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1. Konopleva M, Watt J, Contractor R, Tsao T, Harris D, Estrov Z, Bornmann W, Kantarjian H, Viallet J, Samudio I, Andreeff M: Mechanisms of antileukemic activity of the novel Bcl-2 homology domain-3 mimetic GX15-070 (obatoclax). Cancer Res; 2008 May 1;68(9):3413-20
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  • In this study, we investigated the mechanism of apoptosis induction of obatoclax (GX15-070), a novel Bcl-2 homology domain-3 (BH3) mimetic, in acute myeloid leukemia (AML) cell lines and primary AML samples.
  • Obatoclax inhibited cell growth of HL-60, U937, OCI-AML3, and KG-1 cell lines.
  • We show that obatoclax can promote the release of cytochrome c from isolated leukemia cell mitochondria and that apoptosis induced by this agent is preceded by the release of Bak from Mcl-1, liberation of Bim from both Bcl-2 and Mcl-1, and the formation of an active Bak/Bax complex.
  • Notably, apoptosis was diminished, but not fully prevented, in the absence of Bak/Bax or Bim, suggesting that obatoclax has additional targets that contribute to its cytotoxicity.
  • At growth inhibitory doses that did not induce apoptosis or decrease viability, obatoclax induced an S-G(2) cell-cycle block.
  • Obatoclax induced apoptosis in AML CD34+ progenitor cells with an average IC(50) of 3.59 +/- 1.23 micromol/L although clonogenicity was inhibited at concentrations of 75 to 100 nmol/L.
  • Obatoclax synergized with the novel BH3 mimetic ABT-737 to induce apoptosis in OCI-AML3 cells and synergistically induced apoptosis in combination with AraC in leukemic cell lines and in primary AML samples.
  • In conclusion, we show that obatoclax potently induces apoptosis and decreases leukemia cell proliferation and may be used in a novel therapeutic strategy for AML alone and in combination with other targeted agents and chemotherapeutics.

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  • (PMID = 18451169.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA49639; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA55164; United States / NCI NIH HHS / CA / P01 CA049639; United States / NCI NIH HHS / CA / P01 CA055164
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABT-737; 0 / Antineoplastic Agents; 0 / AraC Transcription Factor; 0 / Biphenyl Compounds; 0 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Nitrophenols; 0 / Piperazines; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrroles; 0 / Sulfonamides; 0 / obatoclax
  • [Other-IDs] NLM/ NIHMS445004; NLM/ PMC4096127
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2. Herry A, Douet-Guilbert N, Morel F, Le Bris MJ, De Braekeleer M: Redefining monosomy 5 by molecular cytogenetics in 23 patients with MDS/AML. Eur J Haematol; 2007 Jun;78(6):457-67
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  • [Title] Redefining monosomy 5 by molecular cytogenetics in 23 patients with MDS/AML.
  • Deletion of the long arm of chromosome 5 [del(5q)] or loss of a whole chromosome 5 (-5) is a common finding, arising de novo in 10% of patients with myelodysplastic syndromes (MDS) or acute myeloid leukemia (AML) and in 40% of patients with therapy-related MDS or AML.
  • We investigated by molecular cytogenetics 23 MDS/AML patients for whom conventional cytogenetics detected a monosomy 5.
  • Sequential fluorescent in situ hybridization studies with whole chromosome paints and region-specific probes, used as a complement to conventional cytogenetic analysis, allow a better interpretation of karyotypes in MDS/AML patients.
  • [MeSH-major] Chromosomes, Human, Pair 5. Leukemia, Myeloid / genetics. Monosomy. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged


3. Yoon S, Benini L, De Micheli G: Finding co-clusters of genes and clinical parameters. Conf Proc IEEE Eng Med Biol Soc; 2005;1:906-12
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  • [Title] Finding co-clusters of genes and clinical parameters.
  • The proposed method was tested with data from an Acute Myelogenous Leukemia (AML) study and identified statistically significant co-clusters of genes and clinical traits.

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  • (PMID = 17282331.001).
  • [ISSN] 1557-170X
  • [Journal-full-title] Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference
  • [ISO-abbreviation] Conf Proc IEEE Eng Med Biol Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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4. Gruschkus SK, Lairson D, Dunn JK, Risser J, Du XL: Use of white blood cell growth factors and risk of acute myeloid leukemia or myelodysplastic syndrome among elderly patients with non-Hodgkin lymphoma. Cancer; 2010 Nov 15;116(22):5279-89
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  • [Title] Use of white blood cell growth factors and risk of acute myeloid leukemia or myelodysplastic syndrome among elderly patients with non-Hodgkin lymphoma.
  • BACKGROUND: The current study was conducted to evaluate the association between colony-stimulating factor (CSF) use and the risk of developing therapy-related myelodysplastic syndromes or acute myeloid leukemia (t-MDS/AML) among a large cohort of elderly patients with non-Hodgkin lymphoma (NHL) who were treated with chemotherapy.
  • Patients were followed from their initial chemotherapy date until the date they were diagnosed with t-MDS/AML, death, or last follow-up (October 31, 2006), whichever occurred first.
  • During the follow-up period (median follow-up, 2.9 years [range, 1-14.7 years]), 272 (5.2%) patients who were treated with CSF developed t-MDS/AML, compared with 230 (2.9%) patients who did not (P < .0001, log-rank test).
  • The 5-year incidence of t-MDS/AML for patients receiving CSF was 14.1 per 1000 person-years compared with 8.3 per 1000 person-years for patients not receiving CSF.
  • In a multivariable Cox regression analysis adjusted for gender, histology, stage, comorbidities, radiotherapy, and chemotherapy agent, CSF use was found to be independently associated with a 53% increased risk of t-MDS/AML (hazard ratio [HR], 1.53; 95% confidence interval [95% CI], 1.26-1.84).
  • The observed association between CSF use and t-MDS/AML persisted across histologic subgroups (ie, diffuse large B-cell lymphoma, follicular lymphoma, and others).
  • Patients who received both CSF and antimetabolite chemotherapy were found to have a 2.5-fold increased risk of t-MDS/AML (HR, 2.49; 95% CI, 1.91-3.26) compared with patients who received neither agent.
  • CONCLUSIONS: The current study, which to our knowledge is the first large population-based study published to date, demonstrated that the administration of CSF among elderly NHL patients receiving chemotherapy was associated with an increased risk of t-MDS/AML, although the absolute risk was low.
  • [MeSH-major] Colony-Stimulating Factors / adverse effects. Leukemia, Myeloid, Acute / epidemiology. Lymphoma, Non-Hodgkin / drug therapy. Myelodysplastic Syndromes / epidemiology


5. Aziz KA: An acquired form of Bernard Soulier syndrome associated with acute myeloid leukemia. Saudi Med J; 2005 Jul;26(7):1095-8
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  • [Title] An acquired form of Bernard Soulier syndrome associated with acute myeloid leukemia.
  • OBJECTIVE: To investigate glycoprotein-1b (GP-1b) expression on platelets from patients with acute myeloid leukemia (AML).
  • METHODS: Purified platelets, obtained from AML-patients and normal control subjects, were examined for surface membrane GP1b-expression by flow cytometry and GP1b-mediated aggregation responses by aggregometry.
  • RESULTS: Platelets from the majority of AML-patients showed reduced GP1b-expression and reduced GP1b-mediated aggregation responses.
  • CONCLUSION: The present study suggests that elastase, released from leukemic blasts, degrades platelet GP1b, resulting in dysfunctional circulating platelets in AML-patients.
  • [MeSH-major] Blood Platelets / metabolism. Leukemia, Myeloid / metabolism. Platelet Glycoprotein GPIb-IX Complex / metabolism
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Bernard-Soulier Syndrome / etiology. Case-Control Studies. Female. Humans. Male. Middle Aged. Pancreatic Elastase / blood

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  • (PMID = 16047060.001).
  • [ISSN] 0379-5284
  • [Journal-full-title] Saudi medical journal
  • [ISO-abbreviation] Saudi Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Saudi Arabia
  • [Chemical-registry-number] 0 / Platelet Glycoprotein GPIb-IX Complex; EC 3.4.21.36 / Pancreatic Elastase
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6. Falini B, Tiacci E, Martelli MP, Ascani S, Pileri SA: New classification of acute myeloid leukemia and precursor-related neoplasms: changes and unsolved issues. Discov Med; 2010 Oct;10(53):281-92
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  • [Title] New classification of acute myeloid leukemia and precursor-related neoplasms: changes and unsolved issues.
  • The World Health Organization (WHO) classification of lympho-hematopoietic neoplasms is increasingly based on genetic criteria.
  • Here, we focus on changes that, as compared to the 2001 edition, were introduced into the 2008 WHO classification of acute myeloid leukemia (AML) and related precursor neoplasms.
  • The category of AML with recurrent genetic abnormalities was expanded to account for 60% of AML by adding three distinct entities, i.e., AML with t(6,9), inv(3), or t(1;22), and two provisional entities, i.e., AML with mutated NPM1 or CEBPA.
  • These changes have greatly modified the approaches to diagnosis and prognostic stratification of AML patients.
  • To emphasize the need of various parameters for diagnosis, including myelodysplasia (MD)-related cytogenetic abnormalities, history of myelodysplasia or myelodysplasia/myeloproliferative neoplasm, and multilineage dysplasia, the category of "AML with multilineage dysplasia" was re-named AML with MD-related changes.
  • Finally, we describe the unique characteristics of myeloid proliferations associated with Down syndrome and blastic plasmacytoid dendritic cell neoplasm.
  • [MeSH-major] Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / pathology. Lymphoproliferative Disorders / classification. Lymphoproliferative Disorders / pathology. Medical Oncology / trends. Neoplasms / classification. Neoplasms / pathology
  • [MeSH-minor] Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Disease Progression. Down Syndrome / complications. Down Syndrome / pathology. Humans. Precancerous Conditions / classification. Precancerous Conditions / genetics. Precancerous Conditions / pathology. World Health Organization

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  • (PMID = 21034669.001).
  • [ISSN] 1944-7930
  • [Journal-full-title] Discovery medicine
  • [ISO-abbreviation] Discov Med
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] United States
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7. Malik E, Cohen SB, Sahar D, Dann EJ, Rund D: The frequencies of NAD(P)H quinone oxidoreductase (NQO1) variant allele in Israeli ethnic groups and the relationship of NQO1*2 to adult acute myeloid leukemia in Israeli patients. Haematologica; 2006 Jul;91(7):956-9
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  • [Title] The frequencies of NAD(P)H quinone oxidoreductase (NQO1) variant allele in Israeli ethnic groups and the relationship of NQO1*2 to adult acute myeloid leukemia in Israeli patients.
  • The NQO1*2 variant enzyme (codon 609 C-->T, encoding a proline to serine substitution) with greatly reduced activity has been reported to predispose to acute myeloid leukemia (AML).
  • Our aim was to examine the relationship between NQO1*2 and AML in Israeli patients.
  • We analyzed for NQO1*2 in 262 adult Israeli patients with de novo AML and 688 controls of the same ethnic groups (Arabs, and Caucasian and Ethiopian Jews).
  • However, NQO1*2 frequencies did not differ between AML patients and controls.
  • Karyotype was not found to be associated with NQO1*2.
  • In Israeli patients, NQO1*2 does not predispose to de novo AML.
  • [MeSH-major] Genetic Variation. Leukemia, Myeloid / genetics. NAD(P)H Dehydrogenase (Quinone) / genetics
  • [MeSH-minor] Acute Disease. Gene Frequency. Israel / epidemiology. Israel / ethnology. Molecular Epidemiology

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  • (PMID = 16818284.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
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8. Bretonnière C, Touzeau C, Guillaume T, Coste-Burel M, Moreau A, Hamidou M, Guitton C, Villers D: [Multiple organ failure and disseminated adenoviral infection]. Med Mal Infect; 2010 May;40(5):296-8
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  • BACKGROUND: Peripheral blood stem cell transplantation is a frequent option, especially for patients with hematological malignancies.
  • CASE REPORTS: A first patient received this treatment for acute myeloblastic leukemia, the second for Richter's syndrome (follicular lymphoma).
  • In both cases, allograft (unrelated donor, non myeloablative conditioning) was followed by graft versus host disease (GVH) requiring an immunosuppressive treatment.
  • The diagnosis was made according to positive blood PCR, positive BAL, and hepatic histological findings.
  • T lymphocyte depletion plays a key role.

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  • [Copyright] Copyright 2009. Published by Elsevier SAS.
  • (PMID = 19616908.001).
  • [ISSN] 1769-6690
  • [Journal-full-title] Médecine et maladies infectieuses
  • [ISO-abbreviation] Med Mal Infect
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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9. Robazzi TC, Barreto JH, Silva LR, Santiago MB, Mendonça N: Osteoarticular manifestations as initial presentation of acute leukemias in children and adolescents in Bahia, Brazil. J Pediatr Hematol Oncol; 2007 Sep;29(9):622-6
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  • [Title] Osteoarticular manifestations as initial presentation of acute leukemias in children and adolescents in Bahia, Brazil.
  • OBJECTIVE: This study was to determine the prevalence and characteristics of the osteoarticular manifestations on initial clinical presentation of acute leukemias (ALs) on childhood in the state of Bahia, Brazil.
  • RESULTS: Acute lymphocytic leukemia (ALL) was diagnosed in 313 (77.1%) patients and acute myeloid leukemia (AML), in 93 (22.9%) patients, including 241 males (59.4%) and 165 females (40.6%).
  • Prior referral to our center, the most frequent initial diagnosis was anemia (15.8%), leukemia (15.0%), amygdalitis (3.7%), and rheumatic fever (2.7%).
  • The presence of joint tenderness (16.2% in ALLx5.4% in AML), arthritis (26.6% in ALLx9.7 in AML), bone tenderness (26.1% in ALLx16.1% in AML), limb tenderness (49.5% in ALLx25.8% in AML), and antalgic gait (32.8% in ALLx9.7% in AML) had higher prevalence on ALL.
  • CONCLUSIONS: AL should be considered on the differential diagnosis of osteoarticular symptoms of unknown etiology in children.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Osteoarthritis / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Brazil. Child. Child, Preschool. Female. Humans. Infant. Male

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  • (PMID = 17805037.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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10. Chen CH, Lee CM, Tung WC, Wang JH, Hung CH, Hu TH, Wang JC, Lu SN, Changchien CS: Evolution of full-length HBV sequences in chronic hepatitis B patients with sequential lamivudine and adefovir dipivoxil resistance. J Hepatol; 2010 Apr;52(4):478-85
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  • BACKGROUND & AIMS: The aim of this study was to determine the evolution of full-length hepatitis B virus (HBV) sequences in chronic hepatitis B (CHB) patients with sequential lamivudine (LAM) and adefovir (ADV) resistance.
  • METHODS: The full-length genomes of HBV were sequenced from 11 CHB patients before LAM treatment and at the emergence of LAM- and ADV-resistant HBV.
  • RESULTS: Besides the known LAM-resistant polymerase gene mutations, 10 of 11 patients who had LAM-resistant HBV variants had additional amino acid changes in the reverse transcriptase (RT) domain, and ADV therapy reversed these additional changes to pre-LAM therapy status.
  • Seven patients had amino acid changes within the known T-cell or B-cell epitopes of HBV surface and core antigens at the emergence of LAM and/or ADV resistance.
  • The frequency of pre-S deletions between nucleotide 3037-56 was higher at the emergence of ADV resistance compared with that at the emergence of LAM resistance (7/11 vs. 1/11; p=0.024).
  • Combined LAM-ADV resistance was detected in one of 11 patients.
  • CONCLUSIONS: In addition to the known LAM- and ADV-resistant mutations accompanying the emergence of LAM and ADV resistance, the changes of nucleotide or amino acid sequences occurred commonly in the HBV surface antigen or RT domain and were scattered along the full-length HBV genomes.
  • [MeSH-minor] Adult. Amino Acid Substitution / genetics. Antiviral Agents / therapeutic use. Epitopes, B-Lymphocyte / genetics. Epitopes, T-Lymphocyte / genetics. Evolution, Molecular. Female. Gene Products, pol / genetics. Genome, Viral / genetics. Genotype. Hepatitis B Core Antigens / genetics. Hepatitis B Surface Antigens / genetics. Hepatitis B e Antigens / genetics. Humans. Male. Middle Aged. Phylogeny. Reverse Transcriptase Inhibitors / therapeutic use. Young Adult

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  • (PMID = 20185198.001).
  • [ISSN] 1600-0641
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Epitopes, B-Lymphocyte; 0 / Epitopes, T-Lymphocyte; 0 / Gene Products, pol; 0 / Hepatitis B Core Antigens; 0 / Hepatitis B Surface Antigens; 0 / Hepatitis B e Antigens; 0 / Organophosphonates; 0 / P protein, Hepatitis B virus; 0 / Reverse Transcriptase Inhibitors; 2T8Q726O95 / Lamivudine; JAC85A2161 / Adenine; U6Q8Z01514 / adefovir dipivoxil
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11. Iwai M, Kiyoi H, Ozeki K, Kinoshita T, Emi N, Ohno R, Naoe T: Expression and methylation status of the FHIT gene in acute myeloid leukemia and myelodysplastic syndrome. Leukemia; 2005 Aug;19(8):1367-75
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  • [Title] Expression and methylation status of the FHIT gene in acute myeloid leukemia and myelodysplastic syndrome.
  • To clarify the role of fragile histidine triad (FHIT) in hematological malignancies, we examined the methylation status and the expression level of the FHIT gene in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) cells in comparison with the methylation of the p15(INK4B) gene.
  • The FHIT methylation was found in 13 of 94 (13.8%) AML and 22 of 40 (55.0%) MDS cases, but not in normal mononuclear cells (MNCs).
  • Both the frequency and density of methylation increased in the advanced-stages MDS and the relapsed AML cases.
  • Although FHIT and p15(INK4B) methylations were not correlated in MDS and AML, increased FHIT methylation at the relapse in AML was associated with p15(INK4B) methylation.
  • The median expression level in AML was significantly higher than in normal MNCs, although the median expression level in those with methylation was significantly lower than in those without methylation.
  • Furthermore, the methylation level at relapse was significantly higher than at diagnosis in AML.
  • These results suggested that FHIT methylation was accumulated through the disease progression of MDS and AML, and the role of the FHIT gene as a tumor suppressor seemed different in AML and MDS.
  • [MeSH-major] Acid Anhydride Hydrolases / genetics. DNA Methylation. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Neoplasm Proteins / genetics
  • [MeSH-minor] Acute Disease. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Bone Marrow / pathology. Cell Cycle Proteins / genetics. Cyclin-Dependent Kinase Inhibitor p15. Genes, Tumor Suppressor. Humans. RNA, Messenger / analysis. Recurrence. Tumor Suppressor Proteins / genetics

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  • [Copyright] Leukemia (2005) 19, 1367-1375.
  • (PMID = 15902282.001).
  • [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 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; 0 / fragile histidine triad protein; 776B62CQ27 / decitabine; EC 3.6.- / Acid Anhydride Hydrolases; M801H13NRU / Azacitidine
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12. Malaise M, Steinbach D, Corbacioglu S: Clinical implications of c-Kit mutations in acute myelogenous leukemia. Curr Hematol Malig Rep; 2009 Apr;4(2):77-82
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  • [Title] Clinical implications of c-Kit mutations in acute myelogenous leukemia.
  • This finding culminated in a two-class model integrating constitutive activating and maturation arrest-inducing mutations as key elements for the pathogenesis of acute myelogenous leukemia (AML).
  • c-Kit is expressed by myeloblasts in about 60% to 80% of patients, and the most frequently observed activating RTK mutations in AML (next to FLT3) are mutations or internal tandem duplications in c-Kit, with an overall incidence of 17%.
  • The identification of small-molecule tyrosine kinase inhibitors capable of blocking key kinase switches introduced a paradigm change in the treatment of diseases like gastrointestinal stromal tumors and chronic myelogenous leukemia.
  • Despite encouraging preclinical data, it appears that a complex clonal disease like AML will probably benefit from a synergistic approach of targeted drugs used (at least for now) in combination with conventional chemotherapy.
  • [MeSH-major] Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics. Mutation. Proto-Oncogene Proteins c-kit / genetics
  • [MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Gene Expression Regulation, Leukemic. Humans. Prognosis. Protein Kinase Inhibitors / administration & dosage. Protein Kinase Inhibitors / therapeutic use. Treatment Outcome


13. Zhang J, Harrison JS, Uskokovic M, Danilenko M, Studzinski GP: Silibinin can induce differentiation as well as enhance vitamin D3-induced differentiation of human AML cells ex vivo and regulates the levels of differentiation-related transcription factors. Hematol Oncol; 2010 Sep;28(3):124-32
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  • [Title] Silibinin can induce differentiation as well as enhance vitamin D3-induced differentiation of human AML cells ex vivo and regulates the levels of differentiation-related transcription factors.
  • Induction of terminal differentiation is a conceptually attractive approach for the therapy of neoplastic diseases.
  • Although vitamin D derivatives (deltanoids) can induce differentiation of AML cells in vitro, so far deltanoids have not been successfully brought to the clinic, due to the likelihood of life-threatening hypercalcemia.
  • Here, we incubated freshly obtained blood cells from patients with AML with a plant antioxidant (PAOx), silibinin (SIL), alone or together with a deltanoid.
  • Twenty patients with AML (all subtypes except M3) were available for this study, and in 14 (70%), SIL (60 µM) either induced differentiation ex vivo, or enhanced differentiation induced by deltanoids, or both.
  • Interestingly, SIL acting alone induced differentiation only in cases in which chromosome aberrations could not be detected.
  • In eleven samples sufficient material was available for a limited analysis of the underlying events.
  • This suggests that although the presence of SIL may not always be sufficient to induce differentiation, it can serve as a differentiation enabling factor for blasts obtained from a large proportion of patients with AML.
  • Thus, SIL/deltanoid combinations warrant further consideration as preventive/therapeutic regimens in human leukaemia.

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  • [Copyright] © 2009 John Wiley & Sons, Ltd.
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  • (PMID = 19866452.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA044722-19; United States / NCI NIH HHS / CA / R01 CA117942-02; United States / NCI NIH HHS / CA / R01-CA 044722; United States / NCI NIH HHS / CA / R01 CA117942; United States / NCI NIH HHS / CA / CA044722-19; United States / NCI NIH HHS / CA / CA117942-02; United States / NCI NIH HHS / CA / R01 CA044722; United States / NCI NIH HHS / CA / R01-CA 117942
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Calcitriol; 0 / Retinoid X Receptor alpha; 0 / Silymarin; 0 / Transcription Factors; 1C6V77QF41 / Cholecalciferol; 4RKY41TBTF / silybin
  • [Other-IDs] NLM/ NIHMS170018; NLM/ PMC2889217
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14. Dellett M, O'Hagan KA, Colyer HA, Mills KI: Identification of gene networks associated with acute myeloid leukemia by comparative molecular methylation and expression profiling. Biomark Cancer; 2010;2:43-55
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  • [Title] Identification of gene networks associated with acute myeloid leukemia by comparative molecular methylation and expression profiling.
  • Around 80% of acute myeloid leukemia (AML) patients achieve a complete remission, however many will relapse and ultimately die of their disease.
  • The association between karyotype and prognosis has been studied extensively and identified patient cohorts as having favourable [e.g. t(8; 21), inv (16)/t(16; 16), t(15; 17)], intermediate [e.g. cytogenetically normal (NK-AML)] or adverse risk [e.g. complex karyotypes].
  • Previous studies have shown that gene expression profiling signatures can classify the sub-types of AML, although few reports have shown a similar feature by using methylation markers.
  • The global methylation patterns in 19 diagnostic AML samples were investigated using the Methylated CpG Island Amplification Microarray (MCAM) method and CpG island microarrays containing 12,000 CpG sites.
  • Mutations in the NPM1 gene occur at a high frequency (40%) within the NK-AML subgroup and are associated with a more favourable prognosis in these patients.
  • This may result in a better classification of the risk groups, improved monitoring targets, or the identification of novel molecular therapies.

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  • (PMID = 24179384.001).
  • [Journal-full-title] Biomarkers in cancer
  • [ISO-abbreviation] Biomark Cancer
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3783331
  • [Keywords] NOTNLM ; AML / NPM / cytogenetics / methylation
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15. Erikci AA, Ozturk A, Karagoz B, Bilgi O, Turken O, Top C, Kandemir EG: Results of combination therapy with amifostine, pentoxifylline, ciprofloxacin and dexamethasone in patients with myelodysplastic syndrome and acute myeloid leukemia. Hematology; 2008 Oct;13(5):289-92
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  • [Title] Results of combination therapy with amifostine, pentoxifylline, ciprofloxacin and dexamethasone in patients with myelodysplastic syndrome and acute myeloid leukemia.
  • Myelodysplastic syndrome (MDS) is a clonal disease of the bone marrow characterized by abnormal hematopoiesis and cytopenias.
  • It has been shown that abnormal cytokine production together with apoptosis are major contributors to the cytopenias associated with the disorder.
  • In this study we report the results of combination therapy of amifostine and PCD in 12 patients with MDS and acute myeloid leukemia (AML).
  • As a result it was found that amifostine + PCD combination may be beneficial in reversing cytopenias in the treatment of MDS and AML and is worth further study.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


16. Li L, Giannopoulos K, Reinhardt P, Tabarkiewicz J, Schmitt A, Greiner J, Rolinski J, Hus I, Dmoszynska A, Wiesneth M, Schmitt M: Immunotherapy for patients with acute myeloid leukemia using autologous dendritic cells generated from leukemic blasts. Int J Oncol; 2006 Apr;28(4):855-61
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  • [Title] Immunotherapy for patients with acute myeloid leukemia using autologous dendritic cells generated from leukemic blasts.
  • Vaccination with dendritic cells (DCs) as professional antigen presenting cells generated from autologous leukemic blasts might elicit anti-leukemic T cell responses in patients with acute myeloid leukemia (AML).
  • To test this hypothesis, autologous AML-DC were generated under good manufacturing practice (GMP) conditions and injected s.c. into five AML patients up to four times at a biweekly interval.
  • Three patients remained in a stable condition for 5.5-13 months and two patients died from rapidly progressive AML.
  • Compared to the initial T cell frequency, enzyme linked immunosorbent spot (ELISPOT) assays revealed a significant increase of granzyme B releasing CD8+ T cells specifically recognizing the PRAME derived peptide (ALYVDSLFFL), a leukemia associated antigen expressed by AML blasts.
  • The cytokine levels in the serum of vaccination AML patients as assessed by cytokine bead assay changed over the period of vaccination to an elevated type 1 T helper cell pattern.
  • In summary, we demonstrated that autologous AML-DC vaccination is well tolerated and can result in an enhanced and specific response of cytotoxic T cells in AML patients.
  • [MeSH-major] Dendritic Cells / immunology. Immunotherapy, Adoptive / methods. Leukemia, Myeloid / therapy. Leukocytes, Mononuclear / immunology
  • [MeSH-minor] Acute Disease. Aged. Antigens, CD / analysis. Antigens, CD86 / analysis. Antigens, Neoplasm / analysis. CD8-Positive T-Lymphocytes / immunology. Female. Flow Cytometry. Granzymes. Hematopoietic Stem Cells / immunology. Humans. Immunoglobulins / analysis. Intercellular Adhesion Molecule-1 / analysis. Interferon-gamma / analysis. Interleukin-10 / analysis. Interleukin-2 / analysis. Interleukin-4 / analysis. Interleukin-5 / analysis. Male. Membrane Glycoproteins / analysis. Middle Aged. Serine Endopeptidases / analysis. Time Factors. Transplantation, Autologous. Treatment Outcome. Tumor Necrosis Factor-alpha / analysis. Vaccination / methods

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  • (PMID = 16525634.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD86; 0 / Antigens, Neoplasm; 0 / CD83 antigen; 0 / Immunoglobulins; 0 / Interleukin-2; 0 / Interleukin-5; 0 / Membrane Glycoproteins; 0 / PRAME protein, human; 0 / Tumor Necrosis Factor-alpha; 126547-89-5 / Intercellular Adhesion Molecule-1; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma; EC 3.4.21.- / GZMB protein, human; EC 3.4.21.- / Granzymes; EC 3.4.21.- / Serine Endopeptidases
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17. Chen RL, Chen MZ, Cai KR, Fang XM, Ye ZL: [Influence of cytochrome C on apoptosis induced by daunorubicine in acute myeloid leukemia (AML) cells]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Apr;13(2):282-5
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  • [Title] [Influence of cytochrome C on apoptosis induced by daunorubicine in acute myeloid leukemia (AML) cells].
  • The purpose was to study the responses of AML cell treated with cytochrome C and to explore the influence of cytochrome C on apoptosis of AML cell induced by daunorudicine (DNR).
  • The differentiation of AML cell was detected by Wright-Giemsa staining and NBT test, the apoptosis of AML cell was assayed by flow cytometry and fluorescence microscopy.
  • (1) different concentrations of cytochrome C could induce different effects on AML cells.
  • Concentration of cytochrome C for differentiation was 10 microl/ml, for apoptosis was 20 microl/ml, and for necrosis was 40 microl/ml. (2) the apoptosis of AML cells decreased with the administration of cytochrome C in 10.0 microg/ml before treating AML cells with DNR (P < 0.01), but no change was shown with the administration of cytochrome C in 20.0 microg/ml (P > 0.05). (3) in reverse sequence, administrating of cytochrome C in 10 microl/ml and 20 microl/ml after treating AML cells with DNR, two different concentrations of cytochrome C could increase the apoptosis of AML cells (P < 0.01).
  • It is suggested that cytochrome C may probably affect the apoptosis of AML cells induced by DNR.

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  • (PMID = 15854293.001).
  • [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 / Antibiotics, Antineoplastic; 9007-43-6 / Cytochromes c; ZS7284E0ZP / Daunorubicin
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18. Staratschek-Jox A, Classen S, Gaarz A, Debey-Pascher S, Schultze JL: Blood-based transcriptomics: leukemias and beyond. Expert Rev Mol Diagn; 2009 Apr;9(3):271-80
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  • [Title] Blood-based transcriptomics: leukemias and beyond.
  • In 1999, Golub et al. proposed for the first time microarray-based transcriptional profiling to be used as a new technology for the differential diagnosis of acute myeloid leukemias and acute lymphocytic leukemias.
  • This very preliminary study sparked great enthusiasm beyond the leukemias.
  • Over the last 10 years, numerous studies addressed the use of gene expression profiling of peripheral blood from patients with malignancies, infectious diseases, autoimmunity and even cardiovascular diseases.
  • Here we highlight the advances in the field of blood transcriptomics during the last 10 years and also critically discuss the issues that need to be resolved before blood transcriptomics will become part of daily diagnostics in the leukemias, as well as in other diseases showing involvement of peripheral blood.
  • [MeSH-major] Blood. Gene Expression Profiling / methods. Leukemia / diagnosis. Leukemia / genetics. Oligonucleotide Array Sequence Analysis / methods
  • [MeSH-minor] Autoimmune Diseases / diagnosis. Autoimmune Diseases / genetics. Humans

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  • (PMID = 19379085.001).
  • [ISSN] 1744-8352
  • [Journal-full-title] Expert review of molecular diagnostics
  • [ISO-abbreviation] Expert Rev. Mol. Diagn.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 57
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19. Haferlach T, Bacher U, Kern W, Schnittger S, Haferlach C: Diagnostic pathways in acute leukemias: a proposal for a multimodal approach. Ann Hematol; 2007 May;86(5):311-27
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  • [Title] Diagnostic pathways in acute leukemias: a proposal for a multimodal approach.
  • Acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) each represent a heterogeneous complex of disorders, which result from diverse mechanisms of leukemogenesis.
  • Modern therapeutic concepts are based on individual risk stratification at diagnosis and during follow-up.
  • For some leukemia subtypes such as AML M3/M3v with t(15;17)/PML-RARA or Philadelphia-positive ALL targeted therapy options are available.
  • Thus, optimal therapeutic conditions are based on exact classification of the acute leukemia subtype at diagnosis and are guided by exact and sensitive quantification of minimal residual disease during complete hematologic remission.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Leukocytes / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Acute Disease. Algorithms. Chromosome Aberrations / classification. Flow Cytometry. Humans. Immunohistochemistry. Molecular Diagnostic Techniques

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  • (PMID = 17375301.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 157
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20. 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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  • [Title] Azacitidine: a review of its use in higher-risk myelodysplastic syndromes/acute myeloid leukaemia.
  • 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.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Combined Modality Therapy. Leukemia, Myeloid, Acute / drug therapy. Prognosis. Risk Assessment
  • [MeSH-minor] Bone Marrow / drug effects. Bone Marrow Cells. Chromosome Inversion. Erythrocyte Transfusion. Erythroid Precursor Cells. Hematopoietic Stem Cell Transplantation / adverse effects. Humans. Myelodysplastic Syndromes. Randomized Controlled Trials as Topic. Remission Induction. Stem Cell Transplantation / adverse effects. Transplantation Conditioning / mortality. Treatment Outcome


21. Tan L, Xu B, Liu R, Liu H, Tan H, Huang W: Gene therapy for acute myeloid leukemia using Sindbis vectors expressing a fusogenic membrane glycoprotein. Cancer Biol Ther; 2010 Mar 1;9(5):350-7
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  • [Title] Gene therapy for acute myeloid leukemia using Sindbis vectors expressing a fusogenic membrane glycoprotein.
  • AML has a dismal prognosis.
  • It was previously shown that the expression of gene coding for the hyperfusogenic gibbon ape leukemia virus envelope glycoprotein (GALV.fus) can efficiently kill leukemic cells.
  • However, target killing effect of GALV.fus on leukemia cells may be limited.
  • Viral vectors, such as retroviruses and adenoviruses, have been developed to deliver heterologous genes into tumors in vivo, but these vectors have some limitations for gene therapy of leukemia.
  • We found that Laminin-R was obviously expressed in HL-60 and primary human AML cells, but weakly expressed in K562 cells and blood samples of normal human.
  • So we reasoned that Sindbis-virus-based vectors might be ideal for target gene transfer of GALV.fus to acute myeloid leukemic cell.
  • It was shown that Sindbis virus efficiently transduced human acute myeloid leukemic cells with high expression of Laminin-R and exhibited potent cytopathic potential.
  • What is more, we found that CFU-GMs were significantly reduced after Sindbis virus carrying GALV.fus transduced human primary AML cells.
  • Sindbis virus carrying GALV.fus was active against human AML xenografts in vivo.
  • Taken together, we concluded that Sindbis virus carrying GALV.fus may be an useful strategy for gene therapy of acute myeloid leukemia.
  • [MeSH-minor] Adenoviridae / genetics. Granulocyte-Macrophage Progenitor Cells. Humans. Leukemia Virus, Gibbon Ape / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Membrane Glycoproteins / genetics


22. Ma LH, Liu H, Xiong H, Chen B, Zhang XW, Wang YY, Le HY, Huang QH, Zhang QH, Li BL, Chen Z, Chen SJ: Aberrant transcriptional regulation of the MLL fusion partner EEN by AML1-ETO and its implication in leukemogenesis. Blood; 2007 Jan 15;109(2):769-77
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  • The EEN (extra eleven nineteen) gene, located on chromosome 19p13, was cloned as a fusion with MLL from a patient with acute myeloid leukemia (AML) with translocation t(11;19)(q23;p13).
  • We found that Sp1 could bind to the guanine-cytosine (GC)-stretch of the EEN promoter and was critical for the normal EEN expression, whereas the leukemia-associated fusion protein AML1-ETO could aberrantly transactivate the EEN gene through an AML1 binding site.
  • Of note, overexpressed EEN showed oncogenic properties, such as transforming potential in NIH3T3 cells, stimulating cell proliferation, and increasing the activity of transcriptional factor AP-1.
  • Moreover, Kasumi-1 and HL60-cell growth was inhibited with down-regulation of EEN by RNAi.
  • These findings demonstrate that EEN might be a common target in 2 major types of AML associated with MLL or AML1 translocations, and overexpression of EEN may play an essential role in leukemogenesis.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Leukemic. Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Transcription, Genetic / genetics
  • [MeSH-minor] Acute Disease. Animals. Cell Transformation, Neoplastic. HL-60 Cells. Humans. K562 Cells. Mammary Neoplasms, Animal. Mice. Mice, Nude. Neoplasm Transplantation. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity. Transcription Factors / metabolism. U937 Cells

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  • (PMID = 16990610.001).
  • [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 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Intracellular Signaling Peptides and Proteins; 0 / Oncogene Proteins, Fusion; 0 / SH3GL1 protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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23. Williams B, Atkins A, Zhang H, Lu D, Jimenez X, Li H, Wang MN, Ludwig D, Balderes P, Witte L, Li Y, Zhu Z: Cell-based selection of internalizing fully human antagonistic antibodies directed against FLT3 for suppression of leukemia cell growth. Leukemia; 2005 Aug;19(8):1432-8
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  • [Title] Cell-based selection of internalizing fully human antagonistic antibodies directed against FLT3 for suppression of leukemia cell growth.
  • FMS-like tyrosine kinase 3 (FLT3) receptor is highly expressed in an array of hematological malignancies including approximately 90% of acute myelogenous leukemia (AML).
  • Ligand stimulation of the receptor promotes the survival and proliferation of leukemia cells.
  • Strategies targeting FLT3 using monoclonal antibodies may therefore constitute an effective therapeutic approach for these leukemia.
  • Towards this, we selected a naïve antibody phage display library on both recombinant FLT3 receptor protein and FLT3-expressing leukemia cells using a tailored selection scheme that was designed to isolate antagonistic phage antibodies that not only interfere with receptor/ligand binding but also trigger receptor internalization upon cell surface binding.
  • Phage antibodies were screened first for their ability to bind to cell surface receptor and induce receptor internalization, followed by their activity in blocking ligand-receptor interaction and neutralizing ligand-stimulated receptor activation and cell proliferation.
  • We identified three fully human antibodies, EB10, A2IN, and D4-3, which bound specifically to both soluble and cell surface-expressed FLT3.
  • All three antibodies were shown to be internalized upon binding to cell surface-expressed receptor in a time-dependent fashion.
  • EB10 and D4-3 blocked ligand binding to the receptor with IC(50)s of 14 and 7 nM, respectively.
  • Further, EB10 and D4-3 inhibited FLT3 ligand-induced receptor phosphorylation and cell proliferation in EOL-1 leukemia cells.
  • Taken together, these results suggest that both EB10 and D4-3 may represent excellent therapeutic candidates for the treatment of FLT3-expressing human leukemia, both as unmodified antibodies and as conjugates of cytotoxic agents.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Leukemia / therapy. Proto-Oncogene Proteins / immunology. Receptor Protein-Tyrosine Kinases / immunology
  • [MeSH-minor] Antigen-Antibody Reactions. Cell Line, Tumor. Cell Proliferation / drug effects. Endocytosis / drug effects. Humans. Immunotherapy. Peptide Library. Phosphorylation / drug effects. fms-Like Tyrosine Kinase 3

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  • [Copyright] Leukemia (2005) 19, 1432-1438.
  • (PMID = 15931264.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Peptide Library; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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24. Zhou GB, Zhang J, Wang ZY, Chen SJ, Chen Z: Treatment of acute promyelocytic leukaemia with all-trans retinoic acid and arsenic trioxide: a paradigm of synergistic molecular targeting therapy. Philos Trans R Soc Lond B Biol Sci; 2007 Jun 29;362(1482):959-71
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  • [Title] Treatment of acute promyelocytic leukaemia with all-trans retinoic acid and arsenic trioxide: a paradigm of synergistic molecular targeting therapy.
  • To turn a disease from highly fatal to highly curable is extremely difficult, especially when the disease is a type of cancer.
  • However, we can gain some insight into how this can be done by looking back over the 50-year history of taming acute promyelocytic leukaemia (APL).
  • APL is the M3 type of acute myeloid leukaemia characterized by an accumulation of abnormal promyelocytes in bone marrow, a severe bleeding tendency and the presence of the chromosomal translocation t(15;17) or variants.
  • APL was considered the most fatal type of acute leukaemia five decades ago and the treatment of APL was a nightmare for physicians.
  • Great efforts have been made by scientists worldwide to conquer this disease.
  • When arsenic trioxide (ATO) was used to treat relapsed APL not only the patients but also the ancient drug were revived.
  • Of note, both ATRA and ATO trigger catabolism of the PML-RARalpha fusion protein which is the key player in APL leukaemogenesis generated from t(15;17), targeting the RARalpha (retinoic acid receptor alpha) or promyelocytic leukaemia (PML) moieties, respectively.
  • Strikingly, a clearance of PML-RARalpha transcript in an earlier and more thorough manner, and a higher quality remission and survival in newly diagnosed APL are achieved when ATRA is combined with ATO, as compared to either monotherapy, making APL a curable disease.
  • Thus, the story of APL can serve as a model for the development of curative approaches for disease; it suggests that molecularly synergistic targeted therapies are powerful tools in cancer, and dissection of disease pathogenesis or anatomy of the cancer genome is critical in developing molecular target-based therapies.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use. Tretinoin / therapeutic use

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  • (PMID = 17317642.001).
  • [ISSN] 0962-8436
  • [Journal-full-title] Philosophical transactions of the Royal Society of London. Series B, Biological sciences
  • [ISO-abbreviation] Philos. Trans. R. Soc. Lond., B, Biol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 90
  • [Other-IDs] NLM/ PMC2435563
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25. Hassan IB, Islam SI, Alizadeh H, Kristensen J, Kambal A, Sonday S, Bernseen RM: Acute leukemia among the adult population of United Arab Emirates: an epidemiological study. Leuk Lymphoma; 2009 Jul;50(7):1138-47
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  • [Title] Acute leukemia among the adult population of United Arab Emirates: an epidemiological study.
  • There is no published data regarding adult acute leukemia (AL) in the United Arab Emirates (UAE).
  • Our objectives were to determine the distribution and incidence of adult AL in UAE (nationals and non-nationals).
  • Acute lymphoblastic leukemia (ALL) was more frequently diagnosed (32%) than in western countries.
  • There is a tendency for lower crude and age-specific incidence rates of AL, acute myeloid leukemia (AML) and ALL in the UAE when compared with those in western countries.
  • We found a statistically significant higher incidence of AML among national females than in national males (p = 0.04).
  • This is reflected in a significantly higher incidence of AL (p = 0.02) and AML (p = 0.02) among the females when compared with the males in the total population of the UAE.
  • This result contradicts the generally known finding that AML and ALL are more common in males.
  • The implication of cumulative risk factors to which females could be exposed, such as vitamin D deficiency as a result of sunlight deprivation and direct exposure to benzene and color enhancement chemicals in henna, could not be excluded and warrant further investigation.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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  • (PMID = 19557635.001).
  • [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
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26. Liu TX, Becker MW, Jelinek J, Wu WS, Deng M, Mikhalkevich N, Hsu K, Bloomfield CD, Stone RM, DeAngelo DJ, Galinsky IA, Issa JP, Clarke MF, Look AT: Chromosome 5q deletion and epigenetic suppression of the gene encoding alpha-catenin (CTNNA1) in myeloid cell transformation. Nat Med; 2007 Jan;13(1):78-83
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  • [Title] Chromosome 5q deletion and epigenetic suppression of the gene encoding alpha-catenin (CTNNA1) in myeloid cell transformation.
  • Interstitial loss of all or part of the long arm of chromosome 5, or del(5q), is a frequent clonal chromosomal abnormality in human myelodysplastic syndrome (MDS, a preleukemic disorder) and acute myeloid leukemia (AML), and is thought to contribute to the pathogenesis of these diseases by deleting one or more tumor-suppressor genes.
  • We focused our analysis of gene expression on RNA from primitive leukemia-initiating cells, which harbor 5q deletions, and analyzed 12 genes within the CDR that are expressed by normal hematopoietic stem cells.
  • Here we show that the gene encoding alpha-catenin (CTNNA1) is expressed at a much lower level in leukemia-initiating stem cells from individuals with AML or MDS with a 5q deletion than in individuals with MDS or AML lacking a 5q deletion or in normal hematopoietic stem cells.
  • Analysis of HL-60 cells, a myeloid leukemia line with deletion of the 5q31 region, showed that the CTNNA1 promoter of the retained allele is suppressed by both methylation and histone deacetylation.
  • Restoration of CTNNA1 expression in HL-60 cells resulted in reduced proliferation and apoptotic cell death.
  • Thus, loss of expression of the alpha-catenin tumor suppressor in hematopoietic stem cells may provide a growth advantage that contributes to human MDS or AML with del(5q).
  • [MeSH-major] Cell Transformation, Neoplastic. Chromosome Deletion. Chromosomes, Human, Pair 5 / genetics. Myeloid Progenitor Cells / pathology. alpha Catenin / genetics
  • [MeSH-minor] Acute Disease. Blotting, Western. Cell Line. Cell Line, Tumor. DNA Methylation / drug effects. Flow Cytometry. Gene Expression Regulation, Neoplastic / drug effects. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. HL-60 Cells. Humans. Hydroxamic Acids / pharmacology. In Situ Hybridization, Fluorescence / methods. K562 Cells. Leukemia, Myeloid / blood. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Mutation. Myelodysplastic Syndromes / blood. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Reverse Transcriptase Polymerase Chain Reaction. Transfection. U937 Cells


27. Miron I, Mihăilă D, Aprodu G, Miron L, Plămădeală P, Moisă SM: Immunoproliferative small intestinal disease versus colonic monoblastic sarcoma in a 2-year-old boy. Rom J Morphol Embryol; 2009;50(4):733-8
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  • [Title] Immunoproliferative small intestinal disease versus colonic monoblastic sarcoma in a 2-year-old boy.
  • The authors present a case of colonic monoblastic sarcoma, previously treated for other digestive abnormalities (malabsorbtion, Hirschprung's disease).
  • Important similitudes with immunoproliferative small intestinal disease (IPSID) lymphoma were demonstrated for this patient (male, 2-year-old).
  • Some particularities of this case are the young age and the extremely rapid development of the malignant disease in a patient with no previous signs of acute non-lymphoblastic leukemia.
  • The initial diagnosis was of malabsorbtion syndrome, based on the clinical exam at presentation, and then the patient was thought to have a form of Hirschprung's disease, due to a functional intestinal disorder (slow transit).
  • After the necropsy, pathologists diagnosed an immunoproliferative small intestinal disease, and four years later, they performed a more appropriate pathological exam, which explained better clinical symptoms associated to this complex case.
  • [MeSH-major] Colonic Neoplasms / diagnosis. Immunoproliferative Small Intestinal Disease / diagnosis. Sarcoma / diagnosis
  • [MeSH-minor] Child, Preschool. Diagnosis, Differential. Hirschsprung Disease / diagnosis. Humans. Malabsorption Syndromes / diagnosis. Male

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  • (PMID = 19942975.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Romania
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28. Laport GG, Sandmaier BM, Storer BE, Scott BL, Stuart MJ, Lange T, Maris MB, Agura ED, Chauncey TR, Wong RM, Forman SJ, Petersen FB, Wade JC, Epner E, Bruno B, Bethge WA, Curtin PT, Maloney DG, Blume KG, Storb RF: Reduced-intensity conditioning followed by allogeneic hematopoietic cell transplantation for adult patients with myelodysplastic syndrome and myeloproliferative disorders. Biol Blood Marrow Transplant; 2008 Feb;14(2):246-55
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  • [Title] Reduced-intensity conditioning followed by allogeneic hematopoietic cell transplantation for adult patients with myelodysplastic syndrome and myeloproliferative disorders.
  • Allogeneic hematopoietic cell transplantation (HCT) is the only curative strategy for patients with myelodysplastic syndrome (MDS) and myeloproliferative disorders (MPD).
  • We report the results of 148 patients (median age = 59 years old) with de novo MDS (n = 40), acute myelogenous leukemia (AML) after antecedent MDS/MPD (n = 49), treatment-related MDS (t-MDS) (n = 25), MPD (n = 27), and chronic myelomonocytic leukemia (CMML) (n = 7) who underwent allogeneic HCT using a conditioning regimen of low-dose total body irradiation (TBI) alone (200 cGy) on day 0 (n = 5) or with the addition of fludarabine (Flu) 30 mg/m(2)/day on days -4 to -2 (n = 143).
  • There was no significant difference in the incidence of acute (gr II-IV) and chronic extensive graft-versus-host disease (aGVHD, cGVHD) between the recipients of related and unrelated donor grafts.
  • By day +28, 75% of patients demonstrated mixed T cell chimerism.
  • The 3-year RFS for the patients with de novo MDS, AML after antecedent MDS/MPD, t-MDS, MPD, and CMML were 22%, 20%, 29%, 37%, and 43%, respectively, and the 3-year OS was 20%, 23%, 27%, 43%, and 43%, respectively.
  • Factors associated with a lower risk of relapse were the development of extensive cGVHD and having a low risk or intermediate-1 risk International Prognostic Score for the de novo MDS patients.
  • Nonmyeloablative HCT confers remissions in patients who otherwise were not eligible for conventional HCT but for whom relapse is the leading cause of treatment failure.

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  • (PMID = 18215785.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA049605-14; United States / NCI NIH HHS / CA / CA18029; United States / NHLBI NIH HHS / HL / HL036444-27; United States / NCI NIH HHS / CA / K23 CA092058-01; United States / NHLBI NIH HHS / HL / HL36444; United States / NCI NIH HHS / CA / P30 CA015704-31; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / P30 CA015704; United States / NCI NIH HHS / CA / CA78902; United States / NCI NIH HHS / CA / CA92058; United States / NCI NIH HHS / CA / CA092058-01; United States / NCI NIH HHS / CA / K23 CA092058; United States / NCI NIH HHS / CA / P01 CA018029-250002; United States / NCI NIH HHS / CA / CA049605-14; United States / NCI NIH HHS / CA / P01 CA018029-270047; United States / NCI NIH HHS / CA / CA15704; United States / NCI NIH HHS / CA / P01 CA078902-09; United States / NCI NIH HHS / CA / CA018029-270047; United States / NCI NIH HHS / CA / CA078902-09; United States / NHLBI NIH HHS / HL / P01 HL036444-27; United States / NCI NIH HHS / CA / CA018029-250002; United States / NHLBI NIH HHS / HL / P01 HL036444; United States / NCI NIH HHS / CA / P01 CA078902; United States / NCI NIH HHS / CA / P01-CA 49605; United States / NCI NIH HHS / CA / CA015704-31; United States / NCI NIH HHS / CA / P01 CA049605
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ NIHMS39955; NLM/ PMC2259225
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29. Palle J, Frost BM, Peterson C, Gustafsson G, Hellebostad M, Kanerva J, Schmiegelow K, Lönnerholm G, Nordic Society for Pediatric Hematology and Oncology: Doxorubicin pharmacokinetics is correlated to the effect of induction therapy in children with acute myeloid leukemia. Anticancer Drugs; 2006 Apr;17(4):385-92
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  • [Title] Doxorubicin pharmacokinetics is correlated to the effect of induction therapy in children with acute myeloid leukemia.
  • We studied the pharmacokinetics of doxorubicin in 41 children treated for newly diagnosed acute myeloid leukemia.
  • Doxorubicin, 75 mg/m2 body surface area, was administered by constant i.v. infusion over 8 h.
  • Four children with Down's syndrome (DS), 1.2-2.3 years old, had a median total body clearance of 523 ml/min/m2.
  • The median clearance in non-DS children, 0.6-1.8 years old (n = 4) and 2.5-17.7 years old (n = 33), was 446 and 538 ml/min/m2, respectively.
  • Patients who went into complete remission (CR) after induction therapy had a significantly higher median plasma concentration of doxorubicin than those who did not, 249 compared with 180 ng/ml, respectively (P = 0.036; analysis restricted to non-DS patients).
  • Doxorubicin plasma concentration was an independent factor for CR, both in univariate (P = 0.031) and multivariate analysis including sex, age and white blood cell count at diagnosis (P = 0.021).
  • Patients who reached CR had a significantly lower doxorubicin clearance than those who did not, 513 and 657 ml/min/m2, respectively (P = 0.017).
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacokinetics. Doxorubicin / pharmacokinetics. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 16549995.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin; HUH05KI4CF / adriamycinol
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30. Olwill SA, McGlynn H, Gilmore WS, Alexander HD: Annexin II cell surface and mRNA expression in human acute myeloid leukaemia cell lines. Thromb Res; 2005;115(1-2):109-14
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  • [Title] Annexin II cell surface and mRNA expression in human acute myeloid leukaemia cell lines.
  • INTRODUCTION: Acute promyelocytic leukaemia (APL) (M3) is associated with both a characteristic t(15;17) and severe bleeding diathesis caused by disseminated intravascular coagulation (DIC) and/or hyperfibrinolysis.
  • MATERIALS AND METHODS: This study examined the level of annexin II cell surface and mRNA expression in a range of acute myeloid leukaemia (AML) cell lines.
  • The evidence that annexin II levels are higher in APL would lend support to the hypothesis that the bleeding disorder seen in APL is caused by hyperfibrinolysis.
  • RESULTS: Cell surface annexin II was found to be expressed at higher levels on NB4 (promyelocytic) cells than on either KG1a (early myeloid) or HL60 (myelocytic) cells.
  • MM6 cells showed a threefold increase in annexin II mRNA compared to any of the other cell lines.
  • CONCLUSIONS: These findings do not fully support the concept of the coagulopathy associated with APL being caused by hyperfibrinolysis alone.
  • Further investigations are required to identify the significance of annexin II expression and regulation in leukaemia.
  • [MeSH-major] Annexin A2 / genetics. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid / metabolism. Leukemia, Promyelocytic, Acute / complications. RNA, Messenger / analysis
  • [MeSH-minor] Cell Line, Tumor. Fibrinolysis. Hemorrhage / etiology. Humans. Membrane Proteins

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  • (PMID = 15567461.001).
  • [ISSN] 0049-3848
  • [Journal-full-title] Thrombosis research
  • [ISO-abbreviation] Thromb. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ANXA2 protein, human; 0 / Annexin A2; 0 / Membrane Proteins; 0 / RNA, Messenger
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31. Kanemura N, Tsurumi H, Kasahara S, Hara T, Yamada T, Sawada M, Goto N, Kitagawa J, Shimizu M, Oyama M, Moriwaki H: Continuous drip infusion of low dose cytarabine and etoposide with granulocyte colony-stimulating factor for elderly patients with acute myeloid leukaemia ineligible for intensive chemotherapy. Hematol Oncol; 2008 Mar;26(1):33-8
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  • [Title] Continuous drip infusion of low dose cytarabine and etoposide with granulocyte colony-stimulating factor for elderly patients with acute myeloid leukaemia ineligible for intensive chemotherapy.
  • BACKGROUNDS AND OBJECTIVES: The optimal strategy for the management of elderly patients with acute myeloid leukaemia (AML) is still controversial.
  • We previously reported the effectiveness of low dose cytarabine (Ara-C) and etoposide (VP-16) (AV therapy) for those elderly AML patients ineligible for intensive chemotherapy.
  • PATIENTS AND METHODS: The eligibility for enrolment was AML patients according to the World Health Organization (WHO) criteria who were over 60 years of age and who had difficulty in tolerating intensive chemotherapy due to their poor performance status (PS) or some comorbidities.
  • They were given continuous drip infusion of Ara-C (20 mg/body) and VP-16 (50 mg/body) for 7-14 days, and were also simultaneously administered G-CSF (150 microg/m2) once daily.
  • The 1-year disease free survival (DFS) rate in CR patients was 44%.
  • CONCLUSION: AVG therapy was therefore found to be an effective and well-tolerated regimen for remission induction in elderly AML patients with poor PS or comorbidity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Monocytic, Acute / drug therapy

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  • (PMID = 17918772.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 6PLQ3CP4P3 / Etoposide
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32. Krogh-Madsen M, Hansen SH, Honoré PH: Simultaneous determination of cytosine arabinoside, daunorubicin and etoposide in human plasma. J Chromatogr B Analyt Technol Biomed Life Sci; 2010 Jul 15;878(22):1967-72
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  • The method was successfully applied to quantification of the three drugs in blood samples from patients undergoing induction treatment for acute myeloid leukaemia, thus demonstrating its suitability for clinical studies.

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  • [Copyright] 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20542475.001).
  • [ISSN] 1873-376X
  • [Journal-full-title] Journal of chromatography. B, Analytical technologies in the biomedical and life sciences
  • [ISO-abbreviation] J. Chromatogr. B Analyt. Technol. Biomed. Life Sci.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZS7284E0ZP / Daunorubicin
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33. Kantarjian H, O'brien S, Cortes J, Giles F, Faderl S, Jabbour E, Garcia-Manero G, Wierda W, Pierce S, Shan J, Estey E: Results of intensive chemotherapy in 998 patients age 65 years or older with acute myeloid leukemia or high-risk myelodysplastic syndrome: predictive prognostic models for outcome. Cancer; 2006 Mar 1;106(5):1090-8
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  • [Title] Results of intensive chemotherapy in 998 patients age 65 years or older with acute myeloid leukemia or high-risk myelodysplastic syndrome: predictive prognostic models for outcome.
  • BACKGROUND: Elderly patients (age > or = 65 years) with acute myeloid leukemia (AML) generally have a poor prognosis.
  • AML-type therapy results are often derived from studies in younger patients and may not apply to elderly AML.
  • However, baseline expectations for outcomes of elderly AML with 'standard' AML-type therapy are not well defined.
  • The aim was to develop prognostic models for complete response (CR), induction (8-week) mortality, and survival rates in elderly AML, which would be used to advise oncologists and patients of expectations with standard AML type therapy, and to establish baseline therapy results against which novel strategies would be evaluated.
  • METHODS: A total of 998 patients age > or = 65 years with AML or high-risk myelodysplastic syndrome (> 10% blasts) treated with intensive chemotherapy between 1980 and 2004 were analyzed.
  • These included age > or = 75 years, unfavorable karyotypes (often complex), poor performance (3-4 ECOG [Eastern Cooperative Oncology Group]), longer duration of antecedent hematologic disorder, treatment outside the laminar airflow room, and abnormal organ functions.
  • CONCLUSIONS: Prognostic models, based on standard readily available baseline characteristics, were developed for elderly patients with AML, which may assist in therapeutic and investigational decisions.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy. Models, Theoretical. Myelodysplastic Syndromes / drug therapy


34. Basara N, Baurmann H, Kolbe K, Yaman A, Labopin M, Burchardt A, Huber C, Fauser AA, Schwerdtfeger R: Antithymocyte globulin for the prevention of graft-versus-host disease after unrelated hematopoietic stem cell transplantation for acute myeloid leukemia: results from the multicenter German cooperative study group. Bone Marrow Transplant; 2005 May;35(10):1011-8
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  • [Title] Antithymocyte globulin for the prevention of graft-versus-host disease after unrelated hematopoietic stem cell transplantation for acute myeloid leukemia: results from the multicenter German cooperative study group.
  • A total of 155 patients with acute myeloid leukemia (AML) received hematopoietic stem cell transplants from unrelated donors after standard conditioning.
  • Clinical outcome after the use of two different antithymocyte globulins for the prevention of graft-versus-host disease (GvHD) was analyzed in a retrospective study as follows: rabbit ATG (Thymoglobulin Sangstat/Genzyme, n=49, median age 42 years, 53% in CR, further ATG-S); rabbit ATG (ATG-Fresenius, n=38, median age 42 years, 58% in CR, further ATG-F) or no ATG (n=68, median age 36 years, 55% in CR).
  • The groups were comparable regarding disease status at transplant, age, CMV status and cytogenetics.
  • Grade III-IV acute GvHD was found in 15% in the ATG and 27% in the no ATG group (P=0.44).
  • The most important independent risk factors for chronic GvHD (cGvHD) were the use of ATG, disease status at transplant and conditioning. cGvHD developed significantly more frequently in no ATG group.
  • [MeSH-major] Antilymphocyte Serum / therapeutic use. Graft vs Host Disease / prevention & control. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid, Acute / therapy


35. Francesconi M, Remondini D, Neretti N, Sedivy JM, Cooper LN, Verondini E, Milanesi L, Castellani G: Reconstructing networks of pathways via significance analysis of their intersections. BMC Bioinformatics; 2008 Apr 25;9 Suppl 4:S9
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  • We apply this method for the reconstruction of networks of pathways to two gene expression datasets: the first one obtained from a c-Myc rat fibroblast cell line expressing a conditional Myc-estrogen receptor oncoprotein; the second one obtained from the comparison of Acute Myeloid Leukemia and Acute Lymphoblastic Leukemia derived from bone marrow samples.
  • We show that groups of genes at the interface between different pathways can be considered as relevant even if the pathways they belong to are not significant by themselves.

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  • (PMID = 18460182.001).
  • [ISSN] 1471-2105
  • [Journal-full-title] BMC bioinformatics
  • [ISO-abbreviation] BMC Bioinformatics
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM041690; United States / NIGMS NIH HHS / GM / R01 GM41690-17
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proteome
  • [Other-IDs] NLM/ PMC2367636
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36. Antón E, Casanova A, Xaubet A, Román A, Villena V, Montero MC, Molina-Molina M, Pérez-Sánchez E, Sueiro A, Morell F, Girón RM, Ancochea J: Lymphangioleiomyomatosis: a study of 72 patients from the Spanish registry. Sarcoidosis Vasc Diffuse Lung Dis; 2009 Jul;26(2):85-91
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  • BACKGROUND: Pulmonary lymphangioleiomyomatosis (LAM) is a rare lung disease that almost exclusively affects young women of childbearing age.
  • The true incidence and prevalence of LAM are unknown.
  • Information about the study and this questionnaire were both sent by e-mail to all the participants of the interstitial disease registry of 2004.
  • Sixty-three patients (87.5%) presented the sporadic LAM and 9 (12.5%) presented LAM associated with tuberous sclerosis (LAM-TS).
  • LAM diagnosis was confirmed with an open lung biopsy in 57 patients (79.2%) and was performed with thoracic HRCT compatible with LAM diagnosis in the other 15 cases.
  • Most patients with LAM-TS (88.8%) had renal angiomyolipomas compared with 31.7% in the sporadic LAM group.
  • CONCLUSION: The characteristics of the Spanish population affected with LAM are similar to those of other countries.

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  • (PMID = 20560288.001).
  • [ISSN] 1124-0490
  • [Journal-full-title] Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG
  • [ISO-abbreviation] Sarcoidosis Vasc Diffuse Lung Dis
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study
  • [Publication-country] Italy
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37. Stornaiuolo G, Stanzione M, Brancaccio G, Cuomo G, Precone V, Di Biase S, Felaco FM, Piccinino F, Gaeta GB: Viral blips during long-term treatment with standard or double dose lamivudine in HBe antigen negative chronic hepatitis B. World J Gastroenterol; 2007 Nov 14;13(42):5642-7
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  • AIM: To evaluate safety and effect on hepatitis B virus (HBV) suppression of a long-term treatment with lamivudine (LAM) at standard (100 mg/d) or double (200 mg/d) dose in chronic hepatitis B.
  • RESULTS: Twelve patients received LAM 200 mg/d and 35 LAM 100 mg/d, for a median of 28 mo.
  • A primary response (PR; i.e. negative HBV-DNA with Amplicor assay) was achieved in 100% of LAM-200 patients and 83% of LAM-100 patients.
  • A virological breakthrough occurred in 16.7 and 24.7%, respectively, of the PR-patients, with the appearance of typical LAM resistance mutations in all but one patient.
  • At the end of the study, 51.4% of LAM-100 patients and 83.3% of LAM-200 patients had remained stably HBV-DNA negative.
  • Double-dose LAM was well tolerated.

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  • (PMID = 17948940.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Hepatitis B e Antigens; 0 / Reverse Transcriptase Inhibitors; 2T8Q726O95 / Lamivudine; EC 2.6.1.2 / Alanine Transaminase
  • [Other-IDs] NLM/ PMC4172745
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38. Johnson GT, Harbison SC, McCluskey JD, Harbison RD: Characterization of cancer risk from airborne benzene exposure. Regul Toxicol Pharmacol; 2009 Dec;55(3):361-6
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  • Alternatively, occupational exposure to significantly elevated levels of benzene is associated with acute myeloid leukemia (AML).
  • Comparative analysis with the epidemiologic literature indicates the association between benzene exposure and AML is related to cumulative exposures far in excess of 1ppm-years, with the likely threshold for benzene-induced leukemogenesis of 50ppm-years cumulative exposure.
  • Based upon the results of this investigation, it is unreasonable to anticipate AML cases in Florida residents as a result of ambient airborne benzene concentrations.
  • [MeSH-major] Air Pollutants / toxicity. Benzene / toxicity. Leukemia, Myeloid, Acute / chemically induced

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  • (PMID = 19703507.001).
  • [ISSN] 1096-0295
  • [Journal-full-title] Regulatory toxicology and pharmacology : RTP
  • [ISO-abbreviation] Regul. Toxicol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Air Pollutants; 0 / Carcinogens; J64922108F / Benzene
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39. Ozdilli K, Oguz FS, Anak S, Kekik C, Carin M, Gedikoglu G: The frequency of HLA class I and II alleles in Turkish childhood acute leukaemia patients. J Int Med Res; 2010 Sep-Oct;38(5):1835-44
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  • [Title] The frequency of HLA class I and II alleles in Turkish childhood acute leukaemia patients.
  • In this study, blood samples were taken from 200 patients with childhood acute leukaemias, including acute lymphoblastic leukaemia (ALL) and acute myeloid leukaemia (AML), and from 100 healthy volunteers (controls).
  • Among patients with AML, the frequency of the HLA-B49 antigen and the HLA-DRB1*15 allele were significantly higher, whereas the frequencies of the HLA-A11 and HLA-B38 antigens were significantly lower compared with controls.
  • The frequency of the HLA-DRB1*04 allele was also significantly higher in male patients with ALL and AML, whereas the HLA-DRB1*13 allele was found significantly less frequently in male AML and female ALL patients than in controls.
  • To date, this is the only study to evaluate the associations between HLA molecules and leukaemia in a Turkish population with acute childhood leukaemia.
  • [MeSH-major] Histocompatibility Antigens Class I / genetics. Histocompatibility Antigens Class II / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 21309500.001).
  • [ISSN] 0300-0605
  • [Journal-full-title] The Journal of international medical research
  • [ISO-abbreviation] J. Int. Med. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class I; 0 / Histocompatibility Antigens Class II
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40. Hou HA, Chou WC, Lin LI, Tang JL, Tseng MH, Huang CF, Yao M, Chen CY, Tsay W, Tien HF: Expression of angiopoietins and vascular endothelial growth factors and their clinical significance in acute myeloid leukemia. Leuk Res; 2008 Jun;32(6):904-12
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  • [Title] Expression of angiopoietins and vascular endothelial growth factors and their clinical significance in acute myeloid leukemia.
  • Angiogenic factors play an essential role in normal and pathologic angiogenesis, but their clinical role in acute myeloid leukemia (AML) remains unclear.
  • We investigated the expression of Ang-1, Ang-2, Tie2, VEGF-A, and VEGF-C genes in bone marrow (BM) mononuclear cells by real-time quantitative PCR (RQ-PCR) in a cohort of 126 patients with newly diagnosed de novo AML and normal marrow donors.
  • Here we show that high pre-treatment levels of Ang-2 in the BM indicate an unfavorable prognosis in AML.
  • Only karyotype (hazard ratio 2.19, 95% CI 1.25-3.42, P=0.005) and expression of Ang-2 (hazard ratio 2.05, 95% CI 1.20-3.52, P=0.009), but not other angiogenic factors, were independent prognostic factors for overall survival by multivariate analysis.
  • Subgroup analysis showed that Ang-2 expression had prognostic impact on patients with low (but not high) Ang-1 or Tie2 levels, and on patients with high (but not low) VEGF-A or VEGF-C levels.
  • [MeSH-major] Angiopoietin-1 / genetics. Angiopoietin-2 / genetics. Gene Expression Regulation, Leukemic / physiology. Leukemia, Myeloid, Acute / genetics. Receptor, TIE-2 / genetics. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor C / genetics

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  • [CommentIn] Leuk Res. 2008 Jun;32(6):843-4 [18207236.001]
  • (PMID = 17904634.001).
  • [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 / ANGPT1 protein, human; 0 / Angiopoietin-1; 0 / Angiopoietin-2; 0 / DNA Primers; 0 / RNA, Messenger; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C; EC 2.7.10.1 / Receptor, TIE-2
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41. Pabst T, Stillner E, Neuberg D, Nimer S, Willman CL, List AF, Melo JV, Tenen DG, Mueller BU: Mutations of the myeloid transcription factor CEBPA are not associated with the blast crisis of chronic myeloid leukaemia. Br J Haematol; 2006 May;133(4):400-2
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  • [Title] Mutations of the myeloid transcription factor CEBPA are not associated with the blast crisis of chronic myeloid leukaemia.
  • The transcription factor CEBPA is crucial for normal myeloid differentiation.
  • CEBPA gene mutations have been reported in patients with acute myeloid leukaemia.
  • The inevitable evolution of chronic myeloid leukaemia (CML) in chronic phase (CP) to a fatal blast crisis (BC) is assumed to result from the acquisition of additional genetic changes in the leukaemic clone.
  • Gain of CEBPA mutations might represent a key event causing the differentiation block observed in myeloid CML-BC, but not in CML-CP.
  • Here, no CEBPA mutation in 95 CML-BC patients was found, suggesting a limited role, if any, of CEBPA mutations in this disorder.
  • [MeSH-major] Blast Crisis / genetics. CCAAT-Enhancer-Binding Protein-alpha / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mutation
  • [MeSH-minor] Cell Differentiation / genetics. Cell Line, Tumor. Disease Progression. Humans

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  • (PMID = 16643447.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha
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42. Wang SN, Tsai KB, Lee KT: Hepatic angiomyolipoma with trace amounts of fat: a case report and literature review. J Clin Pathol; 2006 Nov;59(11):1196-9
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  • Hepatic angiomyolipoma (AML), a rare benign mesenchymal tumour, is characterised by the presence of mature adipose tissue, smooth-muscle cells and thick-walled blood vessels.
  • Increasing attention to hepatic AMLs has led to the discovery that sufficient proportions of fat often allow for definite diagnoses preoperatively.
  • One case of hepatic AML is reported, where the amount of fat was <1%.
  • Abdominal ultrasonography showed a hypoechoic mass measuring 5 cm in diameter and without an obvious capsule in the left lobe of the liver.
  • A dynamic computed tomography scan showed a well-defined and slightly enhanced mass in the medial segment of the left lobe of the liver.
  • Microscopically, the amount of fat was too low to establish a diagnosis of hepatic AML.
  • However, positive homatropine methylbromide 45 immunoreactivity of the smooth-muscle cells seemed to assist in arriving at the diagnosis.
  • [MeSH-major] Adipose Tissue / pathology. Angiomyolipoma / pathology. Liver Neoplasms / pathology

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  • (PMID = 17071805.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
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43. Anagnostopoulos C, Jadwat Y, Wood NH, Meyerov R, Lemmer J, Bouckaert M, Feller L: A report of oral extramedullary acute myeloid leukaemia (AML) in an 8-year-old girl with newly diagnosed AML-M4Eo. SADJ; 2007 Oct;62(9):390, 392-3
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  • [Title] A report of oral extramedullary acute myeloid leukaemia (AML) in an 8-year-old girl with newly diagnosed AML-M4Eo.
  • Acute myeloid leukaemia (AML), characterized by proliferation of immature neoplastic myeloid cells, is uncommon in childhood.
  • We present a case of an 8-year-old girl with AML-M4Eo who had an extramedullary leukaemic tumour in the oral cavity.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / pathology. Mouth Neoplasms / pathology
  • [MeSH-minor] Bone Marrow Neoplasms / pathology. Child. Diagnosis, Differential. Eosinophilia / pathology. Fatal Outcome. Female. Humans. Immunophenotyping / methods. Sepsis / drug therapy

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  • (PMID = 18260548.001).
  • [ISSN] 1029-4864
  • [Journal-full-title] SADJ : journal of the South African Dental Association = tydskrif van die Suid-Afrikaanse Tandheelkundige Vereniging
  • [ISO-abbreviation] SADJ
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] South Africa
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44. Tanvetyanon T, Stiff PJ: Recurrent steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations. Leuk Lymphoma; 2005 Jan;46(1):151-4
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  • Several paraneoplastic inflammatory conditions, particularly autoimmune diseases, have been described in association with myelodysplastic syndromes (MDS).
  • However, to date, recurrent acute pancreatitis has never been described in association with MDS.
  • The vasculitic syndrome responded rapidly to corticosteroids, but soon after tapering of corticosteroids, acute pancreatitis developed.
  • Finally, his MDS transformed into acute myeloid leukemia (AML); severe acute pancreatitis closely accompanied.
  • A subsequent pancreatitis attack with pseudocyst formation occurred, but again was controlled with corticosteroids, although this was followed closely by another relapse of AML.
  • All etiologies for recurrent acute pancreatitis were ruled out.
  • The dramatic response of his pancreatitis attacks to immunosuppression suggested its autoimmune origin, while the close relationship in both the timing and severity of acute pancreatitis and MDS/AML suggested that the autoimmune pancreatitis was a paraneoplastic phenomenon related to MDS.
  • [MeSH-minor] Abdomen / pathology. Adult. Cell Transformation, Neoplastic. Humans. Male. Recurrence. Time Factors


45. Sharma P, Dhingra KK, Roy S, Singh T: An acute myeloid leukemia M6b blast crisis with giant proerythroblasts in chronic myeloid leukemia. J Pediatr Hematol Oncol; 2009 Mar;31(3):220-1
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  • [Title] An acute myeloid leukemia M6b blast crisis with giant proerythroblasts in chronic myeloid leukemia.
  • The case of a 12 yr old female with bcr-abl positive chronic myeloid leukemia who subsequently developed a fatal AML-M6b (pure erythroleukemia) blast crisis is presented.
  • The case is unique for its rarity of occurrence and for the striking resemblance that the circulating proerythroblasts showed to the giant cells characteristically seen in Parvovirus B19-induced acute pure red cell aplasia.
  • This is, to the best of our knowledge, the first description of such cells in a blast crisis of chronic myeloid leukemia.
  • [MeSH-major] Blast Crisis / pathology. Erythroblasts / pathology. Leukemia, Erythroblastic, Acute / pathology. Neoplasms, Multiple Primary / pathology

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  • (PMID = 19262253.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; X6Q56QN5QC / Hydroxyurea
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46. Nimer SD: Is it important to decipher the heterogeneity of "normal karyotype AML"? Best Pract Res Clin Haematol; 2008 Mar;21(1):43-52
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  • [Title] Is it important to decipher the heterogeneity of "normal karyotype AML"?
  • Almost half of adult acute myelogenous leukemia (AML) is normal cytogenetically, and this subgroup shows a remarkable heterogeneity of genetic mutations at the molecular level and an intermediate response to therapy.
  • The finding of recurrent cytogenetic abnormalities has influenced, in a primary way, the understanding and treatment of leukemias.
  • Yet "normal karyotype AML" lacks such obvious abnormalities, but has a variety of prognostically important genetic abnormalities.
  • Thus, the presence of a FLT3-ITD (internal tandem duplication), MLL-PTD (partial tandem duplication), or the increased expression of ERG or EVI1 mRNAs confer a poor prognosis, and an increased risk of relapse.
  • Although resistance to treatment is associated with specific mutations, the degree to which the leukemia resembles a stem cell in its functional properties may provide greater protection from the effects of treatment.
  • Although usually all of the circulating leukemia cells are cleared following treatment, a small residual population of leukemic cells in the bone marrow persists, making this disease hard to eradicate.
  • Increased understanding of the biological consequences of at least some of these mutations in "normal karyotype AML" is leading to more targeted approaches to develop more effective treatments for this disease.

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  • (PMID = 18342811.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK052621; United States / NIDDK NIH HHS / DK / R01 DK052621-08; United States / NIDDK NIH HHS / DK / R56 DK052208-09A1; United States / NCI NIH HHS / CA / R01 CA102202-01; United States / NCI NIH HHS / CA / CA102202-01; United States / NIDDK NIH HHS / DK / R56 DK052208; United States / NCI NIH HHS / CA / R01 CA102202; United States / NIDDK NIH HHS / DK / DK052208-09A1; United States / NIDDK NIH HHS / DK / DK052621-08
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 76
  • [Other-IDs] NLM/ NIHMS44325; NLM/ PMC2654590
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47. Arts J, Angibaud P, Mariën A, Floren W, Janssens B, King P, van Dun J, Janssen L, Geerts T, Tuman RW, Johnson DL, Andries L, Jung M, Janicot M, van Emelen K: R306465 is a novel potent inhibitor of class I histone deacetylases with broad-spectrum antitumoral activity against solid and haematological malignancies. Br J Cancer; 2007 Nov 19;97(10):1344-53
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  • R306465 potently inhibited cell proliferation of all main solid tumour indications, including ovarian, lung, colon, breast and prostate cancer cell lines, with IC50 values ranging from 30 to 300 nM.
  • Haematological cell lines, including acute lymphoblastic leukaemia, acute myeloid leukaemia, chronic lymphoblastic leukaemia, chronic myeloid leukaemia, lymphoma and myeloma, were potently inhibited at a similar concentration range.
  • R306465 induced apoptosis and inhibited angiogenesis in cell-based assays and had potent oral in vivo antitumoral activity in xenograft models.
  • The high activity of R306465 in cell-based assays and in vivo after oral administration makes R306465 a promising novel antitumoral agent with potential applicability in a broad spectrum of human malignancies.
  • [MeSH-minor] Administration, Oral. Angiogenesis Inhibitors / administration & dosage. Angiogenesis Inhibitors / chemistry. Angiogenesis Inhibitors / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Disease Models, Animal. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Histones / drug effects. Histones / metabolism. Humans. Immunohistochemistry. Isoenzymes / antagonists & inhibitors. Male. Mice. Mice, Nude. Promoter Regions, Genetic / drug effects. Promoter Regions, Genetic / genetics. Rats. Rats, Sprague-Dawley. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 18000499.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Hydroxamic Acids; 0 / Isoenzymes; 0 / R 306465; 0 / Sulfones
  • [Other-IDs] NLM/ PMC2360244
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48. Martynkevich IS, Gritsaev SV, Moskalenko MV, Ivanova MP, Aksenova VIu, Tiranova SA, Abdulkadyrov KM: [FLT3 and NPM1 gene mutations in patients with acute myeloid leukemias and the impact of FLT3-ITD mutations on the survival of patients with a normal karyotype]. Ter Arkh; 2010;82(12):33-9
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  • [Title] [FLT3 and NPM1 gene mutations in patients with acute myeloid leukemias and the impact of FLT3-ITD mutations on the survival of patients with a normal karyotype].
  • AIM: To estimate the extent of FLT3 and NPM1 gene mutations and the impact of mutations of FLT3-ITD on the survival of patients with acute myeloid leukemias (AML).
  • MATERIALS AND METHODS: The nucleus-containing cells of bone marrow and blood were studied in 43 patients with AML.
  • In AML patients with a normal karyotype and the FLT3-ITD-/NPM1 and FLT3-ITD+/ NPM-T genotypes, median overall survival was 17.3 versus 8 months (p = 0.069); and event-free survival (EFS) was 11 versus 5 months (p = 0.026).
  • CONCLUSION: The findings allow AML patients with a normal karyotype and the FLT3-ITD-/NPM-genotypes to be identified as a poor prognosis group.
  • [MeSH-major] DNA / genetics. Genetic Predisposition to Disease. Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 21516736.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; 9007-49-2 / DNA; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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49. Zhou J, Khng J, Jasinghe VJ, Bi C, Neo CH, Pan M, Poon LF, Xie Z, Yu H, Yeoh AE, Lu Y, Glaser KB, Albert DH, Davidsen SK, Chen CS: In vivo activity of ABT-869, a multi-target kinase inhibitor, against acute myeloid leukemia with wild-type FLT3 receptor. Leuk Res; 2008 Jul;32(7):1091-100
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  • [Title] In vivo activity of ABT-869, a multi-target kinase inhibitor, against acute myeloid leukemia with wild-type FLT3 receptor.
  • We investigated the in vivo anti-leukemic effect of ABT-869 against AML with wild-type FLT3 using RFP transfected HL60 cells with in vivo imaging technology on both the subcutaneous and systemic leukemia xenograft models.
  • ABT-869 also reduced the leukemia burden and prolonged survival.
  • Our study supports the rationale for clinically testing an anti-angiogenesis agent in AML with wild-type FLT3.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Indazoles / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Phenylurea Compounds / therapeutic use. Protein Kinase Inhibitors / therapeutic use. fms-Like Tyrosine Kinase 3 / metabolism

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  • (PMID = 18160102.001).
  • [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 / Antineoplastic Agents; 0 / Indazoles; 0 / N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N1-(2-fluoro-5-methylphenyl)urea; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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50. de Jonge HJ, Woolthuis CM, de Bont ES, Huls G: Paradoxical down-regulation of p16 mRNA with advancing age in acute myeloid leukemia. Aging (Albany NY); 2009 Nov;1(11):949-53
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  • [Title] Paradoxical down-regulation of p16 mRNA with advancing age in acute myeloid leukemia.
  • Aging is generally considered to be the consequence of stem cell attrition caused by the activity of tumor suppressor pathways that censor potentially malignant clones by eliciting apoptosis or senescence.
  • We recently showed that, unlike healthy cells, acute myeloid leukemia (AML) derived blasts show a down-regulation of p16(INK4a) mRNA with increasing age.
  • [MeSH-major] Aging / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Down-Regulation / genetics. Leukemia, Myeloid, Acute / genetics. RNA, Messenger / genetics

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  • (PMID = 20157576.001).
  • [ISSN] 1945-4589
  • [Journal-full-title] Aging
  • [ISO-abbreviation] Aging (Albany NY)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC2815746
  • [Keywords] NOTNLM ; Acute Myeloid Leukemia / aging / p16INK4a / senescence
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51. Sánchez Y, Amrán D, de Blas E, Aller P: Regulation of genistein-induced differentiation in human acute myeloid leukaemia cells (HL60, NB4) Protein kinase modulation and reactive oxygen species generation. Biochem Pharmacol; 2009 Feb 1;77(3):384-96
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  • [Title] Regulation of genistein-induced differentiation in human acute myeloid leukaemia cells (HL60, NB4) Protein kinase modulation and reactive oxygen species generation.
  • While it has been reported that genistein induces differentiation in multiple tumour cell models, the signalling and regulation of isoflavone-provoked differentiation are poorly known.
  • We here demonstrate that genistein causes G(2)/M cycle arrest and expression of differentiation markers in human acute myeloid leukaemia cells (HL60, NB4), and cooperates with all-trans retinoic acid (ATRA) in inducing differentiation, while ATRA attenuates the isoflavone-provoked toxicity.
  • Genistein rapidly stimulates Raf-1, MEK1/2 and ERK1/2 phosphorylation/activation, but does not stimulate and instead causes a late decrease in Akt phosphorylation/activation which is attenuated by ATRA.
  • Both differentiation and G(2)/M arrest are attenuated by MEK/ERK inhibitors (PD98059, U0126) and ERK1-/ERK2-directed small interfering RNAs (siRNAs), and by the PI3K inhibitor LY294002, but not by the p38-MAPK inhibitor SB203580.
  • Caffeine abrogates the genistein-provoked G(2)/M blockade and alterations in cell cycle regulatory proteins, and also suppresses differentiation.
  • In summary, genistein-induced differentiation in acute myeloid leukaemia cells is a ROS-independent, Raf-1/MEK/ERK-mediated and PI3K-dependent response, which is coupled and co-regulated with G(2)/M arrest, but uncoupled to the pro-apoptotic action of the drug.
  • [MeSH-major] Cell Differentiation / drug effects. Genistein / pharmacology. Leukemia, Myeloid, Acute / pathology. Protein Kinases / metabolism. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Cell Division / drug effects. Cell Line, Tumor. Enzyme Activation. Flow Cytometry. Humans. Phosphorylation. Protein Kinase Inhibitors / pharmacology. RNA, Small Interfering / genetics


52. Thomas X, Raffoux E, Elhamri M, Lobe I, Cannas G, Dombret H: Clofarabine for the treatment of adult acute myeloid leukemia. Future Oncol; 2009 Oct;5(8):1197-210
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  • [Title] Clofarabine for the treatment of adult acute myeloid leukemia.
  • Clofarabine, a next-generation deoxyadenosine analog, has demonstrated significant activity in patients with acute myeloid leukemia (AML).
  • Clofarabine has been safely and effectively combined with other agents and will probably become an integral part of induction and/or consolidation regimens in AML.
  • Current studies are underway to better define the role of clofarabine in younger and elderly patients with AML, and also explore development strategies for an oral formulation.
  • [MeSH-major] Adenine Nucleotides / therapeutic use. Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use. Leukemia, Myeloid, Acute / drug therapy


53. Rong Y, Wang D, Lou W, Kuang T, Jin D: Granulocytic sarcoma of the pancreas: a case report and review of the literatures. BMC Gastroenterol; 2010;10:80
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  • [Title] Granulocytic sarcoma of the pancreas: a case report and review of the literatures.
  • BACKGROUND: Granulocytic sarcoma (GS) is a form of acute myeloid leukemia (AML), also known as extramedullary myeloid tumor or chloroma.
  • We performed surgery and the pathology and immunohistochemistry suggested GS; however the blood test and the bone marrow infiltration showed no evidence of AML.
  • In our review of the published reports of GS, we only found six reports of the GS in the pancreas, and we suggested that immunohistochemical staining should be used to accurately differentiate GS from other pancreatic cancer and other types of leukemia.
  • CONCLUSIONS: The accurate diagnosis of GS is necessary for determining prognosis and deciding appropriate therapy.
  • [MeSH-major] Pancreatic Neoplasms / diagnosis. Sarcoma, Myeloid / diagnosis

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  • (PMID = 20624285.001).
  • [ISSN] 1471-230X
  • [Journal-full-title] BMC gastroenterology
  • [ISO-abbreviation] BMC Gastroenterol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD43; EC 1.11.1.7 / Peroxidase
  • [Number-of-references] 13
  • [Other-IDs] NLM/ PMC2912803
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54. Jin G, Yamazaki Y, Takuwa M, Takahara T, Kaneko K, Kuwata T, Miyata S, Nakamura T: Trib1 and Evi1 cooperate with Hoxa and Meis1 in myeloid leukemogenesis. Blood; 2007 May 1;109(9):3998-4005
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  • [Title] Trib1 and Evi1 cooperate with Hoxa and Meis1 in myeloid leukemogenesis.
  • Cooperative activation of Meis1 and Hoxa9 perturbs myeloid differentiation and eventually leads myeloid progenitors to leukemia, yet it remains to be clarified what kinds of subsequent molecular processes are required for development of overt leukemia.
  • The mice that received Hoxa9/Meis1-transduced bone marrow cells developed acute myeloid leukemia (AML), and Trib1, Evi1, Ahi1, Raralpha, Pitpnb, and AK039950 were identified as candidate cooperative genes located near common retroviral integration sites.
  • Trib1 and Evi1 were up-regulated due to retroviral insertions, and coexpression of these genes significantly accelerated the onset of Hoxa9/Meis1-induced AML, suggesting that Trib1 and Evi1 are the key collaborators.
  • Furthermore, Trib1 by itself is a novel myeloid oncogene, enhancing phosphorylation of ERK, resulting in inhibition of apoptosis.
  • These results demonstrate the importance of specific oncogene interaction in myeloid leukemogenesis.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. DNA-Binding Proteins / metabolism. Homeodomain Proteins / metabolism. Leukemia, Myeloid / metabolism. Microtubule Proteins / metabolism. Neoplasm Proteins / metabolism. Neoplastic Stem Cells / metabolism. Transcription Factors / metabolism

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  • (PMID = 17227832.001).
  • [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 / DNA-Binding Proteins; 0 / Evi1 protein, mouse; 0 / Homeodomain Proteins; 0 / Microtubule Proteins; 0 / Neoplasm Proteins; 0 / Transcription Factors; 0 / Trib protein, mouse; 0 / homeobox protein HOXA9; 0 / myeloid ecotropic viral integration site 1 protein
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55. Frey NV, Leid CE, Nowell PC, Tomczak E, Strauser HT, Kasner M, Goldstein S, Loren A, Stadtmauer E, Luger S, Hexner E, Hinkle J, Porter DL: Trisomy 8 in an allogeneic stem cell transplant recipient representative of a donor-derived constitutional abnormality. Am J Hematol; 2008 Nov;83(11):846-9
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  • [Title] Trisomy 8 in an allogeneic stem cell transplant recipient representative of a donor-derived constitutional abnormality.
  • Trisomy 8 is a common cytogenetic abnormality in myeloid malignancies.
  • We report a case of a 20-year-old woman with acute myelogenous leukemia associated with the 11q23/MLL translocation who underwent allogeneic hematopoietic stem cell transplantation (HSCT) from a healthy, unrelated 26-year-old female.
  • FISH analysis of a cryopreserved sample of the donor graft showed trisomy 8 in 120 of 200 cells examined.
  • This represents the first reported case of a person with constitutional trisomy 8 mosaicism serving as a stem cell donor.
  • The case illustrates the importance of identifying donor-derived constitutional abnormalities to avoid the assumption that these cytogenetic abnormalities after HSCT are representative of malignant disease.

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  • [Copyright] Copyright 2008 Wiley-Liss, Inc.
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  • (PMID = 18819096.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA117879-03; United States / NCI NIH HHS / CA / K24 CA117879; United States / NCI NIH HHS / CA / K24 CA117879-03; United States / NCI NIH HHS / CA / K24 CA11787901
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS74574; NLM/ PMC2610424
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56. Guo Y, Köck K, Ritter CA, Chen ZS, Grube M, Jedlitschky G, Illmer T, Ayres M, Beck JF, Siegmund W, Ehninger G, Gandhi V, Kroemer HK, Kruh GD, Schaich M: Expression of ABCC-type nucleotide exporters in blasts of adult acute myeloid leukemia: relation to long-term survival. Clin Cancer Res; 2009 Mar 01;15(5):1762-9
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  • [Title] Expression of ABCC-type nucleotide exporters in blasts of adult acute myeloid leukemia: relation to long-term survival.
  • PURPOSE: Successful treatment of acute myeloid leukemia (AML) remains a therapeutic challenge, with a high percentage of patients suffering from persistent or relapsed disease.
  • Both mechanisms are mediated by the efflux transporters ABCC4 (MRP4), ABCC5 (MRP5), and ABCC11 (MRP8), which are involved in cellular efflux of endogenous signaling molecules (e.g., cyclic adenosine 3', 5'-monophosphate and cyclic guanosine 3',5'-monophosphate) and nucleoside analogues.
  • The nucleoside analogue cytosine arabinoside (AraC) is administered to all patients with AML.
  • EXPERIMENTAL DESIGN: Expression of ABCC transporters MRP4, MRP5, and MRP8 in blast samples from 50 AML patients was investigated by real-time reverse transcription-PCR analysis and correlated with clinical outcome measures.
  • Furthermore, AraC monophosphate was transported by MRP8-enriched membrane vesicles (116+/-6 versus 65+/-13 pmol/mg/10 minutes by control vesicles), and MRP8-transfected cells were resistant to AraC.
  • CONCLUSION: These data suggest that MRP8 is differentially expressed in AML blasts, that expression of MRP8 serves as a predictive marker for treatment outcome in AML, and that efflux of AraC metabolites by MRP8 is a mechanism that contributes to resistance of AML blasts.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Blast Crisis. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. Multidrug Resistance-Associated Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Cell Membrane / metabolism. Cytarabine / metabolism. Drug Resistance, Neoplasm. Female. Humans. LLC-PK1 Cells. Male. Middle Aged. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Stem Cells / metabolism. Stem Cells / pathology. Survival Rate

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  • (PMID = 19240178.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA057629; United States / NCI NIH HHS / CA / CA113474; United States / NCI NIH HHS / CA / CA73728; United States / NCI NIH HHS / CA / R01 CA114574; United States / NCI NIH HHS / CA / CA57629; United States / NCI NIH HHS / CA / U01 CA073728
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCC11 protein, human; 0 / ABCC4 protein, human; 0 / ABCC5 protein, human; 0 / ATP-Binding Cassette Transporters; 0 / Multidrug Resistance-Associated Proteins; 0 / RNA, Messenger; 04079A1RDZ / Cytarabine
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57. Li X, Du W, Liu W, Li X, Li H, Huang SA: Comprehensive flow cytometry phenotype in acute leukemia at diagnosis and at relapse. APMIS; 2010 May;118(5):353-9
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  • [Title] Comprehensive flow cytometry phenotype in acute leukemia at diagnosis and at relapse.
  • Multiparameter flow cytometry (MFC) plays a vital role in the detection of minimal residual disease (MRD) and diagnosis of relapse in acute leukemia.
  • However, application of a limited panel of antibodies in MFC leads to high rates of false-negative and false-positive results.
  • Thirteen patients with acute lymphoblastic leukemia (ALL) and 12 patients with acute myeloid leukemia (AML) were immunophenotyped by MFC at diagnosis and at relapse using a comprehensive panel of monoclonal antibodies (McAbs) to 27 antigens and CD45/SSC gating.
  • In 23 of 25 patients (92.3%), changes in at least one of progenitor-associated, myeloid and lymphoid antigens between diagnosis and relapse were observed.
  • Antigen changes were observed in 92 of 239 antigens (38.5%) expressed in 25 patients, in 49 of 117 antigens (41.9%) expressed in 13 ALL patients, and in 43 of 122 antigens (35.2%) expressed in 12 AML patients.
  • However, myeloid lineage shift was identified by MFC in two patients with T-ALL.
  • Multiple panels of three or more McAbs are likely to be required in the monitoring of MRD and diagnosis of relapse in acute leukemia by MFC.
  • [MeSH-major] Flow Cytometry / methods. Immunophenotyping / methods. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 20477810.001).
  • [ISSN] 1600-0463
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Neoplasm
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58. Sakamoto KM, Frank DA: CREB in the pathophysiology of cancer: implications for targeting transcription factors for cancer therapy. Clin Cancer Res; 2009 Apr 15;15(8):2583-7
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  • Transcription factors are key regulators of the pattern of gene expression in a cell and directly control central processes such as proliferation, survival, self-renewal, and invasion.
  • Although transcription factors are not often directly modified by mutations in cancer cells, they frequently become activated constitutively through mutations affecting "upstream" pathways.
  • CREB is overexpressed and constitutively phosphorylated in a number of forms of human cancer, including acute myeloid leukemia (AML) and non-small cell lung cancer, and appears to play a direct role in disease pathogenesis and prognosis.
  • Although transcription factors have not been a central focus of drug development, recent advances suggest that CREB and other such proteins may be worthwhile targets for cancer therapy.

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  • (PMID = 19351775.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL075826-03; United States / NHLBI NIH HHS / HL / R01 HL075826; United States / NHLBI NIH HHS / HL / R01 HL083077-03S1; United States / NHLBI NIH HHS / HL / R01 HL083077-04S1; United States / NHLBI NIH HHS / HL / HL083077-03S1; United States / NHLBI NIH HHS / HL / HL083077-01; United States / NHLBI NIH HHS / HL / HL075826-04; United States / NHLBI NIH HHS / HL / R01 HL083077-03; United States / NHLBI NIH HHS / HL / HL075826-01; United States / NHLBI NIH HHS / HL / HL083077-04; United States / NHLBI NIH HHS / HL / HL083077-03; United States / NHLBI NIH HHS / HL / HL075826-03; United States / NHLBI NIH HHS / HL / R01 HL075826-02; United States / NHLBI NIH HHS / HL / R01 HL083077-02; United States / NHLBI NIH HHS / HL / HL83077; United States / NHLBI NIH HHS / HL / HL75826; United States / NHLBI NIH HHS / HL / R01 HL083077; United States / NHLBI NIH HHS / HL / HL075826-02S2; United States / NHLBI NIH HHS / HL / HL075826-02S1; United States / NHLBI NIH HHS / HL / HL083077-02; United States / NHLBI NIH HHS / HL / HL083077-04S1; United States / NHLBI NIH HHS / HL / R01 HL075826-02S2; United States / NHLBI NIH HHS / HL / R01 HL075826-04; United States / NHLBI NIH HHS / HL / R01 HL075826-02S1; United States / NHLBI NIH HHS / HL / HL075826-02; United States / NHLBI NIH HHS / HL / R01 HL083077-01; United States / NHLBI NIH HHS / HL / R01 HL083077-04; United States / NHLBI NIH HHS / HL / R01 HL075826-01
  • [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 / CREB1 protein, human; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Cytokines; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 2.7.- / Protein Kinases
  • [Other-IDs] NLM/ NIHMS184976; NLM/ PMC2883446
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59. Ottmann OG, Bug G, Krauter J: Current status of growth factors in the treatment of acute myeloid and lymphoblastic leukemia. Semin Hematol; 2007 Jul;44(3):183-92
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  • [Title] Current status of growth factors in the treatment of acute myeloid and lymphoblastic leukemia.
  • The safety of granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) in patients with acute leukemia has been well established in numerous clinical trials.
  • The primary aim of these studies was to determine whether CSFs, when used as adjuncts to intensive chemotherapy, reduced the duration of neutropenia, prevented febrile neutropenia, infections, and hospitalization rates, and improved response and overall outcome in patients with acute myeloid leukemia (AML) or acute lymphoblastic leukemia (ALL).
  • Despite considerable efforts in divers clinical settings, the potential advantages of hematopoietic growth factors in the management of these leukemias remain inconclusive.
  • In general, individual published trials have shown declines in the incidence and/or duration of neutropenia but have not consistently demonstrated a reduction in the overall frequency of infectious complications or the duration of hospitalization.
  • Most protocols also have failed to show a benefit in terms of disease-free or overall survival.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Granulocyte Colony-Stimulating Factor / therapeutic use. Granulocyte-Macrophage Colony-Stimulating Factor / therapeutic use. Leukemia, Lymphoid / drug therapy. Leukemia, Myeloid / drug therapy. Neutropenia / drug therapy
  • [MeSH-minor] Acute Disease. Clinical Trials as Topic. Cytokines / blood. Cytokines / therapeutic use. Humans

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  • (PMID = 17631182.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Number-of-references] 71
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60. Cosenza M, Civallero M, Sacchi S, Marcheselli R, Pozzi S: Biological effects of Atra and Arsenic Trioxide on short term cultures of non-M3 leukemic blasts. Leuk Lymphoma; 2005 Feb;46(2):257-63
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  • [Title] Biological effects of Atra and Arsenic Trioxide on short term cultures of non-M3 leukemic blasts.
  • The efficacy of All-Trans Retinoic Acid (Atra) and Arsenic Trioxide (As(2)O(3)) in the treatment of Acute Promyelocytic Leukemia (APL) is well known.
  • Further, these drugs inhibit cell growth and induce apoptosis in several cell lines, but few data are reported on leukemic blasts.
  • The aim of this study was to evaluate the biological effects on non-M3 Acute Myeloid Leukemia (AML) cells.
  • Blasts of six patients, after exposition to Atra and As(2)O(3) were tested for growth inhibition, induction of apoptosis and change in cell cycle distribution, evaluating cell viability, percentage of apoptotic cells and of blasts positive for Ki-67 and BrdU.
  • We did not observe additive or synergistic effects with the combination of the drugs.
  • Further, our results showed that Atra and As(2)O(3) have effects on cell cycle distribution reducing S-phase and proliferating cells.
  • These results should be taken in to account preparing future laboratory and clinical experimental protocols that associate these drugs with antineoplastic agents with different cell cycle specificity.
  • [MeSH-major] Arsenicals / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Oxides / pharmacology. Tretinoin / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Bromodeoxyuridine. Cell Cycle / drug effects. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Drug Interactions. Humans. Ki-67 Antigen / analysis. Kinetics. S Phase. Tumor Cells, Cultured

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  • (PMID = 15621810.001).
  • [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 / Arsenicals; 0 / Ki-67 Antigen; 0 / Oxides; 5688UTC01R / Tretinoin; G34N38R2N1 / Bromodeoxyuridine; S7V92P67HO / arsenic trioxide
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61. Imahashi N, Inamoto Y, Seto A, Watanabe K, Nishiwaki S, Yanagisawa M, Shinba M, Yasuda T, Kuwatsuka Y, Atsuta Y, Kodera Y, Miyamura K: Impact on relapse of corticosteroid therapy after allogeneic hematopoietic stem cell transplantation for acute myeloid leukemia. Clin Transplant; 2010 Nov-Dec;24(6):772-7
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  • [Title] Impact on relapse of corticosteroid therapy after allogeneic hematopoietic stem cell transplantation for acute myeloid leukemia.
  • Corticosteroids are often used following allogeneic hematopoietic stem cell transplantation (HSCT) to control complications such as graft-versus-host disease (GVHD).
  • However, there is some concern that corticosteroids may suppress the graft-versus-leukemia effect and increase leukemia relapse.
  • To evaluate the effect of corticosteroids on relapse, we analyzed 112 adult patients who received their first allogeneic HSCT for acute myeloid leukemia at our institution between 1997 and 2007.
  • In multivariate analysis, with corticosteroid administration entered as a time-dependent covariate, corticosteroid administration was not a risk factor for relapse (p = 1.00, hazard ratio [HR] 1.00, 95% confidence interval [CI] 0.53-1.88), but it was associated with higher non-relapse mortality (NRM) (p < 0.001, HR 55.5, 95% CI 7.42-416) and lower overall survival (p < 0.001, HR 2.68, 95% CI 1.56-4.61).
  • [MeSH-major] Glucocorticoids / therapeutic use. Graft vs Host Disease / prevention & control. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / surgery. Neoplasm Recurrence, Local


62. Petersen FB, Ford CD: Maximum supportive care, standard conditioning and allogeneic stem cell transplantation for elderly patients with acute myelogenous leukemia. Curr Opin Oncol; 2009 Jun;21 Suppl 1:S7-9
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  • [Title] Maximum supportive care, standard conditioning and allogeneic stem cell transplantation for elderly patients with acute myelogenous leukemia.
  • Dose-intense conditioning (DIC) (myeloablative) regimens for allogeneic stem cell transplantation (alloSCT) were previously avoided in patients with acute myelogenous leukemia aged more than 55 years because of the fear of excessive morbidity and mortality.
  • Significant disadvantages remain, however, including the late establishment of a posttransplant graft-versus-leukemia effect and an overrepresentation of poor prognostic factors in elderly patients, resulting in the risk of early relapse/progression before the graft-versus-leukemia effect being disproportionally large.
  • We hypothesize that DIC may be important for the early control of leukemia in elderly patients, and that prospective, randomized trials comparing DIC and RIC-based transplants should be carried out, with the expectation that early transplant-related mortality will be no different.
  • [MeSH-major] Health Services for the Aged. Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation. Transplantation Conditioning / methods


63. van Gosliga D, Schepers H, Rizo A, van der Kolk D, Vellenga E, Schuringa JJ: Establishing long-term cultures with self-renewing acute myeloid leukemia stem/progenitor cells. Exp Hematol; 2007 Oct;35(10):1538-49
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  • [Title] Establishing long-term cultures with self-renewing acute myeloid leukemia stem/progenitor cells.
  • OBJECTIVE: With the emergence of the concept of the leukemia stem cell, assays to study them remain pivotal in understanding (leukemic) stem cell biology.
  • METHODS: We have cultured acute myeloid leukemia CD34(+) cells on bone marrow stroma.
  • Long-term expansion was monitored and self-renewal was addressed by replating of Leukemic-cobblestone area-forming cells (L-CAs).
  • RESULTS: A strong expansion was observed in about 75% of the acute myeloid leukemia cases (n = 30) and long-term cultures could be maintained for up to 24 weeks on MS5 bone marrow stromal cells.
  • Cells that were able to initiate leukemic cobblestone areas resided in the CD34(+) population and were absent from the CD34(-) population.
  • [MeSH-major] Bone Marrow Cells / pathology. Cell Line, Tumor / pathology. Leukemia, Myeloid, Acute / pathology. Neoplastic Stem Cells / pathology. Tumor Stem Cell Assay

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  • (PMID = 17889721.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / homeobox protein HOXA9; 0 / myeloid ecotropic viral integration site 1 protein; EC 6.3.2.19 / Polycomb Repressive Complex 1
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64. Maha A, Cheong SK, Leong CF, Seow HF: Cell viability of acute myeloid leukaemia blasts in culture correlates with treatment outcome. Hematology; 2008 Feb;13(1):13-20
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  • [Title] Cell viability of acute myeloid leukaemia blasts in culture correlates with treatment outcome.
  • Despite the advances in understanding the pathophysiology of acute myeloid leukaemia (AML), the cure rate for acute myeloid leukaemia patients remains low.
  • However, many AML patients still die.
  • Acute myeloid leukaemia blasts demonstrated differing ability to survive in culture.
  • First, cells underwent maturation by increased expression of CD16 and down-regulated CD34 (a haemopoietic stem cell marker).
  • A comparison between results of MTT assay and duration of disease free survival revealed that a higher viability in vitro correlated significantly with shorter survival duration in the patient (R -0.761, p=0.002, n=13).
  • Thus, this study further supports the hypothesis that AML patients with poor survival may be related to having blasts with a biologically more immature or stem cell-like nature.
  • [MeSH-major] Cell Differentiation. Cell Proliferation. Granulocyte Precursor Cells / pathology. Leukemia, Myeloid, Acute / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Apoptosis. Cell Survival. Child. Child, Preschool. Cohort Studies. Female. Humans. In Vitro Techniques. Infant. Male. Middle Aged. Phenotype. Remission Induction. Survival Analysis. Tumor Cells, Cultured

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  • (PMID = 18534060.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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65. Moosavi SA, Sanchez J, Adeyinka A: Marker chromosomes are a significant mechanism of high-level RUNX1 gene amplification in hematologic malignancies. Cancer Genet Cytogenet; 2009 Feb;189(1):24-8
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  • To understand the cytogenetic mechanisms responsible for multiple RUNX1 gene copy numbers in hematologic malignancies, we analyzed the chromosomal and molecular cytogenetic findings in bone marrow or peripheral blood samples of individuals who were diagnosed with acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), or acute lymphoblastic leukemia (ALL).
  • Eight of these had, by interphase FISH, RUNX1/RUNX1T1 or RUNX1/ETV6 fusion, and 19 had three or more RUNX1 signals not related to fusion with RUNX1T1 or ETV6 gene.
  • Four of the five tumors with high-level RUNX1 amplification were myeloid disorders--three cases of AML and one case of MDS.
  • Our findings show that high-level RUNX1 amplification, especially in myeloid disorders, often results from marker chromosomes harboring extra copies of the RUNX1 gene .
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Gene Amplification / genetics. Hematologic Neoplasms / genetics. Leukemia / genetics

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  • (PMID = 19167608.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
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66. Faurschou M, Sorensen IJ, Mellemkjaer L, Loft AG, Thomsen BS, Tvede N, Baslund B: Malignancies in Wegener's granulomatosis: incidence and relation to cyclophosphamide therapy in a cohort of 293 patients. J Rheumatol; 2008 Jan;35(1):100-5
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  • Significantly increased SIR were observed for acute myeloid leukemia (AML; SIR 19.6, 95% CI 4.0-57), bladder cancer (SIR 3.6, 95% CI 1.2-8.3), and non-melanoma skin cancers (SIR 4.7, 95% CI 2.8-7.3).
  • Leukemias and bladder cancers were diagnosed 6.9-18.5 years after initiation of CYC therapy.
  • The risk of these malignancies was not increased for patients who never received CYC or for patients treated with cumulative CYC doses < or = 36 g.
  • In contrast, high risks of AML (SIR 59.0, 95% CI 12-172) and bladder cancer (SIR 9.5, 95% CI 2.6-24) were observed for patients treated with cumulative CYC doses > 36 g.

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  • [CommentIn] Nat Clin Pract Rheumatol. 2008 Jul;4(7):340-1 [18506161.001]
  • [CommentIn] J Rheumatol. 2008 Jan;35(1):11-3 [18176988.001]
  • (PMID = 17937462.001).
  • [ISSN] 0315-162X
  • [Journal-full-title] The Journal of rheumatology
  • [ISO-abbreviation] J. Rheumatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antirheumatic Agents; 0 / Mutagens; 8N3DW7272P / Cyclophosphamide
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67. Dao T, Scheinberg DA: Peptide vaccines for myeloid leukaemias. Best Pract Res Clin Haematol; 2008 Sep;21(3):391-404
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  • [Title] Peptide vaccines for myeloid leukaemias.
  • The development of cancer vaccines directed against myeloid leukaemias has been a research area of intense interest in the past decade.
  • Both human studies in vitro and mouse models in vivo have demonstrated that leukaemia-associated antigens (LAAs), such as the fusion protein BCR-ABL, Wilms' tumour protein and proteinase 3, may serve as effective targets for cellular immunotherapy.
  • Peptide-based vaccines are able to induce cytotoxic T-lymphocyte responses that kill leukaemia cells.
  • Based on these results, pilot clinical trials have been initiated in chronic and acute myeloid leukaemia and other haematological malignancies, which include vaccination of patients with synthetic peptides derived from these LAAs.
  • This chapter will focus mainly on discussing the preclinical studies of peptide vaccines in human systems, the results from clinical trials and the future prospects for vaccine therapy for myeloid leukaemia.
  • [MeSH-major] Leukemia, Myeloid / immunology. Vaccines, Subunit / therapeutic use
  • [MeSH-minor] CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Fusion Proteins, bcr-abl / immunology. Humans. Immunotherapy / methods. Kidney Neoplasms / immunology. Kidney Neoplasms / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / immunology. Myeloblastin / immunology. Neoplasm Proteins / immunology. WT1 Proteins / immunology. Wilms Tumor / immunology. Wilms Tumor / therapy

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  • (PMID = 18790445.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Vaccines, Subunit; 0 / WT1 Proteins; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.4.21.76 / Myeloblastin
  • [Number-of-references] 86
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68. Lee CC, Lin CP, Lee YL, Wang GC, Cheng YC, Liu HE: Meisoindigo is a promising agent with in vitro and in vivo activity against human acute myeloid leukemia. Leuk Lymphoma; 2010 May;51(5):897-905
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  • [Title] Meisoindigo is a promising agent with in vitro and in vivo activity against human acute myeloid leukemia.
  • Meisoindigo, a derivative of Indigo naturalis, has been used in China for chronic myeloid leukemia.
  • In vitro cell line studies have shown that this agent might induce apoptosis and myeloid differentiation of acute myeloid leukemia (AML).
  • In this study, we explored its mechanisms and potential in AML.
  • NB4, HL-60, and U937 cells and primary AML cells were used to examine its effects and the NOD/SCID animal model was used to evaluate its in vivo activity.
  • Meisoindigo inhibited the growth of leukemic cells by inducing marked apoptosis and moderate cell-cycle arrest at the G(0)/G(1) phase.
  • It down-regulated anti-apoptotic Bcl-2, and up-regulated pro-apoptotic Bak and Bax and cell-cycle related proteins, p21and p27.
  • Furthermore, it induced myeloid differentiation, as demonstrated by morphologic changes, up-regulation of CD11b, and increased nitroblue tetrazolium reduction activity in all cell lines tested.
  • As with the results from cell lines, meisoindigo also induced apoptosis, up-regulated p21 and p27, and down-regulated Bcl-2 in primary AML cells.
  • Taking these results together, meisoindigo is a potential agent for AML.
  • [MeSH-major] Apoptosis / drug effects. Cell Cycle / drug effects. Cell Proliferation / drug effects. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 20233051.001).
  • [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 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Indoles; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 97207-47-1 / N-methylisoindigotin; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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69. Alvarez Alvarez C, Fernández Sanromán J, Fernández Castilla M, Antón Badiola I: Sporadic oral angiomyolipoma. Case report. Med Oral Patol Oral Cir Bucal; 2007 Sep;12(5):E391-3
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  • Angiomyolipoma (AML) is a rare, benign tumour composed of a variable proportion of lipocytes, smooth muscle and thick-walled blood vessels.
  • AML is part of a family of tumours arising from perivascular epithelioid cells (PEComas), and many cases are associated with tuberous sclerosis, with the kidney being the most frequent site involved.
  • We report a case of sporadic AML in the hard palate of a 52-year-old male, an extremely unusual location for this tumour.
  • Differentiation from other benign and malignant oral mesenchymal lesions depends on recognition of the three histologic components, and immunohistochemical techniques may be helpful.
  • AML occurring in the head and neck do not express HMB-45, an antibody that identifies immature melanosomes, conversely to the usual immunopositivity shown in AMLs from kidney and liver, suggesting that there are differences among them.

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  • (PMID = 17767105.001).
  • [ISSN] 1698-6946
  • [Journal-full-title] Medicina oral, patología oral y cirugía bucal
  • [ISO-abbreviation] Med Oral Patol Oral Cir Bucal
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Spain
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71. Sun C, Zhang SJ, Li JY, Sheng YF: [Molecular markers related to prognosis of acute myeloid leukemia-review]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Aug;17(4):1083-7
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  • [Title] [Molecular markers related to prognosis of acute myeloid leukemia-review].
  • Numerous genetic abnormalities which can not be identified by cytogenetic detection (e.g., gene mutations, gene expression abnormalities) have been gradually found, which means that the further molecular classification of AML (acute myeloid leukemia) with distinctive prognosis have arrived.
  • This review focuses on the features and relationship of these genetic abnormalities, as well as their influence on the prognosis of AML.

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  • (PMID = 19698266.001).
  • [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; Review
  • [Publication-country] China
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72. Khoury H, Suarez-Saiz F, Wu S, Minden MD: An upstream insulator regulates DLK1 imprinting in AML. Blood; 2010 Mar 18;115(11):2260-3
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  • [Title] An upstream insulator regulates DLK1 imprinting in AML.
  • Using informative coding single nucleotide polymorphisms, we found DLK1 expression to be monoallelic in normal bone marrow, whereas it was biallelic in 76% of acute myeloid leukemia (AML) overexpressing DLK1 (61% of all AML).
  • Quantitative methylation analysis of 7 cytosine-phosphate-guanosine-rich areas (3 upstream of or within DLK1, the putative intergenic-differentially methylated region and 3 upstream of or within MEG3) revealed a strong association between biallelic DLK1 expression and hypermethylation of a cytosine-phosphate-guanosine-rich region 18 kb upstream of DLK1.
  • Allele-specific methylation analysis of this region revealed the alleles to be differentially methylated in normal bone marrow and monoallelic DLK1 AML, whereas there was increased methylation of both alleles in AML with biallelic expression.
  • Moreover, chromatin immunoprecipitation analysis revealed that CCTC-binding factor binds to this region in monoallelic but not biallelic expression samples.
  • [MeSH-major] Genomic Imprinting / genetics. Insulator Elements / genetics. Intercellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Membrane Proteins / genetics
  • [MeSH-minor] Alleles. Base Sequence. Cell Line, Tumor. DNA Methylation / genetics. DNA Mutational Analysis. Gene Expression Regulation, Leukemic. Humans. Molecular Sequence Data

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  • (PMID = 20089961.001).
  • [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 / DLK1 protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins
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73. Castagnola E, Rossi MR, Cesaro S, Livadiotti S, Giacchino M, Zanazzo G, Fioredda F, Beretta C, Ciocchello F, Carli M, Putti MC, Pansini V, Berger M, Licciardello M, Farina S, Caviglia I, Haupt R: Incidence of bacteremias and invasive mycoses in children with acute non-lymphoblastic leukemia: results from a multi-center Italian study. Pediatr Blood Cancer; 2010 Dec 1;55(6):1103-7
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  • [Title] Incidence of bacteremias and invasive mycoses in children with acute non-lymphoblastic leukemia: results from a multi-center Italian study.
  • BACKGROUND: Data on the epidemiology of bacteremias and invasive fungal diseases (IFD) in children with acute myeloid leukemia (AML) are scarce.
  • DESIGN AND METHODS: In a multi-center, retrospective study, we analyzed proportion, rate per 1,000 person-days at risk, and cumulative risk of bacteremias and IFD in children with AML.
  • RESULTS: Between January 1998 and December 2005, 240 children were treated for AML at 8 Italian Centers, for a total of 521 treatment courses and 63,232 person-days at risk.
  • The epidemiology of bacteremias and IFD was different during front-line therapy for M3 as compared to other types of AML, but the differences were not statistically significant.
  • CONCLUSIONS: Severe infectious complications are frequent during the treatment of pediatric AML, especially during relapse treatment, and bacteremias are more frequent than IFD.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Bacteremia / etiology. Leukemia, Myeloid, Acute / microbiology. Mycoses / etiology


74. Kawatani E, Kishikawa Y, Sankoda C, Kuwahara N, Mori D, Osoegawa K, Matsuishi E, Gondo H: [Bacillus cereus sepsis and subarachnoid hemorrhage following consolidation chemotherapy for acute myelogenous leukemia]. Rinsho Ketsueki; 2009 Apr;50(4):300-3
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  • [Title] [Bacillus cereus sepsis and subarachnoid hemorrhage following consolidation chemotherapy for acute myelogenous leukemia].
  • A 64-year-old man with acute myelogenous leukemia (FAB classification, M7) in remission received consolidation chemotherapy with mitoxantrone/cytosine arabinoside.
  • Postmortem examination demonstrated many colonies of B. cereus in the cerebrum, cerebellum, lung, and liver.
  • Hepatocyte necrosis was also observed in the liver.
  • Bacterial aneurysms or septic emboli were not identified in the arachnoid vessels, but necrosis of cerebral vessels was prominent, which was considered to be the cause of subarachnoid hemorrhage.
  • Fatal subarachnoid hemorrhage has been reported to be associated with B. cereus sepsis, which developed at nadir following chemotherapy for leukemia patients.
  • Because of the aggressive clinical course of B. cereus sepsis, including the risk for subarachnoid hemorrhage, early treatment with effective antibiotics for B. cereus sepsis would be important in the management of leukemia patients after chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bacillaceae Infections / complications. Bacillus cereus. Immunocompromised Host. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Opportunistic Infections / complications. Sepsis / complications. Subarachnoid Hemorrhage / etiology

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  • (PMID = 19404024.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone
  • [Number-of-references] 12
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75. Ma Y, Cui W, Yang J, Qu J, Di C, Amin HM, Lai R, Ritz J, Krause DS, Chai L: SALL4, a novel oncogene, is constitutively expressed in human acute myeloid leukemia (AML) and induces AML in transgenic mice. Blood; 2006 Oct 15;108(8):2726-35
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  • [Title] SALL4, a novel oncogene, is constitutively expressed in human acute myeloid leukemia (AML) and induces AML in transgenic mice.
  • Through immunohistochemistry and real-time reverse-transcription-polymerase chain reaction (RT-PCR), we demonstrated that SALL4 was constitutively expressed in human primary acute myeloid leukemia (AML, n = 81), and directly tested the leukemogenic potential of constitutive expression of SALL4 in a murine model.
  • SALL4B transgenic mice developed myelodysplastic syndrome (MDS)-like features and subsequently AML that was transplantable.
  • Our data suggest that the constitutive expression of SALL4 causes MDS/AML, most likely through the Wnt/beta-catenin pathway.
  • Our murine model provides a useful platform to study human MDS/AML transformation, as well as the Wnt/beta-catenin pathway's role in the pathogenesis of leukemia stem cells.


76. Rücker FG, Bullinger L, Schwaenen C, Lipka DB, Wessendorf S, Fröhling S, Bentz M, Miller S, Scholl C, Schlenk RF, Radlwimmer B, Kestler HA, Pollack JR, Lichter P, Döhner K, Döhner H: Disclosure of candidate genes in acute myeloid leukemia with complex karyotypes using microarray-based molecular characterization. J Clin Oncol; 2006 Aug 20;24(24):3887-94
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  • [Title] Disclosure of candidate genes in acute myeloid leukemia with complex karyotypes using microarray-based molecular characterization.
  • PURPOSE: To identify novel genomic regions of interest in acute myeloid leukemia (AML) with complex karyotypes, we applied comparative genomic hybridization to microarrays (array-CGH), allowing high-resolution genome-wide screening of genomic imbalances.
  • PATIENTS AND METHODS: Sixty AML cases with complex karyotypes were analyzed using array-CGH; parallel analysis of gene expression was performed in a subset of cases.
  • CONCLUSION: In conclusion, a large spectrum of genomic imbalances, including novel recurring changes in AML with complex karyotypes, was identified using array-CGH.
  • In addition, the combined analysis of array-CGH data with gene expression profiles allowed the detection of candidate genes involved in the pathogenesis of AML.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genomic Instability. Leukemia, Myeloid / genetics. Microarray Analysis. Nucleic Acid Hybridization
  • [MeSH-minor] Acute Disease. Allelic Imbalance. Chromosome Aberrations. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 20. Chromosomes, Human, Pair 5. Chromosomes, Human, Pair 7. Chromosomes, Human, Pair 8. Genetic Linkage. Humans. Karyotyping. Loss of Heterozygosity. Nucleic Acid Amplification Techniques

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  • [CommentIn] J Clin Oncol. 2007 Mar 20;25(9):1151-2; author reply 1152-3 [17369586.001]
  • (PMID = 16864856.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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77. Alloush HM, Anderson E, Martin AD, Ruddock MW, Angell JE, Hill PJ, Mehta P, Smith MA, Smith JG, Salisbury VC: A bioluminescent microbial biosensor for in vitro pretreatment assessment of cytarabine efficacy in leukemia. Clin Chem; 2010 Dec;56(12):1862-70
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  • [Title] A bioluminescent microbial biosensor for in vitro pretreatment assessment of cytarabine efficacy in leukemia.
  • BACKGROUND: The nucleoside analog cytarabine (Ara-C [cytosine arabinoside]) is the key agent for treating acute myeloid leukemia (AML); however, up to 30% of patients fail to respond to treatment.
  • METHODS: We used transposition mutagenesis to create a cytidine deaminase (cdd)-deficient mutant of E. coli MG1655 that responded to Ara-C.
  • The strain was transformed with the luxCDABE operon and used as a whole-cell biosensor for development an 8-h assay to determine Ara-C uptake and phosphorylation by leukemic cells.
  • Results using AML cell lines with known response to Ara-C showed close correlation between the 8-h assay and a 3-day cytotoxicity test for Ara-C cell killing.
  • In retrospective tests with 24 clinical samples of bone marrow or peripheral blood, the biosensor-based assay predicted leukemic cell response to Ara-C within 8 h.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Biosensing Techniques. Cytarabine / analysis. Escherichia coli. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Bone Marrow Cells / drug effects. Bone Marrow Cells / pathology. Cell Line, Tumor. Cytidine Deaminase. Deoxycytidine Kinase / biosynthesis. Deoxycytidine Kinase / genetics. Drug Resistance, Neoplasm. Humans. Intracellular Space / chemistry. Luminescent Measurements. Mutation. Nucleoside Deaminases / genetics. Phosphorylation

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  • (PMID = 20921267.001).
  • [ISSN] 1530-8561
  • [Journal-full-title] Clinical chemistry
  • [ISO-abbreviation] Clin. Chem.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MR/J005207/1; United Kingdom / Biotechnology and Biological Sciences Research Council / / 330/E19334
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 2.7.1.74 / Deoxycytidine Kinase; EC 3.5.4.- / Nucleoside Deaminases; EC 3.5.4.5 / Cytidine Deaminase; EC 3.5.4.5 / deoxycytidine deaminase
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78. Olaru D, Campos L, Flandrin P, Nadal N, Duval A, Chautard S, Guyotat D: Multiparametric analysis of normal and postchemotherapy bone marrow: Implication for the detection of leukemia-associated immunophenotypes. Cytometry B Clin Cytom; 2008 Jan;74(1):17-24
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  • [Title] Multiparametric analysis of normal and postchemotherapy bone marrow: Implication for the detection of leukemia-associated immunophenotypes.
  • BACKGROUND: The knowledge of normal marrow is mandatory to assess the malignant counterpart of normal cells and define leukemia-associated immunophenotypes (LAIPs).
  • In this study, the expression of a variety of antigens expressed in normal and postchemotherapy bone marrow (BM) was analyzed to provide a frame of reference for the identification of myeloid LAIPs.
  • METHODS: Multiparameter four- and six-color flow cytometry was used to define antigen combinations totally absent or present at very minimal levels in marrow cells of normal individuals (n = 20) and patients receiving chemotherapy for acute lymphoblastic leukemia (n = 20).
  • Fifty-three acute myeloid leukemia (AML) samples were studied in six-color combinations.
  • Using the six-color panel, 58% of the absent or infrequent phenotypes in normal BM were found in at least one of 53 AML samples.
  • All AML cases exhibited at least one LAIP.
  • Furthermore, these absent or infrequent phenotypes in normal BM are identified in AML and can be utilized for minimal residual disease study.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Marrow / pathology. Flow Cytometry / methods. Immunophenotyping. Leukemia, Myeloid, Acute / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • [Copyright] (c) 2007 Clinical Cytometry Society
  • (PMID = 18061947.001).
  • [ISSN] 1552-4957
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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79. Advani AS, Hunger SP, Burnett AK: Acute leukemia in adolescents and young adults. Semin Oncol; 2009 Jun;36(3):213-26
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  • [Title] Acute leukemia in adolescents and young adults.
  • In many areas of medicine adolescents are regarded as a discrete group with specific therapeutic, psychological, educational, and resource needs.
  • In the treatment of acute leukemia age is a predictor of response.
  • Thus, in acute lymphoblastic leukemia (ALL) there is a clearly poorer treatment outcome after puberty, while in acute myeloid leukaemia (AML), which is more common in older adults, age is a continuous variable with poorer outcomes in each successive decade.
  • Here we discuss the outcome of acute leukemia in adolescents and young adults, particularly with respect to whether they respond similarly to children or other adults.
  • [MeSH-major] Leukemia, Myeloid, Acute. Precursor Cell Lymphoblastic Leukemia-Lymphoma
  • [MeSH-minor] Adolescent. Adult. Age Factors. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Leukemia, Promyelocytic, Acute. Stem Cell Transplantation. Survival Rate

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  • (PMID = 19460579.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 66
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80. Solomon PR, Munirajan AK, Tsuchida N, Muthukumarasamy K, Rathinavel A, Selvam GS, Shanmugam G: Promoter hypermethylation analysis in myelodysplastic syndromes: diagnostic & prognostic implication. Indian J Med Res; 2008 Jan;127(1):52-7
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  • BACKGROUND & OBJECTIVE: Myelodysplastic syndromes (MDS) are a heterogenous group of haematopoietic stem cell disorders that are multifactorial in their aetiology.
  • Unique genetic alterations in combinations or in isolation account for a small fraction of MDS suggesting the epigenetic hypermethylation as a possible leading cause for MDS and its transformation to acute myelocytic leukaemia (AML).
  • Therefore, in this study, promoter hypermethylation status of key cell cycle regulators was assessed as markers in MDS patients and association of hypermethylation with clinical progression of disease was also studied.
  • METHODS: Promoter hypermethylation analysis of five tumour associated genes namely p16, p15, MGMT, hMLH1 and E-cadherin were done for 41 MDS patient samples with its various subtype.
  • MGMT gene showed a low 5 per cent (2/41) methylation whereas hMLH1 gene was not methylated in any one of the samples analysed.
  • All the samples analysed showed the absence of a methylator phenotype in MDS.

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  • (PMID = 18316853.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / MLH1 protein, human; 0 / Nuclear Proteins; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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81. Pabst T, Eyholzer M, Haefliger S, Schardt J, Mueller BU: Somatic CEBPA mutations are a frequent second event in families with germline CEBPA mutations and familial acute myeloid leukemia. J Clin Oncol; 2008 Nov 1;26(31):5088-93
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  • [Title] Somatic CEBPA mutations are a frequent second event in families with germline CEBPA mutations and familial acute myeloid leukemia.
  • PURPOSE: The transcription factor CCAAT/enhancer binding protein-alpha (CEBPA) is crucial for normal myeloid differentiation.
  • Mutations in the CEBPA gene are found in subsets of patients with acute myeloid leukemia (AML).
  • Recently, three families were reported in whom several family members had germline CEBPA mutations and subsequently developed AML.
  • Whereas familial AML is considered a rare event, the frequency of CEBPA germline mutations in AML is not known.
  • PATIENTS AND METHODS: In this study, we screened 187 consecutive AML patients for CEBPA mutations at diagnosis.
  • RESULTS: We found that two (11.1%) of 18 AML patients with CEBPA mutations carried a germline N-terminal frameshift CEBPA mutation.
  • Interestingly, additional members in the families of both of these patients have been affected by AML, and the germline CEBPA mutations were also observed in these patients.
  • Additional somatic mutations in AML patients with germline CEBPA mutations in the two families comprised in-frame C-terminal CEBPA mutations in two patients, two nonsilent CEBPA point mutations in one patient, and monosomy 7 in one patient.
  • CONCLUSION: This study shows, for the first time to our knowledge, that germline CEBPA mutations are frequently observed among AML patients with CEBPA mutations.
  • Including the families with germline CEBPA mutations reported previously, additional somatic CEBPA mutations represent a frequent second event in AML with germline CEBPA mutations.
  • Our data strongly indicate that germline CEBPA mutations predispose to AML and that additional somatic CEBPA mutations contribute to the development of the disease.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / genetics. Gene Expression Regulation, Leukemic. Germ-Line Mutation. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. DNA Mutational Analysis. Genetic Predisposition to Disease. Heterozygote. Humans. Middle Aged. Pedigree. Risk Factors


82. Perkhofer S, Lass-Flörl C, Hell M, Russ G, Krause R, Hönigl M, Geltner C, Auberger J, Gastl G, Mitterbauer M, Willinger B, Knöbl P, Resch G, Waldner R, Makrai A, Hartmann G, Girschikofsky M, Greil R: The Nationwide Austrian Aspergillus Registry: a prospective data collection on epidemiology, therapy and outcome of invasive mould infections in immunocompromised and/or immunosuppressed patients. Int J Antimicrob Agents; 2010 Dec;36(6):531-6
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  • A prospective, observational, multicentre study was performed to assess the incidence, diagnosis, epidemiology and outcome of invasive mould infections (IMIs) reported to the Nationwide Austrian Aspergillus Registry.
  • Patients with acute myelogenous leukaemia (34%) and lung transplant recipients (17%) are currently at highest risk for IMI, followed by a mixed population with impaired immunity (14%).
  • Multivariate analysis showed that outcome and survival did not correlate with the status of fungal disease, breakthrough infection, fungal species or age (P>0.05).

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  • [Copyright] Copyright © 2010 Elsevier B.V. and the International Society of Chemotherapy. All rights reserved.
  • (PMID = 20947312.001).
  • [ISSN] 1872-7913
  • [Journal-full-title] International journal of antimicrobial agents
  • [ISO-abbreviation] Int. J. Antimicrob. Agents
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antifungal Agents
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83. Falini B, Martelli MP, Bolli N, Bonasso R, Ghia E, Pallotta MT, Diverio D, Nicoletti I, Pacini R, Tabarrini A, Galletti BV, Mannucci R, Roti G, Rosati R, Specchia G, Liso A, Tiacci E, Alcalay M, Luzi L, Volorio S, Bernard L, Guarini A, Amadori S, Mandelli F, Pane F, Lo-Coco F, Saglio G, Pelicci PG, Martelli MF, Mecucci C: Immunohistochemistry predicts nucleophosmin (NPM) mutations in acute myeloid leukemia. Blood; 2006 Sep 15;108(6):1999-2005
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  • [Title] Immunohistochemistry predicts nucleophosmin (NPM) mutations in acute myeloid leukemia.
  • Nucleophosmin (NPM) exon-12 mutations occur in 50% to 60% of adult acute myeloid leukemia (AML) with normal karyotype and are predictors of favorable prognosis.
  • We evaluated bone marrow or peripheral blood samples from 450 adult patients with AML of the GIMEMA (Gruppo Italiano Malattie Ematologiche Maligne dell'Adulto)/AML12 EORTC (European Organization for Research and Treatment of Cancer) trial to (1) search for new exon-12 NPM mutations;.
  • (2) determine whether NPM immunostaining on paraffin-embedded biopsies predicts NPM mutations; and (3) investigate altered nucleocytoplasmic NPM traffic in primary AML cells.
  • All 200 AML cases expressing cytoplasmic NPM (NPMc(+) AML) carried NPM mutations.
  • None of the 250 cases with nucleus-restricted NPM (NPMc(-) AML) was mutated.
  • The specific Crm1/exportin-1 inhibitor leptomycin-B relocated NPM mutants from cytoplasm to nucleus of primary NPMc(+) AML cells, demonstrating that nuclear export is NES dependent.
  • NPM mutants bound and recruited wild-type NPM into leukemic cell cytoplasm.
  • Because alterations at C-terminus of leukemic NPM mutants are similar, immunohistochemistry detects all exon-12 NPM mutations and is a valuable, inexpensive tool in the diagnostic-prognostic work-up of patients with AML with normal karyotype.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Mutation. Nuclear Proteins / genetics. Nuclear Proteins / metabolism
  • [MeSH-minor] Active Transport, Cell Nucleus. Adolescent. Adult. Amino Acid Sequence. Base Sequence. Cytoplasm / metabolism. DNA, Neoplasm / genetics. Exons. Humans. Immunohistochemistry. Middle Aged. Nuclear Export Signals / genetics. Tryptophan / genetics

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  • (PMID = 16720834.001).
  • [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 / DNA, Neoplasm; 0 / Nuclear Export Signals; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; 8DUH1N11BX / Tryptophan
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84. Lehrnbecher T, Zimmermann M, Reinhardt D, Dworzak M, Stary J, Creutzig U: Prophylactic human granulocyte colony-stimulating factor after induction therapy in pediatric acute myeloid leukemia. Blood; 2007 Feb 1;109(3):936-43
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  • [Title] Prophylactic human granulocyte colony-stimulating factor after induction therapy in pediatric acute myeloid leukemia.
  • Children with acute myelogenous leukemia (AML) have a high risk of infectious complications that might be reduced by prophylactic granulocyte colony-stimulating factor (G-CSF).
  • However, G-CSF could induce AML blast proliferation.
  • The prospective randomized trial AML-BFM 98 investigated the impact of G-CSF on hematopoetic recovery and infectious complications (primary endpoints) and on outcome (secondary endpoint) in children (aged 0-18 years) with de novo AML.
  • Patients with more than 5% blasts in day-15 bone marrow or with FAB M3 were not included.
  • Between 1998 and 2003, 161 children with AML were randomized to receive G-CSF after inductions 1 and 2, whereas 156 patients were assigned to the control group.
  • G-CSF did not decrease the incidence of febrile neutropenia (72 and 36 patients vs 78 and 37 patients, respectively), microbiologically documented infections (27 and 25 patients vs 36 and 19 patients, respectively) and infection-associated mortality (5 vs 2 patients).
  • Since G-CSF does not influence the risk of infectious complications or outcome in children undergoing therapy for AML, one cannot advocate the routine use of G-CSF in this patient group.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / administration & dosage. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adolescent. Cell Proliferation / drug effects. Child. Child, Preschool. Disease-Free Survival. Hematopoiesis / drug effects. Humans. Infant. Infection / drug therapy. Infection / mortality. Infection Control. Neutropenia. Premedication. Remission Induction. Treatment Outcome

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  • (PMID = 17008536.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
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85. Gupta SK, Sazawal S, Mahapatra M, Saxena R: Evaluation of PG-M3 antibody in the diagnosis of acute promyelocytic leukaemia. Eur J Clin Invest; 2010 Oct;40(10):960-2
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  • [Title] Evaluation of PG-M3 antibody in the diagnosis of acute promyelocytic leukaemia.
  • BACKGROUND & OBJECTIVES: Acute promyelocytic leukaemia (APL) is a distinct subtype of acute myeloid leukaemia (AML) characterized by a reciprocal translocation, t(15;17) and a high incidence of life-threatening coagulopathy.
  • APL diagnosis is considered a medical emergency.
  • As reverse transcription-polymerase chain reaction (RT-PCR) for PML-RAR fusion oncoprotein is time consuming, there is a need for a rapid and accurate diagnostic test for APL.
  • This study evaluates the role of PG-M3 monoclonal antibody using immunofluorescence (IF) in the early diagnosis of APL.
  • MATERIALS AND METHODS: Thirty-six new untreated APL cases diagnosed with RT-PCR for PML-RAR as the gold standard and 38 non-APL controls (28 non-APL AMLs and 10 non-leukaemic samples) were evaluated by routine morphology and cytochemistry, RT-PCR and IF using PG-M3 monoclonal antibody.
  • By comparison, two of 28 (7·1%) non-APL AMLs showed microgranular pattern (false positive).
  • All 10 non-leukaemic samples showed a speckled pattern.
  • It can be a useful adjunct for diagnosis of APL especially if facilities for RT-PCR are not available, particularly in resource-limited settings.
  • [MeSH-major] Antibodies, Monoclonal. Leukemia, Promyelocytic, Acute / diagnosis

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  • [Copyright] © 2010 The Authors. European Journal of Clinical Investigation © 2010 Stichting European Society for Clinical Investigation Journal Foundation.
  • (PMID = 20701624.001).
  • [ISSN] 1365-2362
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
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86. Thiede C, Koch S, Creutzig E, Steudel C, Illmer T, Schaich M, Ehninger G: Prevalence and prognostic impact of NPM1 mutations in 1485 adult patients with acute myeloid leukemia (AML). Blood; 2006 May 15;107(10):4011-20
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  • [Title] Prevalence and prognostic impact of NPM1 mutations in 1485 adult patients with acute myeloid leukemia (AML).
  • Mutations of the nucleophosmin (NPM1) gene have recently been described in patients with acute myeloid leukemia (AML).
  • To clarify the prevalence as well as the clinical impact of this mutation, we investigated 1485 patients with AML for NPM1 exon 12 mutations using fragment analysis.
  • NPM1 mutations were most prevalent in patients with normal karyotype (NK) (324 of 709; 45.7%) compared with 58 of 686 with karyotype abnormalities (8.5%; P < .001) and were significantly associated with several clinical parameters (high bone marrow [BM] blasts, high white blood cell [WBC] and platelet counts, female sex).
  • The analysis of the clinical impact in 4 groups (NPM1 and FLT3-ITD single mutants, double mutants, and wild-type [wt] for both) revealed that patients having only an NPM1 mutation had a significantly better overall and disease-free survival and a lower cumulative incidence of relapse.
  • In conclusion, NPM1 mutations represent a common genetic abnormality in adult AML.
  • If not associated with FLT3-ITD mutations, mutant NPM1 appears to identify patients with improved response toward treatment.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics


87. Fouillard L, Labopin M, Gratwohl A, Gluckman E, Frassoni F, Beelen DW, Willemze R, Montserrat E, Blaise D, Atienza AI, Sierra J, Santos M, Gorin NC, Rocha V, Acute Leukemia Working Party of the European Group for Blood and Marrow Transplantation: Results of syngeneic hematopoietic stem cell transplantation for acute leukemia: risk factors for outcomes of adults transplanted in first complete remission. Haematologica; 2008 Jun;93(6):834-41
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  • [Title] Results of syngeneic hematopoietic stem cell transplantation for acute leukemia: risk factors for outcomes of adults transplanted in first complete remission.
  • BACKGROUND: The possibility of performing syngeneic hematopoietic stem cell transplantation is rare and there are concerns about the absence of a graft-versus-leukemia effect following such a strategy.
  • We report the outcomes of a large series of adult patients who underwent syngeneic hematopoietic stem cell transplantation for acute myeloblastic leukemia or acute lymphoblastic leukemia.
  • DESIGN AND METHODS: The outcomes of all syngeneic transplants for acute myeloblastic or lymphoblastic leukemia reported to the European Group for Blood and Marrow Transplantation registry were analyzed; a study of prognostic factors was performed for those transplanted in first complete remission.
  • RESULTS: One hundred and sixty-two patients, 109 with acute myeloblastic leukemia and 53 with acute lymphoblastic leukemia, were identified; 116 were in first complete remission.
  • Most of the patients did not receive prophylaxis against graft-versus-host disease.
  • Nineteen patients developed acute graft-versus-host disease and only three patients developed chronic graft-versus-host disease.
  • At 5 years the non-relapse mortality was 8 +/- 5%, the relapse incidence 49 +/- 8% and the leukemia-free survival 43 +/- 3%.
  • Analysis of patients in first complete remission showed that the number of courses of chemotherapy required to induce first complete remission was the main risk factor: the leukemia-free survival at 5 years was 66 +/- 6% when first complete remission was reached after one induction course of chemotherapy and was only 20 +/- 9% when first complete remission was reached after at least two induction courses of chemotherapy (p = 0.0001); the relapse incidence was 30 +/- 6% and 54 +/- 10%, respectively (p = 0.007).
  • CONCLUSIONS: Outcomes were better for patients transplanted in first complete remission than in second complete remission or a more advanced phase of the disease.
  • When a syngeneic donor is available for patients with high risk acute leukemia, allotransplantation should be performed as soon as the first complete remission has been achieved, ideally with one course of chemotherapy.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / therapeutic use. Diseases in Twins. Female. Graft vs Host Disease. Humans. Male. Middle Aged. Recurrence. Remission Induction. Risk Factors. Treatment Outcome

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  • [CommentIn] Haematologica. 2008 Jun;93(6):801-5 [18515876.001]
  • (PMID = 18469352.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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88. Ito A, Honda H, Kamihira M: [Construction of 3D tissue-like structure using functional magnetite nanoparticles]. Yakugaku Zasshi; 2008 Jan;128(1):21-8
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  • Since these nanoparticles have unique magnetic features not present in other materials, they can be applied to special medical techniques.
  • Magnetite cationic liposomes (MCLs), one group of the cationic magnetic particles, can be used as carriers to introduce magnetite nanoparticles into target cells since their positively charged surface interacts with the negatively charged cell surface.
  • Magnetite nanoparticles conjugated with antibodies (antibody-conjugated magnetoliposomes, AMLs) are applicable to introduce magnetite nanoparticles specifically into target cells, even when target cells coexist with other kinds of cells.
  • Both magnetic force and functionalized magnetite nanoparticles were used in a process of tissue engineering: construction of multilayered cell sheet-like structures and tubular structures.
  • [MeSH-minor] Animals. Antibodies. Capillaries / cytology. Cell Adhesion. Cell Culture Techniques. Epidermis / cytology. Humans. Liposomes. Liver / cytology. Mesenchymal Stromal Cells / cytology. Myocardium / cytology. Nanostructures

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  • (PMID = 18176052.001).
  • [ISSN] 0031-6903
  • [Journal-full-title] Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan
  • [ISO-abbreviation] Yakugaku Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies; 0 / Liposomes; XM0M87F357 / Ferrosoferric Oxide
  • [Number-of-references] 18
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89. Li X, Zhu Z, Mo D, Wang H, Yang S, Zhao S, Li K: Comparative molecular characterization of ADSS1 and ADSS2 genes in pig (Sus scrofa). Comp Biochem Physiol B Biochem Mol Biol; 2007 Jun;147(2):271-7
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  • Moreover, we found that one single nucleotide polymorphism (SNP, T/C(70)) in the ninth intron of ADSS2 gene was significantly associated with average daily gain trait (ADG, P<0.05) and loin muscle area trait (P<0.05).

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  • (PMID = 17347008.001).
  • [ISSN] 1096-4959
  • [Journal-full-title] Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology
  • [ISO-abbreviation] Comp. Biochem. Physiol. B, Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Isoenzymes; EC 6.3.4.4 / Adenylosuccinate Synthase
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90. Platzbecker U, von Bonin M, Goekkurt E, Radke J, Binder M, Kiani A, Stoehlmacher J, Schetelig J, Thiede C, Ehninger G, Bornhäuser M: Graft-versus-host disease prophylaxis with everolimus and tacrolimus is associated with a high incidence of sinusoidal obstruction syndrome and microangiopathy: results of the EVTAC trial. Biol Blood Marrow Transplant; 2009 Jan;15(1):101-8
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  • [Title] Graft-versus-host disease prophylaxis with everolimus and tacrolimus is associated with a high incidence of sinusoidal obstruction syndrome and microangiopathy: results of the EVTAC trial.
  • A calcineurin inhibitor combined with methotrexate is the standard prophylaxis for graft-versus-host disease (GVHD) after allogeneic hematopoietic stem cell transplantation (HSCT).
  • We report on a combination of everolimus and tacrolimus in 24 patients (median age, 62 years) with either myelodysplastic syndrome (MDS; n = 17) or acute myeloid leukemia (AML; n = 7) undergoing intensive conditioning followed by HSCT from related (n = 4) or unrelated (n = 20) donors.
  • Nine patients (37%) developed acute grade II-IV GVHD, and 11 of 17 evaluable patients (64%) developed chronic extensive GVHD.
  • Transplantation-associated microangiopathy (TMA) occurred in 7 patients (29%), with 2 cases of acute renal failure.
  • Although this new combination appears to be effective as a prophylactic regimen for acute GVHD, the incidence of TMA and SOS is considerably higher than seen with other regimens.
  • [MeSH-major] Anemia, Hemolytic / chemically induced. Graft vs Host Disease / prevention & control. Hematopoietic Stem Cell Transplantation / methods. Hepatic Veno-Occlusive Disease / chemically induced. Sirolimus / analogs & derivatives. Tacrolimus / adverse effects
  • [MeSH-minor] Adult. Aged. Everolimus. Female. Humans. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / therapy. Male. Middle Aged. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / therapy. Survival Rate. Transplantation, Homologous

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  • (PMID = 19135948.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9HW64Q8G6G / Everolimus; W36ZG6FT64 / Sirolimus; WM0HAQ4WNM / Tacrolimus
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91. Sarafnejad A, Khosravi F, Alimoghadam K, Dianat S, Ansaripour B, Moradi B, Dorkhosh S, Amirzargar A: HLA class II allele and haplotype frequencies in iranian patients with acute myelogenous leukemia and control group. Iran J Allergy Asthma Immunol; 2006 Sep;5(3):115-9
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  • [Title] HLA class II allele and haplotype frequencies in iranian patients with acute myelogenous leukemia and control group.
  • We have analyzed HLA class II alleles and haplotypes in 60 Iranian patients with acute myelogenous leukemia (AML) and 180 unrelated normal subjects.
  • Significant positive association with the disease was found for HLA-DRB1*11 allele (35% vs. 24.7%, p=0.033).
  • It is suggested that HLA-DRB1*11 allele plays as a presumptive predisposing factor while the HLA-DRB4 and -DQB1*0303 alleles are suggested as protective genetic factors against acute myelogenous leukemia.
  • Larger studies are needed to confirm and establish the role of these associations with acute myelogenous leukemia.
  • [MeSH-major] HLA-DQ Antigens / genetics. HLA-DR Antigens / genetics. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Case-Control Studies. Gene Frequency. Genetic Predisposition to Disease. HLA-DQ alpha-Chains. HLA-DQ beta-Chains. Haplotypes. Humans. Iran / epidemiology

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  • (PMID = 17237562.001).
  • [ISSN] 1735-1502
  • [Journal-full-title] Iranian journal of allergy, asthma, and immunology
  • [ISO-abbreviation] Iran J Allergy Asthma Immunol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Iran
  • [Chemical-registry-number] 0 / HLA-DQ Antigens; 0 / HLA-DQ alpha-Chains; 0 / HLA-DQ beta-Chains; 0 / HLA-DQA1 antigen; 0 / HLA-DQB1 antigen; 0 / HLA-DR Antigens
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92. Molica S: Second neoplasms in chronic lymphocytic leukemia: incidence and pathogenesis with emphasis on the role of different therapies. Leuk Lymphoma; 2005 Jan;46(1):49-54
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  • [Title] Second neoplasms in chronic lymphocytic leukemia: incidence and pathogenesis with emphasis on the role of different therapies.
  • Several surveys have defined chronic lymphocytic leukemia (CLL) patients as a high-risk patient population for developing second neoplasms.
  • As possible mechanisms underlying the increased risk of specific second malignancies in CLL patients the immunodeficiency associated with disease is generally proposed.
  • As far as secondary acute leukemia is concerned, greater insight into the molecular pathogenesis of therapy-related acute myeloid leukemia (AML) developing in CLL would allow to avoid treatment regimens that can lead to this complication.
  • Richter's syndrome continues to be a fatal and highly refractory to chemotherapy disease complicating the clinical course of CLL.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Neoplasms, Second Primary / complications. Neoplasms, Second Primary / therapy
  • [MeSH-minor] Humans. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 15621780.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 44
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93. Ma L, Zhong MH, Feng DR, Long H, Shen J, Ma YG, Huang SZ: [FMS-like tyrosine kinase 3 gene mutation in acute myeloid leukemia detected by denaturing PAGE and its clinical significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Dec;18(6):1386-9
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  • [Title] [FMS-like tyrosine kinase 3 gene mutation in acute myeloid leukemia detected by denaturing PAGE and its clinical significance].
  • The aim of this study was to analyze the frequency of flt3 length mutation (flt3-LM) in de novo acute myeloid leukemia patients and the relationship between flt3-LM and chromosome alterations, FAB subgroups, as well as efficiency of therapy.
  • Genomic DNA was amplified by PCR; 2% agarose gel or 8% denaturing PAGE were used to detect the length mutation of flt3 gene in 99 de novo acute myeloid leukemia patients; karyotyping in 72 AML patients was performed by G banding technique.
  • The flt3-LM was not detected in M(0) (only one patient was available), but flt3-LM occurrence in AML subtypes was as follow: in M(2) (9/30), M(3) (6/27), M(4) (4/14), M(5) (7/19), M(6) (3/8) respectively. flt3-LM in patients with normal karyotypes (39.13%) was more prevalent as compared with patients of abnormal karyotype (24.49%), but there was no statistical difference (p > 0.05).
  • The flt3 mutation represents a common genetic abnormality in AML patients, and the flt3-LM is associated with lower CR rate.

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  • (PMID = 21176335.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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94. Wu J, Li J, Zhu Z, Li J, Huang G, Tang Y, Gao X: Protective effects of echinocystic acid isolated from Gleditsia sinensis Lam. against acute myocardial ischemia. Fitoterapia; 2010 Jan;81(1):8-10
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  • [Title] Protective effects of echinocystic acid isolated from Gleditsia sinensis Lam. against acute myocardial ischemia.
  • Echinocystic acid (EA), a pentacyclic triterpene, was isolated and identified from the fruits of Gleditsia sinensis Lam.
  • The protective effects of EA were evaluated in rat models with acute myocardial ischemia induced by isoproterenol and vasopressin.

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  • (PMID = 19573579.001).
  • [ISSN] 1873-6971
  • [Journal-full-title] Fitoterapia
  • [ISO-abbreviation] Fitoterapia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adrenergic beta-Agonists; 0 / Plant Extracts; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Vasoconstrictor Agents; 11000-17-2 / Vasopressins; 6SMK8R7TGJ / Oleanolic Acid; L4DUW10YOF / echinocystic acid; L628TT009W / Isoproterenol
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95. Secondary leukaemia: after umbilical cord blood stem cell transplantation too. Prescrire Int; 2010 Aug;19(108):166-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary leukaemia: after umbilical cord blood stem cell transplantation too.
  • Ten cases of secondary leukaemia following cord blood stem cell transplantation have been published in detail, including 7 cases of acute myeloid leukaemia.
  • The patients were severely immunodepressed, and analysis showed that the leukaemias were of donor cell origin.
  • Patients receiving cord blood stem cell grafts, like all transplant recipients, should therefore be monitored for secondary leukaemia.
  • [MeSH-major] Cord Blood Stem Cell Transplantation / adverse effects. Leukemia / etiology
  • [MeSH-minor] Hematologic Diseases / therapy. Humans. Risk Factors. Tissue Donors

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  • (PMID = 20939449.001).
  • [ISSN] 1167-7422
  • [Journal-full-title] Prescrire international
  • [ISO-abbreviation] Prescrire Int
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
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96. Spillane JB, Henderson MA: Cancer stem cells: a review. ANZ J Surg; 2007 Jun;77(6):464-8
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  • Research has been increasing in recent years into the application of stem cell biology to clinical medicine, particularly its role in the evolution and metastasis of tumours.
  • Stem cells may be the target cell for malignant transformation, and tumour formation could be considered a disorder of stem cell self-renewal pathways.
  • Cancer stem cells have been identified in acute myeloid leukaemia and in breast and central nervous system tumours.
  • [MeSH-minor] Animals. Cell Division / physiology. Cell Transformation, Neoplastic / pathology. Humans. Microarray Analysis. Neoplasm Metastasis / therapy. Stem Cells / physiology

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  • (PMID = 17501888.001).
  • [ISSN] 1445-1433
  • [Journal-full-title] ANZ journal of surgery
  • [ISO-abbreviation] ANZ J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Australia
  • [Number-of-references] 30
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97. Perl AE, Carroll M: Exploiting signal transduction pathways in acute myelogenous leukemia. Curr Treat Options Oncol; 2007 Aug;8(4):265-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Exploiting signal transduction pathways in acute myelogenous leukemia.
  • Traditional cytotoxic chemotherapy is effective at temporizing AML in the majority of patients but cures a small minority.
  • While signal transduction inhibition is a promising area to advance AML therapy, no agent as monotherapy has demonstrated obvious clinical benefit over traditional cytotoxic chemotherapy.
  • Tipifarnib is perhaps an exception as it is the only signal transduction inhibitor in AML that reproducibly shows clinical benefit using traditional chemotherapy response criteria.
  • Similarly unclear is the benefit of a potent specific kinase inhibitor versus a broad inhibitor of multiple kinases that could prove relevant to leukemia biology.
  • To this end, the extensive measures applied to correlate the biologic activity of FLT3 inhibitors with clinical responses are noteworthy and provide useful lessons for clinical trial design and drug development both in leukemia and other cancers.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Signal Transduction / drug effects


98. Ko M, Huang Y, Jankowska AM, Pape UJ, Tahiliani M, Bandukwala HS, An J, Lamperti ED, Koh KP, Ganetzky R, Liu XS, Aravind L, Agarwal S, Maciejewski JP, Rao A: Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2. Nature; 2010 Dec 9;468(7325):839-43
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  • [Title] Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2.
  • The gene encoding TET2 resides at chromosome 4q24, in a region showing recurrent microdeletions and copy-neutral loss of heterozygosity (CN-LOH) in patients with diverse myeloid malignancies.
  • Somatic TET2 mutations are frequently observed in myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), MDS/MPN overlap syndromes including chronic myelomonocytic leukaemia (CMML), acute myeloid leukaemias (AML) and secondary AML (sAML).
  • We show here that TET2 mutations associated with myeloid malignancies compromise catalytic activity.
  • Our results demonstrate that Tet2 is important for normal myelopoiesis, and suggest that disruption of TET2 enzymatic activity favours myeloid tumorigenesis.
  • Measurement of 5hmC levels in myeloid malignancies may prove valuable as a diagnostic and prognostic tool, to tailor therapies and assess responses to anticancer drugs.


99. Melchert M: Managing acute myeloid leukemia in the elderly. Oncology (Williston Park); 2006 Nov;20(13):1674-82; discussion 1683-4, 1687
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  • [Title] Managing acute myeloid leukemia in the elderly.
  • Acute myeloid leukemia (AML) is a disease of the elderly, with the majority of patients diagnosed in their 6th and 7th decade of life.
  • Older patients with AML are less likely to achieve complete remission after induction chemotherapy, and they suffer from higher rates of leukemia relapse compared to younger cohorts.
  • Suboptimal outcomes are the result of adverse biologic characteristics of leukemia in the elderly, as well as the presence of medical comorbidities and patient or physician preferences as to initiating treatment.
  • In addition, there is a distinct lack of randomized, prospective data to guide management decisions for the treatment of AML in the elderly.
  • Patients who are over age 75, with poor performance status, multiple comorbidities, or poor prognostic features, should be considered for a clinical trial or palliative therapy.
  • Further prospective trials are needed to identify a tolerable, effective treatment regimen for older patients with AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Age Factors. Aged. Clinical Trials as Topic. Humans. Karyotyping. Prognosis. Treatment Outcome

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  • (PMID = 17175744.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 62
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100. Knapper S, Burnett AK, Littlewood T, Kell WJ, Agrawal S, Chopra R, Clark R, Levis MJ, Small D: A phase 2 trial of the FLT3 inhibitor lestaurtinib (CEP701) as first-line treatment for older patients with acute myeloid leukemia not considered fit for intensive chemotherapy. Blood; 2006 Nov 15;108(10):3262-70
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  • [Title] A phase 2 trial of the FLT3 inhibitor lestaurtinib (CEP701) as first-line treatment for older patients with acute myeloid leukemia not considered fit for intensive chemotherapy.
  • Activating mutations of FMS-like tyrosine kinase 3 (FLT3) are present in approximately one third of patients with acute myeloid leukemia (AML) and are associated with adverse prognosis.
  • The important role played by FLT3 in the survival and proliferation of blasts, and its overexpression in most patients with AML, make FLT3 an attractive therapeutic target.
  • We undertook a phase 2 trial of the FLT3-selective tyrosine kinase inhibitor lestaurtinib (CEP701) used as monotherapy in untreated older patients with AML not considered fit for intensive chemotherapy, irrespective of FLT3 mutation status.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Leukemia, Myeloid / drug therapy. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Blood Cell Count. Carbazoles / administration & dosage. Carbazoles / toxicity. Female. Humans. Indoles / administration & dosage. Indoles / toxicity. Male. Treatment Outcome

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  • (PMID = 16857985.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbazoles; 0 / Indoles; DO989GC5D1 / lestaurtinib; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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