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1. 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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  • 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).
  • It compared aza with CCR in 358 patients with higher risk MDS, CMML and AML 20-30% blasts.
  • The outcomes reported in AZA-001 included overall survival, TTP to AML and adverse events.
  • The results showed that: the median overall survival was 24.5 months on aza, compared with 15.0 months in the CCR group (p = 0.0001); the response rates were low (complete remission 17% aza versus 8% CCR); the median time to transformation to AML was greater in the aza group (17.8 versus 11.5 months; p < 0.0001); and of patients who were red blood cell (RBC) transfusion-dependent at baseline, 45% of those on aza became RBC transfusion-independent during the treatment period, compared with 11.8% in the CCR group (p < 0.0001).
  • 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.
  • At the time of writing, the guidance appraisal consultation document issued by NICE on 4 March 2010 states that azacitidine is not recommended as a treatment option for people not eligible for haemopoietic stem cell transplantation with the the following conditions: intermediate-2 and high-risk MDS according to the International Prognostic Scoring System, CMML with 10-29% marrow blasts without myeloproliferative disorder, or with AML with 20-30% blasts and multilineage dysplasia, according to World Health Organization classification.


2. Li YM, Li XX, Ge ML, Shi J, Qian LS, Wang JX, Zheng YZ: [Treatment of severe aplastic anemia with intensified immunosuppressive therapy and two different regimens with recombinant human granulocyte colony-stimulating factor: a retrospective study based on long-term follow-up]. Zhonghua Xue Ye Xue Za Zhi; 2010 Jul;31(7):470-4
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  • There were no differences between two groups in terms of survival and the response rates (P = 0.288, 0.066), but there was an increasing risk of evolving into MDS/AML in Group B (22.3%) when compared with Group A (3.71%) (P = 0.023). (3) By multivariate analysis, the severity of disease (P = 0.010, RR = 1.922) and the early response (P < 0.01, RR = 5.749) were associated with the overall survival.
  • Moreover, the number of days of rhG-CSF therapy was the only significant risk factor for SAA evolving into MDS/AML (P = 0.017, RR = 1.004).
  • CONCLUSIONS: The early initiation of rhG-CSF therapy with proper dose might contribute to a desirable early response and reduced infection-related death rate, but extended administration of rhG-CSF did not improve the long-term outcome of refractory SAA and may further facilitate the progression of SAA into MDS/AML.


3. Lakshmikuttyamma A, Takahashi N, Pastural E, Torlakovic E, Amin HM, Garcia-Manero G, Voralia M, Czader M, DeCoteau JF, Geyer CR: RIZ1 is potential CML tumor suppressor that is down-regulated during disease progression. J Hematol Oncol; 2009 Jul 14;2:28
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  • [Title] RIZ1 is potential CML tumor suppressor that is down-regulated during disease progression.
  • In AML cell lines and patient material, RIZ1 expression is reduced relative to normal bone marrow.
  • RESULTS: In CML patient material, we observed that RIZ1 expression was decreased during progression from chronic phase to blast crisis.
  • Together these results suggest that loss of RIZ1 expression will lead to an increase in myeloid blast cell population resulting in CML progression.

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  • (PMID = 19602237.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / PRDM2 protein, human
  • [Other-IDs] NLM/ PMC2719666
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4. Majhail NS, Brunstein CG, Tomblyn M, Thomas AJ, Miller JS, Arora M, Kaufman DS, Burns LJ, Slungaard A, McGlave PB, Wagner JE, Weisdorf DJ: Reduced-intensity allogeneic transplant in patients older than 55 years: unrelated umbilical cord blood is safe and effective for patients without a matched related donor. Biol Blood Marrow Transplant; 2008 Mar;14(3):282-9
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  • The median age of MRD and UCB cohorts was 58 (range, 55-70) and 59 (range, 55-69) years, respectively. acute myelogenous leukemia/myelodysplastic syndrome (AML/MDS) (50%) was the most common diagnosis.
  • The 3-year probabilities of progression-free survival (PFS; 30% versus 34%, P = .98) and OS (43% versus 34%, P = .57) were similar for recipients of MRD and UCB.

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  • (PMID = 18275894.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA065493-110009; United States / NCI NIH HHS / CA / P01 CA065493; United States / NCI NIH HHS / CA / P01 CA065493-120009; United States / NCI NIH HHS / CA / P01CA65493; United States / NCI NIH HHS / CA / CA065493-120009; United States / NCI NIH HHS / CA / CA065493-110009
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Myeloablative Agonists
  • [Other-IDs] NLM/ NIHMS41246; NLM/ PMC2674378
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5. Solomon PR, Munirajan AK, Tsuchida N, Muthukumarasamy K, Rathinavel A, Selvam GS, Shanmugam G: Promoter hypermethylation analysis in myelodysplastic syndromes: diagnostic & prognostic implication. Indian J Med Res; 2008 Jan;127(1):52-7
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  • Unique genetic alterations in combinations or in isolation account for a small fraction of MDS suggesting the epigenetic hypermethylation as a possible leading cause for MDS and its transformation to acute myelocytic leukaemia (AML).
  • Therefore, in this study, promoter hypermethylation status of key cell cycle regulators was assessed as markers in MDS patients and association of hypermethylation with clinical progression of disease was also studied.

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  • (PMID = 18316853.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / MLH1 protein, human; 0 / Nuclear Proteins; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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6. Bessho F, Imashuku S, Hibi S, Tsuchida M, Nakahata T, Miyazaki S, Kojima S, Tsukimoto I, Hamajima N, Pediatric AA Follow-up Study Group in Japan: Serial morphologic observation of bone marrow in aplastic anemia in children. Int J Hematol; 2005 Jun;81(5):400-4
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  • Recent reports of myelodysplastic syndrome/acute myeloid leukemia (t-MDS/AML) developing after treatment with immunosuppressants and granulocyte colony-stimulating factor (G-CSF) has raised the question of whether previously unrecognized myelodysplastic features had been present or whether actual transformation had occurred.
  • In each case, bone marrow specimens were tested at study entry and every 6 months for 3 years to detect t-MDS/AML as defined by morphologic and molecular/cytogenetic criteria.
  • [MeSH-minor] Bone Marrow Examination. Child. Chromosome Aberrations. Disease Progression. Follow-Up Studies. Granulocyte Colony-Stimulating Factor / adverse effects. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Immunosuppressive Agents / adverse effects. Immunosuppressive Agents / therapeutic use. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / diagnosis. Mast Cells / pathology. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / diagnosis

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  • (PMID = 16158820.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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7. Kikushige Y, Takase K, Sata K, Aoki K, Numata A, Miyamoto T, Fukuda T, Gondo H, Harada M, Nagafuji K: Repeated relapses of acute myelogenous leukemia in the isolated extramedullary sites following allogeneic bone marrow transplantations. Intern Med; 2007;46(13):1011-4
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  • Isolated extramedullary (EM) relapses of acute myelogenous leukemia (AML) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) have been reported to be rare, and are usually followed by bone marrow relapses.
  • We report a 49-year-old man with AML with the unfavorable chromosome abnormality 7q-, who was treated by allo-HSCT.
  • Accordingly, we should be aware that AML relapses can occur repeatedly only in isolated EM sites post allo-HSCT, resulting in treatment failure and a poor prognosis.
  • [MeSH-minor] Biopsy, Needle. Disease Progression. Fatal Outcome. Humans. Immunohistochemistry. Male. Middle Aged. Recurrence. Severity of Illness Index. Transplantation, Homologous

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  • (PMID = 17603242.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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8. Greco M, D'Alò F, Scardocci A, Criscuolo M, Fabiani E, Guidi F, Di Ruscio A, Migliara G, Pagano L, Fianchi L, Chiusolo P, Hohaus S, Leone G, Voso MT: Promoter methylation of DAPK1, E-cadherin and thrombospondin-1 in de novo and therapy-related myeloid neoplasms. Blood Cells Mol Dis; 2010 Oct 15;45(3):181-5
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  • [Title] Promoter methylation of DAPK1, E-cadherin and thrombospondin-1 in de novo and therapy-related myeloid neoplasms.
  • DNA methylation is one of the major epigenetic changes in human cancers, leading to silencing of tumor suppressor genes, with a pathogenetic role in tumor development and progression in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML).
  • We were interested in the characterization of the methylation pattern of AML and MDS de novo and therapy-related.
  • There were 105 MDS, 208 de novo AML and 72 t-MN (45 MDS and 27 AML).
  • DAPK1 was more frequently methylated in t-MDS/AML when compared to de novo MDS and AML (39% vs 15.3% and 24.4%, p=0.0001), while methylation of CDH1 was similar in t-MDS/AML and AML (51% and 53.4%), but less frequent in de novo MDS (29%) (p=0.003).
  • In the t-MDS/AML group, we found that the methylation pattern appeared to be related to the primary tumor, with DAPK1 more frequently methylated in patients with a previous lymphoproliferative disease (75% vs 32%, p=0.006).
  • TSP1 hypermethylation was rare and not characteristic of t-MDS/AML.
  • In 177 patients studied for concurrent methylation of several promoters, t-MN and AML de novo were significantly more frequently hypermethylated in 2 or more promoter regions than de novo MDS (20% vs 12.4%, p<0.001).
  • Chemotherapy and individual genetic predisposition have a role in t-MDS/AML development, the identification of specific epigenetic modifications may explain complexity and genomic instability of these diseases and give the basis for targeted-therapy.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20655775.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / CDH1 protein, human; 0 / Cadherins; 0 / Thrombospondin 1; EC 2.7.11.1 / DAPK1 protein, human; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
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9. 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.
  • 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.
  • 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-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Follow-Up Studies. Humans. Karyotyping. Male. Middle Aged. Remission Induction. Risk Factors. Treatment Failure


10. Antic D, Elezovic I, Bogdanovic A, Vukovic NS, Pavlovic A, Jovanovic MP, Jakovic L, Kraguljac N: Isolated myeloid sarcoma of the gastrointestinal tract. Intern Med; 2010;49(9):853-6
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  • Most patients subsequently develop acute myelogenous leukemia (AML), and their prognosis is poor.
  • Two months after initial presentation, bone marrow tests led to a diagnosis of AML.
  • [MeSH-minor] Adult. Biopsy, Needle. Disease Progression. Duodenum / pathology. Endoscopy, Gastrointestinal / methods. Female. Follow-Up Studies. Humans. Immunohistochemistry. Intestine, Small / pathology. Severity of Illness Index. Treatment Refusal

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  • (PMID = 20453407.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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11. Kracmarova A, Cermak J, Brdicka R, Bruchova H: High expression of ERCC1, FLT1, NME4 and PCNA associated with poor prognosis and advanced stages in myelodysplastic syndrome. Leuk Lymphoma; 2008 Jul;49(7):1297-305
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  • Myelodysplastic syndrome (MDS) represents a good model for research of prognostic/progression markers due to frequent transformation into acute myeloid leukemia (AML).
  • We analysed expression profiles of 26 MDS and 6 AML patients using cDNA arrays comprising 588 gene probes.
  • Our findings demonstrate the progressive up-regulation of the genes along the sequence of 5q-syndrome/RCMD/RAEB/de novo AML, suggesting their association with disease progression.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Disease Progression. Female. Gene Expression. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Nucleoside Diphosphate Kinase D. Oligonucleotide Array Sequence Analysis. Prognosis


12. Mossner M, Hopfer O, Nowak D, Baldus CD, Neumann U, Kmetsch A, Benlasfer O, John T, Perka C, Thiel E, Hofmann WK: Detection of differential mitotic cell age in bone marrow CD34(+) cells from patients with myelodysplastic syndrome and acute leukemia by analysis of an epigenetic molecular clock DNA signature. Exp Hematol; 2010 Aug;38(8):661-5
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  • To determine mitotic cell age in hematopoietic cells of myelodysplastic syndrome (MDS), acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) patients, we assessed differential CSX methylation patterns in these diseases vs age-adjusted healthy controls.
  • MATERIALS AND METHODS: We performed bisulfite pyrosequencing to analyze CSX methylation in CD34(+) and bone marrow (BM) cells from 53 MDS, 62 AML, 77 ALL patients, and 37 controls.
  • RESULTS: Analysis of MDS CD34(+) and BM cells revealed significantly increasing methylation of CSX in controls < MDS low-risk < MDS high-risk < AML.
  • Furthermore, increased differences of CSX methylation between the CD34(+) vs the unselected BM compartment were detected in matched MDS low-risk but not high-risk and AML samples.
  • CONCLUSIONS: Assessment of mitotic cell age by CSX methylation analysis could reveal novel insights into the distinct progression of hematologic diseases.


13. 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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  • 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-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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14. Ika SA, Qi XF, Chen ZX: Protein RAP1GAP in human myelodysplastic syndrome detected by flow cytometry and its clinical relevance. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Jun;17(3):612-7
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  • The results indicated that the expression level of RAP1GAp in MDS patients significantly increased as compared with patients with non-malignant blood diseases or AML (8.42 +/- 8.37% vs 2.97 +/- 4.75% or 2.26 +/- 4.24%).
  • The role played by RAP1GAP expression in the pathogenesis of MDS and its clinical significance during progression of MDS towards AML deserves further studies.


15. Janus A, Linke A, Cebula B, Robak T, Smolewski P: Rapamycin, the mTOR kinase inhibitor, sensitizes acute myeloid leukemia cells, HL-60 cells, to the cytotoxic effect of arabinozide cytarabine. Anticancer Drugs; 2009 Sep;20(8):693-701
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  • Overexpression of the mTOR signaling pathway has been described in several tumor cells, including the majority of acute myeloid leukemia (AML) cases.
  • In AML, however, the potential antineoplastic effect of mTOR inhibitors has received little attention thus far.
  • In this in-vitro study of the human AML cell line, HL-60, we aimed to assess the antileukemic activity of rapamycin (RAPA), an mTOR inhibitor, alone and in combination with cytarabine (Ara-C).
  • The study showed that RAPA in concentrations of 1-10 nmol/l arrested the cell cycle progression of Hl-60 cells in the G1 phase, without evident cytotoxic effect.
  • In conclusion, these data indicate that RAPA might be effective in the treatment of acute leukemia patients, especially in combination with Ara-C, the drug routinely used in AML treatment.
  • On the basis of these results, attempts to combine classical induction chemotherapy with an inhibitor of the mTOR kinase in AML treatment could be warranted.

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  • (PMID = 19584709.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Chromones; 0 / Cyclins; 0 / EIF4EBP1 protein, human; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / Phosphoproteins; 04079A1RDZ / Cytarabine; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; EC 3.4.22.- / Caspase 3; W36ZG6FT64 / Sirolimus
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16. 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.
  • The Patient with AML and BCA had an infection of the treated breast after 4 months and postponed mastectomy to an AML remission status.
  • [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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17. Chou WC, Tang JL, Lin LI, Yao M, Tsay W, Chen CY, Wu SJ, Huang CF, Chiou RJ, Tseng MH, Lin DT, Lin KH, Chen YC, Tien HF: Nucleophosmin mutations in de novo acute myeloid leukemia: the age-dependent incidences and the stability during disease evolution. Cancer Res; 2006 Mar 15;66(6):3310-6
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  • [Title] Nucleophosmin mutations in de novo acute myeloid leukemia: the age-dependent incidences and the stability during disease evolution.
  • Nucleophosmin (NPM) mutations have been found in a significant proportion of adults with de novo acute myeloid leukemia (AML), especially in those of a normal karyotype.
  • These results provide a basis for studies of the pathogenesis in this specific subgroup of AML.
  • In this study, NPM mutations were analyzed in 173 Chinese patients of de novo AML, including adults and children.
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Amino Acid Sequence. Base Sequence. Child. Child, Preschool. Disease Progression. Exons. Female. Humans. Immunophenotyping. Infant. Male. Middle Aged. Molecular Sequence Data

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  • (PMID = 16540685.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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18. Weiss JR, Baer MR, Ambrosone CB, Blanco JG, Hutson A, Ford LA, Moysich KB: Concordance of pharmacogenetic polymorphisms in tumor and germ line DNA in adult patients with acute myeloid leukemia. Cancer Epidemiol Biomarkers Prev; 2007 May;16(5):1038-41
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  • However, genotypes determined in tumor and somatic tissues may differ due to cytogenetic and molecular changes associated with malignant transformation and progression.
  • We compared genotypes determined in DNA extracted from paired pretreatment bone marrow and buccal samples from 80 adult patients with acute myeloid leukemia (AML).
  • Paired AML and buccal DNA samples were genotyped for polymorphisms (21 single nucleotide polymorphisms and 2 gene deletions) on genes encoding proteins involved in drug metabolism (CYP3A4, CYP2C8, CDA, and GSTP1), oxidative stress mechanisms (CAT, MnSOD, GSTT1, GSTM1, GSTA1, and GPX1), drug transport (MDR1, MRP1, and BCRP), and DNA repair (MGMT, XPD, and XRCC1).
  • Concordance of genotypes was tested by kappa statistics. kappa statistics for paired AML and buccal DNA samples ranged between 0.94 and 1.00, indicating excellent agreement.
  • Agreement was also excellent for genes at AML chromosome deletion and translocation breakpoints, including MDR1 at 7q21.1 and MRP1 at 16p13.1.
  • Based on these data, genotypes derived from archived AML bone marrow samples were not likely to differ from those from genomic DNA, and archived bone marrow samples may be useful for the conduct of retrospective pharmacogenetic studies.


19. Chen SH, Hung IJ, Yang CP, Jaing TH, Fang EC, Yang SH, Tseng CK: Allogeneic related bone marrow transplantation in children--a single center experience. Acta Paediatr Taiwan; 2005 Nov-Dec;46(6):352-5
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  • Seven patients died (5 because of relapse and/or disease progression and 2 because of infectious complication).
  • The underlying diseases were acute lymphoblastic leukemia (ALL; 4 cases: 3 CR2, 1 Ph+), acute myeloid leukemia (AML; 2 cases: 1 CR2, 1 refractory), and juvenile chronic myelogenous leukemia (JCML; 1 case).

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  • (PMID = 16640037.001).
  • [ISSN] 1608-8115
  • [Journal-full-title] Acta paediatrica Taiwanica = Taiwan er ke yi xue hui za zhi
  • [ISO-abbreviation] Acta Paediatr Taiwan
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China (Republic : 1949- )
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20. Malcovati L, Nimer SD: Myelodysplastic syndromes: diagnosis and staging. Cancer Control; 2008 Oct;15 Suppl:4-13
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  • Myelodysplastic syndromes (MDS) represent a heterogeneous group of hematologic disorders characterized by ineffective hematopoiesis and an increased risk of developing acute myelogenous leukemia (AML).
  • The WHO classification-based prognostic scoring system (WPSS) permits dynamic estimation of survival and risk of AML transformation at multiple time points during the natural course of MDS.
  • [MeSH-minor] Disease Progression. Humans. Precancerous Conditions / classification. Precancerous Conditions / diagnosis. Prognosis


21. Fard SS, Jeddi-Tehrani M, Akhondi MM, Hashemi M, Ardekani AM: Flow Cytometric Analysis of 4-HPR-induced Apoptosis and Cell Cycle Arrest in Acute Myelocytic Leukemia Cell Line (NB-4). Avicenna J Med Biotechnol; 2010 Jan;2(1):53-61
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  • To test whether this drug has activity in acute myeloid leukemia (AML), we first analyzed the anti-proliferative effect of 4-HPR in one AML cell line (NB-4) using MTT Assay.
  • We also analyzed the cell cycle progression by PI staining using flow cytometry.
  • In total, the results indicate that 4-HPR is a strong inhibitor of AML cell proliferation and a potent inducer of in vitro apoptotic cell death.
  • Further studies are required to evaluate the in vitro effects of 4-HPR in AML blasts derived from AML patients.

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  • (PMID = 23407328.001).
  • [ISSN] 2008-2835
  • [Journal-full-title] Avicenna journal of medical biotechnology
  • [ISO-abbreviation] Avicenna J Med Biotechnol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Iran
  • [Other-IDs] NLM/ PMC3558144
  • [Keywords] NOTNLM ; 4-HPR / Acute myelocytic leukemia / Apoptosis / Cell differentiation / Flow cytometry
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22. Tadmor T, Vadazs Z, Dar H, Laor R, Attias D: Hemophagocytic syndrome preceding acute myeloid leukemia with der t [7:17][q12; q11], monosomy, 17 and 5p-. J Pediatr Hematol Oncol; 2006 Aug;28(8):544-6
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  • We report a case of a child presented with HS, who progressed later to acute myeloid leukemia (AML)-M4, associated with a clonal evolution, from normal to a complex karyotype consisting of t [7:17] and deletions in chromosomes 7, 17, and 5.
  • This is the second report of involvement of 7q rearrangement in a child with HS that has progressed to AML.
  • Additional studies are required to establish the association reported here, between HS with progression to AML and chromosome rearrangements that involve chromosome 7q.

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  • (PMID = 16912598.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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23. Invernizzi R, Travaglino E, Benatti C, Malcovati L, Della Porta M, Cazzola M, Ascari E: Survivin expression, apoptosis and proliferation in chronic myelomonocytic leukemia. Eur J Haematol; 2006 Jun;76(6):494-501
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  • Thirty-four patients with CMML [18 MDS-CMML and 16 myeloproliferative disorder (MPD)-CMML], 90 with MDS, 41 with acute myeloid leukemia (AML), 19 with chronic MPD and 25 control subjects were studied.
  • In CMML survivin levels higher than in MDS and AML (P < 0.0001), but similar to those found in MPD were observed.
  • Proliferation did not differ significantly in normal controls, MDS and CMML; the lowest levels were observed in AML and MPD (P < 0.0001).
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis. Cell Division. Disease Progression. Female. Humans. Inhibitor of Apoptosis Proteins. Leukemia, Myeloid / classification. Leukemia, Myeloid / metabolism. Leukemia, Myeloid / pathology. Male. Middle Aged. Myelodysplastic Syndromes / metabolism. Myelodysplastic Syndromes / pathology

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  • (PMID = 16529600.001).
  • [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 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
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24. Park MJ, Park YH, Ahn HJ, Choi W, Paik KH, Kim JM, Chang YH, Ryoo BY, Yang SH: Secondary hematological malignancies after breast cancer chemotherapy. Leuk Lymphoma; 2005 Aug;46(8):1183-8
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  • According to several reports, the 10 year incidence of secondary acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS) after systemic chemotherapy is approximately 1.5%.
  • We detected 2 cases of secondary AML and 1 case of MDS, 19, 52 and 12 months, respectively, after systemic chemotherapy for breast cancer.
  • Published data on the occurrence of secondary hematological malignancies other than AML or MDS in this setting are scarce.
  • [MeSH-minor] Disease Progression. Dose-Response Relationship, Drug. Fatal Outcome. Female. Follow-Up Studies. Humans. Middle Aged. Treatment Outcome


25. Cheuk AT, Chan L, Czepulkowski B, Berger SA, Yagita H, Okumura K, Farzaneh F, Mufti GJ, Guinn BA: Development of a whole cell vaccine for acute myeloid leukaemia. Cancer Immunol Immunother; 2006 Jan;55(1):68-75
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  • We have been involved in the genetic modification of tumour cells to prepare a whole cell vaccine for nearly a decade and we have a particular interest in acute myeloid leukaemia (AML).
  • AML is an aggressive and difficult to treat disease, especially, for patients for whom haematopoietic stem cell (HSC) transplant is not an option.
  • AML patients who have a suitable donor and meet HSC transplant fitness requirements, have a 5-year survival of 50%; however, for patients with no suitable donor or for who age is a factor, the prognosis is much worse.
  • It would be hoped that immunotherapy would be used to clear residual tumour cells in these patients in the first remission following standard chemotherapy treatments and this will extend the remission and reduce the risk of a second relapse associated with disease progression and poor mortality rates.
  • In this symposia report, we will focus on whole cell vaccines as an immunotherapeutic option with particular reference to their use in the treatment of AML.
  • We will aim to provide a brief overview of the latest data from our group and considerations for the use of this treatment modality in clinical trials for AML.

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  • (PMID = 15891884.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 4-1BB Ligand; 0 / Cancer Vaccines; 0 / TNFSF9 protein, human; 0 / Tnfsf9 protein, mouse; 0 / Tumor Necrosis Factors
  • [Number-of-references] 65
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26. 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.
  • During follow-up, patients with the mutation were more likely to transform into PV but the incidences of AML, MMM, or thrombotic events were similar between patients with and without the mutation.
  • [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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27. Zhou Q, Bucher C, Munger ME, Highfill SL, Tolar J, Munn DH, Levine BL, Riddle M, June CH, Vallera DA, Weigel BJ, Blazar BR: Depletion of endogenous tumor-associated regulatory T cells improves the efficacy of adoptive cytotoxic T-cell immunotherapy in murine acute myeloid leukemia. Blood; 2009 Oct 29;114(18):3793-802
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  • To elucidate host factors contributing to the poor response of adoptively transferred tumor-reactive cytotoxic T lymphocytes (CTLs), we used a systemic model of murine acute myeloid leukemia (AML).
  • AML progression resulted in a progressive regulatory T-cell (Treg) accumulation in disease sites.
  • The adoptive transfer of in vitro-generated, potently lytic anti-AML-reactive CTLs failed to reduce disease burden or extend survival.
  • Compared with non-AML-bearing hosts, transferred CTLs had reduced proliferation in AML sites of metastases.
  • Treg depletion by a brief course of interleukin-2 diphtheria toxin (IL-2DT) transiently reduced AML disease burden but did not permit long-term survival.
  • In contrast, IL-2DT prevented anti-AML CTL hypoproliferation, increased the number of transferred CTLs at AML disease sites, reduced AML tumor burden, and resulted in long-term survivors that sustained an anti-AML memory response.
  • These data demonstrated that Tregs present at AML disease sites suppress adoptively transferred CTL proliferation, limiting their in vivo expansion, and Treg depletion before CTL transfer can result in therapeutic efficacy in settings of substantial pre-existing tumor burden in which antitumor reactive CTL infusion alone has proven ineffective.

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  • (PMID = 19724059.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120409-03; United States / NCI NIH HHS / CA / CA120409-03; United States / NCI NIH HHS / CA / R01 CA120409; United States / NCI NIH HHS / CA / R01 CA72669; United States / NHLBI NIH HHS / HL / R01 HL056067; United States / NCI NIH HHS / CA / R01 CA072669
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins; 0 / interleukin 2-diphtheria toxin
  • [Other-IDs] NLM/ PMC2773484
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28. Shih LY, Liang DC, Huang CF, Wu JH, Lin TL, Wang PN, Dunn P, Kuo MC, Tang TC: AML patients with CEBPalpha mutations mostly retain identical mutant patterns but frequently change in allelic distribution at relapse: a comparative analysis on paired diagnosis and relapse samples. Leukemia; 2006 Apr;20(4):604-9
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  • [Title] AML patients with CEBPalpha mutations mostly retain identical mutant patterns but frequently change in allelic distribution at relapse: a comparative analysis on paired diagnosis and relapse samples.
  • The roles of CEBPalpha mutations and its cooperating mutations in the relapse of acute myeloid leukemia (AML) are not clear.
  • CEBPalpha mutations were analyzed on 149 patients with de novo AML at both diagnosis and relapse.
  • Our study showed that 91% of de novo AML harboring CEBPalpha mutations at diagnosis retained the identical mutant patterns but frequently changed in the allelic distribution at relapse.
  • [MeSH-minor] Adolescent. Adult. Aged. Alleles. Bone Marrow / pathology. Child. Child, Preschool. DNA Mutational Analysis. Disease Progression. Female. Genes, ras / genetics. Humans. Infant. Male. Middle Aged. Recurrence. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16453003.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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29. Duell T, Poleck-Dehlin B, Schmid C, Wunderlich B, Ledderose G, Mittermuller J, Kolb HJ, Schmetzer H: Clonal karyotype evolution involving ring chromosome 1 with myelodysplastic syndrome subtype RAEB-t progressing into acute leukemia. Acta Haematol; 2006;116(2):131-6
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  • Karyotypic evolution is a well-known phenomenon in patients with malignant hematological disorders during disease progression.
  • One month later, the patient progressed to an acute myeloid leukemia (AML), subtype M4 with 40% BM blasts and cytogenetic examination showed clonal evolution by the appearance of additional numerical aberrations in addition to the ring chromosome [46,XY,r(1),+8,-21/45,XY,r(1),+8,-21,-22/46, XY].
  • This is an interesting case of a patient with AML secondary to MDS.
  • This case confirms the value of cytogenetic analysis in characterizing the malignant clone in hematological neoplasias, the importance of controlling the quality of an induced remission and of the detection of a progress of the disease.
  • [MeSH-minor] Acute Disease. Chromosome Banding. Diagnosis, Differential. Disease Progression. Humans. Immunophenotyping. Karyotyping. Male. Middle Aged


30. 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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31. Alyea EP, Kim HT, Ho V, Cutler C, DeAngelo DJ, Stone R, Ritz J, Antin JH, Soiffer RJ: Impact of conditioning regimen intensity on outcome of allogeneic hematopoietic cell transplantation for advanced acute myelogenous leukemia and myelodysplastic syndrome. Biol Blood Marrow Transplant; 2006 Oct;12(10):1047-55
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  • We reviewed 136 patients with advanced acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS) undergoing allogeneic transplantation to assess the impact of conditioning regimen intensity on outcome.
  • Progression-free survival (PFS) at 2 years was 20% for NST and 31% for myeloablative transplantation (P = .31).
  • Despite the high-risk features of patients with advanced AML or MDS undergoing NST, OS and PFS in these patients was similar to those in patients receiving myeloablative transplantation.
  • These results suggest that NST is a reasonable alternative for patients with advanced AML and MDS at high risk for complications after myeloablative transplantation.


32. Eddy JA, Sung J, Geman D, Price ND: Relative expression analysis for molecular cancer diagnosis and prognosis. Technol Cancer Res Treat; 2010 Apr;9(2):149-59
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  • Such tools can enhance our understanding of human health and genetic diseases, such as cancer, by accurately classifying phenotypes, detecting the presence of disease, discriminating among cancer sub-types, predicting clinical outcomes, and characterizing disease progression.
  • We review several studies which demonstrate accurate classification of disease phenotypes (e.g., cancer vs. normal), cancer subclasses (e.g., AML vs. ALL, GIST vs. LMS), disease outcomes (e.g., metastasis, survival), and diverse human pathologies assayed through blood-borne leukocytes.

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  • (PMID = 20218737.001).
  • [ISSN] 1533-0338
  • [Journal-full-title] Technology in cancer research & treatment
  • [ISO-abbreviation] Technol. Cancer Res. Treat.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / UL1 RR025005; United States / NCRR NIH HHS / RR / UL1 RR 025005; United States / NCI NIH HHS / CA / P50 CA83636; United States / NCI NIH HHS / CA / R00 CA126184; United States / NCI NIH HHS / CA / P50 CA083636; United States / NCI NIH HHS / CA / R00 CA126184-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Number-of-references] 37
  • [Other-IDs] NLM/ NIHMS226808; NLM/ PMC2921829
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33. Lorenzo F, Nishii K, Monma F, Kuwagata S, Usui E, Shiku H: Mutational analysis of the KIT gene in myelodysplastic syndrome (MDS) and MDS-derived leukemia. Leuk Res; 2006 Oct;30(10):1235-9
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  • In this study, the role of mutation of the KIT gene in the extracellular membrane, juxtamembrane and tyrosine kinase domains was investigated in 75 patients with MDS or MDS-derived leukemia (MDS-AML).
  • Mutation was detected in 2 of 15 (13.3%) patients with refractory anemia with excess blasts transformation (RAEB-T), in 1 of 15 (6.6%) patients with chronic myelomonocytic leukemia (CMML), and in 5 of 26 (19.2%) patients with MDS-AML.
  • These observations suggest that KIT gene mutations identified in the advanced stage of MDS, and genetic abnormality in the KIT gene, particularly at codon 816, might be additional events that contribute to the progression of MDS to AML.
  • [MeSH-minor] Adult. Aged. Anemia, Refractory, with Excess of Blasts / genetics. Codon / genetics. DNA Mutational Analysis. Disease Progression. Female. Humans. Japan. Karyotyping. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction


34. Ishikawa Y, Xu J, Sakashita G, Urano T, Suzuki T, Tomita A, Kiyoi H, Nakamura S, Naoe T: Abnormal cytoplasmic dyslocalisation and/or reduction of nucleophosmin protein level rarely occurs in myelodysplastic syndromes. Leuk Lymphoma; 2008 Dec;49(12):2359-64
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  • The Nucleophosmin1 (NPM1) gene located in chromosome 5q35 is affected by chromosomal translocation, mutation and deletion in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML).
  • The NPM1 expression levels of mRNA and protein were not related to chromosome 5 abnormalities and were almost the same as those in normal BM and AML cells.
  • However, the protein levels in AML cells with NPM1 mutations were slightly lower than in those without mutation.
  • The increase in the number of nuclear NPM1-positive cells may be related to the progression of MDS.
  • [MeSH-minor] Chromosome Aberrations. Disease Progression. Humans. Mutation. RNA, Messenger / analysis


35. Hou HA, Huang TC, Lin LI, Liu CY, Chen CY, Chou WC, Tang JL, Tseng MH, Huang CF, Chiang YC, Lee FY, Liu MC, Yao M, Huang SY, Ko BS, Hsu SC, Wu SJ, Tsay W, Chen YC, Tien HF: WT1 mutation in 470 adult patients with acute myeloid leukemia: stability during disease evolution and implication of its incorporation into a survival scoring system. Blood; 2010 Jun 24;115(25):5222-31
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  • The impact of WT1 mutations in acute myeloid leukemia (AML) is not completely settled.
  • We aimed to determine the clinical implication of WT1 mutation in 470 de novo non-M3 AML patients and its stability during the clinical course.
  • WT1 mutations were identified in 6.8% of total patients and 8.3% of younger patients with normal karyotype (CN-AML).
  • Multivariate analysis demonstrated that the WT1 mutation was an independent poor prognostic factor for overall survival and relapse-free survival among total patients and the CN-AML group.
  • A scoring system incorporating WT1 mutation, NPM1/FLT3-ITD, CEBPA mutations, and age into survival analysis proved to be very useful to stratify CN-AML patients into different prognostic groups (P < .001).
  • In conclusion, WT1 mutations are correlated with poor prognosis in AML patients.
  • The mutation status may be changed in some patients during AML progression.


36. Panteli KE, Hatzimichael EC, Bouranta PK, Katsaraki A, Seferiadis K, Stebbing J, Bourantas KL: Serum interleukin (IL)-1, IL-2, sIL-2Ra, IL-6 and thrombopoietin levels in patients with chronic myeloproliferative diseases. Br J Haematol; 2005 Sep;130(5):709-15
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  • IL-2, sIL-2Ra and IL-6 levels were raised during the transformation phase of CML, during progression of MMM to AML, and ET and PV to myelofibrosis (P < 0.001).

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  • (PMID = 16115126.001).
  • [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 / Antigens, CD34; 0 / Biomarkers; 0 / Cytokines; 0 / Interleukin-1; 0 / Interleukin-2; 0 / Interleukin-6; 0 / Receptors, Interleukin-2; 9014-42-0 / Thrombopoietin
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37. Andreeva SV, Drozdova VD, Ponochevnaia EV, Kavardakova NV: [Rearrangements of chromosome 9 in different hematological neoplasia]. Tsitol Genet; 2008 Sep-Oct;42(5):72-9
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  • The frequencies of chromosome 9 abnormalities in children with hematological neoplasia have constituted: 25/112 in acute lymphoblastic leukemia (ALL), 10/83--in acute myeloid leukemia (AML), 3/20--in refractory anemia (RA).
  • In AML the translocations were detected with greater frequency than deletions.
  • Multidrug resistance and disease progression during chemotherapy were noted in t (9;22).


38. Kitawaki T, Kadowaki N, Kondo T, Ishikawa T, Ichinohe T, Teramukai S, Fukushima M, Kasai Y, Maekawa T, Uchiyama T: Potential of dendritic-cell immunotherapy for relapse after allogeneic hematopoietic stem cell transplantation, shown by WT1 peptide- and keyhole-limpet-hemocyanin-pulsed, donor-derived dendritic-cell vaccine for acute myeloid leukemia. Am J Hematol; 2008 Apr;83(4):315-7
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  • A 58-year-old woman received Wilms' tumor 1 (WT1) peptide- and keyhole limpet hemocyanin (KLH)-pulsed, donor-derived dendritic cell (DC) vaccination for AML relapse after allogeneic stem cell transplantation.
  • [MeSH-minor] Adjuvants, Immunologic. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Disease Progression. Female. Hematopoietic Stem Cell Transplantation. Humans. Immunosuppressive Agents / therapeutic use. Living Donors. Middle Aged. Phosphoproteins / immunology. Siblings. Transplantation, Homologous. Viral Matrix Proteins / immunology

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 18081032.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Cancer Vaccines; 0 / Immunosuppressive Agents; 0 / Peptide Fragments; 0 / Phosphoproteins; 0 / Viral Matrix Proteins; 0 / WT1 Proteins; 0 / cytomegalovirus matrix protein 65kDa; 04079A1RDZ / Cytarabine; 9013-72-3 / Hemocyanin; FV4Y0JO2CX / keyhole-limpet hemocyanin; ZS7284E0ZP / Daunorubicin
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39. Fiume R, Teti G, Faenza I, Cocco L: Phosphoinositide-specific phospholipase C beta1 signal transduction in the nucleus. Methods Mol Biol; 2010;645:143-64
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  • We now know that nuclear PLCbeta1 is a key player in the control of cell cycle progression; in fact it appears to be involved in the cyclin-mediated regulation of the physiological machinery.
  • Indeed, the recent discovery of a possible involvement of the interstitial deletion of PLCbeta1 gene in the progression of myelodysplastic syndrome (MDS) to acute myeloid leukemia in humans (AML) strengthens this contention.

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  • (PMID = 20645187.001).
  • [ISSN] 1940-6029
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 4L6452S749 / Inositol; EC 3.1.4.11 / Phospholipase C beta
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40. 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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  • 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.
  • The AML blast cells in these elderly patients are often characterised by several unfavourable covariates that predict the poor treatment outcome, including high stem cell marker CD34 expression, minimally or undifferentiated features, high P-glycoprotein expression, high bcl-2/bax ratio, unfavourable karyotype and more frequent internal tandem duplications (ITDs) and mutations of class III receptor-type tyrosine kinase for key haematopoietic cytokines: Flt-3 (receptor for Flt-ligand), c-kit (receptor for stem cell factor) and fms (receptor for M-CSF).
  • Testing the new and more specific molecular-targeted therapeutic approaches in CD34+ AML cells can provide the basis for a more effective combined molecular/chemotherapy regimen and may consequently improve the treatment outcome in elderly AML patients.
  • Therefore, the present study was performed to evaluate whether stem cell factor-antibody (anti-SCF) can enhance the efficacy of the two main chemotherapeutic drugs used in AML therapy: cytarabine and daunorubicin at low doses in human-resistant CD34+ AML cells, in an attempt to identify a novel effective regimen with tolerable side-effects for elderly AML patients.
  • The effect of anti-SCF on each of the two chemotherapeutic drugs-induced apoptosis and necrosis was investigated in KG1a human-resistant CD34+ AML cells expressing P-glycoprotein to determine its enhancing activity.
  • Anti-SCF has significantly enhanced the low dose cytarabine- and daunorubicin-induced apoptosis+necrosis in KG1a CD34+ AML cells from 12.0+/-1.7 to 40.9+/-5.9% and from 16.3+/-0.9 to 48.9+/-1.0%, respectively, p<0.01.
  • It has also exerted its significant enhancement activity on the low dose cytarabine- and daunorubicin-induced apoptosis+necrosis in KG1a CD34+ AML cells in the presence of SCF, p<0.05.
  • Anti-SCF has significantly enhanced the low dose cytarabine- and daunorubicin-induced bcl-2 reduction in KG1a CD34+ AML cells from 26.7+/-0.6 to 64.6+/-1.0% and from 59.8+/-3.1 to 80.1+/-7.9%, respectively, p<0.01.
  • The addition of SCF has not altered the low dose cytarabine- and daunorubicin-induced bcl-2 reduction in KG1a CD34+ AML cells (Table 4).
  • Anti-SCF has also significantly enhanced the low dose cytarabine- and daunorubicin-induced bcl-2 reduction in KG1a CD34+ AML cells in the presence of SCF, p<0.05.
  • The unique potent enhancing activity of anti-SCF on low dose chemotherapy-induced apoptosis and necrosis in extremely resistant AML cells suggest a novel promising role for the treatment of elderly AML patients.
  • Further studies are warranted to evaluate a similar enhancing effect for anti-SCF in blast cells from elderly AML patients in primary cultures before its introduction in a pilot clinical study.
  • In conclusion, the combination of anti-SCF and the low dose cytarabine provides a promising solution for the dilemma of therapy in elderly AML patients.

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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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41. Zatkova A, Merk S, Wendehack M, Bilban M, Muzik EM, Muradyan A, Haferlach C, Haferlach T, Wimmer K, Fonatsch C, Ullmann R: AML/MDS with 11q/MLL amplification show characteristic gene expression signature and interplay of DNA copy number changes. Genes Chromosomes Cancer; 2009 Jun;48(6):510-20
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  • [Title] AML/MDS with 11q/MLL amplification show characteristic gene expression signature and interplay of DNA copy number changes.
  • AML/MDS patients carrying 11q amplifications involving the mixed lineage leukemia gene (MLL) locus are characterized by a complex aberrant karyotype (CAK) frequently including deletions within 5q, 17p, and 7q, older age and fast progression of the disease with extremely poor prognosis.
  • In this study, we investigated 19 patients with AML/MDS and MLL gain/amplification.
  • Furthermore, we demonstrate that the gene expression signature can be used to discriminate AML/MDS with MLL amplification from several other types of AML.


42. Saha MN, Micallef J, Qiu L, Chang H: Pharmacological activation of the p53 pathway in haematological malignancies. J Clin Pathol; 2010 Mar;63(3):204-9
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  • p53 gene mutations are rarely detected at diagnosis in common haematological cancers such as multiple myeloma (MM), acute myeloid leukaemia (AML), chronic lymphocytic leukaemia (CLL) and Hodgkin's disease (HD), although their prevalence may increase with progression to more aggressive or advanced stages.

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  • (PMID = 19955555.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Furans; 0 / Imidazoles; 0 / NSC 652287; 0 / Piperazines; 0 / Tumor Suppressor Protein p53; 0 / nutlin 3; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Number-of-references] 85
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43. Mahadevan D, DiMento J, Croce KD, Riley C, George B, Fuchs D, Mathews T, Wilson C, Lobell M: Transcriptosome and serum cytokine profiling of an atypical case of myelodysplastic syndrome with progression to acute myelogenous leukemia. Am J Hematol; 2006 Oct;81(10):779-86
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  • [Title] Transcriptosome and serum cytokine profiling of an atypical case of myelodysplastic syndrome with progression to acute myelogenous leukemia.
  • The patient ultimately progressed to acute myelogenous leukemia (AML, FAB M2) and had a normal karyotype throughout her course.
  • Transformation to AML was characterized by a BM blast percentage of 49%.
  • [MeSH-minor] Aged. Biomarkers, Tumor / blood. Disease Progression. Enzyme-Linked Immunosorbent Assay / methods. Fatal Outcome. Female. Hepatocyte Growth Factor / blood. Humans. Insulin-Like Growth Factor Binding Protein 1 / blood. Oligonucleotide Array Sequence Analysis / methods. Reverse Transcriptase Polymerase Chain Reaction / methods


44. Gyurkocza B, Storb R, Storer BE, Chauncey TR, Lange T, Shizuru JA, Langston AA, Pulsipher MA, Bredeson CN, Maziarz RT, Bruno B, Petersen FB, Maris MB, Agura E, Yeager A, Bethge W, Sahebi F, Appelbaum FR, Maloney DG, Sandmaier BM: Nonmyeloablative allogeneic hematopoietic cell transplantation in patients with acute myeloid leukemia. J Clin Oncol; 2010 Jun 10;28(17):2859-67
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  • PURPOSE: Allogeneic hematopoietic cell transplantation (HCT) after high-dose conditioning regimens imposes prohibitively high risks of morbidity and mortality for patients with high-risk acute myeloid leukemia (AML) who are older or have comorbid conditions.
  • PATIENTS AND METHODS: Two hundred seventy-four patients (median age, 60 years) with de novo or secondary AML underwent allogeneic HCT from related (n = 118) or unrelated donors (n = 156) after conditioning with 2 Gy of total-body irradiation (TBI) with or without fludarabine.
  • The estimated 5-year relapse/progression and nonrelapse mortality rates were 42% and 26%, respectively.
  • CONCLUSION: Allogeneic HCT from related or unrelated donors after conditioning with low-dose TBI and fludarabine, relying almost exclusively on graft-versus-leukemia effects, can result in long-term remissions in older or medically infirm patients with AML.

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  • (PMID = 20439626.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA18029; United States / NHLBI NIH HHS / HL / HL36444; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / P30 CA015704; United States / NCI NIH HHS / CA / CA78902; United States / NCI NIH HHS / CA / R21 CA106177; United States / NCI NIH HHS / CA / CA15704; United States / NHLBI NIH HHS / HL / P01 HL036444; United States / NCI NIH HHS / CA / CA106177; United States / NCI NIH HHS / CA / P01 CA078902
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2903320
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45. Martelli AM, Nyåkern M, Tabellini G, Bortul R, Tazzari PL, Evangelisti C, Cocco L: Phosphoinositide 3-kinase/Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia. Leukemia; 2006 Jun;20(6):911-28
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  • The phosphoinositide 3-kinase (PI3K)/Akt signaling pathway is crucial to many aspects of cell growth, survival and apoptosis, and its constitutive activation has been implicated in the both the pathogenesis and the progression of a wide variety of neoplasias.
  • Recent studies showed that PI3K/Akt signaling is frequently activated in acute myeloid leukemia (AML) patient blasts and strongly contributes to proliferation, survival and drug resistance of these cells.
  • Upregulation of the PI3K/Akt network in AML may be due to several reasons, including FLT3, Ras or c-Kit mutations.
  • Small molecules designed to selectively target key components of this signal transduction cascade induce apoptosis and/or markedly increase conventional drug sensitivity of AML blasts in vitro.
  • In this review, we summarize the existing knowledge about PI3K/Akt signaling in AML cells and we examine the rationale for targeting this fundamental signal transduction network by means of selective pharmacological inhibitors.

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  • (PMID = 16642045.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Number-of-references] 250
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46. Sharma Poudel B, Karki L: Abnormal hepatic function and splenomegaly on the newly diagnosed acute leukemia patients. JNMA J Nepal Med Assoc; 2007 Oct-Dec;46(168):165-9
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  • The related factors such as peripheral WBC count, bone marrow blasts, peripheral blasts, sex, age, AML, ALL affecting the liver function and splenomegaly were evaluated.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Alanine Transaminase / blood. Aspartate Aminotransferases / blood. Biopsy. Diagnosis, Differential. Disease Progression. Female. Follow-Up Studies. Humans. Leukocyte Count. Male. Middle Aged. Prothrombin Time. Retrospective Studies. Severity of Illness Index. Tomography, X-Ray Computed

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  • (PMID = 18340367.001).
  • [ISSN] 0028-2715
  • [Journal-full-title] JNMA; journal of the Nepal Medical Association
  • [ISO-abbreviation] JNMA J Nepal Med Assoc
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Nepal
  • [Chemical-registry-number] EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase
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47. Chen BG, Zhu M, Luo WD, Yan WH, Zhou MY, Li BL, Tao DD: [The correlation study of PTEN gene expression and Akt phosphorylation in myelodysplastic syndrome]. Zhonghua Xue Ye Xue Za Zhi; 2007 Jul;28(7):470-3
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  • OBJECTIVE: To investigate the relationship between PTEN gene expression and Akt phosphorylation (p-Akt) in myelodysplastic syndrome (MDS) and to explore the progression of MDS and the mechanism of high risk transformation to acute myeloid leukemia.
  • METHODS: RT-PCR was used to detect the PTEN mRNA expression in leukemia cell lines K562 (as negative control) and Jurkat (as positive control) and 65 MDS and MDS/AML patients.
  • Of 65 MDS and MDS/AML patients, 27 (41.5%) expressed PTEN mRNA, being significantly lower than that in normal group (85.7%) (P < 0.01). (2) Jurkat cell showed high expression (86.9%) of p-Akt, while HL-60 cell as negative control did not express.
  • CONCLUSION: The loss of PTEN gene expression is one of the important factors of p-Akt high expression in MDS patients, moreover, it may speed up the progress of the MDS or transformation to acute myeloid leukemia.


48. Pedersen-Bjergaard J, Andersen MK, Andersen MT, Christiansen DH: Genetics of therapy-related myelodysplasia and acute myeloid leukemia. Leukemia; 2008 Feb;22(2):240-8
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  • Myelodysplasia (MDS) and acute myeloid leukemia (AML) are heterogeneous, closely associated diseases arising de novo or following chemotherapy with alkylating agents, topoisomerase II inhibitors, or after radiotherapy.
  • Whereas de novo MDS and AML are almost always subclassified according to cytogenetic characteristics, therapy-related MDS (t-MDS) and therapy-related AML (t-AML) are often considered as separate entities and are not subdivided.
  • Alternative genetic pathways were previously proposed in t-MDS and t-AML based on cytogenetic characteristics.
  • An increasing number of gene mutations are now observed to cluster differently in these pathways with an identical pattern in de novo and in t-MDS and t-AML.
  • Point mutations of AML1 and RAS seem to cooperate and predispose to progression from t-MDS to t-AML.
  • Their association and cooperation with point mutations of p53 and AML1, respectively, extend the scenario of cooperating genetic abnormalities in MDS and AML.
  • As de novo and t-MDS and t-AML are biologically identical diseases, they ought to be subclassified and treated similarly.


49. Yamagami T, Porada CD, Pardini RS, Zanjani ED, Almeida-Porada G: Docosahexaenoic acid induces dose dependent cell death in an early undifferentiated subtype of acute myeloid leukemia cell line. Cancer Biol Ther; 2009 Feb;8(4):331-7
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  • Acute myeloid leukemia (AML) is the most frequently diagnosed adulthood leukemia, yet current therapies offer a cure rate of less than 30%.
  • This may be due in part to the fact that the leukemia-initiating cells in AML reside within the rare and highly primitive CD34(+)CD38(-) hematopoietic stem/progenitor cell (HSC) population that are often resistant to chemotherapy.
  • Docosahexanoic acid (DHA), a major component of fish oil, has previously been shown to inhibit the induction and progression of breast, prostate and colon cancer, and increase the therapeutic effects of numerous chemotherapeutics, often by enhancing apoptosis.
  • In the present studies, we investigated DHA's effect on the primitive and undifferentiated AML cell line KG1a, to explore the potential of this fatty acid to serve as adjuvant therapy for AML.
  • Since we also show that DHA does not have a detrimental effect on normal hematopoiesis our results suggest that DHA could potentially serve as an well-tolerated adjuvant in the treatment of AML patients.

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  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL070566; United States / NHLBI NIH HHS / HL / HL70566; United States / NHLBI NIH HHS / HL / R01 HL073737; United States / NHLBI NIH HHS / HL / HL052955-14A1; United States / NHLBI NIH HHS / HL / R01 HL052955; United States / NHLBI NIH HHS / HL / R01 HL052955-14A1; United States / NHLBI NIH HHS / HL / HL73737
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / bcl-2-Associated X Protein; 25167-62-8 / Docosahexaenoic Acids; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ NIHMS122907; NLM/ PMC3954154
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50. Moore MA: Converging pathways in leukemogenesis and stem cell self-renewal. Exp Hematol; 2005 Jul;33(7):719-37
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  • Furthermore, the progression from chronic leukemia or myelodysplasia to acute leukemia involves accumulation of at least two mutational events that lead to enhancement of stem cell proliferation, or acquisition of stem cell behavior by a progenitor cell, coupled with maturation inhibition.
  • Translocations resulting in development of oncogenic fusion genes are found in AML and the transforming potential of two of these, AML1-ETO and NUP98-HOXA9, will be discussed.
  • Secondary, constitutively activating mutations of the Flt3 and c-kit receptors and of K- and N-ras are found with high frequency in AML, and the transforming potential of mutated FLT3 and the role of STAT5A activation in human stem cell transformation will be reviewed.

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  • (PMID = 15963848.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytokines
  • [Number-of-references] 214
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51. Bacher U, Haferlach T, Kern W, Haferlach C, Schnittger S: A comparative study of molecular mutations in 381 patients with myelodysplastic syndrome and in 4130 patients with acute myeloid leukemia. Haematologica; 2007 Jun;92(6):744-52
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  • BACKGROUND AND OBJECTIVES: The precise relationship between myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) is unclear and the role of molecular mutations in leukemic transformation in MDS is controversial.
  • The aim of this study was to clarify the relationship between AML and MDS by comparing the frequency of molecular mutations in the two conditions.
  • DESIGN AND METHODS: We compared the frequency of FLT3-length mutations (FLT3-LM), FLT3-TKD, MLL-partial tandem duplications (MLL-PTD), NRAS, and KITD816 in 381 patients with MDS refractory anemia with excess blasts [RAEB] n=49; with ringed sideroblasts [RARS] n=310; chronic monomyelocytic leukemia [CMML] n=22) and in 4130 patients with AML (de novo: n=3139; secondary AML [s-AML] following MDS: n=397; therapy-related [t-AML]: n=233; relapsed: n=361).
  • RESULTS: All mutations were more frequent in s-AML than in MDS and all but the FLT3-TKD were more frequent in RAEB than in RA/RARS.
  • The higher incidences in s-AML were significant for FLT3-TKD (p=0.032), MLL-PTD (p=0.034), and FLT3-LM (RA/RARS: 0/45; RAEB: 8/293; 2.7%; s-AML: 45/389; 11.6%; p<0.0001).
  • The incidence of NRAS-mutations increased from 17/272 (6.3%) in MDS to 41/343 in s-AML (12.0%) and that of KITD816-mutations from 2/290 (0.7%) to 5/341 (1.5%) (p=n.s.).
  • FLT3-LM and MLL-PTD were more frequent in AML relapse than in de novo AML or s-AML (p<0.0001).
  • INTERPRETATION AND CONCLUSIONS: The increase of molecular mutations from low- to high-risk MDS, to s-AML, and to relapsed AML emphasizes the value of these mutations as markers of progressing disease.
  • [MeSH-minor] Acute Disease. Disease Progression. Gene Frequency. Histone-Lysine N-Methyltransferase. Humans. Molecular Epidemiology. Myeloid-Lymphoid Leukemia Protein / genetics. Proto-Oncogene Proteins c-kit / genetics. fms-Like Tyrosine Kinase 3 / genetics. ras Proteins / genetics


52. Meshinchi S, Alonzo TA, Stirewalt DL, Zwaan M, Zimmerman M, Reinhardt D, Kaspers GJ, Heerema NA, Gerbing R, Lange BJ, Radich JP: Clinical implications of FLT3 mutations in pediatric AML. Blood; 2006 Dec 1;108(12):3654-61
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  • [Title] Clinical implications of FLT3 mutations in pediatric AML.
  • FLT3 mutation status of 630 children with de novo acute myeloid leukemia (AML) treated on CCG-2941 and -2961 was determined, and ITD-AR was calculated for patients with FLT3/ITD.
  • Progression-free survival (PFS) was similar in patients with FLT3/ALM and FLT3/WT (51% versus 55%, P = .862).
  • ITD-AR defines the prognostic significance in FLT3/ITD-positive AML, and ITD-AR greater than 0.4 is a significant and independent prognostic factor for relapse in pediatric AML.

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  • (PMID = 16912228.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K23 CA092405; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / R01 CA114563-01; United States / NCI NIH HHS / CA / R21 CA10262-01
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC1895470
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53. 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.
  • METHODS: Twenty-nine patients who had been diagnosed of MDS/AML and had undergone chemotherapy between April 2001 and March 2008 were retrospectively analyzed.
  • Twenty-four patients were administered a low-dose AraC containing regimen and 5 received an AML-like regimen as the initial chemotherapy.
  • CONCLUSION: In MDS/AML, patients with a normal karyotype tended to have a better response to chemotherapy.


54. Wihlidal P, Varga F, Pfeilstöcker M, Karlic H: Expression and functional significance of osteocalcin splicing in disease progression of hematological malignancies. Leuk Res; 2006 Oct;30(10):1241-8
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  • [Title] Expression and functional significance of osteocalcin splicing in disease progression of hematological malignancies.
  • We analysed bone marrow obtained from two patients with chronic myeloid leukemia (CML), seven patients with other myeloproliferative diseases (MPD) and four patients with acute myeloid leukemia (AML).
  • [MeSH-minor] Bone Marrow Cells / pathology. DNA Primers. Disease Progression. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Myeloproliferative Disorders / genetics. Protein Biosynthesis. Proto-Oncogene Proteins c-kit / genetics. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Stem Cells / pathology. Transcription, Genetic

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  • (PMID = 16387359.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 104982-03-8 / Osteocalcin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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55. Huang Y, Li WJ, Wei CX, Zhou Z, Nie B: [Expression of HoxA10 in acute leukemia and its significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Dec;13(6):959-63
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  • HoxA(10) gene appeared to be more strongly expressed in AML-M(1) and -M(2) subtypes than in AML-M(4) and -M(5) subtypes, and the gene was notable high expressed in acute promyelocytic leukemia.
  • The level of HoxA(10) is related with load of leukemic cells and curative effect, and can affect occurrence and development of leukemia in combination with many cytokines, HoxA(10) may facilitate the leukemia progression with another cofactors.

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  • (PMID = 16403259.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Homeodomain Proteins; 0 / RNA, Messenger; 140441-81-2 / HOXA10 protein, human
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56. Licht JD, Sternberg DW: The molecular pathology of acute myeloid leukemia. Hematology Am Soc Hematol Educ Program; 2005;:137-42
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  • The pathogenesis of acute myelogenous leukemia (AML) involves an array of molecular alterations that disrupt almost every facet of cell transformation.
  • This overview describes some of the critical molecular alterations and implicates the rogue leukemogenic proteins in the onset and progression of AML.

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  • (PMID = 16304371.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA82261; United States / NCI NIH HHS / CA / R01 CA59936
  • [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 / Neoplasm Proteins; 0 / Transcription Factors
  • [Number-of-references] 40
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57. Plass C, Oakes C, Blum W, Marcucci G: Epigenetics in acute myeloid leukemia. Semin Oncol; 2008 Aug;35(4):378-87
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  • Acute myeloid leukemia (AML) is a disease characterized by uncontrolled proliferation of clonal neoplastic hematopoietic precursor cells.
  • Major breakthroughs in the past have contributed to our understanding of the genetic failures and the changed biology in AML cells that underlie the initiation and progression of the disease.
  • In this review, we will discuss our current understanding of normal epigenetic processes, outline our knowledge of epigenetic alterations in AML, and discuss how this information is being used to improve current therapy of this disease.

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  • (PMID = 18692688.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 93548; United States / NCI NIH HHS / CA / R01 CA102031; United States / NCI NIH HHS / CA / P01 CA101956; United States / NCI NIH HHS / CA / R01 CA093548; United States / NCI NIH HHS / CA / CA 101956; United States / NCI NIH HHS / CA / CA 102031; United States / NCI NIH HHS / CA / P30 CA 16058; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / R01 CA093548-05
  • [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; 0 / RNA, Untranslated
  • [Number-of-references] 99
  • [Other-IDs] NLM/ NIHMS66042; NLM/ PMC3463865
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58. Pinheiro RF, de Sá Moreira E, Silva MR, Alberto FL, Chauffaille Mde L: FLT3 internal tandem duplication during myelodysplastic syndrome follow-up: a marker of transformation to acute myeloid leukemia. Cancer Genet Cytogenet; 2008 Jun;183(2):89-93
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  • Some molecular abnormalities related to acute myeloid leukemia (AML) transformation have been reported, such as FLT3 (FMS-like tyrosine kinase 3) mutations.
  • We studied FLT3 ITD, prospectively, in 50 MDS patients at diagnosis, at 6 and 12 months follow-up, and at any other time-point if AML transformation was detected.
  • Of these, one case exhibited FLT3 ITD at the end of the 6 months of follow-up in approximately 8% of bone marrow cells; this case evolved into AML at 8 months, at which time FLT3 ITD was present in approximately 85% of bone marrow cells.
  • The other case exhibited FLT3 ITD in 68% of bone marrow cells at 7 months, precisely at the time of AML transformation.
  • Although rare in MDS, FLT3 ITD is associated with a high probability of evolution to AML.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Follow-Up Studies. Humans. Karyotyping. Male. Middle Aged


59. El-Zawahry HM, Zeeneldin AA, Samra MA, Mattar MM, El-Gammal MM, Abd El-Samee A, Darwish T: Cost and outcome of treatment of adults with acute myeloid leukemia at the National Cancer Institute-Egypt. J Egypt Natl Canc Inst; 2007 Jun;19(2):106-13
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  • BACKGROUND: Despite important advances in the therapy of acute myeloid leukemia (AML), the majority of patients die of their disease, unless bone marrow transplantation (BMT) is done.
  • Infection and hemorrhage are still the major causes of mortality in AML patients.
  • Progress in therapy and supportive care has led to gradual improvement in the overall results, but further improvements are still needed.
  • PATIENTS AND METHODS: The aim of this study is to identify the outcome and costs of adult AML patients treated with conventional chemotherapy (CCT) at the National Cancer Institute (NCI), Cairo University during the time period from April 1999 to January 2002.
  • RESULTS: The median age of 82 identified AML patients was 34 years.
  • Infections were the major mortality cause, followed by disease progression then bleeding (65% , 28% and 7% respectively).
  • CONCLUSIONS: Outcome of patients with AML treated at NCI- Cairo University can be enhanced by improvement of supportive therapy; mainly infection control and expanding BMT programs to accommodate all eligible patients.

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  • (PMID = 19034340.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
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60. Drexler HG, Dirks WG, Macleod RA: Many are called MDS cell lines: one is chosen. Leuk Res; 2009 Aug;33(8):1011-6
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  • Myelodysplastic syndromes (MDS) comprise a heterogenous group of clonal disorders of hematopoietic progenitors, showing genetic instability and in many cases progression to acute myeloid leukemia (AML).
  • When MDS progress towards AML (AML/MDS), additional genetic lesions cause a block in differentiation and an accumulation of blast cells.
  • Hence, both pathophysiologically and clinically the MDS and AML/MDS phases are distinguishable.
  • Most remaining ("authentic") MDS cell lines were established during the leukemic phase of the disease progression rather than during the MDS phase.
  • (2) malignant cell lines established in the AML/MDS leukemic phase; and (3) apparently legitimate MDS cell lines established during the MDS phase.
  • While MDS and AML/MDS cell lines both provide singular resources for modelling pathology, mining oncogenically modified macromolecules, and testing druggability, we contend these groups should be considered separately.


61. 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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62. Occhipinti E, Correa H, Yu L, Craver R: Comparison of two new classifications for pediatric myelodysplastic and myeloproliferative disorders. Pediatr Blood Cancer; 2005 Mar;44(3):240-4
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  • Resolution, stability, progression, and death in the subcategories of each system were compared.
  • Eight developed acute myelogenous leukemia (AML) (seven died), one juvenile myelomonocytic leukemia (JMML) (died), one chronic myelomonocytic leukemia (CMML) (currently in relapse), two died of complications, two responded to BMT, three have stable disease, one resolved.
  • Eleven patients were not classifiable by the pediatric WHO system, one of which progressed to AML and died.
  • Nine developed AML (8 died), 1 died of complications, 10 responded to treatment (BMT and/or chemotherapy).
  • Children meeting these criteria are more likely to progress to AML or death.
  • [MeSH-minor] Adult. Child. Disease Progression. Humans. Leukemia / classification. Leukemia / mortality. Prognosis. Retrospective Studies


63. Vieira L, Sousa AC, Matos P, Marques B, Alaiz H, Ribeiro MJ, Braga P, da Silva MG, Jordan P: Three-way translocation involves MLL, MLLT3, and a novel cell cycle control gene, FLJ10374, in the pathogenesis of acute myeloid leukemia with t(9;11;19)(p22;q23;p13.3). Genes Chromosomes Cancer; 2006 May;45(5):455-69
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  • The MLL gene, at 11q23, undergoes chromosomal translocation with a large number of partner genes in both acute lymphoblastic and acute myeloid leukemia (AML).
  • We report a novel t(9;11;19)(p22;q23;p13.3) disrupting MLL in an infant AML patient.
  • These results indicate that FLJ10374 negatively regulates cell cycle progression and proliferation.
  • Thus, a single chromosomal rearrangement resulting in formation of the MLL-MLLT3 fusion gene and haplo-insufficiency of FLJ10374 may have cooperated to promote leukemogenesis in AML with t(9;11;19).

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  • [Copyright] 2006 Wiley-Liss, Inc
  • (PMID = 16450356.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / MLLT3 protein, human; 0 / Nuclear Proteins; 0 / RNA, Messenger; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 9007-49-2 / DNA; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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64. Tibes R, Keating MJ, Ferrajoli A, Wierda W, Ravandi F, Garcia-Manero G, O'Brien S, Cortes J, Verstovsek S, Browning ML, Faderl S: Activity of alemtuzumab in patients with CD52-positive acute leukemia. Cancer; 2006 Jun 15;106(12):2645-51
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  • Because CD52 also is expressed on acute leukemic blasts, the authors investigated the safety and efficacy of alemtuzumab in patients with acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL).
  • METHODS: Fifteen patients with CD52-positive (> or = 20%), recurrent or refractory acute leukemia (9 patients with AML and 6 patients with ALL) received alemtuzumab at a dose of 30 mg intravenously given 3 times a week (dose escalation during Week 1) for a total of 4 to 12 weeks.
  • Ten patients developed disease progression while on study.
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antibodies, Monoclonal, Humanized. Bacteremia / diagnosis. Bacteremia / etiology. Bone Marrow / drug effects. Bone Marrow / pathology. Disease Progression. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Female. Fungemia / diagnosis. Fungemia / etiology. Humans. Male. Middle Aged. Pneumonia / diagnosis. Pneumonia / etiology. Treatment Outcome

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  • [Copyright] Copyright 2006 American Cancer Society.
  • (PMID = 16688777.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
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65. Follo MY, Finelli C, Clissa C, Mongiorgi S, Bosi C, Martinelli G, Baccarani M, Manzoli L, Martelli AM, Cocco L: Phosphoinositide-phospholipase C beta1 mono-allelic deletion is associated with myelodysplastic syndromes evolution into acute myeloid leukemia. J Clin Oncol; 2009 Feb 10;27(5):782-90
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  • Kaplan-Meier analysis revealed a significant association (P < .0001) between the PI-PLCbeta1 mono-allelic deletion and a higher risk of evolution into acute myeloid leukemia (AML), since 23 of 35 MDS patients (65.7%) bearing the PI-PLCbeta1 mono-allelic deletion evolved into AML.
  • Even in multivariate analysis, the PI-PLCbeta1 mono-allelic deletion retained a higher significance, with a P < .001, as a prognostic factor of evolution into AML (odds ratio [OR] 1.83; 95% CI, 2.26 to 17.24; P = .00045).
  • CONCLUSION: PI-PLCbeta1 mono-allelic deletion is associated with a worse clinical outcome in MDS patients, hinting at the identification of a new group at higher risk of AML evolution and representing a reliable prognostic tool.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Gene Deletion. Gene Expression. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction


66. Zhang L, Gajewski TF, Kline J: PD-1/PD-L1 interactions inhibit antitumor immune responses in a murine acute myeloid leukemia model. Blood; 2009 Aug 20;114(8):1545-52
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  • In contrast to available data in solid tumors, little is known regarding involvement of the PD-1/PD-L1 pathway in immune escape by hematopoietic cancers, such as acute myeloid leukemia (AML).
  • PD-1(-/-) mice challenged with C1498 cells generated augmented antitumor T-cell responses, showed decreased AML burden in the blood and other organs, and survived significantly longer than did wild-type mice.
  • [MeSH-minor] Animals. Antigens, CD274. Disease Models, Animal. Disease Progression. Down-Regulation / immunology. Humans. Mice. Mice, Inbred C57BL. Mice, Knockout. Neoplasm Transplantation / pathology. Programmed Cell Death 1 Receptor. Protein Binding. Tumor Cells, Cultured. Tumor Escape / immunology

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  • (PMID = 19417208.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K23 CA133196; United States / NCI NIH HHS / CA / R01 CA127475
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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  • [Other-IDs] NLM/ PMC2731636
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67. Saccà L: The uncontrolled clinical trial: scientific, ethical, and practical reasons for being. Intern Emerg Med; 2010 Jun;5(3):201-4
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  • If two extreme disease conditions for nature and progression are analyzed, such as acute myeloid leukemia (AML) and chronic heart failure (CHF), the difference in the prevalence of uncontrolled trials is very striking.
  • The number of uncontrolled trials is only 13% in CHF, whereas it reaches 66% in the AML group.

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68. Bachas C, Schuurhuis GJ, Hollink IH, Kwidama ZJ, Goemans BF, Zwaan CM, van den Heuvel-Eibrink MM, de Bont ES, Reinhardt D, Creutzig U, de Haas V, Assaraf YG, Kaspers GJ, Cloos J: High-frequency type I/II mutational shifts between diagnosis and relapse are associated with outcome in pediatric AML: implications for personalized medicine. Blood; 2010 Oct 14;116(15):2752-8
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  • [Title] High-frequency type I/II mutational shifts between diagnosis and relapse are associated with outcome in pediatric AML: implications for personalized medicine.
  • Although virtually all pediatric patients with acute myeloid leukemia (AML) achieve a complete remission after initial induction therapy, 30%-40% of patients will encounter a relapse and have a dismal prognosis.
  • To determine relevance of established AML type I/II mutations that may serve as therapeutic targets, we assessed frequencies of these mutations and their persistence during disease progression in a large group (n = 69) of paired diagnosis and relapse pediatric AML specimens.
  • These findings suggest that mutational shifts affect disease progression.

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  • [CommentIn] Blood. 2010 Oct 14;116(15):2622-3 [20947687.001]
  • (PMID = 20592250.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA Primers; 0 / DNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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69. Guidez F, Parks S, Wong H, Jovanovic JV, Mays A, Gilkes AF, Mills KI, Guillemin MC, Hobbs RM, Pandolfi PP, de Thé H, Solomon E, Grimwade D: RARalpha-PLZF overcomes PLZF-mediated repression of CRABPI, contributing to retinoid resistance in t(11;17) acute promyelocytic leukemia. Proc Natl Acad Sci U S A; 2007 Nov 20;104(47):18694-9
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  • RARalpha-PLZF confers RA resistance to a retinoid-sensitive acute myeloid leukemia (AML) cell line in a CRABPI-dependent fashion.
  • [MeSH-minor] Base Sequence. Binding Sites. Cell Line. Chromatin / genetics. DNA Methylation. Disease Progression. Drug Resistance, Neoplasm / drug effects. Gene Expression Regulation, Neoplastic. Humans. Molecular Sequence Data. Retinoids / pharmacology. Up-Regulation

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  • (PMID = 18000064.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE8510
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromatin; 0 / Kruppel-Like Transcription Factors; 0 / Receptors, Retinoic Acid; 0 / Retinoids; 0 / retinoic acid binding protein I, cellular; 0 / retinoic acid receptor alpha; 147855-37-6 / ZBTB16 protein, human
  • [Other-IDs] NLM/ PMC2141839
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70. Lightfoot T: Aetiology of childhood leukemia. Bioelectromagnetics; 2005;Suppl 7:S5-S11
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  • The major morphological subtypes of leukemia, acute lymphoblastic leukemia (ALL), and acute myeloblastic leukemia (AML), are characterized by chromosomal translocations involving over 200 genes including mixed lineage leukemia (MLL), TEL, and AML1.
  • Accordingly, it is important to identify exposures that cause DNA damage and induce chromosome breaks which are inadequately repaired, ultimately leading to the initiation and disease progression.

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc
  • (PMID = 16059922.001).
  • [ISSN] 0197-8462
  • [Journal-full-title] Bioelectromagnetics
  • [ISO-abbreviation] Bioelectromagnetics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 54
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71. Gotlib J, Berubé C, Growney JD, Chen CC, George TI, Williams C, Kajiguchi T, Ruan J, Lilleberg SL, Durocher JA, Lichy JH, Wang Y, Cohen PS, Arber DA, Heinrich MC, Neckers L, Galli SJ, Gilliland DG, Coutré SE: Activity of the tyrosine kinase inhibitor PKC412 in a patient with mast cell leukemia with the D816V KIT mutation. Blood; 2005 Oct 15;106(8):2865-70
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  • The patient died after 3 months of therapy due to progression of her MDS/MPD to acute myeloid leukemia (AML).

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  • (PMID = 15972446.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA66996; United States / NIDDK NIH HHS / DK / DK50654; United States / NHLBI NIH HHS / HL / K23HL04409; United States / NIAID NIH HHS / AI / AI-41995; United States / NIAID NIH HHS / AI / AI-23990; United States / NCI NIH HHS / CA / CA-72074
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 120685-11-2 / 4'-N-benzoylstaurosporine; 30KYC7MIAI / Aspartic Acid; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; H88EPA0A3N / Staurosporine
  • [Other-IDs] NLM/ PMC1895309
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72. Stock W: Controversies in treatment of AML: case-based discussion. Hematology Am Soc Hematol Educ Program; 2006;:185-91
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  • [Title] Controversies in treatment of AML: case-based discussion.
  • Treatment of acute myeloid leukemia (AML) in older adults remains a tremendous challenge.
  • Standard approaches to treatment have resulted in progression-free survival in only a small minority of patients with AML over the age of 60.
  • Elucidation of the molecular genetic events that contribute to the pathogenesis of AML in older patients are providing insights into mechanisms of resistance.

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  • (PMID = 17124059.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 38
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73. 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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  • 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.
  • 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.

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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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74. Klimek VM, Fircanis S, Maslak P, Guernah I, Baum M, Wu N, Panageas K, Wright JJ, Pandolfi PP, Nimer SD: Tolerability, pharmacodynamics, and pharmacokinetics studies of depsipeptide (romidepsin) in patients with acute myelogenous leukemia or advanced myelodysplastic syndromes. Clin Cancer Res; 2008 Feb 1;14(3):826-32
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  • The purpose of this study was to evaluate the toxicity, pharmacokinetic profile, and selected pharmacodynamic properties of the histone deacetylase inhibitor depsipeptide in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML).
  • EXPERIMENTAL DESIGN: Depsipeptide was administered to MDS or AML patients at a (solid tumor) phase I dose of 18 mg/m(2) i.v. on days 1 and 5 every 3 weeks.
  • RESULTS: Twelve patients (nine with AML, three with MDS) received one to five cycles of depsipeptide.
  • The best response of 11 assessed patients was one complete remission in a patient with AML, stable disease in six patients, and progression of disease in four patients.
  • Depsipeptide monotherapy has limited clinical activity in unselected AML/MDS patients.


75. Rigolin GM, Mauro E, Ciccone M, Fraulini C, Sofritti O, Castoldi G, Cuneo A: Neoplastic circulating endothelial-like cells in patients with acute myeloid leukaemia. Eur J Haematol; 2007 May;78(5):365-73
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  • In this report, we showed that, in seven acute myeloid leukaemia (AML) patients with known cytogenetic abnormalities, CEC levels were significantly increased in comparison with controls and that a significant proportion of these CECs carried the same chromosomal aberration as blast cells (20-78%, mean value 42.1% of CECs).
  • These findings suggest a possible direct contribution of AML-related CECs to tumour vasculogenesis and possibly to the spreading and progression of the disease.

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  • (PMID = 17391308.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
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76. Passamonti F, Rumi E, Pietra D, Elena C, Boveri E, Arcaini L, Roncoroni E, Astori C, Merli M, Boggi S, Pascutto C, Lazzarino M, Cazzola M: A prospective study of 338 patients with polycythemia vera: the impact of JAK2 (V617F) allele burden and leukocytosis on fibrotic or leukemic disease transformation and vascular complications. Leukemia; 2010 Sep;24(9):1574-9
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  • We studied the relationship between JAK2 (V617F) mutant allele burden and clinical phenotype, disease progression and survival in patients with polycythemia vera (PV).
  • During the study period, eight patients progressed to post-PV myelofibrosis (MF) (all carrying >50% mutant alleles), while 10 patients developed acute myeloid leukemia (AML).
  • By contrast, the risk of developing AML as well as that of thrombosis was not significantly related to mutant allele burden.
  • In conclusion, a JAK2 (V617F) allele burden >50% represents a risk factor for progression to MF in PV.


77. Weisberg E, Kung AL, Wright RD, Moreno D, Catley L, Ray A, Zawel L, Tran M, Cools J, Gilliland G, Mitsiades C, McMillin DW, Jiang J, Hall-Meyers E, Griffin JD: Potentiation of antileukemic therapies by Smac mimetic, LBW242: effects on mutant FLT3-expressing cells. Mol Cancer Ther; 2007 Jul;6(7):1951-61
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  • Studies suggest that these proteins may be a viable target in leukemia because they have been found to be variably expressed in acute leukemias and are associated with chemosensitivity, chemoresistance, disease progression, remission, and patient survival.
  • Another promising therapeutic target, FLT3, is mutated in about one third of acute myelogenous leukemia (AML) patients; promising results have recently been achieved in clinical trials investigating the effects of the protein tyrosine kinase inhibitor PKC412 on AML patients harboring mutations in the FLT3 protein.

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  • (PMID = 17620426.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA36167; United States / NCI NIH HHS / CA / CA66996; United States / NIDDK NIH HHS / DK / DK50654
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / Diablo protein, mouse; 0 / Inhibitor of Apoptosis Proteins; 0 / LBW242; 0 / Mitochondrial Proteins; 0 / Mutant Proteins; 0 / Oligopeptides; 120685-11-2 / 4'-N-benzoylstaurosporine; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; H88EPA0A3N / Staurosporine
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78. Lim CK, Goh YT, Hwang WY, Ho LP, Sun L: Studies of Wilms' Tumor (WT1) Gene Expression in Adult Acute Leukemias in Singapore. Biomark Insights; 2007 Aug 08;2:293-8
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  • In the study, we have used the Wilms' tumor gene (WT1) as a biomarker to evaluate its expression in local adult patients with newly diagnosed acute leukemia, including both acute myeloid and lymphoid leukemias (AML and ALL).
  • There were fifteen AML and three ALL cases aged from 18 to 71 years old.
  • RESULTS: WT1 gene was exclusively expressed in all eighteen, including three ALL and fifteen AML, patients.
  • It may be used as a potential molecular marker for diagnosis, clinical progression of the diseases or monitoring the response to treatment, as well as a target for the development of novel therapeutic approaches.

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  • (PMID = 19662212.001).
  • [Journal-full-title] Biomarker insights
  • [ISO-abbreviation] Biomark Insights
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2717842
  • [Keywords] NOTNLM ; HLA-A / WT1 / adulthood acute leukemia / gene expression
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79. 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).
  • Cumulative incidence of MDS/AML was 8% at 10 years, with a significant correlation with both G-CSF cumulative dose and second IST.
  • [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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80. 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.
  • None of the patients in Group 3 progressed to AML or MDS.
  • CONCLUSION: AA patients with CA at initial diagnosis or follow-up may not be at greater risk for evolution to AML or MDS, or show shorter survival periods.

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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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81. 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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  • Severe congenital neutropenia (SCN) is a heterogeneous bone marrow failure syndrome predisposing to myelodysplastic syndrome and acute myeloid leukaemia (MDS/AML).
  • There was no significant difference in the risk of MDS/AML in patients with mutant versus wild-type ELA2: the respective cumulative incidences at 15 years were 36% and 25% (P = 0.96).

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  • [Cites] Blood. 2000 Oct 1;96(7):2317-22 [11001877.001]
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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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82. Keating GM: Azacitidine: a review of its use in higher-risk myelodysplastic syndromes/acute myeloid leukaemia. Drugs; 2009;69(17):2501-18
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  • Subcutaneous azacitidine was recently approved in the EU for the treatment of adults who are not eligible for haematopoietic stem cell transplantation and who have intermediate-2-risk or high-risk myelodysplastic syndromes (MDS) [according to International Prognostic Scoring System (IPSS) criteria], chronic myelomonocytic leukaemia (CMML) with 10-29% marrow blasts without myeloproliferative disorder, or acute myeloid leukaemia (AML) with 20-30% blasts and multilineage dysplasia (according to the WHO classification).
  • Subcutaneous azacitidine is the only drug shown to significantly prolong survival in patients with higher-risk MDS or WHO-defined AML, compared with conventional care (i.e. best supportive care, low-dose cytarabine or intensive chemotherapy).
  • In addition, azacitidine is associated with a lower risk of AML progression and higher rates of complete remission, partial remission, haematological improvement and red blood cell (RBC) transfusion independence.
  • Thus, azacitidine is a valuable option for the first-line treatment of patients with higher-risk MDS/AML.


83. Lü X, Qiu HX, Qiu HR, Zhang SJ, Xu J, Xu W, Wu HX, Li JY, Shao JZ: [A case of myelodysplastic syndrome with aberrant evolution of chromosome 1 and 11 in 6 years of follow-up]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Apr;18(2):469-72
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  • This study was aimed to investigate the relationship between cytogenetic evolution and disease progression in patient with MDS-RAEB.
  • The results indicated that this patient was failed with conventional chemotherapy of AML, but had response to ATRA and 6-MP in the 72 months follow-up.
  • It is concluded that karyotype evolution is perhaps associated with progression of MDS.


84. Li Y, Li XY, Wang L, Tian Z, Rao Q, Jia HR, Wang HJ, Wang M, Mi YC: [Biological characteristics of Wt1 gene in relation to Ph(+) leukemia cell line K562]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Jun;18(3):564-9
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  • This gene is highly expressed in acute myeloid leukemia (AML) and the progression of chronic myelogenous leukemia (CML).

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  • (PMID = 20561402.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / WT1 Proteins; IT942ZTH98 / Curcumin
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85. Ko RM, Kim HG, Wolff L, Klug CA: Roles of p15Ink4b and p16Ink4a in myeloid differentiation and RUNX1-ETO-associated acute myeloid leukemia. Leuk Res; 2008 Jul;32(7):1101-11
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  • Inactivation of p15(Ink4b) expression by promoter hypermethylation occurs in up to 80% of acute myeloid leukemia (AML) cases and is particularly common in the FAB-M2 subtype of AML, which is characterized by the presence of the RUNX1-ETO translocation in 40% of cases.
  • To establish whether the loss of p15(Ink4b) contributes to AML progression in association with RUNX1-ETO, we have expressed the RUNX1-ETO fusion protein from a retroviral vector in hematopoietic progenitor cells isolated from wild-type, p15(Ink4b) or p16(Ink4a) knockout bone marrow.
  • Analysis of lethally irradiated recipient mice reconstituted with RUNX1-ETO-expressing cells showed that neither p15(Ink4b) or p16(Ink4a) loss significantly accelerated disease progression over the time period of one year post-transplantation.
  • These results strongly suggest that p15(Ink4b) loss must be accompanied by additional oncogenic changes for RUNX1-ETO-associated AML to develop.

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  • (PMID = 18037485.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096798; United States / NCI NIH HHS / CA / R01 CA087549; United States / NCI NIH HHS / CA / R01CA087549; United States / NCI NIH HHS / CA / CA096798-05; United States / NCI NIH HHS / CA / R01 CA096798-05; United States / NCI NIH HHS / CA / R01CA096798
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA Primers; 0 / Runx1 protein, mouse
  • [Other-IDs] NLM/ NIHMS49471; NLM/ PMC2430055
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86. Shuai X, Zhou D, Shen T, Wu Y, Zhang J, Wang X, Li Q: Overexpression of the novel oncogene SALL4 and activation of the Wnt/beta-catenin pathway in myelodysplastic syndromes. Cancer Genet Cytogenet; 2009 Oct 15;194(2):119-24
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  • Myelodysplastic syndromes (MDS) are a group of heterogeneous clonal stem cell diseases with a tendency to progress to leukemic transformation.
  • Overexpression of SALL4 induces MDS-like features and subsequent leukemic progression in transgenic mice.
  • Here, we examined SALL4 expression levels in bone marrow mononuclear cells from MDS patients, acute myeloid leukemia (AML) patients, and normal control subjects using a semiquantitative reverse transcription polymerase chain reaction.
  • Higher levels of SALL4 expression were seen in MDS and AML samples than in control samples.


87. 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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  • 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.
  • The article illustrates which children may benefit most from MRD analysis in AML and explores practical issues that should be addressed in the design of clinical trials.

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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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88. Mihara K, Takihara Y, Kimura A: Genetic and epigenetic alterations in myelodysplastic syndrome. Cytogenet Genome Res; 2007;118(2-4):297-303
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  • Myelodysplastic syndrome (MDS) is a clonal disorder characterized by dyshematopoiesis and high susceptibility to acute myeloid leukemia (AML).
  • As patients with MDS have widely variable prognosis, we need to stratify them according to chromosomal abnormalities, genetic alterations, and epigenetic deregulations associated with progression to AML in order to treat these patients appropriately.
  • We have reported that the expression of BMI1, a member of PcG, in hematopoietic stem cells or progenitor cells predicts the prognosis of patients with MDS and progression to acute leukemia.
  • Thus PcG not only provides a molecular marker for monitoring disease progression of MDS, but also provides a clue for elucidating a molecular mechanism underlying the disease progression, which may help in the development of a new therapeutic strategy against MDS.


89. 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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90. Stelljes M, Bornhauser M, Kroger M, Beyer J, Sauerland MC, Heinecke A, Berning B, Scheffold C, Silling G, Buchner T, Neubauer A, Fauser AA, Ehninger G, Berdel WE, Kienast J, Cooperative German Transplant Study Group: Conditioning with 8-Gy total body irradiation and fludarabine for allogeneic hematopoietic stem cell transplantation in acute myeloid leukemia. Blood; 2005 Nov 1;106(9):3314-21
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  • Seventy-one patients with acute myeloid leukemia (AML), most of them (63/71) considered ineligible for conventional allogeneic hematopoietic stem cell transplantation (HSCT), were enrolled into a phase 2 study on reduced-intensity myeloablative conditioning with fractionated 8-Gy total body irradiation (TBI) and fludarabine (120 mg/m2).
  • Outcome data in this poor-risk population indicate that allogeneic HSCT from related or unrelated donors with 8-Gy TBI/fludarabine conditioning is feasible with low NRM and preserved antileukemic activity in AML patients in first or later CR.
  • [MeSH-minor] Adult. Aged. Disease Progression. Female. Humans. Male. Middle Aged. Survival Rate. Treatment Outcome


91. Krejci O, Wunderlich M, Geiger H, Chou FS, Schleimer D, Jansen M, Andreassen PR, Mulloy JC: p53 signaling in response to increased DNA damage sensitizes AML1-ETO cells to stress-induced death. Blood; 2008 Feb 15;111(4):2190-9
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  • Intriguingly, microarray data indicate that t(8;21) patient samples exhibit decreased expression of DNA repair genes and increased expression of p53 response genes compared with other acute myeloid leukemia (AML) patient samples.
  • It is possible that the superior outcome of t(8;21) patients is partly due to an activated p53 pathway, and that loss of the p53 response pathway is associated with disease progression.

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  • (PMID = 17975013.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R21 DK071103; United States / NHLBI NIH HHS / HL / R01 HL076604; United States / NIDDK NIH HHS / DK / DK071103; United States / NHLBI NIH HHS / HL / HL076604; United States / NCRR NIH HHS / RR / M01 RR 08084; United States / NCRR NIH HHS / RR / M01 RR008084; United States / NIDDK NIH HHS / DK / DK071103-02; United States / NIDDK NIH HHS / DK / R21 DK071103-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC2234055
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92. Loges S, Tinnefeld H, Metzner A, Jücker M, Butzal M, Bruweleit M, Fischer U, Draab E, Schuch G, O'-Farrel AM, Hossfeld DK, Bokemeyer C, Fiedler W: Downregulation of VEGF-A, STAT5 and AKT in acute myeloid leukemia blasts of patients treated with SU5416. Leuk Lymphoma; 2006 Dec;47(12):2601-9
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  • In acute myeloid leukemia (AML), autocrine or paracrine activation of receptor tyrosine kinases such as c-kit and FLT3 contributes to proliferation and apoptosis resistance of leukemic blasts.
  • This provided the rationale for a multicenter clinical trial in patients with refractory AML with SU5416, a small molecule kinase inhibitor which blocks phosphorylation of c-kit, FLT3, VEGFR-1, VEGFR-2 (KDR) and VEGFR-3.
  • The levels of VEGF mRNA expression were investigated in peripheral blood leukemic blasts taken from AML patients before and during treatment with SU5416.
  • Rapid down regulation of VEGF was observed in AML blasts from 72% (13 of 18) of patients analysed.
  • In the AML patient samples, parallel downregulation of both STAT5 and AKT was observed in several cases (STAT5 in four of 15; AKT in three of six examined patients).
  • In summary, our data show suppression of the expression of VEGF and key signal transduction intermediates in AML blasts during treatment with SU5416.
  • [MeSH-minor] Angiogenesis Inhibitors / pharmacology. Cell Line, Tumor. Cell Separation. DNA Primers / chemistry. Disease Progression. Flow Cytometry. Humans. Protein Kinase Inhibitors / pharmacology. Signal Transduction. Treatment Outcome

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  • (PMID = 17169805.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / DNA Primers; 0 / Indoles; 0 / Protein Kinase Inhibitors; 0 / Pyrroles; 0 / STAT5 Transcription Factor; 0 / Vascular Endothelial Growth Factor A; 71IA9S35AJ / Semaxinib; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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93. Dayyani F, Conley AP, Strom SS, Stevenson W, Cortes JE, Borthakur G, Faderl S, O'Brien S, Pierce S, Kantarjian H, Garcia-Manero G: Cause of death in patients with lower-risk myelodysplastic syndrome. Cancer; 2010 May 01;116(9):2174-9
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  • BACKGROUND: The authors have recently shown that a majority of patients with myelodysplastic syndrome (MDS) classified by the International Prognostic Scoring System as lower risk die without transformation to acute myelogenous leukemia (AML).
  • MDS-related death was defined as infection, bleeding, transformation to AML, or disease progression.
  • The most common disease-related CODs were infection (38%), transformation to AML (15%), and hemorrhage (13%).
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Hemorrhage / complications. Humans. Infection / complications. Male. Middle Aged. Prognosis. Risk

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  • [Copyright] (c) 2010 American Cancer Society.
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  • (PMID = 20162709.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5P011CA108631; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / P01 CA108631-05; United States / NCI NIH HHS / CA / P01 CA108631; United States / NCI NIH HHS / CA / T32 CA009666
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS247751; NLM/ PMC3753205
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94. Feldman EJ: Farnesyltransferase inhibitors in myelodysplastic syndrome. Curr Hematol Rep; 2005 May;4(3):186-90
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  • The most promising activity to date has been demonstrated in patients with hematological malignancies, in particular acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
  • In addition, the presence of an activating Ras mutation has not predicted response to therapy with FTIs in MDS and AML.
  • Despite this, significant clinical efficacy of the FTIs in MDS, on par with that of currently available chemotherapeutic agents, has been observed, leading to further development of this new class of drugs in MDS and AML.
  • [MeSH-minor] Acute Disease. Aged. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Disease Progression. Farnesyltranstransferase. Genes, ras. Hematologic Neoplasms / drug therapy. Hematologic Neoplasms / enzymology. Humans. Leukemia, Myeloid / etiology. Leukemia, Myeloid / genetics. Middle Aged. Protein Prenylation / drug effects. Protein Processing, Post-Translational / drug effects. Proto-Oncogene Proteins p21(ras) / chemistry. Proto-Oncogene Proteins p21(ras) / metabolism. Remission Induction. Signal Transduction / drug effects. Treatment Outcome

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  • (PMID = 15865870.001).
  • [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 / Enzyme Inhibitors; 0 / Piperidines; 0 / Pyridines; 0 / Quinolones; 192185-72-1 / tipifarnib; 193275-84-2 / lonafarnib; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase; EC 3.6.5.2 / HRAS protein, human; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Number-of-references] 37
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95. Stone R, Sekeres M, Garcia-Manero G: Evolving strategies in the treatment of MDS and AML. Clin Adv Hematol Oncol; 2009 Aug;7(8):1-14; quiz 2 p following 14
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  • [Title] Evolving strategies in the treatment of MDS and AML.
  • The treatment of MDS involves improving patient survival and quality of life while decreasing the likelihood of progression to acute myelogenous leukemia (AML).
  • In addition, multiple agents and novel combinations are currently in development to treat both MDS AML.


96. Kakihana K, Kubo F, Wakabayashi S, Kurosu T, Miki T, Murakami N, Miura O: A novel variant form of MLL-ELL fusion transcript with t(11;19)(q23;p13.1) in chronic myelomonocytic leukemia transforming to acute myeloid leukemia. Cancer Genet Cytogenet; 2008 Jul 15;184(2):109-12
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  • Here we report a case of chronic myelomonocytic leukemia (CMML) with a 46,XY,t(11;19)(q23;p13.1) karyotype that transformed to acute myeloid leukemia (AML) without showing any karyotypic evolution.
  • MLL has been fused to ELL exon 2 in all the previously reported MLL-ELL transcripts, which have always been associated with AML.
  • [MeSH-minor] Aged. Base Sequence. Disease Progression. Humans. Male


97. 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.
  • At a median follow-up of 17.2 months, all patients within this 'high CIN' subgroup had died or progressed to AML, while 80% of MDS patients with normal CIN levels had stable disease (P < 0.001).
  • Furthermore, in all three MDS patients for whom serial measurements were available, development of AML was preceded by increasing CIN levels.
  • 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


98. Yao DM, Qian J, Xu WR, Lin J, Jiang YW, Fei X, Han LX, Wang Y, Cen JN, Chen ZX: [Alteration of methylation status of fragile histidine triad gene promoter in patients with myelodysplastic syndrome]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2008 Feb;25(1):36-9
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  • Although significant difference was not observed in the frequencies of FHIT gene hypermethylation among patients with refractory anemia/refractory anemia with ringed sideroblasts (RA/RAS) (1/6, 16.7%), refractory anemia/refractory anemia with ringed sideroblasts (RCMD) and refractory cytopenia with multilineage dysplasia with ringed blasts (RCMD-RS) (6/19, 31.6%), refractory anemia with excess blasts-1 (RAEB-1) (7/11, 63.6%), refractory anemia with excess blasts-2 (RAEB-2) (4/7, 57.1%) and refractory anemia with excess blasts in transformation/acute myeloid leukemia (RAEBt/AML) (8/11, 72.7%)(chi-square=8.417, P=0.077), it was observed in patients in early stages (RA/RAS and RCMD) (7/25, 28.0%), advanced stages (RAEB-1 and RAEB-2)(11/18, 61.1%) and RAEBt/AML (8/11, 72.7%) (chi-square=7.938, P=0.019).
  • CONCLUSION: FHIT gene hypermethylation might be one of the molecular events involved in the disease progression of MDS.

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  • (PMID = 18247301.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / fragile histidine triad protein; EC 3.6.- / Acid Anhydride Hydrolases
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99. Makishima H, Cazzolli H, Szpurka H, Dunbar A, Tiu R, Huh J, Muramatsu H, O'Keefe C, Hsi E, Paquette RL, Kojima S, List AF, Sekeres MA, McDevitt MA, Maciejewski JP: Mutations of e3 ubiquitin ligase cbl family members constitute a novel common pathogenic lesion in myeloid malignancies. J Clin Oncol; 2009 Dec 20;27(36):6109-16
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  • METHODS: We applied high-density SNP-A karyotyping to identify loss of heterozygosity of 11q in 442 patients with MDS, MDS/MPN, MPN, sAML evolved from these conditions, and primary AML.
  • CONCLUSION: Mutations in the Cbl family RING finger domain or linker sequence constitute important pathogenic lesions associated with not only preleukemic CMML, JMML, and other MPN, but also progression to AML, suggesting that impairment of degradation of activated tyrosine kinases constitutes an important cancer mechanism.

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  • (PMID = 19901108.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K24 HL077522; United States / NHLBI NIH HHS / HL / R01 HL082983; United States / NCRR NIH HHS / RR / U54 RR019391; United States / NHLBI NIH HHS / HL / K24 HL-077522; United States / NHLBI NIH HHS / HL / R01HL-082983; United States / NCRR NIH HHS / RR / S10 RR019391
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Other-IDs] NLM/ PMC3040009
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100. Qian J, Chen Z, Lin J, Wang W, Cen J: Decreased expression of CCAAT/enhancer binding protein zeta (C/EBPzeta) in patients with different myeloid diseases. Leuk Res; 2005 Dec;29(12):1435-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • C/EBPzeta, also known as GADD153, CHOP10, and DDIT3 has been found associated with the development of myxoid liposarcoma and the progression of melanoma.
  • To investigate the correlation of C/EBPzeta transcript levels with the development of leukemia, samples from 187 patients with myelodysplastic syndrome (MDS), acute myeloid leukemia (AML), and chronic myeloid leukemia (CML) were examined for C/EBPzeta mRNA using real-time quantitative PCR (RQ-PCR).
  • RQ-PCR analysis demonstrated the median levels of C/EBPzeta were significantly decreased in MDS, AML, and CML patients compared with normal controls (1.40, 0.96, 2.60 versus 14.69, P<0.0001).
  • Significant differences were also observed between patients with CML and with AML or MDS.






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