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1. Mao G, Yuan F, Absher K, Jennings CD, Howard DS, Jordan CT, Gu L: Preferential loss of mismatch repair function in refractory and relapsed acute myeloid leukemia: potential contribution to AML progression. Cell Res; 2008 Feb;18(2):281-9
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  • [Title] Preferential loss of mismatch repair function in refractory and relapsed acute myeloid leukemia: potential contribution to AML progression.
  • Acute myeloid leukemia (AML) is an aggressive hematological cancer.
  • The molecular mechanisms underlying AML development and relapse remain incompletely defined.
  • To explore whether loss of DNA mismatch repair (MMR) function is involved in AML, we screened two key MMR genes, MSH2 and MLH1, for mutations and promoter hypermethylation in leukemia specimens from 53 AML patients and blood from 17 non-cancer controls.
  • We show here that whereas no amino acid alteration or promoter hypermethylation was detected in all control samples, 18 AML patients exhibited either mutations in MMR genes or hypermethylation in the MLH1 promoter.
  • MMR defects were significantly more frequent in patients with refractory or relapsed AML compared with newly diagnosed patients.
  • These observations suggest for the first time that the loss of MMR function is associated with refractory and relapsed AML and may contribute to disease pathogenesis.

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  • (PMID = 18227862.001).
  • [ISSN] 1748-7838
  • [Journal-full-title] Cell research
  • [ISO-abbreviation] Cell Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA104333
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / MLH1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein
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2. 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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3. 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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4. Kantarjian H, Issa JP, Rosenfeld CS, Bennett JM, Albitar M, DiPersio J, Klimek V, Slack J, de Castro C, Ravandi F, Helmer R 3rd, Shen L, Nimer SD, Leavitt R, Raza A, Saba H: Decitabine improves patient outcomes in myelodysplastic syndromes: results of a phase III randomized study. Cancer; 2006 Apr 15;106(8):1794-803
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  • Patients treated with decitabine had a trend toward a longer median time to acute myelogenous leukemia (AML) progression or death compared with patients who received supportive care alone (all patients, 12.1 mos vs. 7.8 mos [P = 0.16]; those with International Prognostic Scoring System intermediate-2/high-risk disease, 12.0 mos vs. 6.8 mos [P = 0.03]; those with de novo disease, 12.6 mos vs. 9.4 mos [P = 0.04]; and treatment-naive patients, 12.3 mos vs. 7.3 mos [P = 0.08]).
  • CONCLUSIONS: Decitabine was found to be clinically effective in the treatment of patients with MDS, provided durable responses, and improved time to AML transformation or death.
  • [MeSH-minor] Acute Disease. Aged. DNA Methylation / drug effects. Disease Progression. Disease-Free Survival. Female. Humans. Leukemia, Myeloid / etiology. Male. Middle Aged. Palliative Care. Quality of Life. Survival Rate


5. 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

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  • (PMID = 19855965.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide
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6. Kroeger H, Jelinek J, Estécio MR, He R, Kondo K, Chung W, Zhang L, Shen L, Kantarjian HM, Bueso-Ramos CE, Issa JP: Aberrant CpG island methylation in acute myeloid leukemia is accentuated at relapse. Blood; 2008 Aug 15;112(4):1366-73
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  • Its impact in leukemia progression is not fully understood.
  • We performed genomewide screening for methylated CpG islands and identified 8 genes frequently methylated in leukemia cell lines and in patients with acute myeloid leukemia (AML): NOR1, CDH13, p15, NPM2, OLIG2, PGR, HIN1, and SLC26A4.
  • We assessed the methylation status of these genes and of the repetitive element LINE-1 in 30 patients with AML, both at diagnosis and relapse.
  • We observed concordance in methylation of several genes, confirming the presence of a hypermethylator pathway in AML.
  • DNA methylation levels increased at relapse in 25 of 30 (83%) patients with AML.
  • Our data suggest that DNA methylation is involved in AML progression and provide a rationale for the use of epigenetic agents in remission maintenance.

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  • (PMID = 18523155.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA108631; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / 5P01CA108631-03; United States / NCI NIH HHS / CA / 5P50CA100632-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2515110
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7. Shih LY, Huang CF, Lin TL, Wu JH, Wang PN, Dunn P, Kuo MC, Tang TC: Heterogeneous patterns of CEBPalpha mutation status in the progression of myelodysplastic syndrome and chronic myelomonocytic leukemia to acute myelogenous leukemia. Clin Cancer Res; 2005 Mar 1;11(5):1821-6
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  • [Title] Heterogeneous patterns of CEBPalpha mutation status in the progression of myelodysplastic syndrome and chronic myelomonocytic leukemia to acute myelogenous leukemia.
  • PURPOSE: We aimed to assess the role of CEBPalpha mutations in the progression of myelodysplastic syndrome (MDS) to acute myelogenous leukemia (AML) and their cooperating mutations.
  • EXPERIMENTAL DESIGN: Mutational analysis of CEBPalpha with direct sequencing for each PCR product was done on matched bone marrow samples obtained from 50 adult patients with MDS at diagnosis and at AML transformation.
  • At AML transformation, three patients retained the identical mutant clones as their initial diagnosis, three acquired the mutations, and one lost CEBPalpha mutation when she gained FLT3/ITD mutation.
  • CEBPalpha mutations had no influence on the time to AML progression or overall survival.
  • The mutation status was heterogeneous, exhibiting identical clone, clonal change, or clonal evolution during the progression to AML.
  • [MeSH-minor] Adult. Aged. Alleles. DNA Mutational Analysis. Disease Progression. Female. Humans. Leucine Zippers. Male. Middle Aged


8. 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.

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  • (PMID = 20368469.001).
  • [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 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Nuclear Proteins; 0 / WT1 Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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9. Bernasconi P, Klersy C, Boni M, Cavigliano PM, Calatroni S, Giardini I, Rocca B, Zappatore R, Caresana M, Quarna J, Lazzarino M, Bernasconi C: Incidence and prognostic significance of karyotype abnormalities in de novo primary myelodysplastic syndromes: a study on 331 patients from a single institution. Leukemia; 2005 Aug;19(8):1424-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence and prognostic significance of karyotype abnormalities in de novo primary myelodysplastic syndromes: a study on 331 patients from a single institution.
  • The impact of clinical parameters, International Prognostic Scoring System (IPSS) scores/cytogenetic categories, and some single cytogenetic defects on overall survival (OS) and time to myelodysplastic syndromes (MDS)/AML progression (progression-free interval (PFI)) was evaluated in 331 MDS patients.
  • In multivariate analysis OS was significantly influenced by age, marrow blast cell percentage, number of cytopenias and either modified or standard IPSS cytogenetic categories; hazard ratios for MDS/AML progression were influenced by all the former, except for age and cytopenias.


10. Kuo MC, Liang DC, Huang CF, Shih YS, Wu JH, Lin TL, Shih LY: RUNX1 mutations are frequent in chronic myelomonocytic leukemia and mutations at the C-terminal region might predict acute myeloid leukemia transformation. Leukemia; 2009 Aug;23(8):1426-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • There was no difference in overall survival between patients with and without RUNX1 mutations, but a trend of higher risk of acute myeloid leukemia (AML) progression was observed in mutation-positive patients (16/30 vs 17/51, P=0.102), especially in patients with C-terminal mutations (P=0.023).
  • The median time to AML progression was 6.8 months in patients with C-terminal mutations compared with 28.3 months in those without mutations (P=0.022).
  • C-terminal mutations might be associated with a more frequent and rapid AML transformation.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease Progression. Female. Genes, ras. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. Protein Structure, Tertiary. fms-Like Tyrosine Kinase 3 / genetics


11. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.


12. Ma L, Kowalski D, Javed K, Hui P: Atypical angiomyolipoma of kidney in a patient with tuberous sclerosis: a case report with p53 gene mutation analysis. Arch Pathol Lab Med; 2005 May;129(5):676-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Angiomyolipoma (AML) is the most common benign mesenchymal tumor of the kidney.
  • Results of recent studies suggest that p53 mutation may play an important role in AML progression.
  • Here, we describe a locally destructive renal AML in a patient with tuberous sclerosis.
  • The diagnosis of atypical epithelioid AML was made.
  • Our finding indicates no definite link between p53 abnormalities and the atypical appearance of AML.
  • To the best of our knowledge, this is the second renal AML case investigated for p53 mutations.

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  • (PMID = 15859641.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm
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13. List A: Lenalidomide--a transforming therapeutic agent in myelodysplastic syndromes. Clin Lymphoma Myeloma; 2009;9 Suppl 3:S302-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Long-term outcome data indicate that cytogenetic response to lenalidomide might confer a survival advantage compared with cytogenetic nonresponders, with a corresponding reduced risk for acute myeloid leukemia (AML) progression.
  • Combination strategies are now in both MDS and AML that could further broaden the therapeutic potential of lenalidomide.
  • [MeSH-minor] Chromosome Deletion. Clinical Trials as Topic. Disease Progression. Humans. Immunosuppression. Karyotyping. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Medical Oncology / methods. Medical Oncology / trends. Risk. Treatment Outcome


14. Kadia TM, Faderl S, Estrov Z, Konopleva M, George S, Lee W, Puzanov I, Chen A, Kantarjian H, Ravandi F: Final results of phase I and pharmacokinetic study of SJG-136 administered on a daily x 5 schedule. J Clin Oncol; 2009 May 20;27(15_suppl):e13506

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Previously treated pts with R/R acute leukemias (AML, ALL, high risk MDS, CML blast phase) or R/R CLL with adequate organ function and ECOG performance status of ≤ 2 were eligible for the study.
  • Thirteen (81%) pts had R/R AML, and 3 (19%) had R/R ALL of which 5 (31%) had diploid and 6 (38%) had adverse cytogenetics.
  • One pt had a PR, 8 pts had stable disease, and 6 had progression.

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  • (PMID = 27961262.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Naik SG, Negrin R, Laport G, Miklos D, Shizuru J, Arai S, Blume K, Wong R, Lowsky R, Johnston L: Long-term outcomes of high-dose therapy using busulfan, etoposide, and cyclophosphamide followed by allogeneic hematopoietic cell transplantation for patients with high-risk or advanced stages of myeloid malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):7033

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Disease status at transplantation was induction failure (IF) acute myeloid leukemia (AML) (n = 10), HR AML in 1st complete remission (CR1) n = 11, in CR2 (n = 5), in CR3 (n = 2), relapsed refractory (RR) AML (n = 14), chronic myeloid leukemia (CML) in second chronic phase (n = 6), blast crisis (n = 2), myelofibrosis (n = 6), myeloproliferative disorders (n = 2), and MDS (n = 38).
  • With a median follow up of 5.6 yrs (1.6-14.6 yrs) actuarial 5-year overall survival (OS) was 32% (95% CI 22-42%) and 5-year probability for freedom from progression (FFP) was 64% (95% CI 52%-76%).
  • There was no statistically significant difference in OS; 31% versus 32% (p = 0.89) or FFP 71% versus 60% (p = 0.29) for recipients of BM versus PBMC with similar results in IF and RR AML.

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  • (PMID = 27961395.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Steensma D, Kantarjian H, Wijermans P: Clinical experience with different dosing schedules of decitabine in patients with myelodysplastic syndromes (MDS). J Clin Oncol; 2009 May 20;27(15_suppl):7011

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Data from each clinical trial supporting overall improvement, duration of improvement, time to AML or death, progression-free survival (PFS), and transfusion independence was assessed.
  • RESULTS: Patients had IPSS classification scores of intermediate-2 or high-risk (D-0007, 70%; EORTC-06011, 93%; ID03-0180, 66%; DACO-020, 46%) and de novo MDS (D-0007, 87%; EORTC-06011, 88%; ID03-0180, 70%; DACO-020, 89%).
  • Comparable overall improvement (complete response [CR] + partial response [PR] + hematologic improvement [HI]), time to AML or death, and PFS was observed across all trials (Table).

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  • (PMID = 27961372.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Armstrong GT, Pan Z, Ness K, Srivastava D, Robison LL: Temporal trends in cause-specific late mortality among five-year survivors of childhood cancer. J Clin Oncol; 2009 May 20;27(15_suppl):10004

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cause-specific mortality was categorized as death from recurrence/progression of primary disease, external causes, and non-recurrence/non-external causes (Non-Recur/Ext) (i.e., deaths from health conditions including sequelae of cancer therapy).
  • Additionally, all-cause mortality was significantly lower in more recent eras for 5-year survivors of ALL, AML, Hodgkin, NHL, and CNS tumors, but not neuroblastoma and Ewing's Sarcoma where an increase in cumulative incidence of late mortality was seen in more recent eras.
  • CONCLUSIONS: All-cause late mortality has improved with more recent eras, attributable to reduced rates of mortality from progression of primary disease (i.e., durable remission).

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  • (PMID = 27962548.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Sekeres M, Kantarjian H, Fenaux P, Becker P, Boruchov A, Guerci-Bresler A, Hu K, Franklin J, Berger D: Subcutaneous or intravenous administration of romiplostim in thrombocytopenic patients with myelodysplastic syndrome (MDS). J Clin Oncol; 2009 May 20;27(15_suppl):7009

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Five pts experienced serious AEs, and there were 2 cases of disease progression to AML: one pt in the QWSC cohort who received romiplostim for 4 weeks and one in the Q2WSC cohort who received romiplostim for 20 weeks.

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  • (PMID = 27961381.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Medeiros BC, Gotlib JR, Coutre SE, Jones C, Khan SA, Rajwanshi R, Rajwanshi R, Zehnder J, Zehnder J: Interim results of protracted low doses of temozolomide in high-risk acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7052

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Phase II clinical trial of tailored temozolomide therapy to high-risk AML patients according to AGAT methylation promoter status.
  • De novo AML was diagnosed in eight patients and five patients had s-AML.
  • Seven patients have died from disease progression, while two patients died of neutropenic sepsis (early deaths).
  • CONCLUSIONS: These preliminary results suggest that temozolomide therapy may be individually tailored to elderly patients with AML according to AGAT promoter status.

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  • (PMID = 27961417.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Schuch G, Oliveira-Ferrer L, Loges S, Laack E, Bokemeyer C, Hossfeld DK, Fiedler W, Ergun S: Antiangiogenic treatment with endostatin inhibits progression of AML in vivo. Leukemia; 2005 Aug;19(8):1312-7
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  • [Title] Antiangiogenic treatment with endostatin inhibits progression of AML in vivo.
  • Using microencapsulation technology, we studied the therapeutic effect of ES in AML.
  • Taken together, ES has inhibitory effects on neo-angiogenesis in the bone marrow and on progression of leukemia in vivo.
  • These experiments suggest a possible therapeutic role of antiangiogenic gene therapy with ES in AML.

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  • [Copyright] Leukemia (2005) 19, 1312-1317.
  • (PMID = 15931265.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD31; 0 / Endostatins
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21. Jiang Y, Dunbar A, Gondek LP, Mohan S, Rataul M, O'Keefe C, Sekeres M, Saunthararajah Y, Maciejewski JP: Aberrant DNA methylation is a dominant mechanism in MDS progression to AML. Blood; 2009 Feb 5;113(6):1315-25
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  • [Title] Aberrant DNA methylation is a dominant mechanism in MDS progression to AML.
  • Myelodysplastic syndromes (MDSs) are clonal hematologic disorders that frequently represent an intermediate disease stage before progression to acute myeloid leukemia (AML).
  • As such, study of MDS/AML can provide insight into the mechanisms of neoplastic evolution.
  • In 184 patients with MDS and AML, DNA methylation microarray and high-density single nucleotide polymorphism array (SNP-A) karyotyping were used to assess the relative contributions of aberrant DNA methylation and chromosomal deletions to tumor-suppressor gene (TSG) silencing during disease progression.
  • Aberrant methylation was seen in every sample, on average affecting 91 of 1505 CpG loci in early MDS and 179 of 1505 loci after blast transformation (refractory anemia with excess blasts [RAEB]/AML).
  • In contrast, chromosome aberrations were seen in 79% of early MDS samples and 90% of RAEB/AML samples, and were not as widely distributed over the genome.
  • However, the ubiquity, extent, and correlation with disease progression suggest that aberrant DNA methylation is the dominant mechanism for TSG silencing and clonal variation in MDS evolution to AML.

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  • (PMID = 18832655.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K24 HL077522; United States / NHLBI NIH HHS / HL / R01 HL082983; United States / NCRR NIH HHS / RR / S10 RR019391; United States / NCRR NIH HHS / RR / U54 RR019391
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FZD3 protein, human; 0 / Frizzled Receptors; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC2637194
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22. Barresi V, Palumbo GA, Musso N, Consoli C, Capizzi C, Meli CR, Romano A, Di Raimondo F, Condorelli DF: Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML. Leuk Res; 2010 Nov;34(11):1539-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML.
  • By conventional metaphase and SNP array cytogenetics we serially studied a patient affected by high-risk myelodysplastic syndrome (MDS), documenting the conversion from partial trisomy 8q to trisomy 8 and partial tetrasomy 8q during progression to acute myeloid leukemia (AML).
  • Moreover, the serial application of high resolution genomic array analysis at different disease stages allowed the description of cryptic abnormalities and the demonstration of their enrichment in the AML phase.
  • In particular the detection and quantification of a copy-neutral loss of heterozygosity region located in chromosome 11q guided the search for point mutations in the CBL gene, thus allowing the escription of the novel missense mutation K382E and the demonstration of its selection during progression to secondary AML.
  • [MeSH-minor] Chromosomes, Human, Pair 8. Clone Cells. Disease Progression. Humans. Male. Mutation. Neoplasms, Second Primary. Trisomy

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20674974.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
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23. Preiss BS, Bergmann OJ, Friis LS, Sørensen AG, Frederiksen M, Gadeberg OV, Mourits-Andersen T, Oestergaard B, Kerndrup GB, AML Study Group of Southern Denmark: Cytogenetic findings in adult secondary acute myeloid leukemia (AML): frequency of favorable and adverse chromosomal aberrations do not differ from adult de novo AML. Cancer Genet Cytogenet; 2010 Oct 15;202(2):108-22
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  • [Title] Cytogenetic findings in adult secondary acute myeloid leukemia (AML): frequency of favorable and adverse chromosomal aberrations do not differ from adult de novo AML.
  • During a 15-year period, 161 adult patients were diagnosed with secondary acute myeloid leukemia (s-AML) in the region of Southern Denmark.
  • In 73 patients, the AML diagnosis was preceded by myelodysplastic syndrome (MDS-AML), in 31 patients by an antecedent hematologic disease, and in 57 patients by treatment with chemotherapy and/or irradiation (t-AML).
  • MDS-AML correlated to a normal karyotype (P < 0.001).
  • t-AML correlated to abnormal clones with numerical and structural aberrations (P = 0.03), five or more unrelated aberrations (P = 0.03), marker chromosomes (P = 0.006), abnormal mitoses only (P = 0.01), female sex (P < 0.001), and -7 (P = 0.006).
  • The frequencies of aberrations in s-AML patients were compared with an age-matched group of de novo AML patients diagnosed in the same area and period.
  • In this comparison, s-AML only correlated to -7 (P = 0.02).
  • In 42 patients, we found that MDS patients with an abnormal karyotype were more likely to show cytogenetic evolution during progression to AML than MDS patients with a normal karyotype (P = 0.01).
  • We conclude that population-based cytogenetic studies of adult s-AML and age- and sex-matched de novo AML show comparable distributions of chromosome abnormalities.


24. Wang Z, Lu QY, Niu XQ, Zhang P, Zhao JN, Zhang KJ, Li P, Hu JS: [Expression of pituitary tumor transforming gene in patients with AML]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Dec;18(6):1427-30
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  • [Title] [Expression of pituitary tumor transforming gene in patients with AML].
  • The aim of study was to explore the expression of pituitary tumor-transforming gene (pttg) in acute myeloid leukemia (AML) and its relationship with the pathogenesis of AML, simultaneously to investigate the difference of the pttg expression among AML different subtypes.
  • The expressions of pttg mRNA were quantitatively detected by real-time fluorescence quantitative polymerase chain reaction (real-time PCR) in bone marrow from 47 patients with AML and 28 normal controls.
  • The results indicated that the expression of pttg mRNA was significantly higher in AML patients [(1.1323 ± 1.3934) × 10(5)] than that in normal controls [(4.5766 ± 1.1817) × 10(3)] (p < 0.05).
  • The expression of pttg mRNA was higher in M(3) patients than that in other AML subtypes, such as M(1), M(2), M(4), M(5).
  • It is concluded that the overexpression of pttg may be related to the pathogenesis and progression of AML, in which the overexpression of pttg may be more intimately related to the pathogenesis and progression of M(3).
  • This study provides a new idea to research the pathogenesis and targeted gene therapy of AML.

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  • (PMID = 21176344.001).
  • [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 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Securin; 0 / pituitary tumor-transforming protein 1, human
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25. Römermann D, Hasemeier B, Metzig K, Schlegelberger B, Länger F, Kreipe H, Lehmann U: [Methylation status of LINE-1 sequences in patients with MDS or secondary AML]. Verh Dtsch Ges Pathol; 2007;91:338-42
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  • [Title] [Methylation status of LINE-1 sequences in patients with MDS or secondary AML].
  • [Transliterated title] Methylierungszustand von LINE-1-Sequenzen bei Patienten mit MDS oder sekundärer AML.
  • OBJECTIVES: This study analyzes changes in the degree of global methylationlevel in myelodysplastic syndrome during progression of the disease.
  • RESULTS: We detected an increase of methylation level of LINE-1 sequences using pyrosequencing and an increase of methylation in the HpaII recognition site employing LUMA during the progression of MDS.

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  • (PMID = 18314632.001).
  • [ISSN] 0070-4113
  • [Journal-full-title] Verhandlungen der Deutschen Gesellschaft für Pathologie
  • [ISO-abbreviation] Verh Dtsch Ges Pathol
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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26. Oki Y, Issa JP: Epigenetic mechanisms in AML - a target for therapy. Cancer Treat Res; 2010;145:19-40
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  • [Title] Epigenetic mechanisms in AML - a target for therapy.
  • In acute myelogenous leukemia (AML), aberrant DNA methylation can be observed in multiple functionally relevant genes such as p15, p 73, E-cadherin, ID 4, RARbeta2.
  • Abnormal activities of histone tail-modifying enzymes have also been seen in AML, frequently as a direct result of chromosomal translocations.
  • It is now clear that these epigenetic changes play a significant role in development and progression of AML, and thus constitute important targets of therapy.

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  • (PMID = 20306243.001).
  • [ISSN] 0927-3042
  • [Journal-full-title] Cancer treatment and research
  • [ISO-abbreviation] Cancer Treat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Neoplasm Proteins; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase
  • [Number-of-references] 174
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27. Moreau-Gachelin F: Lessons from models of murine erythroleukemia to acute myeloid leukemia (AML): proof-of-principle of co-operativity in AML. Haematologica; 2006 Dec;91(12):1644-52
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  • [Title] Lessons from models of murine erythroleukemia to acute myeloid leukemia (AML): proof-of-principle of co-operativity in AML.
  • This review highlights recent findings demonstrating the key roles of the co-operation of two mutations occurring during leukemic progression, a mutation interfering with differentiation and a mutation conferring a proliferative advantage to cells.
  • Through their multi-step evolution, these mouse erythroleukemia models resemble the two phases of human acute myeloid leukemia (AML).


28. Disperati P, Ichim CV, Tkachuk D, Chun K, Schuh AC, Wells RA: Progression of myelodysplasia to acute lymphoblastic leukaemia: implications for disease biology. Leuk Res; 2006 Feb;30(2):233-9
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  • [Title] Progression of myelodysplasia to acute lymphoblastic leukaemia: implications for disease biology.
  • Approximately 30% of cases of MDS eventually progress to acute myelogenous leukemia (AML), while progression of MDS into acute lymphoblastic leukemia (ALL) is rare.

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  • (PMID = 16046234.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 60
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29. 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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30. Advani AS, Rodriguez C, Jin T, Jawde RA, Saber W, Baz R, Kalaycio M, Sobecks R, Sekeres M, Tripp B, Hsi E: Increased C-kit intensity is a poor prognostic factor for progression-free and overall survival in patients with newly diagnosed AML. Leuk Res; 2008 Jun;32(6):913-8
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  • [Title] Increased C-kit intensity is a poor prognostic factor for progression-free and overall survival in patients with newly diagnosed AML.
  • C-kit, a tyrosine kinase receptor, is expressed on most myeloid blasts and is thought to be important in the pathogenesis of AML.
  • Here, we discuss the prognostic impact of c-kit intensity, measured using the mean fluorescent index (MFI) in patients with newly diagnosed AML.
  • On multivariate analysis, c-kit MFI>20.3 correlated with a decreased progression-free survival and overall survival, independent of known prognostic factors (age, white blood count at diagnosis and cytogenetics).
  • Whether inhibiting c-kit in patients with AML will alter prognosis is the basis of ongoing clinical trials.
  • [MeSH-minor] Adolescent. Adult. Aged. Disease Progression. Disease-Free Survival. Female. Fluorescence. Humans. Male. Middle Aged. Retrospective Studies. Survival Rate

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  • [CommentIn] Leuk Res. 2008 Jun;32(6):845-6 [18023867.001]
  • (PMID = 17928050.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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31. Konieczna I, Horvath E, Wang H, Lindsey S, Saberwal G, Bei L, Huang W, Platanias L, Eklund EA: Constitutive activation of SHP2 in mice cooperates with ICSBP deficiency to accelerate progression to acute myeloid leukemia. J Clin Invest; 2008 Mar;118(3):853-67
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  • [Title] Constitutive activation of SHP2 in mice cooperates with ICSBP deficiency to accelerate progression to acute myeloid leukemia.
  • Development of a block in myeloid differentiation is associated with progression of MPD to acute myeloid leukemia (AML) and portends poor prognosis.
  • In mice, ICSBP deficiency induces an MPD that progresses to AML over time, suggesting that ICSBP deficiency is sufficient for myeloproliferation, but additional genetic lesions are necessary for AML.
  • Since activity of ICSBP is influenced by tyrosine phosphorylation state, we hypothesized that mutations in molecular pathways that regulate this process might synergize with ICSBP deficiency for progression to AML.
  • Consistent with this, we found that constitutive activation of SHP2 protein tyrosine phosphatase synergized with ICSBP haploinsufficiency to facilitate cytokine-induced myeloproliferation, apoptosis resistance, and rapid progression to AML in a murine bone marrow transplantation model.
  • Since SHP2 activation and ICSBP deficiency may coexist in human myeloid malignancies, our studies have identified a molecular mechanism potentially involved in disease progression in such diseases.

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  • (PMID = 18246201.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095266; United States / NCI NIH HHS / CA / R01-CA095266
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-8; 42HK56048U / Tyrosine; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
  • [Other-IDs] NLM/ PMC2214847
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32. 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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33. 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.


34. Zuber J, Radtke I, Pardee TS, Zhao Z, Rappaport AR, Luo W, McCurrach ME, Yang MM, Dolan ME, Kogan SC, Downing JR, Lowe SW: Mouse models of human AML accurately predict chemotherapy response. Genes Dev; 2009 Apr 1;23(7):877-89
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  • [Title] Mouse models of human AML accurately predict chemotherapy response.
  • The genetic heterogeneity of cancer influences the trajectory of tumor progression and may underlie clinical variation in therapy response.
  • To model such heterogeneity, we produced genetically and pathologically accurate mouse models of common forms of human acute myeloid leukemia (AML) and developed methods to mimic standard induction chemotherapy and efficiently monitor therapy response.
  • We see that murine AMLs harboring two common human AML genotypes show remarkably diverse responses to conventional therapy that mirror clinical experience.
  • Our studies highlight the importance of genetic information in guiding the treatment of human AML, functionally establish the p53 network as a central determinant of chemotherapy response in AML, and demonstrate that genetically engineered mouse models of human cancer can accurately predict therapy response in patients.

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  • (PMID = 19339691.001).
  • [ISSN] 1549-5477
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA008748; United States / Howard Hughes Medical Institute / /
  • [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 / AML1-ETO fusion protein, human; 0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL-ENL oncoprotein, human; 0 / Oncogene Proteins, Fusion; 0 / Tumor Suppressor Protein p53; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC2666344
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35. Ryningen A, Stapnes C, Paulsen K, Lassalle P, Gjertsen BT, Bruserud O: In vivo biological effects of ATRA in the treatment of AML. Expert Opin Investig Drugs; 2008 Nov;17(11):1623-33
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  • [Title] In vivo biological effects of ATRA in the treatment of AML.
  • Experimental studies suggest that ATRA can induce differentiation and apoptosis in leukaemia cells also for other acute myelogenous leukaemia (AML) subtypes, but the clinical observations are conflicting.
  • DESIGN AND METHODS: Twenty-two AML patients with non-APL disease received oral ATRA alone (22.5 mg/m2 twice daily) for two days, the patients thereafter continued ATRA together with valproic acid and theophylline.
  • Serum/plasma samples were collected before and after 2 days of ATRA, peripheral blood AML cells were collected from all 12 patients with circulating leukaemia cells (ClinicalTrials.gov NCT00175812; EudraCT no. 2004-001663-22).
  • RESULTS: AML cells collected during therapy had altered flow cytometric forward and right angle light scatters but no morphological signs of differentiation.
  • ATRA increased the percentage of circulating AML cells in G0/G1 phase for 9 out of 12 patients (p = 0.043).
  • CONCLUSIONS: In vivo ATRA treatment in AML affects leukaemic cell morphology, regulation of cell cycle progression and apoptosis, and possibly also microvascular endothelial cell functions.

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  • (PMID = 18922099.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00175812
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Histone Deacetylase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Transcription Factors; 5688UTC01R / Tretinoin; EC 3.5.1.98 / Histone Deacetylases
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36. Ryningen A, Wergeland L, Glenjen N, Gjertsen BT, Bruserud O: In vitro crosstalk between fibroblasts and native human acute myelogenous leukemia (AML) blasts via local cytokine networks results in increased proliferation and decreased apoptosis of AML cells as well as increased levels of proangiogenic Interleukin 8. Leuk Res; 2005 Feb;29(2):185-96
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  • [Title] In vitro crosstalk between fibroblasts and native human acute myelogenous leukemia (AML) blasts via local cytokine networks results in increased proliferation and decreased apoptosis of AML cells as well as increased levels of proangiogenic Interleukin 8.
  • Interactions between native human acute myelogenous leukemia (AML) blasts and nonleukemic cells in the bone marrow microenvironment seem important both for disease development chemosensitivity.
  • Native human AML blasts from consecutive patients were cultured with normal human bone marrow stromal cells and two fibroblast lines (HFL1 and Hs27) separated by a semipermeable membrane.
  • This bidirectional crosstalk via the cytokine network between AML blasts and fibroblasts caused (i) increased proliferation, (ii) mediated antiapoptotic signalling and (iii) increased local levels of proangiogenic IL8.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis / physiology. Cell Line, Tumor. Cell Proliferation. Coculture Techniques. Disease Progression. Female. Humans. Male. Middle Aged. Signal Transduction. Stromal Cells / physiology

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  • (PMID = 15607368.001).
  • [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 / Cytokines; 0 / Interleukin-8
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37. Popat U, Heslop HE, Durett A, May R, Krance RA, Brenner MK, Carrum G: Outcome of reduced-intensity allogeneic hematopoietic stem cell transplantation (RISCT) using antilymphocyte antibodies in patients with high-risk acute myeloid leukemia (AML). Bone Marrow Transplant; 2006 Mar;37(6):547-52
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  • [Title] Outcome of reduced-intensity allogeneic hematopoietic stem cell transplantation (RISCT) using antilymphocyte antibodies in patients with high-risk acute myeloid leukemia (AML).
  • It is therefore particularly unsuited to older individuals, who are most at risk of developing acute myeloid leukemia (AML).
  • We report 17 consecutive patients with high-risk AML whose median age was 58 years and who received stem cells from HLA-matched siblings (n=5), or alternative donors (n=12).
  • Both progression-free survival and overall survival are 40% (95% CI, 17-64%).
  • Hence, RISCT using lymphodepleting antibodies may be of value for older patients with AML, even in those with active or high-risk disease, and even if they lack an MHC-identical sibling donor.

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  • (PMID = 16462757.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Immunosuppressive Agents
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38. Mills KI, Kohlmann A, Williams PM, Wieczorek L, Liu WM, Li R, Wei W, Bowen DT, Loeffler H, Hernandez JM, Hofmann WK, Haferlach T: Microarray-based classifiers and prognosis models identify subgroups with distinct clinical outcomes and high risk of AML transformation of myelodysplastic syndrome. Blood; 2009 Jul 30;114(5):1063-72
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  • [Title] Microarray-based classifiers and prognosis models identify subgroups with distinct clinical outcomes and high risk of AML transformation of myelodysplastic syndrome.
  • Discordant samples of MDS were classified either into acute myeloid leukemia (AML) or "none-of-the-targets" (neither leukemia nor MDS) categories.
  • However, a significant correlation was noted between the AML and "none-of-the-targets" categories and prognosis, leading to a prognostic classification model to predict for time-dependent probability of leukemic transformation.
  • The prognostic classification model accurately discriminated patients with a rapid transformation to AML within 18 months from those with more indolent disease.
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Disease Progression. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. RNA, Messenger / genetics. Single-Blind Method. Treatment Outcome


39. Watanabe-Okochi N, Kitaura J, Ono R, Harada H, Harada Y, Komeno Y, Nakajima H, Nosaka T, Inaba T, Kitamura T: AML1 mutations induced MDS and MDS/AML in a mouse BMT model. Blood; 2008 Apr 15;111(8):4297-308
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  • [Title] AML1 mutations induced MDS and MDS/AML in a mouse BMT model.
  • Myelodysplastic syndrome (MDS) is a hematopoietic stem-cell disorder characterized by trilineage dysplasia and susceptibility to acute myelogenous leukemia (AML).
  • Recently, mutations of the transcription factor AML1/RUNX1 have been identified in 15% to 40% of MDS-refractory anemia with excess of blasts (RAEB) and MDS/AML.
  • Most mice developed MDS and MDS/AML-like symptoms within 4 to 13 months after BMT.
  • Interestingly, among integration sites identified, Evi1 seemed to collaborate with an AML1 mutant harboring a point mutation in the Runt homology domain (D171N) to induce MDS/AML with an identical phenotype characterized by marked hepatosplenomegaly, myeloid dysplasia, leukocytosis, and biphenotypic surface markers.
  • On the other hand, a C-terminal truncated AML1 mutant (S291fsX300) induced pancytopenia with erythroid dysplasia in transplanted mice, followed by progression to MDS-RAEB or MDS/AML.
  • Thus, we have developed a useful mouse model of MDS/AML that should help in the understanding of the molecular basis of MDS and the progression of MDS to overt leukemia.


40. 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.

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  • (PMID = 19306356.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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41. Lübbert M, Bertz H, Rüter B, Marks R, Claus R, Wäsch R, Finke J: Non-intensive treatment with low-dose 5-aza-2'-deoxycytidine (DAC) prior to allogeneic blood SCT of older MDS/AML patients. Bone Marrow Transplant; 2009 Nov;44(9):585-8
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  • [Title] Non-intensive treatment with low-dose 5-aza-2'-deoxycytidine (DAC) prior to allogeneic blood SCT of older MDS/AML patients.
  • Novel, non-intensive treatment options in older MDS/AML patients planned for allografting, with the goal of down-staging the underlying disease and bridging time to transplantation, are presently being developed.
  • 5-azacytidine and decitabine (DAC) are of particular interest, as they can be given repetitively, with very limited non-hematologic toxicity and result in responses both in MDS and AML even at low doses.
  • We describe 15 consecutive patients (median age 69 years, range 60-75 years) with MDS (n=10) or AML (n=5) who all received first-line treatment with DAC and subsequent allografting (from sibling donor in four patients, unrelated donor in 11) after reduced-intensity conditioning with the FBM regimen.
  • We conclude that allografting after low-dose DAC and subsequent conditioning with FBM is feasible, with no unexpected toxicities and appears as a valid alternative to standard chemotherapy ('InDACtion instead of induction') in elderly patients with MDS/AML.
  • [MeSH-minor] Aged. Combined Modality Therapy. Disease Progression. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. Risk Factors. Survival Rate. Transplantation Conditioning / methods

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  • (PMID = 19363531.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
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42. Balgobind BV, Van Vlierberghe P, van den Ouweland AM, Beverloo HB, Terlouw-Kromosoeto JN, van Wering ER, Reinhardt D, Horstmann M, Kaspers GJ, Pieters R, Zwaan CM, Van den Heuvel-Eibrink MM, Meijerink JP: Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis. Blood; 2008 Apr 15;111(8):4322-8
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  • [Title] Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis.
  • Patients with NF1 have a higher risk to develop juvenile myelomonocytic leukemia (JMML) with a possible progression toward acute myeloid leukemia (AML).
  • In an oligo array comparative genomic hybridization-based screening of 103 patients with pediatric T-cell acute lymphoblastic leukemia (T-ALL) and 71 patients with MLL-rearranged AML, a recurrent cryptic deletion, del(17)(q11.2), was identified in 3 patients with T-ALL and 2 patients with MLL-rearranged AML.
  • Since the NF1 protein is a negative regulator of the RAS pathway (RAS-GTPase activating protein), homozygous NF1 inactivation represent a novel type I mutation in pediatric MLL-rearranged AML and T-ALL with a predicted frequency that is less than 10%.

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  • (PMID = 18172006.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neurofibromin 1; 0 / RNA, Messenger
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43. Pinheiro RF, Moreira Ede S, Silva MR, Greggio B, Alberto FL, Chauffaille Mde L: FLT3 mutation and AML/ETO in a case of Myelodysplastic syndrome in transformation corroborates the two hit model of leukemogenesis. Leuk Res; 2007 Jul;31(7):1015-8
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  • [Title] FLT3 mutation and AML/ETO in a case of Myelodysplastic syndrome in transformation corroborates the two hit model of leukemogenesis.
  • The aim of this report is to present a case of Myelodysplastic syndrome (MDS) who presented, during AML transformation, a step-wise genetic progression that corroborates the two hit model of leukemogenesis.
  • A RCDM-RS (WHO)/RARS (FAB) patient with normal karyotype at diagnosis, evolved into AML after six months of follow up.
  • At transformation, AML/ETO fusion was detected, although marrow blast cells were not increased until 21 days later, when FLT3-ITD was also demonstrated pointing out that the overgrowth of the FLT3/ITD clone was concomitant with the outburst of marrow blasts.
  • These findings corroborates the two hit model of leukemogenesis in which one class of mutations (Class I) (FLT3/ITD) confers a proliferative or survival advantage to cells, and a second class of mutations (Class II) (AML/ETO) interferes with hematopoietic differentiation.
  • [MeSH-minor] Bone Marrow / pathology. Disease Progression. Female. Humans. Middle Aged. Tandem Repeat Sequences

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  • (PMID = 17079011.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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44. Petrovici K, Graf M, Hecht K, Reif S, Pfister K, Schmetzer H: Use of NG2 (7.1) in AML as a tumor marker and its association with a poor prognosis. Cancer Genomics Proteomics; 2010 Jul-Aug;7(4):173-80
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  • [Title] Use of NG2 (7.1) in AML as a tumor marker and its association with a poor prognosis.
  • We analyzed 70 bone marrow (BM) samples from acute myeloid leukemia (AML) patients for 11q23 aberrations and reactivity with the monoclonal antibody NG2.
  • We detected NG2(+) cells in AML cases with normal karyotype, however, not in healthy BM cells.
  • This means that NG2 qualifies as a reliable AML blast tumor marker, enabling monitoring of the course of AML independently of, although often associated with, 11q23-aberrations.
  • Patients with more than 10% NG2(+) cells showed a tendency to have a shorter progression-free survival (mean: 7 months) than patients with fewer than 10% NG2(+) cells (mean survival: 17 months; p=0.08).

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  • (PMID = 20656983.001).
  • [ISSN] 1790-6245
  • [Journal-full-title] Cancer genomics & proteomics
  • [ISO-abbreviation] Cancer Genomics Proteomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens; 0 / Biomarkers, Tumor; 0 / Proteoglycans; 0 / chondroitin sulfate proteoglycan 4
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45. Carter BZ, Mak DH, Woessner R, Gross S, Schober WD, Estrov Z, Kantarjian H, Andreeff M: Inhibition of KSP by ARRY-520 induces cell cycle block and cell death via the mitochondrial pathway in AML cells. Leukemia; 2009 Oct;23(10):1755-62
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  • [Title] Inhibition of KSP by ARRY-520 induces cell cycle block and cell death via the mitochondrial pathway in AML cells.
  • Kinesin spindle protein (KSP), a microtubule-associated motor protein essential for cell cycle progression, is overexpressed in many cancers and is a potential anti-tumor target.
  • We found that inhibition of KSP by a selective inhibitor, ARRY-520, blocked cell cycle progression, leading to apoptosis in acute myeloid leukemia cell lines that express high levels of KSP.
  • ARRY-520 significantly inhibited tumor growth of xenografts in SCID mice and inhibited AML blast but not normal colony formation, supporting a critical role for KSP in proliferation of leukemic progenitor cells.
  • These results demonstrate that ARRY-520 potently induces cell cycle block and subsequent death in leukemic cells via the mitochondrial pathway and has the potential to eradicate AML progenitor cells.

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  • (PMID = 19458629.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P01 CA049639; United States / NCI NIH HHS / CA / P01 CA55164; United States / NCI NIH HHS / CA / P01 CA49639; United States / NCI NIH HHS / CA / P01 CA055164
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ARRY 520; 0 / Antineoplastic Agents; 0 / KIF11 protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Thiadiazoles; 0 / Tumor Suppressor Protein p53; 0 / X-Linked Inhibitor of Apoptosis Protein; EC 3.4.22.- / Caspase 8; EC 3.6.1.- / Kinesin
  • [Other-IDs] NLM/ NIHMS445013; NLM/ PMC3593228
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46. 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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47. Maeda T, Yagasaki F, Ishikawa M, Takahashi N, Bessho M: Transforming property of TEL-FGFR3 mediated through PI3-K in a T-cell lymphoma that subsequently progressed to AML. Blood; 2005 Mar 1;105(5):2115-23
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  • [Title] Transforming property of TEL-FGFR3 mediated through PI3-K in a T-cell lymphoma that subsequently progressed to AML.
  • Disease in this patient subsequently progressed to acute myelogenous leukemia (AML) with the same translocation.
  • [MeSH-minor] Acute Disease. Animals. Cell Line. Cell Proliferation. Disease Progression. Female. Humans. Mice. Middle Aged. Receptor, Fibroblast Growth Factor, Type 3. Signal Transduction. Transfection

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  • (PMID = 15514005.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ETV6-FGFR3 protein, human; 0 / Oncogene Proteins, Fusion; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 3
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48. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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49. Busse A, Letsch A, Scheibenbogen C, Nonnenmacher A, Ochsenreither S, Thiel E, Keilholz U: Mutation or loss of Wilms' tumor gene 1 (WT1) are not major reasons for immune escape in patients with AML receiving WT1 peptide vaccination. J Transl Med; 2010 Jan 21;8:5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutation or loss of Wilms' tumor gene 1 (WT1) are not major reasons for immune escape in patients with AML receiving WT1 peptide vaccination.
  • Here, we analyzed 10 HLA-A2 positive patients with acute myeloid leukemia (AML) for loss or mutations of the WT1 epitope or epitope flanking sequences that may abolish proper T cell recognition or epitope presentation.
  • Blood and bone marrow samples prior to vaccination and during progression were analyzed for mRNA expression level of WT1.
  • RESULTS: Only in one patient, downregulation of WT1 mRNA by 1 log and loss of WT1 detection on protein level at time of disease progression was observed.
  • [MeSH-minor] Antigen Presentation / immunology. Clinical Trials, Phase II as Topic. Disease Progression. Epitopes. HLA-A2 Antigen / genetics. HLA-A2 Antigen / immunology. Humans. Mutation. T-Lymphocytes / immunology

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  • [Cites] Adv Immunol. 2000;74:181-273 [10605607.001]
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  • (PMID = 20092642.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Epitopes; 0 / HLA-A2 Antigen; 0 / Vaccines, Subunit; 0 / WT1 Proteins
  • [Other-IDs] NLM/ PMC2844374
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50. Timek TA, Lai DT, Liang D, Daughters GT, Ingels NB Jr, Miller DC: Determinants of evolution and progression of acute ovine ischemic mitral regurgitation. J Heart Valve Dis; 2010 Jul;19(4):420-5; discussion 426

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Determinants of evolution and progression of acute ovine ischemic mitral regurgitation.
  • Thus, radiopaque markers were implanted on valvular structures to investigate the geometric and hemodynamic variables associated with the evolution and progression of acute ovine IMR.
  • METHODS: Eight adult sheep underwent implantation of five radiopaque markers on the edge of the posterior mitral leaflet (PML), and five on the edge of the anterior mitral leaflet (AML).
  • CONCLUSION: The initiation of moderate IMR was associated with significant alterations in annular and leaflet geometry, but only a small decrease in LV systolic function, was needed for IMR progression.
  • These data suggest that the surgical repair and optimization of LV function may be important in combination to treat moderate IMR, as only small hemodynamic deterioration and perturbations in valvular geometry are necessary for significant IMR progression.
  • [MeSH-minor] Animals. Disease Models, Animal. Disease Progression. Echocardiography, Transesophageal. Fluoroscopy. Heart Ventricles / physiopathology. Hemodynamics. Risk Assessment. Risk Factors. Sheep. Time Factors. Ventricular Function, Left. Ventricular Pressure. Video Recording

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  • (PMID = 20845887.001).
  • [ISSN] 0966-8519
  • [Journal-full-title] The Journal of heart valve disease
  • [ISO-abbreviation] J. Heart Valve Dis.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL-10452; United States / NHLBI NIH HHS / HL / HL-29589; United States / NHLBI NIH HHS / HL / HL-67025
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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51. Keilholz U, Letsch A, Busse A, Asemissen AM, Bauer S, Blau IW, Hofmann WK, Uharek L, Thiel E, Scheibenbogen C: A clinical and immunologic phase 2 trial of Wilms tumor gene product 1 (WT1) peptide vaccination in patients with AML and MDS. Blood; 2009 Jun 25;113(26):6541-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A clinical and immunologic phase 2 trial of Wilms tumor gene product 1 (WT1) peptide vaccination in patients with AML and MDS.
  • This study investigated the immunogenicity of Wilms tumor gene product 1 (WT1)-peptide vaccination in WT1-expressing acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) patients without curative treatment option.
  • Seventeen AML patients and 2 refractory anemia with excess blasts patients received a median of 11 vaccinations.
  • Objective responses in AML patients were 10 stable diseases (SDs) including 4 SDs with more than 50% blast reduction and 2 with hematologic improvement.
  • An additional 4 patients had clinical benefit after initial progression, including 1 complete remission and 3 SDs.
  • This WT1 vaccination study provides immunologic, molecular, and preliminary evidence of potential clinical efficacy in AML patients, warranting further investigations.

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  • (PMID = 19389880.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Cancer Vaccines; 0 / Neoplasm Proteins; 0 / Peptide Fragments; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / WT1 (126-134), human; 0 / WT1 Proteins
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52. Suemitsu R, Fukuyama S, Ondo K, Ueda H: Resection of mediastinal granulocytic sarcoma triggered the rapid progression of acute myeloid leukemia. Ann Thorac Cardiovasc Surg; 2008 Jun;14(3):181-3
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  • [Title] Resection of mediastinal granulocytic sarcoma triggered the rapid progression of acute myeloid leukemia.
  • We experienced a case of acute myeloid leukemia (AML) that took a rapid turn for the worse after the resection of a mediastinal GS.
  • His WBC count was 77,240 at its peak on POD 9, at which point the patient was diagnosed with AML by bone marrow aspiration.
  • Despite chemotherapy, the patient died on POD 28 as a result of rapid disease progression.
  • [MeSH-minor] Disease Progression. Fatal Outcome. Humans. Male. Middle Aged. Sternum / surgery. Tomography, X-Ray Computed

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  • (PMID = 18577899.001).
  • [ISSN] 1341-1098
  • [Journal-full-title] Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia
  • [ISO-abbreviation] Ann Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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53. Kim HG, Kojima K, Swindle CS, Cotta CV, Huo Y, Reddy V, Klug CA: FLT3-ITD cooperates with inv(16) to promote progression to acute myeloid leukemia. Blood; 2008 Feb 01;111(3):1567-74
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  • [Title] FLT3-ITD cooperates with inv(16) to promote progression to acute myeloid leukemia.
  • The inversion of chromosome 16 in the inv(16)(p13q22) is one of the most frequent cytogenetic abnormalities observed in acute myeloid leukemia (AML).
  • Expression of CBFbeta-SMMHC in mice does not promote AML in the absence of secondary mutations.
  • To test whether an activating mutation of FLT3 (FLT3-ITD) would cooperate with CBFbeta-SMMHC to promote AML, we coexpressed both mutations in hematopoietic progenitor cells used to reconstitute lethally irradiated mice.
  • FLT3-ITD also accelerated disease progression in all CBFbeta-SMMHC/FLT3-ITD-reconstituted animals, which died of a highly aggressive and transplantable AML within 3 to 5 months.
  • These results indicate that FLT3-activating mutations can cooperate with CBFbeta-SMMHC in an animal model of inv(16)-associated AML.
  • [MeSH-minor] Animals. Core Binding Factor beta Subunit / genetics. Core Binding Factor beta Subunit / metabolism. Disease Progression. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Lymphopoiesis. Mice. Mutation / genetics. Myelopoiesis. Smooth Muscle Myosins / genetics. Smooth Muscle Myosins / metabolism. Survival Rate

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  • (PMID = 17967943.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K01 DK067186; United States / NCI NIH HHS / CA / R01 CA096798; United States / NIAID NIH HHS / AI / T32 AI007051; United States / NCI NIH HHS / CA / R01CA96798
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor beta Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.1.- / Smooth Muscle Myosins
  • [Other-IDs] NLM/ PMC2214774
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54. Pollyea DA, Artz AS, Stock W, Daugherty C, Godley L, Odenike OM, Rich E, Smith SM, Zimmerman T, Zhang Y, Huo D, Larson R, van Besien K: Outcomes of patients with AML and MDS who relapse or progress after reduced intensity allogeneic hematopoietic cell transplantation. Bone Marrow Transplant; 2007 Dec;40(11):1027-32
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  • [Title] Outcomes of patients with AML and MDS who relapse or progress after reduced intensity allogeneic hematopoietic cell transplantation.
  • Most deaths were due to disease progression (17/20, 85%).

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  • (PMID = 17846595.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
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55. 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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56. Sun Q, So CC, Yip SF, Wan TS, Ma SK, Chan LC: Functional alterations of Lin-CD34+CD38+ cells in chronic myelomonocytic leukemia and on progression to acute leukemia. Leuk Res; 2008 Sep;32(9):1374-81
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  • [Title] Functional alterations of Lin-CD34+CD38+ cells in chronic myelomonocytic leukemia and on progression to acute leukemia.
  • The functional behavior of hematopoietic stem cell (HSC) and progenitors in chronic myelomonocytic leukemia (CMML) and on disease progression is little known.
  • We performed cell proliferation, apoptosis, hematopoietic colony forming/replating and differentiation potential studies in the purified subpopulations of Lin(-)CD34(+)CD38(-) and Lin(-)CD34(+)CD38(+) cells from 16 CMML with 6 cases after acute myeloid leukemia transformation (AML-t).
  • We observed an expansion of the hematopoietic progenitor pool (Lin(-)CD34(+) cells) in AML-t comprising mainly Lin(-)CD34(+)CD38(+) cells.
  • The Lin(-)CD34(+)CD38(+) cells in AML-t displayed high proliferative activity, resistance to apoptosis, enhanced myeloid colony formation/replating ability and a complete dendritic cell (DC) differentiation block.
  • Our findings suggest Lin(-)CD34(+)CD38(+) cells instead of Lin(-)CD34(+)CD38(-) cells could be the target(s) of secondary genetic lesions underpinning progression from CMML to AML, which have implications for the further study of the biology of leukemic transformation and the design of new strategies for the effective treatment of CMML.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis / physiology. Cell Cycle / physiology. Cell Proliferation. Cell Transformation, Neoplastic. Colony-Forming Units Assay. Dendritic Cells / metabolism. Disease Progression. Flow Cytometry. Granulocyte Colony-Stimulating Factor / administration & dosage. Hematopoietic Stem Cells. Humans. Middle Aged. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 18372040.001).
  • [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 / Antigens, CD34; 0 / Membrane Glycoproteins; 0 / Tumor Necrosis Factor-alpha; 143011-72-7 / Granulocyte Colony-Stimulating Factor; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
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57. Nakamura S, Okinaka K, Hirano I, Ono T, Sugimoto Y, Shigeno K, Fujisawa S, Shinjo K, Ohnishi K: KIS induces proliferation and the cell cycle progression through the phosphorylation of p27Kip1 in leukemia cells. Leuk Res; 2008 Sep;32(9):1358-65
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  • [Title] KIS induces proliferation and the cell cycle progression through the phosphorylation of p27Kip1 in leukemia cells.
  • These data demonstrated that the KIS activity was induced during G0/G1, and it promotes cell cycle progression by phosphorylation of S10 on p27(Kip1).
  • We showed that KIS mRNA expression was increased in primary leukemia specimens (acute myelogenous leukemia (AML); 37, myelodysplastic syndrome (MDS); 72, acute lymphoblastic leukemia (ALL); 23), and the mean ratios of KIS to G3PDH in AML, MDS and ALL specimens were 3.62+/-0.68, 3.27+/-0.73 and 3.17+/-0.58, respectively.
  • Moreover, we found that KIS protein was overexpressed in all 132 adults cases of various leukemias, including 37 AML (8 M1, 12 M2, 2 M3, 7 M4, 8 M5), 72 MDS (42 RAEB-I, 30 REAB-II) and 23 ALL (23 L2).
  • This study demonstrates that the elevated levels of KIS protein in leukemia cells promote the cell cycle progression in leukemia cells.

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  • (PMID = 18384876.001).
  • [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 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / UHMK1 protein, human
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58. Kuchenbauer F, Morin RD, Argiropoulos B, Petriv OI, Griffith M, Heuser M, Yung E, Piper J, Delaney A, Prabhu AL, Zhao Y, McDonald H, Zeng T, Hirst M, Hansen CL, Marra MA, Humphries RK: In-depth characterization of the microRNA transcriptome in a leukemia progression model. Genome Res; 2008 Nov;18(11):1787-97
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  • [Title] In-depth characterization of the microRNA transcriptome in a leukemia progression model.
  • MicroRNAs (miRNAs) have been shown to play important roles in physiological as well as multiple malignant processes, including acute myeloid leukemia (AML).
  • In an effort to gain further insight into the role of miRNAs in AML, we have applied the Illumina massively parallel sequencing platform to carry out an in-depth analysis of the miRNA transcriptome in a murine leukemia progression model.
  • This model simulates the stepwise conversion of a myeloid progenitor cell by an engineered overexpression of the nucleoporin 98 (NUP98)-homeobox HOXD13 fusion gene (ND13), to aggressive AML inducing cells upon transduction with the oncogenic collaborator Meis1.
  • The large number of miRNAs expressed and the nature of differential expression suggest that leukemic progression as modeled here is dictated by the repertoire of shared, but differentially expressed miRNAs.
  • A stringent target prediction analysis coupled with in vitro target validation revealed the potential for miRNA-mediated release of oncogenes that facilitates leukemic progression from the preleukemic to leukemia inducing state.

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  • (PMID = 18849523.001).
  • [ISSN] 1088-9051
  • [Journal-full-title] Genome research
  • [ISO-abbreviation] Genome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Hoxd13 protein, mouse; 0 / MicroRNAs; 0 / Neoplasm Proteins; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm; 0 / Transcription Factors; 0 / myeloid ecotropic viral integration site 1 protein; 0 / nuclear pore complex protein 98
  • [Other-IDs] NLM/ PMC2577858
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59. Jones D, Yao H, Romans A, Dando C, Pierce S, Borthakur G, Hamilton A, Bueso-Ramos C, Ravandi F, Garcia-Manero G, Kantarjian H: Modeling interactions between leukemia-specific chromosomal changes, somatic mutations, and gene expression patterns during progression of core-binding factor leukemias. Genes Chromosomes Cancer; 2010 Feb;49(2):182-91
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  • [Title] Modeling interactions between leukemia-specific chromosomal changes, somatic mutations, and gene expression patterns during progression of core-binding factor leukemias.
  • In cancer genomes, changes observed during tumor progression can be difficult to separate from nonspecific accumulation of cytogenetic changes due to cancer-associated genetic instability.
  • Expression profiles for DNA replication/repair genes and the mutation status of KRAS, NRAS, FLT3, and KIT were compared with the karyotypic changes at diagnosis and relapse(s) in 94 cases of inv(16)(p13.1q22)-AML and 82 cases of t(8;21)(q22;q22)-AML.
  • The majority of both AML types demonstrated a simple aneuploid pattern of cytogenetic progression, with highly distinctive patterns of chromosome copy number changes, such as +22 and +13 exclusively in inv(16)-AML and -Y and -X in t(8;21)-AML.
  • Selection of certain cytogenetic changes correlated with particular somatic mutations, such as +8 with RAS mutation, and absence of kinase pathway mutations in t(8;21)-AML with localized deletions at chromosome band 9q22.
  • Alterations in transcript levels of mitotic spindle kinases such as CHEK1, AURKA, and AURKB were associated with the aneuploid progression pattern, particularly in t(8;21) cases.
  • Despite the similarity in the initiating genetics of the two CBF AML types, highly tumor-specific patterns of limited aneuploidy are noted that persist and continue to accumulate at relapse.

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  • (PMID = 19908318.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA100707; United States / NCI NIH HHS / CA / 1P50CA100707-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factors
  • [Other-IDs] NLM/ NIHMS155604; NLM/ PMC4161977
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60. Vélez-Ruelas MA, Martínez-Jaramillo G, Arana-Trejo RM, Mayani H: Hematopoietic changes during progression from Fanconi anemia into acute myeloid leukemia: case report and brief review of the literature. Hematology; 2006 Oct;11(5):331-4
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  • [Title] Hematopoietic changes during progression from Fanconi anemia into acute myeloid leukemia: case report and brief review of the literature.
  • Around 9% of FA patients develop acute myeloid leukemia (AML), which makes FA a good genetic model to study leukemogenesis.
  • To date, however, no information exists on the functional integrity of the hematopoietic system of FA patients during the period in which they develop AML.
  • Herein, we report on the characterization of hematopoietic progenitor cells from a pediatric FA patient that developed AML.
  • Our results show that significant changes occurred in the hematopoietic system of the patient from the time he presented with FA to the time he developed AML.
  • Interestingly, no significant changes in the karyotype of marrow cells were observed, indicating that progression from FA into AML may proceed without major chromosomal alterations (i.e. translocations and/or deletions).
  • This study represents one of the first steps towards the cellular characterization of the hematopoietic system in FA patients that develop AML.
  • [MeSH-minor] Bone Marrow Cells / pathology. Child. Disease Progression. Humans. Karyotyping. Male

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  • (PMID = 17607582.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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61. Hentschel N, Krusch M, Kiener PA, Kolb HJ, Salih HR, Schmetzer HM: Serum levels of sCD137 (4-1BB) ligand are prognostic factors for progression in acute myeloid leukemia but not in non-Hodgkin's lymphoma. Eur J Haematol; 2006 Aug;77(2):91-101
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  • [Title] Serum levels of sCD137 (4-1BB) ligand are prognostic factors for progression in acute myeloid leukemia but not in non-Hodgkin's lymphoma.
  • Recently, we demonstrated that low levels of soluble (s) CD137L and high levels of sCD178 correlate significantly with a long progression free survival in patients with myelodysplastic syndrome (MDS).
  • In this study, we correlated sCD137L and sCD178 levels in sera of 42 samples of patients with acute myeloid leukemia (AML) and 46 samples of patients with non-Hodgkin's lymphoma (NHL) with stages, subtypes, and the clinical course of the diseases and determined cut-off values with maximum probability for significant differentiation between cases with higher/lower probability for progress free survival.
  • In contrast to patients with MDS, surprisingly no correlation between sCD178 levels and different subtypes and stages or with prognosis in AML or NHL were observed.
  • Regarding sCD137L, NHL-patients displayed lower levels compared with AML.
  • Statistically significant higher median levels of sCD137L are present in patients with undifferentiated AML (M1/M2, 1,470 pg/mL), poor cytogenetic risk (288 pg/mL) and higher levels of BM-blasts (186 pg/mL) compared with patients with monocytoid AML (M4/M5, 89 pg/mL), intermediate cytogenetic risk (59 pg/mL) and lower levels of BM-blasts (14 pg/mL) respectively.
  • Furthermore, in AML patients sCD137L levels correlate significantly with the probabilities to achieve complete remission (CR), stay in CR or with progress of the disease.
  • Taken together, our data demonstrate that sCD137L can be used as a prognostic factor not only in MDS but also in AML.
  • [MeSH-minor] 4-1BB Ligand. Acute Disease. Adult. Aged. Aged, 80 and over. Blast Crisis / blood. Child, Preschool. Disease Progression. Disease-Free Survival. Fas Ligand Protein. Female. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / blood. Lymphoma, B-Cell / blood. Lymphoma, T-Cell / blood. Male. Middle Aged. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / blood. Prognosis. Retrospective Studies. Solubility. Survival Analysis

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  • (PMID = 16800841.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / 4-1BB Ligand; 0 / Biomarkers, Tumor; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / TNFSF9 protein, human; 0 / Tumor Necrosis Factors
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62. Mihara K, Chowdhury M, Nakaju N, Hidani S, Ihara A, Hyodo H, Yasunaga S, Takihara Y, Kimura A: Bmi-1 is useful as a novel molecular marker for predicting progression of myelodysplastic syndrome and patient prognosis. Blood; 2006 Jan 1;107(1):305-8
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  • [Title] Bmi-1 is useful as a novel molecular marker for predicting progression of myelodysplastic syndrome and patient prognosis.
  • Here, we analyzed the expression of Bmi-1, which is required to regulate the self-renewal in CD34+ cells from 51 patients with cases of MDS and acute myeloid leukemia preceded by MDS (MDS-AML).
  • Higher positivity rate of Bmi-1 was preferentially seen in refractory anemia with excess blasts (RAEB), RAEB in transformation (RAEB-T), and MDS-AML compared with refractory anemia (RA) and RA with ringed sideroblasts (RARS).
  • Patients with RA and RARS with a higher percentage of Bmi-1+ cells showed disease progression to RAEB.
  • Here, we propose Bmi-1 as a novel molecular marker to predict the progression and prognosis of MDS.
  • [MeSH-minor] Aged. Aged, 80 and over. Anemia, Refractory / diagnosis. Antigens, CD34. Biomarkers / analysis. Bone Marrow / chemistry. Bone Marrow / pathology. Case-Control Studies. Cell Proliferation. Disease Progression. Female. Humans. Leukemia, Myeloid. Male. Middle Aged. Polycomb Repressive Complex 1. Prognosis

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  • (PMID = 16160010.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / BMI1 protein, human; 0 / Biomarkers; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; EC 6.3.2.19 / Polycomb Repressive Complex 1
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63. 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.


64. Agerstam H, Lilljebjörn H, Lassen C, Swedin A, Richter J, Vandenberghe P, Johansson B, Fioretos T: Fusion gene-mediated truncation of RUNX1 as a potential mechanism underlying disease progression in the 8p11 myeloproliferative syndrome. Genes Chromosomes Cancer; 2007 Jul;46(7):635-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fusion gene-mediated truncation of RUNX1 as a potential mechanism underlying disease progression in the 8p11 myeloproliferative syndrome.
  • EMS is associated with a high risk of transformation to acute myeloid leukemia (AML), but the mechanisms underlying the disease progression are unknown.
  • In the present study, we have investigated a case of EMS harboring a t(8;22)(p11;q11)/BCR-FGFR1 rearrangement as well as a t(9;21)(q34;q22) at the time of AML transformation.
  • The most likely functional outcome of the rearrangement was haploinsufficiency of RUNX1, which thus may be one mechanism by which EMS transforms to AML.
  • [MeSH-minor] Aged. Amino Acid Sequence. Base Sequence. Blotting, Northern. Blotting, Southern. DNA, Complementary. Disease Progression. Female. Humans. Male. Middle Aged. Molecular Sequence Data. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17394134.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Complementary; 0 / RUNX1 protein, human
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65. Nakamura S, Hirano I, Okinaka K, Takemura T, Yokota D, Ono T, Shigeno K, Shibata K, Fujisawa S, Ohnishi K: The FOXM1 transcriptional factor promotes the proliferation of leukemia cells through modulation of cell cycle progression in acute myeloid leukemia. Carcinogenesis; 2010 Nov;31(11):2012-21
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  • [Title] The FOXM1 transcriptional factor promotes the proliferation of leukemia cells through modulation of cell cycle progression in acute myeloid leukemia.
  • However, it is not clearly understood how FOXM1 contributes to acute myeloid leukemia (AML) cell proliferation.
  • In this study, we investigated the cellular and molecular function of FOXM1 in AML cells.
  • The FOXM1 messenger RNA (mRNA) expressed in AML cell lines was predominantly the FOXM1B isoform, and its levels were significantly higher than in normal high aldehyde dehydrogenase activity (ALDH(hi)) cells.
  • Reduction of FOXM1 expression in AML cells inhibited cell proliferation compared with control cells, through induction of G(2)/M cell cycle arrest, a decrease in the protein expression of Aurora kinase B, Survivin, Cyclin B1, S-phase kinase-associated protein 2 and Cdc25B and an increase in the protein expression of p21(Cip1) and p27(Kip1).
  • FOXM1 messenger RNA (mRNA) was overexpressed in all 127 AML clinical specimens tested (n = 21, 56, 32 and 18 for M1, M2, M4 and M5 subtypes, respectively).
  • Compared with normal ALDH(hi) cells, FOXM1 gene expression was 1.65- to 2.26-fold higher in AML cells.
  • Moreover, the FOXM1 protein was more strongly expressed in AML-derived ALDH(hi) cells compared with normal ALDH(hi) cells.
  • In addition, depletion of FOXM1 reduced colony formation of AML-derived ALDH(hi) cells due to inhibition of Cdc25B and Cyclin B1 expression.
  • In summary, we found that FOXM1B mRNA is predominantly expressed in AML cells and that aberrant expression of FOXM1 induces AML cell proliferation through modulation of cell cycle progression.
  • Thus, inhibition of FOXM1 expression represents an attractive target for AML therapy.
  • [MeSH-minor] Adult. Aged. Aldehyde Dehydrogenase / genetics. Aldehyde Dehydrogenase / metabolism. Apoptosis. Aurora Kinase B. Aurora Kinases. Blotting, Western. Cells, Cultured. Cyclin B1 / genetics. Cyclin B1 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27. Disease Progression. Fluorescent Antibody Technique. Humans. Inhibitor of Apoptosis Proteins. Intracellular Signaling Peptides and Proteins / genetics. Intracellular Signaling Peptides and Proteins / metabolism. Lymphocytes / metabolism. Microtubule-Associated Proteins / genetics. Microtubule-Associated Proteins / metabolism. Middle Aged. Protein-Serine-Threonine Kinases / genetics. Protein-Serine-Threonine Kinases / metabolism. RNA, Messenger / genetics. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. S-Phase Kinase-Associated Proteins / genetics. S-Phase Kinase-Associated Proteins / metabolism

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  • (PMID = 20823107.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / CCNB1 protein, human; 0 / CDKN1A protein, human; 0 / CDKN1B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin B1; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / FOXM1 protein, human; 0 / Forkhead Transcription Factors; 0 / Inhibitor of Apoptosis Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Microtubule-Associated Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / S-Phase Kinase-Associated Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 1.2.1.3 / Aldehyde Dehydrogenase; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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66. Hultdin M, Sundström G, Wahlin A, Lundström B, Samuelsson J, Birgegård G, Engström-Laurent A: Progression of bone marrow fibrosis in patients with essential thrombocythemia and polycythemia vera during anagrelide treatment. Med Oncol; 2007;24(1):63-70
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  • [Title] Progression of bone marrow fibrosis in patients with essential thrombocythemia and polycythemia vera during anagrelide treatment.
  • Adequate bone marrow biopsies were obtained from 53 of the CMPD patients [36 essential thrombocythemia (ET), 16 polycythemia vera (PV), 1 chronic idiopathic myelofibrosis (CIMF)] before treatment and compared with biopsies from 30 healthy volunteers and 34 patients with acute myeloid leukemia (AML).
  • Higher reticulin and hyaluronan (HYA) scores were found before anagrelide therapy in the CMPD patients than in the normal controls (p < 0.001 and p < 0.001, respectively) and AML patients (p < 0.001 and p = 0.011, respectively).
  • The increase of reticulin and HYA in the bone marrow after 2 yr of treatment with anagrelide indicated progression of fibrosis.
  • Although anagrelide is a valuable drug for reduction of platelet levels, it seems unable to stop progression of bone marrow fibrosis and hypercellularity in ET and PV.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Disease Progression. Female. Humans. Hyaluronic Acid / metabolism. Male. Middle Aged. Prognosis. Prospective Studies. Reticulin / metabolism. Thrombocytosis

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  • (PMID = 17673813.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fibrinolytic Agents; 0 / Quinazolines; 0 / Reticulin; 0 / anagrelide; 9004-61-9 / Hyaluronic Acid
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67. Berasain C, Sampedro A, Mauleón I, Goñi S, Latasa MU, Matscheko N, García-Bravo M, Unzu C, Corrales FJ, Enríquez de Salamanca R, Prieto J, Avila MA, Fontanellas A: Epidermal growth factor receptor ligands in murine models for erythropoietic protoporphyria: potential novel players in the progression of liver injury. Cell Mol Biol (Noisy-le-grand); 2009;55(1):29-37
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  • [Title] Epidermal growth factor receptor ligands in murine models for erythropoietic protoporphyria: potential novel players in the progression of liver injury.
  • However its chronic activation participates in the progression of liver disease, including fibrogenesis and malignant transformation.
  • Interestingly, protoporphyrin accumulation in cultured hepatic AML-12 cells readily elicited the expression of these three EGFR ligands.

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  • (PMID = 19267999.001).
  • [ISSN] 1165-158X
  • [Journal-full-title] Cellular and molecular biology (Noisy-le-Grand, France)
  • [ISO-abbreviation] Cell. Mol. Biol. (Noisy-le-grand)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Amphiregulin; 0 / Areg protein, mouse; 0 / Betacellulin; 0 / Btc protein, mouse; 0 / EGF Family of Proteins; 0 / Epgn protein, mouse; 0 / Epigen; 0 / Epiregulin; 0 / Ereg protein, mouse; 0 / Glycoproteins; 0 / Hbegf protein, mouse; 0 / Heparin-binding EGF-like Growth Factor; 0 / Intercellular Signaling Peptides and Proteins; 0 / Protoporphyrins; 0 / Transforming Growth Factor alpha; 32HRV3E3D5 / Griseofulvin; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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68. Jiang JG, Roman E, Nandula SV, Murty VV, Bhagat G, Alobeid B: Congenital MLL-positive B-cell acute lymphoblastic leukemia (B-ALL) switched lineage at relapse to acute myelocytic leukemia (AML) with persistent t(4;11) and t(1;6) translocations and JH gene rearrangement. Leuk Lymphoma; 2005 Aug;46(8):1223-7
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  • [Title] Congenital MLL-positive B-cell acute lymphoblastic leukemia (B-ALL) switched lineage at relapse to acute myelocytic leukemia (AML) with persistent t(4;11) and t(1;6) translocations and JH gene rearrangement.
  • [MeSH-minor] Cell Lineage. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. Chromosomes, Human, Pair 6 / genetics. Cytogenetic Analysis. Disease Progression. Fatal Outcome. Female. Histone-Lysine N-Methyltransferase. Humans. Immunoglobulin Heavy Chains / genetics. Immunoglobulin J-Chains / genetics. Immunophenotyping. Infant, Newborn. Prognosis. Recurrence

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  • (PMID = 16085566.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin J-Chains; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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69. Amadori S, Suciu S, Selleslag D, Stasi R, Alimena G, Baila L, Rizzoli V, Borlenghi E, Gaidano G, Magro D, Torelli G, Muus P, Venditti A, Cacciola E, Lauria F, Vignetti M, de Witte T: Randomized trial of two schedules of low-dose gemtuzumab ozogamicin as induction monotherapy for newly diagnosed acute myeloid leukaemia in older patients not considered candidates for intensive chemotherapy. A phase II study of the EORTC and GIMEMA leukaemia groups (AML-19). Br J Haematol; 2010 May;149(3):376-82
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  • [Title] Randomized trial of two schedules of low-dose gemtuzumab ozogamicin as induction monotherapy for newly diagnosed acute myeloid leukaemia in older patients not considered candidates for intensive chemotherapy. A phase II study of the EORTC and GIMEMA leukaemia groups (AML-19).
  • Primary endpoint was the rate of disease non-progression (DnP), defined as the proportion of patients either achieving a response or maintaining a stable disease following GO induction in each arm.
  • [MeSH-minor] Aged. Antibodies, Monoclonal, Humanized. Disease Progression. Drug Administration Schedule. Feasibility Studies. Female. Humans. Male. Middle Aged. Treatment Outcome

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  • [Cites] Blood. 2001 May 15;97(10):3197-204 [11342449.001]
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  • (PMID = 20230405.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U10 CA011488; United States / NCI NIH HHS / CA / U10 CA011488-33
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 93NS566KF7 / gemtuzumab
  • [Other-IDs] NLM/ NIHMS189126; NLM/ PMC2864316
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70. Cocco L, Manzoli L, Palka G, Martelli AM: Nuclear phospholipase C beta1, regulation of the cell cycle and progression of acute myeloid leukemia. Adv Enzyme Regul; 2005;45:126-35
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  • [Title] Nuclear phospholipase C beta1, regulation of the cell cycle and progression of acute myeloid leukemia.
  • PLC beta1 is a well-known example, given that it has been shown that only the enzyme located in the nucleus targets the cyclin D3/cdk4 complex, playing, in turn, a key role in the control of normal progression through the G1 phase of the cell cycle.
  • Moreover, non-specific alterations in chromosome 20 have been found in patients affected by MDS and acute myeloid leukemia AML.
  • MDS is an adult hematological disease that evolves into AML in about 30% of the cases.
  • The availability of a highly specific probe gave an opportunity to perform in patients affected with MDS/AML, associated with normal karyotype, painting and FISH analysis aimed to check the PLC beta1 gene, given that this signaling molecule is a key player in the control of some checkpoints of the normal progression through the cell cycle.
  • FISH analysis disclosed in a small group of MDS/AML patients with normal karyotype the monoallelic deletion of the PLC beta1 gene.
  • The MDS patients, bearing the deletion, rapidly evolved to AML, whilst the normal karyotype MDS patients, showing non-deletion of PLC beta1 gene, are still alive at least 24 months after the diagnosis.
  • The immunocytochemical analysis using an anti PLC beta1 monoclonal antibody showed that all the AML/MDS patients who were normal at FISH analysis also had normal staining of the nucleus, which is a preferential site for PLC beta1.
  • The reported data strengthen the contention of a key role played by PLC beta1 in the nucleus, suggest a possible involvement of PLC beta1 in the progression of MDS to AML and pave the way for a larger investigation aimed at identifying a possible high risk group among MDS patients with a normal karyotype.


71. Rassool FV, Gaymes TJ, Omidvar N, Brady N, Beurlet S, Pla M, Reboul M, Lea N, Chomienne C, Thomas NS, Mufti GJ, Padua RA: Reactive oxygen species, DNA damage, and error-prone repair: a model for genomic instability with progression in myeloid leukemia? Cancer Res; 2007 Sep 15;67(18):8762-71
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  • [Title] Reactive oxygen species, DNA damage, and error-prone repair: a model for genomic instability with progression in myeloid leukemia?
  • Myelodysplastic syndromes (MDS) comprise a heterogeneous group of disorders characterized by ineffective hematopoiesis, with an increased propensity to develop acute myelogenous leukemia (AML).
  • The molecular basis for MDS progression is unknown, but a key element in MDS disease progression is loss of chromosomal material (genomic instability).
  • Using our two-step mouse model for myeloid leukemic disease progression involving overexpression of human mutant NRAS and BCL2 genes, we show that there is a stepwise increase in the frequency of DNA damage leading to an increased frequency of error-prone repair of double-strand breaks (DSB) by nonhomologous end-joining.
  • There is a concomitant increase in reactive oxygen species (ROS) in these transgenic mice with disease progression.
  • Our data link gene abnormalities to constitutive DNA damage and increased DSB repair errors in vivo and provide a mechanism for an increase in the error rate of DNA repair with MDS disease progression.
  • These data suggest treatment strategies that target RAS/RAC pathways and ROS production in human MDS/AML.
  • [MeSH-minor] Animals. Disease Models, Animal. Disease Progression. Genes, bcl-2. Genes, ras. Mice. Mice, Transgenic


72. 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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73. Chandra P, Luthra R, Zuo Z, Yao H, Ravandi F, Reddy N, Garcia-Manero G, Kantarjian H, Jones D: Acute myeloid leukemia with t(9;11)(p21-22;q23): common properties of dysregulated ras pathway signaling and genomic progression characterize de novo and therapy-related cases. Am J Clin Pathol; 2010 May;133(5):686-93
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  • [Title] Acute myeloid leukemia with t(9;11)(p21-22;q23): common properties of dysregulated ras pathway signaling and genomic progression characterize de novo and therapy-related cases.
  • We compared pathogenetic features of 32 de novo and 29 therapy-related (t) t(9;11)(p21-22;q23)/MLLT3-MLL acute myeloid leukemia (AML) cases to identify progression factors and to assess whether distinction between these manifestations is warranted.
  • Ras point mutations were common in both groups (overall, 18/50 [36%]) and associated with monocytic phenotype and aneuploid progression.
  • Outcome for both groups was poor (relapsed or refractory in 49/61 [80%] cases); however, patients with t-AML were generally older and female, with worse outcome (P = .03), likely secondary to t-AML mostly arising in patients with breast cancer following topoisomerase inhibitor-containing chemotherapy.
  • Ras activation seems to complement the MLLT3-MLL oncogene in transformation with features of de novo and t-AML with MLLT3-MLL being similar.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Disease Progression. Female. Gene Expression Profiling. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Infant. Male. MicroRNAs / genetics. MicroRNAs / metabolism. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Point Mutation. Signal Transduction. Survival Rate. Texas / epidemiology. Young Adult

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  • (PMID = 20395514.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / MLLT3 protein, human; 0 / MicroRNAs; 0 / Nuclear Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.6.5.2 / ras Proteins
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74. 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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75. 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


76. Pigazzi M, Ricotti E, Germano G, Faggian D, Aricò M, Basso G: cAMP response element binding protein (CREB) overexpression CREB has been described as critical for leukemia progression. Haematologica; 2007 Oct;92(10):1435-7
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  • [Title] cAMP response element binding protein (CREB) overexpression CREB has been described as critical for leukemia progression.
  • CREB has been described as critical for leukemia progress.
  • We investigated CREB expression in ALL and AML pediatric patients.
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Chromosomes, Human / genetics. Disease Progression. Humans. Infant. Middle Aged

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  • (PMID = 18024382.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Cyclic AMP Response Element-Binding Protein
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77. Thepot S, Itzykson R, Seegers V, Raffoux E, Quesnel B, Chait Y, Sorin L, Dreyfus F, Cluzeau T, Delaunay J, Sanhes L, Eclache V, Dartigeas C, Turlure P, Harel S, Salanoubat C, Kiladjian JJ, Fenaux P, Adès L, Groupe Francophone des Myelodysplasies (GFM): Treatment of progression of Philadelphia-negative myeloproliferative neoplasms to myelodysplastic syndrome or acute myeloid leukemia by azacitidine: a report on 54 cases on the behalf of the Groupe Francophone des Myelodysplasies (GFM). Blood; 2010 Nov 11;116(19):3735-42
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  • [Title] Treatment of progression of Philadelphia-negative myeloproliferative neoplasms to myelodysplastic syndrome or acute myeloid leukemia by azacitidine: a report on 54 cases on the behalf of the Groupe Francophone des Myelodysplasies (GFM).
  • Transformation of Philadelphia (Ph)-negative myeloproliferative neoplasms (MPNs) to myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML) is associated with poor response to chemotherapy and short survival.
  • Fifty-four patients with Ph-negative MPN (including 21 essential thrombocythemia [ET], 21 polycythemia vera [PV], 7 primary myelofibrosis, and 5 unclassified MPN) who had progressed to AML (n = 26) or MDS (n = 28) were treated with azacitidine in a patient-named program.
  • Prognostic factors were for overall response the underlying MPN (71% vs 33% responses in ET and PV, respectively; P = .016); prognostic factors for CR achievement were the underlying MPN (14% CR for PV vs 43% for ET; P = .040) and World Health Organization classification at transformation (36% vs 12% CR in MDS and AML, respectively, P = .038).
  • Azacitidine gives encouraging results in Ph-negative MPN having progressed to AML or MDS, but response duration is short, and consolidation treatments have to be evaluated.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. France / epidemiology. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Philadelphia Chromosome. Prognosis. Treatment Outcome


78. Liu JM, Bignon J, Ilic V, Briscoe C, Lallemand JY, Riches A, Wdzieczak-Bakala J: Evidence for an association of high levels of endogenous Acetyl-Ser-Asp-Lys-Pro, a potent mediator of angiogenesis, with acute myeloid leukemia development. Leuk Lymphoma; 2006 Sep;47(9):1915-20
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  • Evidence from clinical and laboratory studies suggests that angiogenesis is important in the progression of solid tumours and hematologic malignancies.
  • Levels of AcSDKP in the plasma and bone marrow (BM) cells from mice bearing an acute myeloid leukemia (AML) were five- to ten-fold greater than those in non-leukemic mice.
  • Furthermore, a strong correlation between the concentration of endogenous AcSDKP and the progression of AML was demonstrated.
  • [MeSH-minor] Animals. Disease Progression. Immunoenzyme Techniques. Male. Mice. Mice, Inbred CBA. Spleen / cytology

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  • [CommentIn] Leuk Lymphoma. 2006 Sep;47(9):1732-3 [17064980.001]
  • (PMID = 17065006.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Growth Inhibitors; 0 / Oligopeptides; H041538E9P / goralatide
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79. 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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80. Kalinkovich A, Tavor S, Avigdor A, Kahn J, Brill A, Petit I, Goichberg P, Tesio M, Netzer N, Naparstek E, Hardan I, Nagler A, Resnick I, Tsimanis A, Lapidot T: Functional CXCR4-expressing microparticles and SDF-1 correlate with circulating acute myelogenous leukemia cells. Cancer Res; 2006 Nov 15;66(22):11013-20
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  • Stromal cell-derived factor-1 (SDF-1/CXCL12) and its receptor CXCR4 are implicated in the pathogenesis and prognosis of acute myelogenous leukemia (AML).
  • In the present study, we investigated the putative relationships between the SDF-1/CXCR4 axis and microparticles in AML.
  • We detected CXCR4-expressing microparticles (CXCR4(+) microparticles) in the peripheral blood and bone marrow plasma samples of normal donors and newly diagnosed adult AML patients.
  • In samples from AML patients, levels of CXCR4(+) microparticles and total SDF-1 were elevated compared with normal individuals.
  • The majority of CXCR4(+) microparticles in AML patients were CD45(+), whereas in normal individuals, they were mostly CD41(+).
  • Importantly, we found a strong correlation between the levels of CXCR4(+) microparticle and WBC count in the peripheral blood and bone marrow plasma obtained from the AML patients.
  • Furthermore, our data indicate NH(2)-terminal truncation of the CXCR4 molecule in the microparticles of AML patients.
  • However, such microparticles were capable of transferring the CXCR4 molecule to AML-derived HL-60 cells, enhancing their migration to SDF-1 in vitro and increasing their homing to the bone marrow of irradiated NOD/SCID/beta2m(null) mice.
  • Our findings suggest that functional CXCR4(+) microparticles and SDF-1 are involved in the progression of AML.
  • We propose that their levels are potentially valuable as an additional diagnostic AML variable.

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  • (PMID = 17108140.001).
  • [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 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Receptors, CXCR4
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81. Gross M, Mkrtchyan H, Glaser M, Fricke HJ, Höffken K, Heller A, Weise A, Liehr T: Delineation of yet unknown cryptic subtelomere aberrations in 50% of acute myeloid leukemia with normal GTG-banding karyotype. Int J Oncol; 2009 Feb;34(2):417-23
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  • Acute myeloid leukemia (AML) is a heterogeneous disease with respect to clinical prognosis and acquired chromosomal aberrations.
  • After routine banding cytogenetic analysis 45% of AML patients show a normal karyotype (NK-AML).
  • For a better understanding of development and progression in AML, it is important to find markers which could be primary genetic aberrations.
  • Therefore, in this study 31 patients with NK-AML were analyzed by new high resolution molecular cytogenetic approaches.
  • According to these results, locus-specific probes for the subtelomeric regions of chromosomes 5, 9, 11, 12 and 13 were applied on 22 of the studied 31 NK-AML cases.
  • These results implicate that aberrations in the subtelomeric regions of NK-AML occur quite often and may be considered as primary genetic changes, and should not be neglected in future diagnostic approaches.

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  • (PMID = 19148476.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
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82. 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.

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  • [Copyright] Copyright (c) 2007 S. Karger AG, Basel.
  • (PMID = 18000383.001).
  • [ISSN] 1424-859X
  • [Journal-full-title] Cytogenetic and genome research
  • [ISO-abbreviation] Cytogenet. Genome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers
  • [Number-of-references] 66
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83. Willis MS, McKenna RW, Peterson LC, Coad JE, Kroft SH: Low blast count myeloid disorders with Auer rods: a clinicopathologic analysis of 9 cases. Am J Clin Pathol; 2005 Aug;124(2):191-8
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  • In 5 patients, acute myelogenous leukemia (AML) developed 6, 6, 5, 13, and 24 months after diagnosis; the patients subsequently died.
  • Three patients died at 1, 1, and 8 months without progression to AML, and only 1 was alive at 10 months.
  • MDSs with fewer than 5% blasts and Auer rods seem to be a heterogeneous group, but rapid progression to death or AML in most cases suggests that Auer rods signify an aggressive biology in MDSs with a low blast count.

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  • (PMID = 16040288.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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84. Wang H, Lindsey S, Konieczna I, Bei L, Horvath E, Huang W, Saberwal G, Eklund EA: Constitutively active SHP2 cooperates with HoxA10 overexpression to induce acute myeloid leukemia. J Biol Chem; 2009 Jan 23;284(4):2549-67
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  • Sustained HoxA10 expression during differentiation has been described in poor prognosis human acute myeloid leukemia (AML).
  • Consistent with this, engineered overexpression of HoxA10 in murine bone marrow induces a myeloproliferative disorder that progresses to AML over time.
  • This murine model suggests that HoxA10 overexpression is sufficient for myeloproliferation but that differentiation block, and therefore AML, requires acquisition of additional mutations.
  • HoxA10 is de-phosphorylated by SHP2 protein-tyrosine phosphatase in myeloid progenitors.
  • Constitutively active SHP2 mutants have been described in human AML, which dephosphorylate HoxA10 throughout myelopoiesis.
  • In this study, we hypothesize that constitutive SHP2 activation synergizes with HoxA10 overexpression to accelerate progression to AML.
  • Because both HoxA10 overexpression and constitutive SHP2 activation are found in poor prognosis human AML, these studies contribute to understanding biochemical aspects of disease progression in myeloid malignancy.

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  • (PMID = 19022774.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / 01 HL87717
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Homeodomain Proteins; 140441-81-2 / HOXA10 protein, human; 42HK56048U / Tyrosine; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
  • [Other-IDs] NLM/ PMC2629090
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85. Preudhomme C, Renneville A, Bourdon V, Philippe N, Roche-Lestienne C, Boissel N, Dhedin N, André JM, Cornillet-Lefebvre P, Baruchel A, Mozziconacci MJ, Sobol H: High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder. Blood; 2009 May 28;113(22):5583-7
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  • Familial platelet disorder (FPD), a rare autosomal dominant disorder characterized by quantitative and qualitative platelet abnormalities, is considered as a model of genetic predisposition to acute myeloid leukemia (AML).
  • In addition to the germline RUNX1 mutation, we identified a second RUNX1 alteration in 6 AML cases (acquired point mutations in 4 cases and duplication of the altered RUNX1 allele associated with acquired trisomy 21 in 2 other cases).
  • Although haploinsufficiency of RUNX1 causes FPD, our findings suggest that a second genetic event involving RUNX1 is often associated with progression to AML.


86. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.


87. 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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88. Haus O, Kotlarek-Haus S, Potoczek S, Czarnecka M, Duszenko E, Makowska I, Mirowska N, Kuliczkowski K: Myelodysplastic syndromes according to FAB and WHO classification. Single center experience. Neoplasma; 2006;53(2):136-43
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  • The progression to AML was more common in less favorable groups, with p=0.0001 for FAB and p=0.00016 for WHO.


89. Weisberg E, Roesel J, Furet P, Bold G, Imbach P, Flörsheimer A, Caravatti G, Jiang J, Manley P, Ray A, Griffin JD: Antileukemic Effects of Novel First- and Second-Generation FLT3 Inhibitors: Structure-Affinity Comparison. Genes Cancer; 2010 Oct;1(10):1021-32

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Constitutively activated mutant FLT3 has emerged as a promising target for therapy for the subpopulation of acute myeloid leukemia (AML) patients who harbor it.
  • However, the identification of PKC412-resistant leukemic blast cells in the bone marrow of AML patients has propelled the development of novel and structurally distinct FLT3 inhibitors that have the potential to override drug resistance and more efficiently prevent disease progression or recurrence.

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  • (PMID = 21779428.001).
  • [ISSN] 1947-6027
  • [Journal-full-title] Genes & cancer
  • [ISO-abbreviation] Genes Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R37 CA036167; United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / R37 CA036167-19; United States / NCI NIH HHS / CA / P01 CA066996-14; United States / NIDDK NIH HHS / DK / P01 DK050654; United States / NCI NIH HHS / CA / R01 CA036167
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3092267
  • [Keywords] NOTNLM ; AML / FLT3 inhibitor / drug potency / drug resistance / leukemia / neoplasia / structure affinity
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90. Gery S, Gombart AF, Yi WS, Koeffler C, Hofmann WK, Koeffler HP: Transcription profiling of C/EBP targets identifies Per2 as a gene implicated in myeloid leukemia. Blood; 2005 Oct 15;106(8):2827-36
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  • Per2 levels were reduced in lymphoma cell lines and in acute myeloid leukemia (AML) patient samples.
  • These results suggest that Per2 is a downstream C/EBPalpha-target gene involved in AML, and its disruption might be involved in initiation and/or progression of AML.

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  • (PMID = 15985538.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [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.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / Cell Cycle Proteins; 0 / Nuclear Proteins; 0 / PER2 protein, human; 0 / Per2 protein, mouse; 0 / Period Circadian Proteins; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1895299
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91. Silverman LR: Clinical roundtable monograph. Overall survival and maintenance of MDS patients. Clin Adv Hematol Oncol; 2009 Jul;7(7):S3-5
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  • The disease is marked by gradually worsening cytopenias and a variable risk for the eventual transformation to acute myelogenous leukemia (AML).
  • The International Prognostic Scoring System (IPSS) was developed to aid in determining the prognosis of patients with MDS; this system categorizes patients into four risk groups for both overall survival and transformation to AML: low, intermediate-1, intermediate-2, and high.
  • The management of MDS is based on the goal of controlling cytopenia-related symptoms, improving survival, improving quality of life, and decreasing risk of progression to AML.

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  • (PMID = 19708287.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
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92. Rosenfeld CS: Clinical development of decitabine as a prototype for an epigenetic drug program. Semin Oncol; 2005 Oct;32(5):465-72
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  • A clinical development program with low-dose decitabine in malignant diseases is focused on myelodysplastic syndrome (MDS), acute myelogenous leukemia (AML), and chronic myelogenous leukemia (CML).
  • A phase III trial in MDS showed objective responses (complete [CR] plus partial [PR] remission) and longer median time to progression to AML or death with decitabine than with supportive care alone.

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  • (PMID = 16210087.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / DNA Adducts; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
  • [Number-of-references] 72
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93. Choi SW, Boxer LA, Pulsipher MA, Roulston D, Hutchinson RJ, Yanik GA, Cooke KR, Ferrara JL, Levine JE: Stem cell transplantation in patients with severe congenital neutropenia with evidence of leukemic transformation. Bone Marrow Transplant; 2005 Mar;35(5):473-7
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  • With appropriate treatment using recombinant human granulocyte-colony-stimulating factor (r-HuG-CSF), SCN patients are now surviving longer, but are at increased risk of developing myelodysplastic syndrome (MDS)/acute myeloid leukemia (AML).
  • We report results for six patients with SCN who underwent HSCT for MDS or AML between 1997 and 2001 at two transplant centers.
  • Four patients, who all received induction chemotherapy for AML prior to HSCT, died.
  • Rapid transplantation should be the goal for the SCN patient once the diagnosis of MDS/AML is established.
  • SCN patients should be monitored carefully for progression to MDS in order to be treated with HSCT as soon as they have progressed and before developing AML.
  • For SCN patients who progress to AML, HSCT should still be considered, even though the risks appear to be greater.
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Bone Marrow Examination. Child. Child, Preschool. Disease Progression. Female. Humans. Infant. Karyotyping. Male. Myelodysplastic Syndromes / etiology. Myelodysplastic Syndromes / therapy. Retrospective Studies. Survival Rate. Transplantation Conditioning. Treatment Outcome

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  • (PMID = 15640815.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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94. Omidvar N, Kogan S, Beurlet S, le Pogam C, Janin A, West R, Noguera ME, Reboul M, Soulie A, Leboeuf C, Setterblad N, Felsher D, Lagasse E, Mohamedali A, Thomas NS, Fenaux P, Fontenay M, Pla M, Mufti GJ, Weissman I, Chomienne C, Padua RA: BCL-2 and mutant NRAS interact physically and functionally in a mouse model of progressive myelodysplasia. Cancer Res; 2007 Dec 15;67(24):11657-67
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  • Myelodysplastic syndromes (MDS) are clonal stem cell hematologic disorders that evolve to acute myeloid leukemia (AML) and thus model multistep leukemogenesis.
  • Activating RAS mutations and overexpression of BCL-2 are prognostic features of MDS/AML transformation.
  • Using NRASD12 and BCL-2, we created two distinct models of MDS and AML, where human (h)BCL-2 is conditionally or constitutively expressed.
  • Our novel transplantable in vivo models show that expression of hBCL-2 in a primitive compartment by mouse mammary tumor virus-long terminal repeat results in a disease resembling human MDS, whereas the myeloid MRP8 promoter induces a disease with characteristics of human AML.
  • Expanded leukemic stem cell (Lin(-)/Sca-1(+)/c-Kit(+)) populations and hBCL-2 in the increased RAS-GTP complex within the expanded Sca-1(+) compartment are described in both MDS/AML-like diseases.
  • This represents the first in vivo progression model of MDS/AML dependent on the formation of a BCL-2:RAS-GTP complex.
  • The colocalization of BCL-2 and RAS in the bone marrow of MDS/AML patients offers targeting either oncogene as a therapeutic strategy.
  • [MeSH-minor] Animals. Bone Marrow Transplantation. Cell Transplantation. Colony-Forming Units Assay. Disease Models, Animal. Disease Progression. Immunophenotyping. Leukemia / genetics. Leukemia, Myeloid / genetics. Mice. Mice, Transgenic. Microscopy, Confocal. Spleen


95. Kessler T, Fehrmann F, Bieker R, Berdel WE, Mesters RM: Vascular endothelial growth factor and its receptor as drug targets in hematological malignancies. Curr Drug Targets; 2007 Feb;8(2):257-68
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  • While this has been accepted for solid forms of cancer there is now emerging evidence that progression of hematological malignancies also requires the induction of new blood vessels.
  • Complete remissions in acute myeloid leukemia (AML) have been reported by targeting the receptor tyrosine kinase system of VEGF.
  • While the pathophysiology behind the contribution of VEGF to leukemia progression is not yet completely understood, VEGF and its receptors may provide promising targets not only in solid tumors but also hematological malignancies such as AML.
  • [MeSH-minor] Cell Proliferation. Cell Survival. Disease Progression. Humans

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  • (PMID = 17305503.001).
  • [ISSN] 1873-5592
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 226
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96. 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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97. Caudill JS, Sternberg AJ, Li CY, Tefferi A, Lasho TL, Steensma DP: C-terminal nucleophosmin mutations are uncommon in chronic myeloid disorders. Br J Haematol; 2006 Jun;133(6):638-41
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  • C-terminal somatic mutations in nucleophosmin (NPM), a nucleolar shuttling protein that binds p53 and p19(Arf), were recently described in karyotypically normal acute myeloid leukaemia (AML).
  • NPM1 mutations (tetranucleotide duplication) were detected in three patients, all of whom had chronic myelomonocytic leukaemia (CMML) and a short (<1 year) survival, with rapid progression to overt AML.
  • [MeSH-minor] Base Sequence. Cell Transformation, Neoplastic / genetics. Chronic Disease. DNA Mutational Analysis / methods. DNA, Neoplasm / genetics. Disease Progression. Humans. Molecular Sequence Data. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics. Prognosis

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  • (PMID = 16704439.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K12 CA090628
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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98. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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

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  • (PMID = 18604718.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / NM23 Nucleoside Diphosphate Kinases; 0 / Neoplasm Proteins; 0 / Proliferating Cell Nuclear Antigen; EC 2.7.10.1 / FLT1 protein, human; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.4.6 / NME4 protein, human; EC 2.7.4.6 / Nucleoside Diphosphate Kinase D; EC 3.1.- / ERCC1 protein, human; EC 3.1.- / Endonucleases
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99. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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


100. Finazzi G, Caruso V, Marchioli R, Capnist G, Chisesi T, Finelli C, Gugliotta L, Landolfi R, Kutti J, Gisslinger H, Marilus R, Patrono C, Pogliani EM, Randi ML, Villegas A, Tognoni G, Barbui T, ECLAP Investigators: Acute leukemia in polycythemia vera: an analysis of 1638 patients enrolled in a prospective observational study. Blood; 2005 Apr 1;105(7):2664-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Progression to acute myeloid leukemia/myelodysplastic syndromes (AML/MDS) is a possible evolution of polycythemia vera (PV), but whether some patients are at increased natural risk for this complication and how much the contribution of pharmacologic cytoreduction can affect the natural course of the disease remain uncertain.
  • AML/MDS was diagnosed in 22 patients after a median of 2.5 years from recruitment in the study and a median of 8.4 years from the diagnosis of PV.
  • Variables associated with progression to AML/MDS were assessed using different models of multivariate analysis.
  • Exposure to P32, busulphan, and pipobroman (HR, 5.46; 95% CI, 1.84-16.25; P = .0023), but not to hydroxyurea (HU) alone (HR, 0.86; 95% CI, 0.26-2.88; P = .8021), had an independent role in producing an excess risk for progression to AML/MDS compared with treatment with phlebotomy or interferon.
  • [MeSH-minor] Acute Disease. Adult. Aged. Aspirin / therapeutic use. Databases, Factual. Disease Progression. Disease-Free Survival. Female. Humans. Male. Middle Aged. Multivariate Analysis. Platelet Aggregation Inhibitors / therapeutic use. Prospective Studies. Risk Factors

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  • [CommentIn] Curr Hematol Rep. 2005 May;4(3):211-2 [15865873.001]
  • (PMID = 15585653.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Platelet Aggregation Inhibitors; R16CO5Y76E / Aspirin
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