New targets for Ph+ leukaemia therapy. Best Pract Res Clin Haematol; 2009 Sep;22(3):445-54
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  • [Title] New targets for Ph+ leukaemia therapy.
  • The outcome for adults with Philadelphia chromosome (Ph+) leukaemias (chronic myeloid leukaemia (CML) and acute lymphoblastic leukaemia (ALL)) has been dramatically improved with the use of tyrosine kinase inhibitors (TKIs), but progression and/or relapse are still present in the majority of patients.
  • Some emerging aurora kinase inhibitors, such as VX-680, PHA-739358, MK-0457 and AS703569, and Smo1 and Hedgehog (Hh) inhibitors promise clinical efficacy against the Bcr-Ab T315I mutant form and leukaemia stem cells, respectively.
  • [MeSH-major] Drug Delivery Systems / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy

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  • (PMID = 19959093.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 88
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38. Kalff A, Shortt J, Farr J, McLennan R, Lui A, Scott J, Spencer A: Laboratory tumor lysis syndrome complicating LBH589 therapy in a patient with acute myeloid leukaemia. Haematologica; 2008 Jan;93(1):e16-7
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  • [Title] Laboratory tumor lysis syndrome complicating LBH589 therapy in a patient with acute myeloid leukaemia.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Hydroxamic Acids / pharmacology. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Tumor Lysis Syndrome / etiology
  • [MeSH-minor] Disease Progression. Electrolytes / metabolism. Fatal Outcome. Humans. Indoles. Male. Middle Aged

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  • (PMID = 18166770.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Electrolytes; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Indoles; 9647FM7Y3Z / panobinostat
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39. Galimberti S, Ghio F, Guerrini F, Ciabatti E, Grassi S, Ferreri MI, Petrini M: WT1 expression levels at diagnosis could predict long-term time-to-progression in adult patients affected by acute myeloid leukaemia and myelodysplastic syndromes. Br J Haematol; 2010 May;149(3):451-4
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  • [Title] WT1 expression levels at diagnosis could predict long-term time-to-progression in adult patients affected by acute myeloid leukaemia and myelodysplastic syndromes.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Leukemia, Myeloid, Acute / diagnosis. Myelodysplastic Syndromes / diagnosis. WT1 Proteins / biosynthesis
  • [MeSH-minor] Aged. Disease Progression. Female. Follow-Up Studies. Humans. Male. Middle Aged. Prognosis. Survival Analysis


40. Komrokji RS, Bennett JM: Evolving classifications of the myelodysplastic syndromes. Curr Opin Hematol; 2007 Mar;14(2):98-105
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  • The International Prognostic Scoring System is very important to define patient risk of progression to acute myeloid leukemia and predict overall survival.

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  • (PMID = 17255786.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 31
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41. Rajić Z, Colović N, Sretenović M, Plecić M, Janković S, Bakrac M, Colović M: [Hepatosplenic candidiasis in acute leukaemia patients]. Srp Arh Celok Lek; 2008 Jul-Aug;136(7-8):414-8
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  • [Title] [Hepatosplenic candidiasis in acute leukaemia patients].
  • INTRODUCTION: Hepatosplenic candidiasis is a disseminated invasive fungal infection that may affects patients with acute leukaemia.
  • CASE OUTLINE: The authors present three patients, two women and one men, aged 23, 26 and 33 years, with acute leukaemia; one with acute myeloblastic and two with acute lymphoblastic leukaemia who developed hepatosplenic candidiasis.
  • Two patients died due to progression of leukaemia.
  • CONCLUSION: If leukaemia patient in remission after chemotherapy develops a prolonged fever of unknown origin, hepatosplenic candidiasis has to be considered and all efforts should be done to diagnose it.
  • [MeSH-major] Candidiasis / complications. Immunocompromised Host. Leukemia, Myeloid, Acute / complications. Liver Diseases / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Splenic Diseases / complications


42. Ryningen A, Stapnes C, Paulsen K, Lassalle P, Gjertsen BT, Bruserud O: In vivo biological effects of ATRA in the treatment of AML. Expert Opin Investig Drugs; 2008 Nov;17(11):1623-33
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  • BACKGROUND: All-trans retinoic acid (ATRA) is mandatory in the treatment of acute promyelocytic leukaemia (APL).
  • Experimental studies suggest that ATRA can induce differentiation and apoptosis in leukaemia cells also for other acute myelogenous leukaemia (AML) subtypes, but the clinical observations are conflicting.
  • Serum/plasma samples were collected before and after 2 days of ATRA, peripheral blood AML cells were collected from all 12 patients with circulating leukaemia cells (ClinicalTrials.gov NCT00175812; EudraCT no. 2004-001663-22).
  • Circulating leukaemia cells derived during therapy had increased intracellular levels of P21 (mean increase in mean fluorescence intensity (MFI) being 18.2%, p = 0.017), and decreased levels of Gata-2 (mean decrease in MFI 19%, p = 0.026), NF-kappaB p65 (mean decrease in MFI 15.4%, p = 0.033) and Bcl-2 (mean decrease in MFI 7.2%, p = 0.005).
  • CONCLUSIONS: In vivo ATRA treatment in AML affects leukaemic cell morphology, regulation of cell cycle progression and apoptosis, and possibly also microvascular endothelial cell functions.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Tretinoin / therapeutic use

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  • (PMID = 18922099.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00175812
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Histone Deacetylase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Transcription Factors; 5688UTC01R / Tretinoin; EC 3.5.1.98 / Histone Deacetylases
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43. Amadori S, Suciu S, Selleslag D, Stasi R, Alimena G, Baila L, Rizzoli V, Borlenghi E, Gaidano G, Magro D, Torelli G, Muus P, Venditti A, Cacciola E, Lauria F, Vignetti M, de Witte T: Randomized trial of two schedules of low-dose gemtuzumab ozogamicin as induction monotherapy for newly diagnosed acute myeloid leukaemia in older patients not considered candidates for intensive chemotherapy. A phase II study of the EORTC and GIMEMA leukaemia groups (AML-19). Br J Haematol; 2010 May;149(3):376-82
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  • [Title] Randomized trial of two schedules of low-dose gemtuzumab ozogamicin as induction monotherapy for newly diagnosed acute myeloid leukaemia in older patients not considered candidates for intensive chemotherapy. A phase II study of the EORTC and GIMEMA leukaemia groups (AML-19).
  • This study compared two schedules of low-dose gemtuzumab ozogamicin (GO) as induction monotherapy for untreated acute myeloid leukaemia in older patients unfit for intensive chemotherapy, to identify the more promising regimen for further study.
  • Primary endpoint was the rate of disease non-progression (DnP), defined as the proportion of patients either achieving a response or maintaining a stable disease following GO induction in each arm.
  • [MeSH-major] Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antineoplastic Agents / administration & dosage. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Aged. Antibodies, Monoclonal, Humanized. Disease Progression. Drug Administration Schedule. Feasibility Studies. Female. Humans. Male. Middle Aged. Treatment Outcome

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  • (PMID = 20230405.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U10 CA011488; United States / NCI NIH HHS / CA / U10 CA011488-33
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] England
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44. Park S, Grabar S, Kelaidi C, Beyne-Rauzy O, Picard F, Bardet V, Coiteux V, Leroux G, Lepelley P, Daniel MT, Cheze S, Mahé B, Ferrant A, Ravoet C, Escoffre-Barbe M, Adès L, Vey N, Aljassem L, Stamatoullas A, Mannone L, Dombret H, Bourgeois K, Greenberg P, Fenaux P, Dreyfus F, GFM group (Groupe Francophone des Myélodysplasies): Predictive factors of response and survival in myelodysplastic syndrome treated with erythropoietin and G-CSF: the GFM experience. Blood; 2008 Jan 15;111(2):574-82
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  • Multivariate adjusted comparisons of survival between our cohort and the untreated MDS cohort used to design IPSS showed similar rate of progression to acute myeloid leukemia in both cohorts, but significantly better overall survival in our cohort, suggesting that epoetin or DAR treatment may have a favorable survival impact in MDS.


45. Teachey DT, Grupp SA, Brown VI: Mammalian target of rapamycin inhibitors and their potential role in therapy in leukaemia and other haematological malignancies. Br J Haematol; 2009 Jun;145(5):569-80
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  • [Title] Mammalian target of rapamycin inhibitors and their potential role in therapy in leukaemia and other haematological malignancies.
  • The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that functions as a key regulator of cell growth, protein synthesis, and cell-cycle progression through interactions with a number of signalling pathways, including PI3K/AKT, ras, TCL1, and BCR/ABL.
  • Promising early clinical data suggests activity of mTOR inhibitors in a number of haematological diseases, including acute lymphoblastic leukaemia, chronic myeloid leukaemia, mantle cell lymphoma, anaplastic large cell lymphoma, and lymphoproliferative disorders.
  • This review describes the rationale for using mTOR inhibitors in a variety of haematological diseases with a focus on their use in leukaemia.
  • [MeSH-minor] Autoimmune Diseases / drug therapy. Autoimmune Diseases / metabolism. Humans. Leukemia / drug therapy. Leukemia / metabolism. Lymphoproliferative Disorders / drug therapy. Lymphoproliferative Disorders / metabolism. Signal Transduction / drug effects. TOR Serine-Threonine Kinases

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  • (PMID = 19344392.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K08 CA104882; United States / NCI NIH HHS / CA / 1K08 CA1 04882-01A1; United States / NCI NIH HHS / CA / R01 CA102646; United States / NCI NIH HHS / CA / CA 1116660; United States / NCI NIH HHS / CA / K08 CA104882-01A1; United States / NCI NIH HHS / CA / CA 102646
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; W36ZG6FT64 / Sirolimus
  • [Number-of-references] 104
  • [Other-IDs] NLM/ NIHMS139949; NLM/ PMC2784662
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46. Ponassi R, Biasotti B, Tomati V, Bruno S, Poggi A, Malacarne D, Cimoli G, Salis A, Pozzi S, Miglino M, Damonte G, Cozzini P, Spyrakis F, Campanini B, Bagnasco L, Castagnino N, Tortolina L, Mumot A, Frassoni F, Daga A, Cilli M, Piccardi F, Monfardini I, Perugini M, Zoppoli G, D'Arrigo C, Pesenti R, Parodi S: A novel Bim-BH3-derived Bcl-XL inhibitor: biochemical characterization, in vitro, in vivo and ex-vivo anti-leukemic activity. Cell Cycle; 2008 Oct;7(20):3211-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The antiapoptotic molecule Bcl-X(L), involved in cancer development/progression and tumour resistance to cytotoxic drugs, is a target for Bim.
  • Multiparameter flow cytometry demonstrated that the 072RB dose-dependent growth inhibition of leukaemia cell lines was due to apoptotic cell death.
  • Ex-vivo derived leukemic cells from acute myeloid leukaemia (AML) patients underwent cell death when cultured in vitro in the presence of 072RB.
  • [MeSH-minor] Amino Acid Sequence. Animals. Apoptosis / physiology. Cells, Cultured. Female. Humans. Leukemia, Myeloid, Acute / metabolism. Lymphocytes / cytology. Lymphocytes / physiology. Mice. Mice, Inbred NOD. Mice, SCID. Molecular Sequence Data. Neoplasm Transplantation. Protein Structure, Tertiary. Transplantation, Heterologous. Tumor Cells, Cultured. bcl-2-Associated X Protein / genetics. bcl-2-Associated X Protein / metabolism

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  • [CommentIn] Cell Cycle. 2008 Oct;7(20):3111 [18843203.001]
  • [ErratumIn] Cell Cycle. 2012 Oct 1;11(19):3703. Spyraki, Francesca [corrected to Spyrakis, Francesca]
  • (PMID = 18843207.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 072RB peptide; 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Membrane Proteins; 0 / Peptides; 0 / Proto-Oncogene Proteins; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein
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47. Wolanskyj AP, Lasho TL, Schwager SM, McClure RF, Wadleigh M, Lee SJ, Gilliland DG, Tefferi A: JAK2 mutation in essential thrombocythaemia: clinical associations and long-term prognostic relevance. Br J Haematol; 2005 Oct;131(2):208-13
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  • During this period, thrombotic complications were documented in 62 patients (41.3%) and transformation into acute myeloid leukaemia (AML), polycythaemia vera (PV), or myelofibrosis with myeloid metaplasia (MMM) occurred in 4 (2.7%), 8 (5.3%), and 15 (10%) patients, respectively.
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. DNA Mutational Analysis. Disease Progression. Female. Follow-Up Studies. Hemoglobins / analysis. Humans. Janus Kinase 2. Leukemia, Myeloid, Acute / genetics. Leukocyte Count. Male. Middle Aged. Multivariate Analysis. Polycythemia Vera / genetics. Primary Myelofibrosis / genetics. Risk Factors. Thrombosis / complications

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  • (PMID = 16197451.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hemoglobins; 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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48. Sirohi B, Cunningham D, Powles R, Murphy F, Arkenau T, Norman A, Oates J, Wotherspoon A, Horwich A: Long-term outcome of autologous stem-cell transplantation in relapsed or refractory Hodgkin's lymphoma. Ann Oncol; 2008 Jul;19(7):1312-9
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  • Median overall survival (OS)/progression-free survival (PFS) from ASCT was 9 years/2.9 years.
  • Twenty (10%) patients developed second cancer (seven secondary acute myeloid leukaemia (AML)/myelodysplastic syndrome (MDS)).

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  • (PMID = 18356139.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; Q41OR9510P / Melphalan; U68WG3173Y / Carmustine
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49. Heilig CE, Löffler H, Mahlknecht U, Janssen JW, Ho AD, Jauch A, Krämer A: Chromosomal instability correlates with poor outcome in patients with myelodysplastic syndromes irrespectively of the cytogenetic risk group. J Cell Mol Med; 2010 Apr;14(4):895-902
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  • As for aneuploidy itself, the role of CIN in the evolution and progression of malignancy is a matter still open to debate.
  • Thereby, CIN was measured in 65 patients with myelodysplastic syndromes (MDS), acute myeloid leukaemia (AML) and control subjects.
  • In conclusion, elevated CIN levels may be valuable as an early indicator of poor prognosis in MDS, hence corroborating the concept of CIN as a driving force in tumour progression.
  • [MeSH-minor] Adult. Aged. Disease Progression. Female. Humans. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Male. Middle Aged. Risk Factors. Treatment Outcome. Tumor Cells, Cultured


50. Chevallier P, Hunault-Berger M, Larosa F, Dauriac C, Garand R, Harousseau JL: A phase II trial of high-dose imatinib mesylate for relapsed or refractory c-kit positive and Bcr-Abl negative acute myeloid leukaemia: the AFR-15 trial. Leuk Res; 2009 Aug;33(8):1124-6
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  • [Title] A phase II trial of high-dose imatinib mesylate for relapsed or refractory c-kit positive and Bcr-Abl negative acute myeloid leukaemia: the AFR-15 trial.
  • This was a phase II investigation of high-dose imatinib in 15 adult patients with relapsed or refractory c-kit positive and Bcr-Abl negative acute myeloid leukaemia (AML).
  • No clinical responses were reported with early death due to disease progression reported in 7 patients.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Genes, abl. Leukemia, Myeloid, Acute / drug therapy. Piperazines / administration & dosage. Proto-Oncogene Proteins c-kit. Pyrimidines / administration & dosage

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  • (PMID = 18990444.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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51. Nikolousis E, Nagra S, Paneesha S, Delgado J, Holder K, Bratby L, Chaganti S, Lovell R, Milligan D: Allogeneic transplant outcomes are not affected by body mass index (BMI) in patients with haematological malignancies. Ann Hematol; 2010 Nov;89(11):1141-5
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  • A total of 105 patients had acute myeloid leukaemia, 83 had non-Hodgkin's lymphoma, three had myeloma, 21 had Hodgkin's lymphoma, 34 had acute lymphoblastic leukaemia, 19 had chronic myeloid leukaemia, 22 had chronic lymphocytic leukaemia, 24 had myelodysplasia, seven had T cell non-Hodgkin's lymphoma, six had aplastic leukaemia and seven had myelofibrosis.
  • The mean progression free survival (PFS) in patients undergoing allograft with normal BMI was 33 months as compared to 38 with high BMI (p = 0.13).
  • Of the patients in the high and obese BMI group, 16% developed acute GvHD with 8% grade III-IV and 28% in the normal BMI group with 14% grade III-IV acute GvHD (p = 0.11).

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  • (PMID = 20544351.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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52. Maserati E, Pressato B, Valli R, Minelli A, Sainati L, Patitucci F, Marletta C, Mastronuzzi A, Poli F, Lo Curto F, Locatelli F, Danesino C, Pasquali F: The route to development of myelodysplastic syndrome/acute myeloid leukaemia in Shwachman-Diamond syndrome: the role of ageing, karyotype instability, and acquired chromosome anomalies. Br J Haematol; 2009 Apr;145(2):190-7
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  • [Title] The route to development of myelodysplastic syndrome/acute myeloid leukaemia in Shwachman-Diamond syndrome: the role of ageing, karyotype instability, and acquired chromosome anomalies.
  • (iii) the deletion del(20)(q11) involved the minimal region of deletion typical of myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML);.
  • [MeSH-major] Aging / genetics. Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Adolescent. Adult. Bone Marrow Cells / ultrastructure. Child. Child, Preschool. Chromosome Breakage. Chromosomes, Human, Pair 20. Chromosomes, Human, Pair 7. DNA Mutational Analysis. Disease Progression. Female. Follow-Up Studies. Humans. In Situ Hybridization, Fluorescence. Isochromosomes. Karyotyping. Male. Proteins / genetics. Young Adult


53. Papadavid E, Panayiotides I, Katoulis A, Pappa V, Dervenoulas I, Stavrianeas N: Stasis dermatitis-like leukaemic infiltration in a patient with myelodysplastic syndrome. Clin Exp Dermatol; 2008 May;33(3):298-300
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  • We report a case of leukaemia cutis presenting as stasis dermatitis-like eruption in a patient with myelodysplastic syndrome progressing to acute myelogenic leukaemia.
  • [MeSH-major] Dermatitis / pathology. Leukemia, Myeloid, Acute / pathology. Leukemic Infiltration / pathology. Myelodysplastic Syndromes / pathology. Skin / pathology
  • [MeSH-minor] Aged, 80 and over. Disease Progression. Fatal Outcome. Humans. Hyperpigmentation / etiology. Hyperpigmentation / pathology. Male


54. Keller G, Brassat U, Braig M, Heim D, Wege H, Brümmendorf TH: Telomeres and telomerase in chronic myeloid leukaemia: impact for pathogenesis, disease progression and targeted therapy. Hematol Oncol; 2009 Sep;27(3):123-9
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  • [Title] Telomeres and telomerase in chronic myeloid leukaemia: impact for pathogenesis, disease progression and targeted therapy.
  • However, elevated telomerase activity has also been reported in the majority of solid tumours as well as in acute and chronic leukaemia.
  • Chronic myeloid leukaemia (CML) serves as a model disease to study telomere biology in clonal myeloproliferative disorders.
  • In addition, telomerase activity (TA) is already increased in CP CML and further upregulated with disease progression to accelerated phase and blast crisis (BC).
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Telomerase / antagonists & inhibitors. Telomerase / metabolism. Telomere / pathology
  • [MeSH-minor] Animals. Disease Progression. Humans

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  • (PMID = 19569255.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
  • [Number-of-references] 67
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55. Li H, Diao YT, Li HQ, Ma Q, Cui J, Zhou YZ, Li D: The association between serum levels of oxLDL-lgG and oxLDL-lgM autoantibody with adult acute myeloblastic leukaemia. Lipids Health Dis; 2010;9:11
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  • [Title] The association between serum levels of oxLDL-lgG and oxLDL-lgM autoantibody with adult acute myeloblastic leukaemia.
  • AIM: To evaluate the relationship between serum antibodies against ox-LDL levels and adult acute myeloblastic leukemia (AML).
  • Future studies need to confirm the hypothesis whether they related to the development and progression of adult AML.
  • [MeSH-major] Autoantibodies / immunology. Immunoglobulin G / blood. Immunoglobulin M / blood. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / immunology. Lipoproteins, LDL / blood
  • [MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. Disease Progression. Enzyme-Linked Immunosorbent Assay / methods. Female. Humans. Male. Middle Aged

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  • (PMID = 20113525.001).
  • [ISSN] 1476-511X
  • [Journal-full-title] Lipids in health and disease
  • [ISO-abbreviation] Lipids Health Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Lipoproteins, LDL; 0 / oxidized low density lipoprotein
  • [Other-IDs] NLM/ PMC2834680
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56. Krauze E, Brzezińska-Wcisło L, Kamińska-Winciorek G, Wygledowska-Kania M, Sygula E: Pyoderma gangrenosum coexisting with acute myelogenous leukaemia. J Eur Acad Dermatol Venereol; 2005 Sep;19(5):589-92
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  • [Title] Pyoderma gangrenosum coexisting with acute myelogenous leukaemia.
  • The aim of the study was to report a 26-year-old male patient with pyoderma gangrenosum coexisting with acute myelogenous leukaemia.
  • On the clinical and biochemical picture, the diagnosis of pyoderma gangrenosum within acute myelogenous leukaemia was made.
  • Although chemotherapy leukaemia was performed, the patient died after 4 months of the confirmation of the acute myelogenous leukaemia diagnosis.
  • [MeSH-major] Leg Ulcer / etiology. Leg Ulcer / therapy. Leukemia, Myeloid, Acute / complications. Pyoderma Gangrenosum / etiology. Pyoderma Gangrenosum / therapy
  • [MeSH-minor] Adult. Anti-Bacterial Agents / therapeutic use. Antineoplastic Agents / therapeutic use. Blood Transfusion. Combined Modality Therapy. Disease Progression. Fatal Outcome. Humans. Male. Risk Assessment. Severity of Illness Index

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  • (PMID = 16164714.001).
  • [ISSN] 0926-9959
  • [Journal-full-title] Journal of the European Academy of Dermatology and Venereology : JEADV
  • [ISO-abbreviation] J Eur Acad Dermatol Venereol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antineoplastic Agents
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57. Carlsten M, Baumann BC, Simonsson M, Jädersten M, Forsblom AM, Hammarstedt C, Bryceson YT, Ljunggren HG, Hellström-Lindberg E, Malmberg KJ: Reduced DNAM-1 expression on bone marrow NK cells associated with impaired killing of CD34+ blasts in myelodysplastic syndrome. Leukemia; 2010 Sep;24(9):1607-16
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  • Myelodysplastic syndromes (MDS) comprise a heterogeneous group of clonal stem-cell disorders characterized by ineffective hematopoiesis and risk of progression to acute myeloid leukemia.
  • Thus, given the emerging evidence for NK cell-mediated immune surveillance of neoplastic cells, we speculate that reduced expression of DNAM-1 on bone marrow NK cells may facilitate disease progression in patients with MDS.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Flow Cytometry. Humans. Male. Middle Aged


58. Xiao W, Jiang F, Wang Z: ELL binding regulates U19/Eaf2 intracellular localization, stability, and transactivation. Prostate; 2006 Jan 1;66(1):1-12
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  • Eleven-nineteen Lysine-rich Leukemia (ELL) is an RNA polymerase II transcription elongation factor, initially identified as a fusion partner gene of MLL in the t(11;.
  • 19) (q23; p13.1) chromosomal translocation in acute myeloid leukemia.
  • These findings suggest that ELL-U19/Eaf2 interaction is potentially important in prostate cancer progression and/or acute myeloid leukemia.

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  • (PMID = 16114057.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA90386; United States / NIDDK NIH HHS / DK / R01 DK51193
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EAF1 protein, human; 0 / EAF2 protein, human; 0 / Oligodeoxyribonucleotides; 0 / Transcription Factors; EC 1.13.12.- / Luciferases
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59. Rosenberg PS, Alter BP, Link DC, Stein S, Rodger E, Bolyard AA, Aprikyan AA, Bonilla MA, Dror Y, Kannourakis G, Newburger PE, Boxer LA, Dale DC: Neutrophil elastase mutations and risk of leukaemia in severe congenital neutropenia. Br J Haematol; 2008 Jan;140(2):210-3
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  • [Title] Neutrophil elastase mutations and risk of leukaemia in severe congenital neutropenia.
  • Severe congenital neutropenia (SCN) is a heterogeneous bone marrow failure syndrome predisposing to myelodysplastic syndrome and acute myeloid leukaemia (MDS/AML).

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  • (PMID = 18028488.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01DK54369; United States / NIAID NIH HHS / AI / K08 AI049392; United States / NIDDK NIH HHS / DK / R01 DK054369; United States / Intramural NIH HHS / / Z99 CA999999; United States / NIDDK NIH HHS / DK / R01 DK054369-09; United States / NIAID NIH HHS / AI / 1R24AI049392; United States / NIDDK NIH HHS / DK / DK054369-09
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor; EC 3.4.21.37 / Leukocyte Elastase
  • [Other-IDs] NLM/ NIHMS306469; NLM/ PMC3143022
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60. Götze K, Platzbecker U, Giagounidis A, Haase D, Lübbert M, Aul C, Ganser A, Germing U, Hofmann WK: Azacitidine for treatment of patients with myelodysplastic syndromes (MDS): practical recommendations of the German MDS Study Group. Ann Hematol; 2010 Sep;89(9):841-50
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  • Myelodysplastic syndromes (MDS) are a group of common bone marrow disorders characterized by ineffective hematopoiesis, peripheral cytopenias, and a substantial risk of progression to acute myeloid leukemia (AML).


61. Pons A, Nomdedeu B, Navarro A, Gaya A, Gel B, Diaz T, Valera S, Rozman M, Belkaid M, Montserrat E, Monzo M: Hematopoiesis-related microRNA expression in myelodysplastic syndromes. Leuk Lymphoma; 2009 Nov;50(11):1854-9
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  • The present study sought to link hematopoiesis-relevant miRNAs with myelodysplastic syndromes (MDS) and MDS progression to acute myeloid leukemia (AML).
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Bone Marrow / metabolism. Bone Marrow / pathology. Disease Progression. Female. Humans. Leukemia, Myeloid / blood. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction

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  • [CommentIn] Leuk Lymphoma. 2009 Nov;50(11):1735-6 [19883302.001]
  • (PMID = 19883312.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MIRN15 microRNA, human; 0 / MIRN16 microRNA, human; 0 / MIRN222 microRNA, human; 0 / MIrn181 microRNA, human; 0 / MicroRNAs
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62. Zainina S, Cheong SK: Myelodysplastic syndrome transformed into Acute Lymphoblastic Leukaemia (FAB:L3). Clin Lab Haematol; 2006 Aug;28(4):282-3
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  • [Title] Myelodysplastic syndrome transformed into Acute Lymphoblastic Leukaemia (FAB:L3).
  • Myelodysplastic syndrome (MDS) is recognized as a preleukaemic disorder with a variable risk of transformation to acute myeloid leukaemia.
  • Usually the blast cells in leukaemia are transformed after MDS displays a myeloid phenotype.
  • Even though lymphoid progression had been reported previously, most displayed myeloid-lymphoid hybrid or early B phenotype.
  • We report a case of an elderly man who had MDS transformed into Acute Lymphoblastic Leukaemia (ALL:L3) which is a rare lymphoid transformation.


63. Tamura H, Dan K, Tamada K, Nakamura K, Shioi Y, Hyodo H, Wang SD, Dong H, Chen L, Ogata K: Expression of functional B7-H2 and B7.2 costimulatory molecules and their prognostic implications in de novo acute myeloid leukemia. Clin Cancer Res; 2005 Aug 15;11(16):5708-17
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  • [Title] Expression of functional B7-H2 and B7.2 costimulatory molecules and their prognostic implications in de novo acute myeloid leukemia.
  • Their roles in the progression of human cancers, however, are not well established.
  • The aim of this study was to examine whether leukemic cells of acute myeloid leukemia express functional B7 family molecules and, if so, whether such expression has any clinical significance.
  • EXPERIMENTAL DESIGN: The expression of four B7 family molecules, B7.1, B7.2, B7-H1, and B7-H2, on leukemic cells from acute myeloid leukemia patients was analyzed by flow cytometry.
  • RESULTS: Although B7.1 and B7-H1 expressions were rare, the cells from a substantial number of acute myeloid leukemia cases expressed B7.2 and B7-H2 molecules [mean percentages of B7.2- and B7-H2-positive cells were 28.9% (n = 58) and 15.3% (n = 59), respectively].
  • Consistent with this finding, acute myeloid leukemia cells expressing B7.2 and B7-H2 induced allogeneic CD4+ T cells to proliferate and secrete interleukin-4 and interleukin-10 in vitro, effects that were partially blocked by antibodies against B7.2 and B7-H2.
  • CONCLUSIONS: Our results indicate the expression of functional B7.2 and B7-H2 molecules, and these molecules may facilitate progression of acute myeloid leukemia.
  • [MeSH-major] Antigens, CD86 / genetics. Leukemia, Myeloid / pathology. Proteins / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Analysis of Variance. Antigens, CD. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. CD4-Positive T-Lymphocytes / cytology. CD4-Positive T-Lymphocytes / metabolism. Cell Line, Tumor. Cell Proliferation. Coculture Techniques. Culture Media, Conditioned / chemistry. Culture Media, Conditioned / metabolism. Female. Flow Cytometry. Gene Expression Regulation, Neoplastic. HL-60 Cells. Humans. Inducible T-Cell Co-Stimulator Ligand. Interferon-gamma / metabolism. Interleukin-10 / metabolism. Interleukin-2 / metabolism. Interleukin-4 / metabolism. Jurkat Cells. K562 Cells. Male. Middle Aged. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. U937 Cells

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  • (PMID = 16115907.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD86; 0 / CD86 protein, human; 0 / Culture Media, Conditioned; 0 / ICOSLG protein, human; 0 / Inducible T-Cell Co-Stimulator Ligand; 0 / Interleukin-2; 0 / Proteins; 0 / RNA, Messenger; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
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64. de Melo Campos P, Traina F, da Silva Santos Duarte A, Lorand-Metze I, Costa FF, Saad ST: Reduced expression of FLIP SHORT in bone marrow of low risk myelodysplastic syndrome. Leuk Res; 2007 Jun;31(6):853-7
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  • Apoptosis is dysregulated in patients with myelodysplastic syndrome (MDS) and acute myelogenous leukaemia (AML).
  • Furthermore, FLIP(SHORT) mRNA expression was significantly lower in low risk MDS, compared to MDS-AML/AML de novo (P=0.0006), according to FAB classification.
  • Increased levels of FLIP(SHORT) in RAEB and AML may be related to apoptosis resistance in these diseases and to MDS progression.
  • [MeSH-major] Apoptosis. Apoptosis Regulatory Proteins / biosynthesis. CASP8 and FADD-Like Apoptosis Regulating Protein / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism


65. Göhring G, Giagounidis A, Büsche G, Kreipe HH, Zimmermann M, Hellström-Lindberg E, Aul C, Schlegelberger B: Patients with del(5q) MDS who fail to achieve sustained erythroid or cytogenetic remission after treatment with lenalidomide have an increased risk for clonal evolution and AML progression. Ann Hematol; 2010 Apr;89(4):365-74
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  • [Title] Patients with del(5q) MDS who fail to achieve sustained erythroid or cytogenetic remission after treatment with lenalidomide have an increased risk for clonal evolution and AML progression.
  • Thirty-six percent of patients progressed into acute myeloid leukaemia.
  • However, erythroid and cytogenetic responders had a significantly decreased risk of progression to acute myeloid leukaemia (p = 0.001 and p = 0.009, respectively) compared to non-responders.
  • Three and 5 years after study entry, the cumulative incidence of acute myeloid leukaemia for patients with a cytogenetic response was 10% and 21%, respectively, and for patients without cytogenetic response, it was 46% and 60%.
  • Patients with del(5q) myelodysplastic syndromes without erythroid or cytogenetic remission after treatment with lenalidomide have a high risk for clonal evolution and acute myeloid leukaemia progression.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 5. Erythroid Cells / drug effects. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / pathology. Thalidomide / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Follow-Up Studies. Humans. Karyotyping. Male. Middle Aged. Remission Induction. Risk Factors. Treatment Failure


66. Ngo N, Lampert IA, Naresh KN: Bone marrow trephine findings in acute myeloid leukaemia with multilineage dysplasia. Br J Haematol; 2008 Feb;140(3):279-86
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  • [Title] Bone marrow trephine findings in acute myeloid leukaemia with multilineage dysplasia.
  • Acute myeloid leukaemia (AML) with multilineage dysplasia (MD) is one of the four main categories of AML in the World Health Organization (WHO) classification.
  • With respect to conforming to the WHO definition of AML, documentation of an increased proportion of immature myeloid cells was possible on morphology and counting of immature cells following immunostaining with CD34, CD117 or HLA-DR antibodies.
  • [MeSH-major] Bone Marrow Cells / pathology. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD34 / analysis. Biomarkers / analysis. Biopsy / methods. Bone Marrow Examination / methods. Cytogenetics. Disease Progression. Erythroblasts / pathology. Female. Humans. Immunohistochemistry. Immunophenotyping. Male. Megakaryocytes / pathology. Middle Aged. Myeloid Cells / pathology. Proto-Oncogene Proteins c-kit / analysis

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  • (PMID = 17973948.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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67. Robinson BW, Behling KC, Gupta M, Zhang AY, Moore JS, Bantly AD, Willman CL, Carroll AJ, Adamson PC, Barrett JS, Felix CA: Abundant anti-apoptotic BCL-2 is a molecular target in leukaemias with t(4;11) translocation. Br J Haematol; 2008 Jun;141(6):827-39
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  • Anti-apoptotic BCL-2 expression and target modulation were characterized in cell lines with t(4;11) and BCL-2 expression was examined in MLL and non-MLL infant/paediatric leukaemia cases by Western blot analysis and/or real-time polymerase chain reaction.
  • Variable, sometimes substantial BCL2 mRNA was detected in other leukaemia subtypes.
  • Low G3139 concentrations sensitized RS4:11 and MV4-11 cells to select anti-leukaemia cytotoxic drugs.
  • In RS4:11 cells, combining G3139 with doxorubicin (ADR) increased active caspase 3 and TUNEL staining compared to ADR alone, indicating greater apoptosis, and G3139 increased S-phase progression.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 18422996.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098543
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Thionucleotides; 80168379AG / Doxorubicin; 85J5ZP6YSL / oblimersen
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68. Varga G, Kiss J, Várkonyi J, Vas V, Farkas P, Pálóczi K, Uher F: Inappropriate Notch activity and limited mesenchymal stem cell plasticity in the bone marrow of patients with myelodysplastic syndromes. Pathol Oncol Res; 2007;13(4):311-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Myelodysplastic syndromes (MDSs) are a heterogeneous group of hematological disorders characterized by ineffective hematopoiesis, enhanced bone marrow apoptosis and frequent progression to acute myeloid leukemia.


69. Najfeld V, Tripodi J, Scalise A, Silverman LR, Silver RT, Fruchtman S, Hoffman R: Jumping translocations of the long arms of chromosome 1 in myeloid malignancies is associated with a high risk of transformation to acute myeloid leukaemia. Br J Haematol; 2010 Nov;151(3):288-91
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  • [Title] Jumping translocations of the long arms of chromosome 1 in myeloid malignancies is associated with a high risk of transformation to acute myeloid leukaemia.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 1 / genetics. Leukemia, Myeloid, Acute / genetics. Myeloproliferative Disorders / genetics. Translocation, Genetic
  • [MeSH-minor] Disease Progression. Follow-Up Studies. Humans. Karyotyping. Myelodysplastic Syndromes / genetics

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  • (PMID = 20738298.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA1108671
  • [Publication-type] Letter; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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70. Vener C, Soligo D, Berti E, Gianelli U, Servida F, Ceretti E, Caputo R, Passoni E, Lambertenghi Deliliers G: Indeterminate cell histiocytosis in association with later occurrence of acute myeloblastic leukaemia. Br J Dermatol; 2007 Jun;156(6):1357-61
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  • [Title] Indeterminate cell histiocytosis in association with later occurrence of acute myeloblastic leukaemia.
  • We describe a 39-year-old man who developed diffuse ICH and, 6 years later, acute myeloblastic leukaemia (AML).
  • ICH has previously been reported in association with B-cell malignancy, but only one case has shown systemic progression.
  • [MeSH-major] Histiocytosis / pathology. Leukemia, Myeloid, Acute / pathology. Skin Diseases / pathology


71. Musolino C, Sant'antonio E, Penna G, Alonci A, Russo S, Granata A, Allegra A: Epigenetic therapy in myelodysplastic syndromes. Eur J Haematol; 2010 Jun;84(6):463-73
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  • The wide spectrum of clonal hematopoietic disorders that fall under the broad diagnostic category of myelodysplastic syndromes (MDS) consist of a family of bone marrow malignancies - with ineffective, inadequate, and dysplastic hematopoiesis, and with an increased risk of life-threatening infections, bleeding, and progression to acute myeloid leukemia (AML) - that are characterized by a deep heterogeneity on the clinical, biologic and prognostic level.

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  • (PMID = 20192987.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Neoplasm Proteins; 0 / fragile histidine triad protein; 776B62CQ27 / decitabine; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 3.6.- / Acid Anhydride Hydrolases; M801H13NRU / Azacitidine
  • [Number-of-references] 76
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72. Goulden N, Virgo P, Grimwade D: Minimal residual disease directed therapy for childhood acute myeloid leukaemia: the time is now. Br J Haematol; 2006 Aug;134(3):273-82
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  • [Title] Minimal residual disease directed therapy for childhood acute myeloid leukaemia: the time is now.
  • The continued improvement in the prognosis of childhood acute myeloid leukaemia (AML) has been paralleled by the use of increasingly intensive therapy.
  • This annotation proposes that the introduction of protocols based on the measurement of minimal residual disease (MRD) holds the key to progression from an era of 'cure at all costs' to a more individualised approach.
  • [MeSH-major] Immunosuppressive Agents / therapeutic use. Neoplasm, Residual / drug therapy. Patient Selection. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16848770.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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73. Kumar L, Gangadharan VP, Rao DR, Saikia T, Shah S, Malhotra H, Bapsy PP, Singh K, Rao R: Safety and efficacy of an indigenous recombinant interferon-alpha-2b in patients with chronic myelogenous leukaemia: results of a multicentre trial from India. Natl Med J India; 2005 Mar-Apr;18(2):66-70
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  • [Title] Safety and efficacy of an indigenous recombinant interferon-alpha-2b in patients with chronic myelogenous leukaemia: results of a multicentre trial from India.
  • BACKGROUND: Compared to hydroxyurea, treatment with interferon-alpha (IFN-alpha) is known to prolong survival in patients with chronic phase of chronic myelogenous leukaemia (CML) and was considered as first-line therapy till recently.
  • Nineteen patients had progression (blast crisis n=15, accelerated phase n=4) while on treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Interferon-alpha / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • [ErratumIn] Natl Med J India. 2005 May-Jun;18(3):130
  • (PMID = 15981440.001).
  • [ISSN] 0970-258X
  • [Journal-full-title] The National medical journal of India
  • [ISO-abbreviation] Natl Med J India
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 99210-65-8 / interferon alfa-2b
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74. Gilby DC, Sung HY, Winship PR, Goodeve AC, Reilly JT, Kiss-Toth E: Tribbles-1 and -2 are tumour suppressors, down-regulated in human acute myeloid leukaemia. Immunol Lett; 2010 May 4;130(1-2):115-24
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  • [Title] Tribbles-1 and -2 are tumour suppressors, down-regulated in human acute myeloid leukaemia.
  • Constitutive MAPK signalling is observed in approximately 50% of acute myeloid leukaemia (AML) cases.
  • Tribbles proteins (trb-1, trb-2 and trb-3) are potent negative regulators of MAPK pathways influencing apoptosis, differentiation and cell-cycle progression.
  • Myeloid cell proliferation and apoptosis were assayed in response to trb-1/trb-2 gene knockdown and overexpression, as well as a physical and functional interaction between trb and C/EBPalpha.
  • [MeSH-major] Down-Regulation. Intracellular Signaling Peptides and Proteins / metabolism. Leukemia, Myeloid, Acute / metabolism. Protein-Serine-Threonine Kinases / metabolism

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  • [Copyright] Copyright 2009 Elsevier B.V. All rights reserved.
  • (PMID = 20005259.001).
  • [ISSN] 1879-0542
  • [Journal-full-title] Immunology letters
  • [ISO-abbreviation] Immunol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Messenger; 0 / TRIB1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 2.7.11.17 / TRIB2 protein, human
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75. Georgiou G, Karali V, Zouvelou C, Kyriakou E, Dimou M, Chrisochoou S, Greka P, Dufexis D, Vervesou E, Dimitriadou E, Efthymiou A, Petrikkos L, Dima K, Lilakos K, Panayiotidis P: Serial determination of FLT3 mutations in myelodysplastic syndrome patients at diagnosis, follow up or acute myeloid leukaemia transformation: incidence and their prognostic significance. Br J Haematol; 2006 Aug;134(3):302-6
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  • [Title] Serial determination of FLT3 mutations in myelodysplastic syndrome patients at diagnosis, follow up or acute myeloid leukaemia transformation: incidence and their prognostic significance.
  • Forty-two patients progressed to acute myeloid leukaemia (AML), including the three patients with FLT3 mutations at MDS diagnosis.
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. DNA Mutational Analysis. Disease Progression. Female. Humans. Leukemia, Myeloid / genetics. Male. Middle Aged. Prognosis. Proportional Hazards Models. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Survival Rate


76. Parker TM, Klaassen RJ, Johnston DL: Spontaneous remission of myelodysplastic syndrome with monosomy 7 in a young boy. Cancer Genet Cytogenet; 2008 Apr 15;182(2):122-5
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  • Myelodysplastic syndrome (MDS) is a clonal hematopoietic disorder that often results in progression to acute myeloid leukemia (AML), particularly when additional genetic abnormalities are present, such as monosomy 7.


77. Nowicki M, Ostalska-Nowicka D, Miśkowiak B: Prognostic significance of Ki67-negative blast cell clone in the high risk group of children treated for acute myeloid leukaemia. Folia Histochem Cytobiol; 2006;44(1):49-52
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  • [Title] Prognostic significance of Ki67-negative blast cell clone in the high risk group of children treated for acute myeloid leukaemia.
  • The aim of this study was to demonstrate the value of immunocytochemical staining of Ki67 antigen expression in blast cells of children with acute myeloid leukemia (AML) and to evaluate its correlation with treatment failure.

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  • (PMID = 16584092.001).
  • [ISSN] 0239-8508
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen
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78. Drury NE, Ali A, Mussa S, Webb ST, Rege KP, Wallwork J: Acute leukaemoid reaction following cardiac surgery. J Cardiothorac Surg; 2007;2:3
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  • [Title] Acute leukaemoid reaction following cardiac surgery.
  • Chronic myelomonocytic leukaemia is an atypical myeloproliferative disorder with a natural history of progression to acute myeloid leukaemia, a complex and poorly understood response by the bone marrow to stress.
  • We present a case of undiagnosed chronic myelomonocytic leukaemia who developed rapidly fatal multi-organ dysfunction following cardiac surgery due to an acute leukaemoid reaction.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemoid Reaction / etiology. Myocardial Revascularization / adverse effects

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  • (PMID = 17212818.001).
  • [ISSN] 1749-8090
  • [Journal-full-title] Journal of cardiothoracic surgery
  • [ISO-abbreviation] J Cardiothorac Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1774565
  • [General-notes] NLM/ Original DateCompleted: 20070802
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79. Melo JV, Barnes DJ: Chronic myeloid leukaemia as a model of disease evolution in human cancer. Nat Rev Cancer; 2007 Jun;7(6):441-53
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  • [Title] Chronic myeloid leukaemia as a model of disease evolution in human cancer.
  • Chronic myeloid leukaemia (CML) can be considered as a paradigm for neoplasias that evolve through a multi-step process.
  • If not cured at this stage, CML invariably progresses and transforms into an acute-type leukaemia undergoing a 'blast crisis'.
  • What mechanisms underlie this progression, and are they shared by other common cancers?
  • [MeSH-major] Blast Crisis. Disease Progression. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Models, Biological

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  • (PMID = 17522713.001).
  • [ISSN] 1474-175X
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 153
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80. Rodríguez Pérez A, López Carrizosa MC, Villalón Blanco L, Samper Ots PM, Ortiz Cruz E: Granulocytic sarcoma of the right humerus in a non-leukaemia patient. Clin Transl Oncol; 2008 Nov;10(11):758-60
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  • [Title] Granulocytic sarcoma of the right humerus in a non-leukaemia patient.
  • Granulocytic sarcoma (GS), an uncommon solid extramedullary tumour, should be considered even in the absence of leukaemia, as delay in diagnosis and treatment worsens the prognosis.
  • We present a GS (single humeral bone lesion) in a non-leukaemia patient, treated with intensive AML (Acute Myeloid Leukaemia) chemotherapy and sequential radiotherapy, in complete response 26 months after diagnosis, confirmed by histopathology and without leukaemia progression.
  • [MeSH-major] Bone Neoplasms / diagnosis. Humerus / pathology. Sarcoma, Myeloid / diagnosis

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  • (PMID = 19015073.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
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81. Chehensse C, Braun T, Morin AS, Stirnemann J, Agranat P, Boukari L, Aras N, Kiladjian JJ, Ziol M, Fenaux P, Fain O: [Extramedullary blastic transformation revealed by a prolonged fever during the course of a 5q- syndrome]. Rev Med Interne; 2009 Oct;30(10):886-9
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  • INTRODUCTION: Fever during a myelodysplastic syndrome can be due to infectious complications, systemic disease or acute transformation with clonal evolution.
  • Neither bone marrow nor blood blasts were detected, but liver biopsy demonstrated significant blast infiltration compatible with the diagnosis of acute myeloid leukaemia (AML).
  • Tissue biopsy may be necessary to confirm the leukaemic progression.


82. Perz JB, Szydlo R, Sergeant R, Sanz J, O'Shea D, Khan T, Davey N, Loaiza S, Davis J, Apperley JF, Olavarria E: Impact of HLA class I and class II DNA high-resolution HLA typing on clinical outcome in adult unrelated stem cell transplantation after in vivo T-cell depletion with alemtuzumab. Transpl Immunol; 2007 Nov;18(2):179-85
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  • Patients received SCT for good risk [chronic myeloid leukaemia in first chronic phase (CML-CP1), n=55] or poor risk (n=45) diseases after myeloablative conditioning and T-cell depletion with alemtuzumab.
  • Acute graft versus host disease (GvHD) grades III-IV occurred in 11%, whilst extensive chronic GvHD in 13% of evaluable patients.
  • In the poor risk group, HLA mismatches had a negative impact on survival (p=0.003) and progression free survival (p=0.009) contrary to CML-CP1 patients, in whom HLA mismatches at molecular or serological level did not have any impact.

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  • (PMID = 18005865.001).
  • [ISSN] 0966-3274
  • [Journal-full-title] Transplant immunology
  • [ISO-abbreviation] Transpl. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Histocompatibility Antigens Class I; 0 / Histocompatibility Antigens Class II; 3A189DH42V / alemtuzumab
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83. Szpecht D, Derwich K, Wachowiak J, Konatkowska B, Dworacki G: [Lineage switch - conversion of acute lymphoblastic leukaemia to acute myeloid leukaemia in 4 years old girl]. Med Wieku Rozwoj; 2008 Oct-Dec;12(4 Pt 2):1041-4
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  • [Title] [Lineage switch - conversion of acute lymphoblastic leukaemia to acute myeloid leukaemia in 4 years old girl].
  • We report a case of a 4-year-old girl with diagnosed proB acute lymphoblastic leukaemia with co-expression CD33 antigen, treated according to Acute Lymphoblastic Leukaemia Intercontinental - Berlin Frankfurt Münster 2002 (ALL-IC BFM 2002) protocol for standard risk group.
  • The late isolated bone marrow relapse of acute myeloid leukaemia, type 7 was noted in our patient.
  • We recognized this case as a lineage switch acute lymphoblastic leukaemia to acute myeloid leukaemia.
  • In spite of Ida Flag regimen and following Acute Myeloid Leukaemia - Berlin Frankfurt Münster 2004 (AML-BFM 2004) protocol were administered, the clinical and haematological remission was not achieved and the patient died because of disease progression (circulatory and respiratory insufficiency).
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / therapeutic use. Cell Lineage. Cell Transformation, Neoplastic. Child, Preschool. Daunorubicin / therapeutic use. Disease Progression. Fatal Outcome. Female. Humans. Prednisone / therapeutic use. Remission Induction. Vincristine / therapeutic use

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  • (PMID = 19531823.001).
  • [Journal-full-title] Medycyna wieku rozwojowego
  • [ISO-abbreviation] Med Wieku Rozwoj
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; PVDA protocol
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84. Bolufer P, Barragan E, Collado M, Cervera J, López JA, Sanz MA: Influence of genetic polymorphisms on the risk of developing leukemia and on disease progression. Leuk Res; 2006 Dec;30(12):1471-91
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  • [Title] Influence of genetic polymorphisms on the risk of developing leukemia and on disease progression.
  • BACKGROUND: Recent studies have provided evidence that common genetic variations with low penetrance could account for a proportion of leukemia and could also influence disease outcome, although the results obtained are still controversial.
  • MATERIAL AND METHODS: We reviewed 54 recent reports focused on the contribution of genetic polymorphisms to the risk of developing leukemia and to disease progression.
  • RESULTS: There was a good agreement on the influence of NQO1*2 polymorphism and those of the enzymes involved in DNA repair with the increased risk of therapy-related leukemia/myelodysplastic syndrome.
  • Most studies found a strong association between the polymorphisms MTHFR, C677T or A1298C, and NQO1*2 or *3 and the risk of acute lymphoblastic leukemia (ALL).
  • In addition, most of the studies reported an association between GSTT1 deletions and an increased risk of de novo acute myeloid leukemia.
  • CONCLUSION: The reports reviewed support the hypothesis that several low-penetrance genes with multiplicative effects together with dietary effects, ambient exposition, and individual immune system responses, may account for the risk of leukaemia.
  • [MeSH-major] Enzymes / genetics. Leukemia / genetics. Polymorphism, Genetic
  • [MeSH-minor] Animals. DNA Repair / genetics. Disease Progression. Folic Acid / metabolism. Genetic Variation. Humans. Risk Factors


85. Saracco P, Quarello P, Iori AP, Zecca M, Longoni D, Svahn J, Varotto S, Del Vecchio GC, Dufour C, Ramenghi U, Bacigalupo A, Locasciulli A, Bone Marrow Failure Study Group of the AIEOP (Italian Association of Paediatric Haematology Oncology): Cyclosporin A response and dependence in children with acquired aplastic anaemia: a multicentre retrospective study with long-term observation follow-up. Br J Haematol; 2008 Jan;140(2):197-205
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  • This study, of 42 consecutive children with AAA treated with IST, assessed the incidence of CyA-dependence, CyA and granulocyte colony-stimulating factor (G-CSF) tapering schedules and the impact of drug accumulation on progression to myelodysplasia/acute myeloid leukaemia (MDS/AML).
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease Progression. Drug Administration Schedule. Drug Evaluation. Drug Therapy, Combination. Epidemiologic Methods. Female. Granulocyte Colony-Stimulating Factor / administration & dosage. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Infant. Male. Recurrence. Treatment Outcome

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  • (PMID = 18173756.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 83HN0GTJ6D / Cyclosporine
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86. Sanada M, Uike N, Ohyashiki K, Ozawa K, Lili W, Hangaishi A, Kanda Y, Chiba S, Kurokawa M, Omine M, Mitani K, Ogawa S: Unbalanced translocation der(1;7)(q10;p10) defines a unique clinicopathological subgroup of myeloid neoplasms. Leukemia; 2007 May;21(5):992-7
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  • [Title] Unbalanced translocation der(1;7)(q10;p10) defines a unique clinicopathological subgroup of myeloid neoplasms.
  • The unbalanced translocation, der(1;7)(q10;p10), is one of the characteristic cytogenetic abnormalities found in myelodysplastic syndromes (MDS) and other myeloid neoplasms.
  • In contrast with other -7/7q- cases, where the abnormality tends to be found in one or more partial karyotypes, der(1;7)(q10;p10) represents the abnormality common to all the abnormal clones and usually appears as a sole chromosomal abnormality during the entire clinical courses, or if not, is accompanied only by a limited number and variety of additional abnormalities, mostly trisomy 8 and/or loss of 20q. der(1;7)(q10;p10)-positive MDS cases showed lower blast counts (P<0.0001) and higher hemoglobin concentrations (P<0.0075) at diagnosis and slower progression to acute myeloid leukemia (P=0.0043) than other -7/7q- cases. der(1;7)(q10;p10) cases showed significantly better clinical outcome than other -7/7q cases (P<0.0001).
  • In conclusion, der(1;7)(q10;p10) defines a discrete entity among myeloid neoplasms, showing unique clinical and cytogenetic characteristics.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics. Translocation, Genetic


87. Konieczna I, Horvath E, Wang H, Lindsey S, Saberwal G, Bei L, Huang W, Platanias L, Eklund EA: Constitutive activation of SHP2 in mice cooperates with ICSBP deficiency to accelerate progression to acute myeloid leukemia. J Clin Invest; 2008 Mar;118(3):853-67
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  • [Title] Constitutive activation of SHP2 in mice cooperates with ICSBP deficiency to accelerate progression to acute myeloid leukemia.
  • Development of a block in myeloid differentiation is associated with progression of MPD to acute myeloid leukemia (AML) and portends poor prognosis.
  • Interferon consensus sequence binding protein (ICSBP, also known as IRF8) is an interferon-regulatory transcription factor that functions as a leukemia tumor suppressor.
  • Since activity of ICSBP is influenced by tyrosine phosphorylation state, we hypothesized that mutations in molecular pathways that regulate this process might synergize with ICSBP deficiency for progression to AML.
  • Consistent with this, we found that constitutive activation of SHP2 protein tyrosine phosphatase synergized with ICSBP haploinsufficiency to facilitate cytokine-induced myeloproliferation, apoptosis resistance, and rapid progression to AML in a murine bone marrow transplantation model.
  • Constitutive SHP2 activation cooperated with ICSBP deficiency to increase the number of progenitors in the bone marrow and myeloid blasts in circulation, indicating a block in differentiation.
  • Since SHP2 activation and ICSBP deficiency may coexist in human myeloid malignancies, our studies have identified a molecular mechanism potentially involved in disease progression in such diseases.

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  • (PMID = 18246201.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095266; United States / NCI NIH HHS / CA / R01-CA095266
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-8; 42HK56048U / Tyrosine; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
  • [Other-IDs] NLM/ PMC2214847
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88. Bernasconi P, Boni M, Cavigliano PM, Calatroni S, Giardini I, Rocca B, Zappatore R, Dambruoso I, Caresana M: Clinical relevance of cytogenetics in myelodysplastic syndromes. Ann N Y Acad Sci; 2006 Nov;1089:395-410
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  • In addition, chromosome abnormalities are independent prognostic factors predicting overall survival and the likelihood of progression in acute myeloid leukemia.


89. Paupert J, Mansat-De Mas V, Demur C, Salles B, Muller C: Cell-surface MMP-9 regulates the invasive capacity of leukemia blast cells with monocytic features. Cell Cycle; 2008 Apr 15;7(8):1047-53
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  • [Title] Cell-surface MMP-9 regulates the invasive capacity of leukemia blast cells with monocytic features.
  • The importance of this variant pro-form in tumor progression remains poorly defined.
  • We previously showed that the DNA repair protein Ku interacts at the cell surface of leukaemia cell lines with the 85 Kda pro-form of MMP-9 and these Ku/MMP-9 complexes regulates cell invasion, highlighting their importance in haematological malignancies.
  • We demonstrate here that all samples of acute myeloid leukaemia (AML) blasts purified from bone marrow of 16 affected patients express the 85 Kda form of MMP-9.
  • These results might have important functional significance in the occurrence of extra-medullar infiltrates of leukaemia cells that occurs frequently during the onset of monocyte-related AML sub-types.
  • [MeSH-major] DNA Helicases / metabolism. Leukemia, Myeloid, Acute / metabolism. Matrix Metalloproteinase 9 / metabolism. Membrane Proteins / metabolism. Monocytes / metabolism. Neoplasm Invasiveness / physiopathology

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  • (PMID = 18414048.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / XRCC5 protein, human; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.6.4.- / DNA Helicases
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90. Claxton DF, Ehmann C, Rybka W: Control of advanced and refractory acute myelogenous leukaemia with sirolimus-based non-myeloablative allogeneic stem cell transplantation. Br J Haematol; 2005 Jul;130(2):256-64
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  • [Title] Control of advanced and refractory acute myelogenous leukaemia with sirolimus-based non-myeloablative allogeneic stem cell transplantation.
  • A total of 23 patients with acute myelogenous leukaemia (AML) were treated, with a median age of 59 years (range: 28-72) at transplant.
  • Nine patients were in chemotherapy-refractory progression and seven were primarily refractory to induction therapy.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Immunosuppressive Agents / administration & dosage. Leukemia, Myeloid, Acute / therapy. Sirolimus / administration & dosage
  • [MeSH-minor] Adult. Aged. Antibiotics, Antineoplastic / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chronic Disease. Cyclophosphamide / administration & dosage. Disease Progression. Follow-Up Studies. Graft Survival. Graft vs Host Disease / prevention & control. Humans. Middle Aged. Survival Analysis. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 16029454.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Immunosuppressive Agents; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; W36ZG6FT64 / Sirolimus
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91. Rau R, Brown P: Nucleophosmin (NPM1) mutations in adult and childhood acute myeloid leukaemia: towards definition of a new leukaemia entity. Hematol Oncol; 2009 Dec;27(4):171-81
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  • [Title] Nucleophosmin (NPM1) mutations in adult and childhood acute myeloid leukaemia: towards definition of a new leukaemia entity.
  • It plays key roles in ribosome biogenesis, centrosome duplication, genomic stability, cell cycle progression and apoptosis.
  • Somatic mutations in exon 12 of the NPM gene (NPM1) are the most frequent genetic abnormality in adult acute myeloid leukaemia (AML), found in approximately 35% of all cases and up to 60% of patients with normal karyotype (NK) AML.

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  • [Copyright] Copyright (c) 2009 John Wiley & Sons, Ltd.
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  • (PMID = 19569254.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA111728-05; United States / NCI NIH HHS / CA / K23 CA111728; United States / NCI NIH HHS / CA / T32 CA060441; United States / NCI NIH HHS / CA / K23 CA111728-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  • [Number-of-references] 102
  • [Other-IDs] NLM/ NIHMS234930; NLM/ PMC3069851
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92. Caudill JS, Sternberg AJ, Li CY, Tefferi A, Lasho TL, Steensma DP: C-terminal nucleophosmin mutations are uncommon in chronic myeloid disorders. Br J Haematol; 2006 Jun;133(6):638-41
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  • [Title] C-terminal nucleophosmin mutations are uncommon in chronic myeloid disorders.
  • C-terminal somatic mutations in nucleophosmin (NPM), a nucleolar shuttling protein that binds p53 and p19(Arf), were recently described in karyotypically normal acute myeloid leukaemia (AML).
  • We analysed primary marrow samples from 150 patients with various chronic myeloid disorders for mutations in the NPM1 gene encoding NPM.
  • NPM1 mutations (tetranucleotide duplication) were detected in three patients, all of whom had chronic myelomonocytic leukaemia (CMML) and a short (<1 year) survival, with rapid progression to overt AML.
  • In conclusion, C-terminal NPM mutations are uncommon in chronic myeloid neoplasia, but if present may represent an evolving leukaemic clone.
  • [MeSH-major] Bone Marrow Diseases / genetics. Leukemia, Myelomonocytic, Chronic / genetics. Mutation. Nuclear Proteins / genetics
  • [MeSH-minor] Base Sequence. Cell Transformation, Neoplastic / genetics. Chronic Disease. DNA Mutational Analysis / methods. DNA, Neoplasm / genetics. Disease Progression. Humans. Molecular Sequence Data. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics. Prognosis

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  • (PMID = 16704439.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K12 CA090628
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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93. Vyas P, Sternberg A: Characterization of the hemopoietic defect in early stages of the myelodysplastic syndromes. Adv Enzyme Regul; 2006;46:98-112
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  • Myelodysplasia (MDS) is a heterogeneous disorder characterised by bone marrow failure and progression to acute myeloid leukaemia where the molecular and cellular haematopoietic defects are poorly understood.


94. Lindberg EH: Strategies for biology- and molecular-based treatment of myelodysplastic syndromes. Curr Drug Targets; 2005 Sep;6(6):713-25
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  • The myelodysplastic syndromes (MDS) constitute a group of clonal stem cell disorders characterized by cytopenia, ineffective hematopoiesis, bone marrow dysplasia, and a risk of progression to acute myeloid leukemia (AML).
  • Disease mechanisms can be divided into two main groups; those underlying the increased apoptosis of bone marrow progenitors, and those associated with progressive blast proliferation, and transformation to acute myeloid leukemia.
  • Important mechanisms for disease progression are DNA hypermethylation, histone deacetylation, and possibly RAS mutations.
  • Two new DNA hypomethylating agents, azacytidine and decitabine, have shown efficacy in patients with high-risk MDS, and may prolong time to progression.
  • In conclusion, recent advances in the pathogenetic understanding of MDS have led to significant therapeutic progress.


95. Jädersten M, Hellström-Lindberg E: Myelodysplastic syndromes: biology and treatment. J Intern Med; 2009 Mar;265(3):307-28
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  • This review focuses on low-risk MDS, for which chronic anaemia and eventual progression to acute myeloid leukaemia are the main concerns.
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Blood Transfusion. Chromosomes, Human, Pair 5 / genetics. Disease Progression. Erythropoietin / therapeutic use. Female. Humans. Immunosuppressive Agents / therapeutic use. Iron Chelating Agents / therapeutic use. Male. Recombinant Proteins. Sequence Deletion. Thalidomide / analogs & derivatives. Thalidomide / therapeutic use. World Health Organization


96. Candiloro IL, Mikeska T, Hokland P, Dobrovic A: Rapid analysis of heterogeneously methylated DNA using digital methylation-sensitive high resolution melting: application to the CDKN2B (p15) gene. Epigenetics Chromatin; 2008;1(1):7
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  • We used this approach to study methylation of the CDKN2B (p15) cell cycle progression inhibitor gene which is inactivated by DNA methylation in haematological malignancies of the myeloid lineage.
  • RESULTS: MS-HRM was used to assess CDKN2B methylation in acute myeloid leukaemia (AML) samples.

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  • (PMID = 19014416.001).
  • [ISSN] 1756-8935
  • [Journal-full-title] Epigenetics & chromatin
  • [ISO-abbreviation] Epigenetics Chromatin
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2590600
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97. Teramoto H, Miwa H, Patel V, Letwin N, Castellone MD, Imai N, Shikami M, Imamura A, Gutkind JS, Nitta M, Lee NH: Gene expression changes in a patient presenting nonleukaemic nasal granulocytic sarcoma to acute myelogenous leukaemia using 40 K cDNA microarray. Clin Lab Haematol; 2006 Aug;28(4):262-6
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  • [Title] Gene expression changes in a patient presenting nonleukaemic nasal granulocytic sarcoma to acute myelogenous leukaemia using 40 K cDNA microarray.
  • This is a case report of granulocytic sarcoma occurring as a nasal lesion prior to the onset of acute myelogenous leukaemia (AML).
  • To understand this case in more detail, we used 40,000 human cDNA microarray to identify the gene expression patterns of nonleukaemic stage bone marrow (BM), AML stage BM and AML stage peripheral blood cells and subsequently define the molecular basis of this disease progression.
  • Of significance, we have tracked the expression profile of BM samples during the course of nonleukaemic to leukaemic progression, and identified a number of genes that may account for the growth potential of leukaemia cells and indicate poor prognosis of this case.
  • [MeSH-major] Gene Expression Regulation, Leukemic / genetics. Leukemia, Myeloid, Acute / genetics. Nose Neoplasms / genetics. Sarcoma, Myeloid / genetics
  • [MeSH-minor] Aged, 80 and over. Disease Progression. Down-Regulation / genetics. Fatal Outcome. Female. Humans. Oligonucleotide Array Sequence Analysis / methods. Up-Regulation / genetics

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  • (PMID = 16898967.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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98. Bai J, Xue Y, Ye L, Yao J, Zhou C, Shao Z, Qian L, Yang R, Li H, Zhang H, Zheng Y: Risk factors of long-term incidences of thrombosis, myelofibrosis and evolution into malignance in polycythemia vera: a single center experience from China. Int J Hematol; 2008 Dec;88(5):530-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To find out risk factors of incidences of long-term complications of thrombosis, myelofibrosis with myeloid metaplasia (MMM) and evolution into malignance in Chinese PV patients, we evaluated 320 PV patients referred to our center from April 1984 to June 2005 by Kaplan-Meier estimation and Cox proportional hazards models.
  • A total of 43 patients progressed into MMM at a median time of 84 (7-240) months, higher white blood cell (WBC) count, splenomegaly, receiving alkylating agent and hydroxycarbamide were associated with the progression into MMM.
  • During the follow-up time, 11 and 2 patients died of fatal complications of thrombosis and acute myeloid leukaemia (AML), respectively.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Polycythemia Vera / mortality. Primary Myelofibrosis / mortality. Thromboembolism / mortality


99. Leung EW, Rujkijyanont P, Beyene J, Wei K, Abdelhaleem M, Freedman MH, Dror Y: Shwachman-Diamond syndrome: an inherited model of aplastic anaemia with accelerated angiogenesis. Br J Haematol; 2006 Jun;133(5):558-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Bone marrow angiogenesis is increased in myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML), but has not been studied in inherited or acquired marrow failure syndromes.
  • Future studies should investigate the mechanism for increased angiogenesis in SDS, and whether SDS marrow, with its increased angiogenesis, promotes progression of malignant clones.
  • [MeSH-minor] Acute Disease. Adolescent. Anemia, Aplastic / genetics. Anemia, Aplastic / pathology. Bone Marrow Cells / pathology. Child. Child, Preschool. Female. Gene Expression / genetics. Humans. Infant. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Male. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Neovascularization, Pathologic / genetics. Syndrome. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism


100. Lu C, Hassan HT: Human stem cell factor-antibody [anti-SCF] enhances chemotherapy cytotoxicity in human CD34+ resistant myeloid leukaemia cells. Leuk Res; 2006 Mar;30(3):296-302
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human stem cell factor-antibody [anti-SCF] enhances chemotherapy cytotoxicity in human CD34+ resistant myeloid leukaemia cells.
  • Acute myeloid leukaemia (AML) is a heterogenous malignant disease with diverse biological features in which disease progression at the level of CD34+ cells has a major impact on the resistance to chemotherapy and relapse.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, CD34. Antineoplastic Agents / pharmacology. Biomarkers, Tumor. Cytarabine / pharmacology. Daunorubicin / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Stem Cell Factor / antagonists & inhibitors

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
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  • (PMID = 16112192.001).
  • [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 / Antibodies, Monoclonal; 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / P-Glycoprotein; 0 / Receptors, Cytokine; 0 / Stem Cell Factor; 0 / bcl-2-Associated X Protein; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
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