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6. Papiez MA, Dybala M, Sowa-Kucma M, Krzysciak W, Taha H, Jozkowicz A, Nowak G: Evaluation of oxidative status and depression-like responses in Brown Norway rats with acute myeloid leukemia. Prog Neuropsychopharmacol Biol Psychiatry; 2009 Jun 15;33(4):596-604
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of oxidative status and depression-like responses in Brown Norway rats with acute myeloid leukemia.
  • It has been proved that oxidative stress increases when leukemia is accompanied by depression.
  • The aim of this study was to determine whether the acute myeloid leukemia of Brown Norway rats, which is accompanied by oxidative stress, evoked behavioral and receptor changes resembling alterations characteristic of rat models of depression.
  • Leukemia was induced through intraperitoneal injection of 10(7) promyelocytic leukemia cells to the Brown Norway rats.
  • Radioligand binding assay was used to assess of the effect of leukemia on cortical receptors.
  • Leukemia influenced locomotory activity as well as forced swim test behavior in a 34-day series of experiments.
  • Signs of oxidative stress in leukemic rats were observed in each examined stage of leukemia development.
  • Upregulation of 5-HT(2A) receptors was observed in rat cortex after 30 days of leukemia development but not in 34-days series compared with the control.
  • It is concluded that disturbances in antioxidant system in brain cortex were accompanied by an activation of glycine sites of the NMDA receptor complex, regardless of stage of leukemia development, which are characteristic of model of depression.
  • Findings of our study demonstrate the link between glutamatergic activity, oxidative stress and leukemia.
  • [MeSH-major] Depression / etiology. Disease Models, Animal. Leukemia, Myeloid, Acute / complications. Oxidative Stress / physiology

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  • (PMID = 19268504.001).
  • [ISSN] 1878-4216
  • [Journal-full-title] Progress in neuro-psychopharmacology & biological psychiatry
  • [ISO-abbreviation] Prog. Neuropsychopharmacol. Biol. Psychiatry
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Biogenic Amine; 9007-73-2 / Ferritins; EC 1.14.99.3 / Heme Oxygenase (Decyclizing); GAN16C9B8O / Glutathione; O9MIA842K9 / Biliverdine
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7. Bacher U, Haferlach T, Alpermann T, Zenger M, Kröger N, Beelen DW, Kern W, Schnittger S, Haferlach C: Comparison of cytogenetic clonal evolution patterns following allogeneic hematopoietic transplantation versus conventional treatment in patients at relapse of AML. Biol Blood Marrow Transplant; 2010 Dec;16(12):1649-57
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  • [Title] Comparison of cytogenetic clonal evolution patterns following allogeneic hematopoietic transplantation versus conventional treatment in patients at relapse of AML.
  • Relapse of acute myelogenous leukemia has been associated with clonal cytogenetic evolution, but no study focused specifically on relapse after allogeneic hematopoietic stem cell transplantation (HSCT).
  • We compared karyotypes in 160 patients at both diagnosis and relapse either after allo-HSCT (n = 26) or standard chemotherapy (n = 134) using chromosome banding analysis combined with fluorescein in situ hybridization.
  • At diagnosis, aberrant karyotypes were more frequent in the HSCT than in the chemotherapy cohort (16 of 26; 61.5% versus 63 of 134; 47.0%).
  • Differences in the karyotypes between diagnosis and relapse were more frequent in the allo-cohort (14 of 26; 53.8% versus 49 of 134; 36.6%) than in the conventional cohort (n.s.
  • The mean number of cytogenetic alterations per patient was increasing from 2.0 at diagnosis to 4.0 at relapse in the allo-cohort, in the conventionally treated patients from 0.9 to 1.3 (both P < .001).
  • Thus, higher frequencies of clonal evolution and increasing cytogenetic complexity were observed in the stem cell recipients probably related to the more unfavorable cytogenetic profiles already depicted at diagnosis.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy

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  • [Copyright] Copyright © 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20558312.001).
  • [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] Journal Article
  • [Publication-country] United States
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8. Suzuki K, Irie M, Kadowaki H, Shibata T, Kumagai M, Nishida A: Genetic parameter estimates of meat quality traits in Duroc pigs selected for average daily gain, longissimus muscle area, backfat thickness, and intramuscular fat content. J Anim Sci; 2005 Sep;83(9):2058-65
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  • [Title] Genetic parameter estimates of meat quality traits in Duroc pigs selected for average daily gain, longissimus muscle area, backfat thickness, and intramuscular fat content.
  • Using a multitrait animal model BLUP, selection was conducted over seven generations for growth rate (ADG), real-time ultrasound LM area (LMA), backfat thickness (BF), and intramuscular fat content (IMF) to develop a new line of purebred Duroc pigs with enhanced meat production and meat quality.
  • Genetic correlations of IMF with ADG and BF were low and positive, but low and negative with LMA.
  • Tenderness was correlated negatively with ADG (-0.44) and BF (-0.59), but positively correlated with LMA (0.32).
  • The genetic correlation between LMA and DL was positive and high (0.64).

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  • (PMID = 16100060.001).
  • [ISSN] 1525-3163
  • [Journal-full-title] Journal of animal science
  • [ISO-abbreviation] J. Anim. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-34-5 / Collagen
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9. Møller T, Nielsen OJ, Welinder P, Dünweber A, Hjerming M, Moser C, Kjeldsen L: Safe and feasible outpatient treatment following induction and consolidation chemotherapy for patients with acute leukaemia. Eur J Haematol; 2010 Apr;84(4):316-22
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  • [Title] Safe and feasible outpatient treatment following induction and consolidation chemotherapy for patients with acute leukaemia.
  • Traditionally, patients with acute leukaemia are admitted to hospital during chemotherapy-induced pancytopenia, although a few recent reports have reported the feasibility and safety of outpatient treatment.
  • We have developed an outpatient treatment programme for patients with acute leukaemia incorporating comprehensive patient education for self-care management at home during pancytopenia and involvement of patients in care of their tunnelled central venous catheter (CVC).
  • Herein, we report the results of outpatient treatment of 60 patients with acute leukaemia (54 with acute myeloid leukaemia) followed prospectively in the period from March 2004 to 2007.
  • We conclude that outpatient treatment of patients with acute leukaemia is feasible and safe.
  • [MeSH-major] Ambulatory Care / methods. Anti-Infective Agents / administration & dosage. Leukemia / drug therapy. Neutropenia / drug therapy. Pancytopenia / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Prospective Studies

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  • (PMID = 20002732.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Infective Agents
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10. Palmisano M, Grafone T, Renzulli M, Ottaviani E, Testoni N, Paolini S, Papayannidis C, Baccarani M, Martinelli G: Molecular and chromosomal alterations: new therapies for relapsed acute myeloid leukemia. Hematology; 2008 Feb;13(1):1-12
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  • [Title] Molecular and chromosomal alterations: new therapies for relapsed acute myeloid leukemia.
  • Acute myeloid leukemia (AML) remains the most common form of leukemia and the most common cause of leukemia death.
  • Although conventional chemotherapy can cure between 25 and 45% of AML patients, the majority of patients die after relapse or of complications associated with treatment.
  • Thus, more specific and less toxic treatments for AML patients are needed, especially for elderly patients.
  • An indispensable prerequisite to investigate tailored approaches for AML is the recent progress in the understanding the molecular features that distinguish leukemia progenitors from normal hematopoietic counterparts and the identification of a variety of dysregulated molecular pathways.
  • In this review, we describe some of the signaling pathways that are aberrantly regulated in AML, with a specific focus on their pathogenetic and therapeutic significance, and we examine some recent therapies directed against these targets, used in clinical trial for relapsed patients or unfit for conventional chemotherapy.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Signal Transduction / drug effects
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Drug Design. Genetic Predisposition to Disease / genetics. Humans. Immunologic Factors / pharmacology. Remission Induction. Translocation, Genetic

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  • (PMID = 18534059.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunologic Factors; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Number-of-references] 126
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11. Kang HJ, Hong SH, Kim IH, Park BK, Han KS, Cho HI, Shin HY, Ahn HS: Prognostic significance of FLT3 mutations in pediatric non-promyelocytic acute myeloid leukemia. Leuk Res; 2005 Jun;29(6):617-23
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  • [Title] Prognostic significance of FLT3 mutations in pediatric non-promyelocytic acute myeloid leukemia.
  • This is the first study of FLT3 mutations in pediatric non-promyelocytic AML patients that received the same treatment scheme in single institute.
  • Patients with FLT3/TKD remain alive after autologous stem cell transplantation.
  • The disease-free survival (DFS) of patients with FLT3/ITD (0%) was significantly lower than that of the others (52%).
  • New therapeutic scheme such as stem cell transplantation with more intensive conditioning just after complete remission could be applied in pediatric non-promyelocytic AML patients with the FLT3/ITD mutation.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics

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  • (PMID = 15863200.001).
  • [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 / 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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12. Madlambayan GJ, Meacham AM, Hosaka K, Mir S, Jorgensen M, Scott EW, Siemann DW, Cogle CR: Leukemia regression by vascular disruption and antiangiogenic therapy. Blood; 2010 Sep 2;116(9):1539-47
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  • [Title] Leukemia regression by vascular disruption and antiangiogenic therapy.
  • Acute myelogenous leukemias (AMLs) and endothelial cells depend on each other for survival and proliferation.
  • Monotherapy antivascular strategies such as targeting vascular endothelial growth factor (VEGF) has limited efficacy in treating AML.
  • Thus, in search of a multitarget antivascular treatment strategy for AML, we tested a novel vascular disrupting agent, OXi4503, alone and in combination with the anti-VEGF antibody, bevacizumab.
  • Using xenotransplant animal models, OXi4503 treatment of human AML chloromas led to vascular disruption in leukemia cores that displayed increased leukemia cell apoptosis.
  • However, viable rims of leukemia cells remained and were richly vascular with increased VEGF-A expression.
  • To target this peripheral reactive angiogenesis, bevacizumab was combined with OXi4503 and abrogated viable vascular rims, thereby leading to enhanced leukemia regression.
  • In a systemic model of primary human AML, OXi4503 regressed leukemia engraftment alone and in combination with bevacizumab.
  • Differences in blood vessel density alone could not account for the observed regression, suggesting that OXi4503 also exhibited direct cytotoxic effects on leukemia cells.
  • Together, these data show that OXi4503 alone is capable of regressing AML by a multitargeted mechanism and that the addition of bevacizumab mitigates reactive angiogenesis.

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  • (PMID = 20472832.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK067359; United States / NCI NIH HHS / CA / CA084408; United States / NCI NIH HHS / CA / CA089655; United States / NCI NIH HHS / CA / R01 CA089655; United States / NHLBI NIH HHS / HL / R01 HL070738; United States / NCI NIH HHS / CA / R01 CA084408
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Diphosphates; 0 / Il2rg protein, mouse; 0 / Interleukin Receptor Common gamma Subunit; 0 / Oxi 4503; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Stilbenes; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 2S9ZZM9Q9V / Bevacizumab
  • [Other-IDs] NLM/ PMC2938842
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13. Preudhomme C, Renneville A, Bourdon V, Philippe N, Roche-Lestienne C, Boissel N, Dhedin N, André JM, Cornillet-Lefebvre P, Baruchel A, Mozziconacci MJ, Sobol H: High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder. Blood; 2009 May 28;113(22):5583-7
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  • [Title] High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder.
  • Familial platelet disorder (FPD), a rare autosomal dominant disorder characterized by quantitative and qualitative platelet abnormalities, is considered as a model of genetic predisposition to acute myeloid leukemia (AML).
  • So far, monoallelic RUNX1 germline mutations have been found in 19 of 20 families with reported FPD, and the analysis of blast cells from only 5 patients at acute leukemia (AL) stage has shown no additional RUNX1 abnormality.
  • In addition to the germline RUNX1 mutation, we identified a second RUNX1 alteration in 6 AML cases (acquired point mutations in 4 cases and duplication of the altered RUNX1 allele associated with acquired trisomy 21 in 2 other cases).
  • Although haploinsufficiency of RUNX1 causes FPD, our findings suggest that a second genetic event involving RUNX1 is often associated with progression to AML.
  • [MeSH-major] Blood Platelet Disorders / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics


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4. Petersen WC, Schlis KD, Braverman RS, Carlson I, Liang X, Wang M: Pseudohypopyon: Extramedullary relapse of acute myelogenous leukemia with poor prognosis. Pediatr Blood Cancer; 2009 Jul;52(7):885-7
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  • [Title] Pseudohypopyon: Extramedullary relapse of acute myelogenous leukemia with poor prognosis.
  • She was diagnosed with acute myelogenous leukemia.
  • [MeSH-major] Anterior Chamber / pathology. Eye Diseases / diagnosis. Leukemia, Myelomonocytic, Acute / diagnosis. Neoplasm Recurrence, Local / diagnosis
  • [MeSH-minor] Antimetabolites, Antineoplastic / therapeutic use. Cytarabine / therapeutic use. Female. Humans. Infant. Injections, Spinal. Prognosis. Suppuration / diagnosis

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 19090546.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine
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15. Papamanthos MK, Kolokotronis AE, Skulakis HE, Fericean AM, Zorba MT, Matiakis AT: Acute myeloid leukaemia diagnosed by intra-oral myeloid sarcoma. A case report. Head Neck Pathol; 2010 Jun;4(2):132-5
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  • [Title] Acute myeloid leukaemia diagnosed by intra-oral myeloid sarcoma. A case report.
  • Myeloid sarcoma (MS) is a rare extramedullary malignant tumor composed of immature myeloid cells.
  • It is strongly associated with a well known or covert acute myeloid leukaemia, chronic myeloproliferative diseases or myelodysplastic syndromes.
  • An unusual case of acute myeloid leukaemia, which was diagnosed by mandibular MS that was developed in the alveolar socket after a dental extraction, is reported.
  • The histological examination (including immunohistochemical analysis) of a subsequent biopsy showed infiltration of the oral mucosa by neoplastic cells.
  • This lesion was therefore classified as acute myeloid leukaemia.
  • The patient was referred to oncologists that confirmed the initial diagnosis.
  • Forty days later, a relapse of the disease, which appeared as a great-ulcerated lesion, was developed in the hard palate.
  • Review of the literature shows no report of intraoral relapse and particularly multiple relapse of a MS that involves the oral cavity.
  • Even though MS is encountered infrequently in the oral cavity, it should be considered in the differential diagnosis of conditions (especially tumors) with a similar clinical appearance.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Neoplasms, Multiple Primary / diagnosis. Sarcoma, Myeloid / diagnosis
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Biopsy. Diagnosis, Differential. Etoposide / therapeutic use. Fatal Outcome. Female. Humans. Mouth Mucosa / pathology. Mouth Neoplasms

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  • (PMID = 20512638.001).
  • [ISSN] 1936-0568
  • [Journal-full-title] Head and neck pathology
  • [ISO-abbreviation] Head Neck Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 6PLQ3CP4P3 / Etoposide
  • [Other-IDs] NLM/ PMC2878628
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16. Coppage M, Belanger T, Zauderer M, Sahasrabudhe D: In vitro generation of tumor specific T cells that recognize a shared antigen of AML: molecular characterization of TCR genes. Leuk Res; 2007 Feb;31(2):195-202
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  • [Title] In vitro generation of tumor specific T cells that recognize a shared antigen of AML: molecular characterization of TCR genes.
  • We present data demonstrating in vitro induction of autologous acute myelogenous leukemia (AML)-specific CTL.
  • The specific T cell receptor has been identified and cloned.
  • The CTL demonstrated specific lysis to autologous tumor blasts, but not to autologous BLCL or the NK-sensitive target K562.
  • The clone secreted GM-CSF, TNFa, and IFNg when stimulated with AML blasts from 3 of 11 patients or cell lines tested, but not with K562 or autologous B-LCL.
  • These three AML samples share a single HLA Class I antigen, HLA-A24.
  • The T cell receptor genes identified by molecular methods are Vbeta7.9-J2.3-Cbeta2 and Valpha17-J49-Calpha.
  • [MeSH-major] Antigens, Neoplasm / immunology. HLA Antigens / immunology. Leukemia, Myeloid / immunology. Receptors, Antigen, T-Cell / genetics. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Acute Disease. Amino Acid Sequence. CD8-Positive T-Lymphocytes / immunology. Cell Line, Tumor. Humans. Molecular Sequence Data

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  • [CommentIn] Leuk Res. 2007 Feb;31(2):127-8 [17137625.001]
  • (PMID = 16750565.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / HLA Antigens; 0 / Receptors, Antigen, T-Cell
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17. Renneville A, Boissel N, Zurawski V, Llopis L, Biggio V, Nibourel O, Philippe N, Thomas X, Dombret H, Preudhomme C: Wilms tumor 1 gene mutations are associated with a higher risk of recurrence in young adults with acute myeloid leukemia: a study from the Acute Leukemia French Association. Cancer; 2009 Aug 15;115(16):3719-27
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  • [Title] Wilms tumor 1 gene mutations are associated with a higher risk of recurrence in young adults with acute myeloid leukemia: a study from the Acute Leukemia French Association.
  • BACKGROUND: Wilms tumor 1 (WT1) is a transcription factor that is overexpressed in most acute myeloid leukemias (AMLs).
  • Recently, 2 groups reported that WT1 mutations occur in approximately 10% of normal karyotype AMLs and are an independent predictor of poor outcome in this subgroup of patients with AML.
  • METHODS: The authors studied a cohort of 268 young adults (ages 15-50 years) with AML who were treated on the Acute Leukemia French Association 9802 trial.
  • Within the subgroup of patients who had normal karyotype AML (n = 106), WT1 mutation was identified as an independent adverse prognostic factor for the risk of recurrence.
  • CONCLUSIONS: The current results indicted that WT1 mutations represent an adverse prognostic factor in young adults with AML.
  • Prospective trials should confirm the clinical relevance of WT1 mutations in relation to other prognostic factors in patients with AML.
  • [MeSH-major] Genes, Wilms Tumor. Leukemia, Myeloid, Acute / genetics


18. El-Shemy HA, Aboul-Enein AM, Aboul-Enein KM, Fujita K: Willow leaves' extracts contain anti-tumor agents effective against three cell types. PLoS One; 2007;2(1):e178
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  • [Title] Willow leaves' extracts contain anti-tumor agents effective against three cell types.
  • Many non-natural, synthetic drugs cause severe side effects that were not acceptable except as treatments of last resort for terminal diseases such as cancer.
  • In vitro the willow extract could kill the majority (75%-80%) of abnormal cells among primary cells harvested from seven patients with acute lymphoblastic leukemia (ALL) and 13 with AML (acute myeloid leukemia).
  • DNA fragmentation patterns within treated cells inferred targeted cell death by apoptosis had occurred.
  • The metabolites within the willow extract may act as tumor inhibitors that promote apoptosis, cause DNA damage, and affect cell membranes and/or denature proteins.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Cell Line, Tumor / drug effects. Plant Extracts / pharmacology. Plant Leaves / chemistry. Salix

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  • (PMID = 17264881.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Benzyl Alcohols; 0 / Glucosides; 0 / Plant Extracts; 4649620TBZ / salicin; FA1N0842KB / salicyl alcohol
  • [Other-IDs] NLM/ PMC1779808
  • [General-notes] NLM/ Original DateCompleted: 20070723
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19. Rawat VP, Thoene S, Naidu VM, Arseni N, Heilmeier B, Metzeler K, Petropoulos K, Deshpande A, Quintanilla-Martinez L, Bohlander SK, Spiekermann K, Hiddemann W, Feuring-Buske M, Buske C: Overexpression of CDX2 perturbs HOX gene expression in murine progenitors depending on its N-terminal domain and is closely correlated with deregulated HOX gene expression in human acute myeloid leukemia. Blood; 2008 Jan 1;111(1):309-19
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  • [Title] Overexpression of CDX2 perturbs HOX gene expression in murine progenitors depending on its N-terminal domain and is closely correlated with deregulated HOX gene expression in human acute myeloid leukemia.
  • The mechanisms underlying deregulation of HOX gene expression in AML are poorly understood.
  • Deletion of the N-terminal domain of Cdx2 abrogated its ability to perturb Hox gene expression and to cause acute myeloid leukemia (AML) in mice.
  • In contrast inactivation of the putative Pbx interacting site of Cdx2 did not change the leukemogenic potential of the gene.
  • In an analysis of 115 patients with AML, expression levels of CDX2 were closely correlated with deregulated HOX gene expression.
  • All patients with AML with normal karyotype tested were negative for CDX1 and CDX4 expression.
  • They furthermore correlate the level of CDX2 expression with HOX gene expression in human AML and support a potential role of CDX2 in the development of human AML with aberrant Hox gene expression.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adult. Animals. Bone Marrow Cells / cytology. Bone Marrow Cells / physiology. Bone Marrow Transplantation. Cell Line, Tumor. Gene Expression Profiling. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / physiology. Humans. Karyotyping. Mice. Mutagenesis. NIH 3T3 Cells. Protein Structure, Tertiary. Translocation, Genetic. Up-Regulation / physiology

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  • (PMID = 17855634.001).
  • [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 / CDX2 protein, human; 0 / Cdx2 protein, mouse; 0 / Homeodomain Proteins; 0 / Transcription Factors
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20. O'Brien MM, Lacayo NJ, Lum BL, Kshirsagar S, Buck S, Ravindranath Y, Bernstein M, Weinstein H, Chang MN, Arceci RJ, Sikic BI, Dahl GV: Phase I study of valspodar (PSC-833) with mitoxantrone and etoposide in refractory and relapsed pediatric acute leukemia: a report from the Children's Oncology Group. Pediatr Blood Cancer; 2010 May;54(5):694-702
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  • [Title] Phase I study of valspodar (PSC-833) with mitoxantrone and etoposide in refractory and relapsed pediatric acute leukemia: a report from the Children's Oncology Group.
  • BACKGROUND: Valspodar, a non-immunosuppressive analog of cylosporine, is a potent P-glycoprotein (MDR1) inhibitor.
  • As MDR1-mediated efflux of chemotherapeutic agents from leukemic blasts may contribute to drug resistance, a phase 1 study of valspodar combined with mitoxantrone and etoposide in pediatric patients with relapsed or refractory leukemias was performed.
  • Three of 11 patients with acute lymphoblastic leukemia (ALL) had complete responses while no patient with acute myeloid leukemia (AML) had an objective response.

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  • (PMID = 20209646.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA052168-12S1; United States / NCI NIH HHS / CA / U10 CA98413; United States / PHS HHS / / R01 52168; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCRR NIH HHS / RR / M01 RR 00070; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / R01 CA052168; United States / NCRR NIH HHS / RR / M01 RR000070; United States / NCI NIH HHS / CA / U10 CA98543
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclosporins; 0 / P-Glycoprotein; 121584-18-7 / valspodar; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone
  • [Other-IDs] NLM/ NIHMS155713; NLM/ PMC2838930
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21. Yang L, Zhang Y, Zhang MR, Xiao ZJ: [Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and acute myeloid leukemia and recurrent chromosome translocations]. Zhonghua Yi Xue Za Zhi; 2005 Aug 31;85(33):2312-6
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  • [Title] [Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and acute myeloid leukemia and recurrent chromosome translocations].
  • OBJECTIVE: To investigate the impact of GSTM1, GSTT1 and NQO1 genotypes on susceptibility to acute myeloid leukemia (AML) and recurrent chromosome translocations of AML.
  • METHODS: GSTT1, GSTM1 and NQO1 genotypes were detected in 228 adult patients with de novo AML and 241 controls by PCR or PCR-RFLP.
  • RESULTS: The frequency of GSTM1 null genotype in the AML patients was 62.3%, significantly higher than that in the normal controls (52.7%, P = 0.036), however, no significant difference was found in the incidence of GSTT1 null genotype.
  • The frequencies of NQO1(C609T) C/T and T/T genotypes were 53.1% and 25.0% respectively among the total AML patients (53.1% and 25.0% respectively), 64.3% and 25.0% respectively among the AML patients with t (8;.
  • 21) (q22; q22)/AML-ETO fusion gene, and 57.1% and 26.0% respectively among the AML patient with t (15;.
  • 21) (q22; q22)/AML-ETO (+) AML was 4.487 (95% CI: 1.282-15.705) for the subjects with NQO1(C609T) C/T genotype, and was 6.293 (95% CI: 1.536-25.782) for the subjects with NQO1(C609T) T/T genotype.
  • 17) (q22; q11)/PML-RARalpha (+) AML was 2.531 (95% CI: 1.286-4.981) for the subjects with NQO1(C609T) C/T genotype, and was 4.149 (95% CI: 1.856-9.275) for the subjects with NQO1(C609T) T/T genotype.
  • CONCLUSION: Determination of the NQO1(C609T) genotypes may be used as a stratification marker to predict high-risk individuals for AML, especially for AML with t (8;.
  • 21) (q22; q22)/AML-ETO fusion gene and t (15;.
  • [MeSH-major] Chromosome Aberrations. Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 16321221.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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22. Mann C, Parkinson N, Bleetman A: Endotracheal tube and laryngeal mask airway cuff volume changes with altitude: a rule of thumb for aeromedical transport. Emerg Med J; 2007 Mar;24(3):165-7
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  • Most of these patients are ventilated through endotracheal tubes (ETTs), others through laryngeal mask airways (LMAs).
  • The cuffs of both ETTs and LMAs inflate with increases in altitude as barometric pressure decreases (30 mbar/1000 feet).
  • METHODS: The change in dimensions of the inflated cuffs of a size 8 ETT and a size 5 LMA were measured with digital callipers at 1000 feet intervals in the unpressurised cabin of an Agusta 109 helicopter used by the Warwickshire and Northamptonshire Air Ambulance.
  • RESULTS: A linear expansion in cuff dimensions as a function of altitude increase was identified.
  • CONCLUSION: The data for LMA cuff expansion failed to show significant correlation with altitude change.
  • Further work is required to determine a similar rule of thumb for LMA cuff deflation.

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  • (PMID = 17351218.001).
  • [ISSN] 1472-0213
  • [Journal-full-title] Emergency medicine journal : EMJ
  • [ISO-abbreviation] Emerg Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2660019
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23. Beluffi G, Bernardo ME, Meloni G, Spinazzola A, Locatelli F: Spinal osteomyelitis due to Aspergillus flavus in a child: a rare complication after haematopoietic stem cell transplantation. Pediatr Radiol; 2008 Jun;38(6):709-12
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  • [Title] Spinal osteomyelitis due to Aspergillus flavus in a child: a rare complication after haematopoietic stem cell transplantation.
  • We report the case of a child affected by acute myeloid leukaemia who was treated with allogeneic haematopoietic stem cell transplantation and developed cervicothoracic spinal osteomyelitis due to Aspergillus flavus.
  • The diagnosis was difficult on a clinical basis, but made possible by conventional radiography and MRI.
  • [MeSH-major] Aspergillosis / complications. Hematopoietic Stem Cell Transplantation / adverse effects. Osteomyelitis / microbiology. Spinal Diseases / microbiology
  • [MeSH-minor] Aspergillus flavus / isolation & purification. Bronchoalveolar Lavage. Diagnosis, Differential. Fatal Outcome. Fever / etiology. Humans. Hydrocephalus / etiology. Infant. Leukemia, Myeloid, Acute / surgery. Magnetic Resonance Imaging. Male. Radiography. Rare Diseases. Recurrence. Spine / diagnostic imaging. Spine / pathology


24. Ye Y, McDevitt MA, Guo M, Zhang W, Galm O, Gore SD, Karp JE, Maciejewski JP, Kowalski J, Tsai HL, Gondek LP, Tsai HC, Wang X, Hooker C, Smith BD, Carraway HE, Herman JG: Progressive chromatin repression and promoter methylation of CTNNA1 associated with advanced myeloid malignancies. Cancer Res; 2009 Nov 1;69(21):8482-90
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  • [Title] Progressive chromatin repression and promoter methylation of CTNNA1 associated with advanced myeloid malignancies.
  • Complete loss or deletion of the long arm of chromosome 5 is frequent in myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML).
  • This study is a comprehensive analysis of previously implicated and novel genes for epigenetic inactivation in AML and MDS.
  • In 146 AML cases, methylation of CTNNA1 was frequent, and more common in AML patients with 5q deletion (31%) than those without 5q deletion (14%), whereas no methylation of other 5q genes was observed.
  • In 31 MDS cases, CTNNA1 methylation was only found in high-risk MDS (>or=RAEB2), but not in low-risk MDS (<RAEB2), indicating that CTNNA1 methylation might be important in the transformation of MDS to AML.
  • CTNNA1 expression was lowest in AML/MDS patients with CTNNA1 methylation, although reduced expression was found in some patients without promoter methylation.
  • Repressive chromatin marks (H3K27me3) at the promoter were identified in CTNNA1-repressed AML cell lines and primary leukemias, with the most repressive state correlating with DNA methylation.
  • These results suggest progressive, acquired epigenetic inactivation at CTNNA1, including histone modifications and promoter CpG methylation, as a component of leukemia progression in patients with both 5q- and non-5q- myeloid malignancies.

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  • (PMID = 19826047.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA058184-090013; United States / NCI NIH HHS / CA / P50 CA058184; United States / NCI NIH HHS / CA / P50 CA058184-090013
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNA1 protein, human; 0 / Chromatin; 0 / RNA, Messenger; 0 / alpha Catenin; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ NIHMS142652; NLM/ PMC3081599
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25. Kohlschütter J, Michelfelder S, Trepel M: Drug delivery in acute myeloid leukemia. Expert Opin Drug Deliv; 2008 Jun;5(6):653-63
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  • [Title] Drug delivery in acute myeloid leukemia.
  • BACKGROUND: Acute myeloid leukemia was among the first malignancies to be cured by drug therapy alone, but overall survival rates remain unsatisfactory and have changed little over the past 20 years.
  • OBJECTIVE: We have chosen acute myeloid leukemia as a disease prototype to review established and novel targeted approaches in leukemia treatment.
  • CONCLUSION: While the toxicity profile of chemotherapeutics has been improved by liposomal formulations and antibody conjugation for leukemia-directed uptake, their efficacy has probably not changed significantly.
  • Further improvements may result from the characterization of novel acute myeloid leukemia (AML) cell surface receptors and of leukemic stem cells, as well as from the design of leukemia-targeted gene therapy vectors.
  • [MeSH-minor] Antibodies, Monoclonal / administration & dosage. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Drug Delivery Systems. Genetic Therapy. Humans. Integrin alpha4beta1 / antagonists & inhibitors. Leukemia, Myeloid, Acute / drug therapy. Liposomes. Neoplastic Stem Cells / drug effects. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 18532921.001).
  • [ISSN] 1742-5247
  • [Journal-full-title] Expert opinion on drug delivery
  • [ISO-abbreviation] Expert Opin Drug Deliv
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Integrin alpha4beta1; 0 / Liposomes; 0 / Sialic Acid Binding Ig-like Lectin 3
  • [Number-of-references] 114
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26. Vyas HK, Pal R, Vishwakarma R, Lohiya NK, Talwar GP: Selective killing of leukemia and lymphoma cells ectopically expressing hCGbeta by a conjugate of curcumin with an antibody against hCGbeta subunit. Oncology; 2009;76(2):101-11
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  • [Title] Selective killing of leukemia and lymphoma cells ectopically expressing hCGbeta by a conjugate of curcumin with an antibody against hCGbeta subunit.
  • EXPERIMENTAL DESIGN: The study was carried out on MOLT-4 and U-937 cells expressing hCGbeta and on peripheral blood leukocytes of acute myeloid leukemia (AML) patients.
  • RESULTS: The antibody did not impair the growth of MOLT-4 and U-937 cells in culture.
  • Its conjugate with curcumin, however, was lethal to both cell lines.
  • The immunoconjugate killed tumor cells bearing the CD33 marker of an AML patient expressing hCGbeta but did not have a similar action on cells of another AML patient with the CD13 marker but who was negative for hCGbeta.
  • [MeSH-major] Chorionic Gonadotropin, beta Subunit, Human / metabolism. Curcumin / metabolism. Leukemia / drug therapy. Lymphoma / drug therapy
  • [MeSH-minor] Aged. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Cell Separation. Drug Design. Female. Humans. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Sialic Acid Binding Ig-like Lectin 3. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology. U937 Cells

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  • (PMID = 19127081.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; IT942ZTH98 / Curcumin
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27. O'Sullivan AK, Pandya A, Papadopoulos G, Thompson D, Langston A, Perfect J, Weinstein MC: Cost-effectiveness of posaconazole versus fluconazole or itraconazole in the prevention of invasive fungal infections among neutropenic patients in the United States. Value Health; 2009 Jul-Aug;12(5):666-73
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  • METHODS: We used modeling techniques to assess the cost-effectiveness of posaconazole versus FLU or ITRA in the prevention of IFIs among patients with acute myelogenous leukemia (AML) or myelodysplastic syndromes (MDS) and chemotherapy-induced neutropenia.
  • CONCLUSIONS: We conclude that posaconazole is very likely to be a cost-effective alternative to FLU or ITRA in the prevention of IFIs among neutropenic patients with AML and MDS, and may result in cost savings.

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  • (PMID = 19508661.001).
  • [ISSN] 1524-4733
  • [Journal-full-title] Value in health : the journal of the International Society for Pharmacoeconomics and Outcomes Research
  • [ISO-abbreviation] Value Health
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 304NUG5GF4 / Itraconazole; 8VZV102JFY / Fluconazole
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28. Raffegerst SH, Hoelzlwimmer G, Kunder S, Mysliwietz J, Quintanilla-Martinez L, Schendel DJ: Diverse hematological malignancies including hodgkin-like lymphomas develop in chimeric MHC class II transgenic mice. PLoS One; 2009;4(12):e8539
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  • The majority of malignancies were distributed equally between T and B cell neoplasms and included lymphoblastic T cell lymphoma (LTCL), lymphoblastic B cell lymphoma (LBCL), diffuse large B cell lymphoma (DLBCL), the histiocyte/T cell rich variant of DLBCL (DLBCL-HA/T cell rich DLBCL), splenic marginal zone lymphoma (SMZL), follicular B cell lymphoma (FBL) and plasmacytoma (PCT).
  • Most of these neoplasms were highly similar to human diseases.
  • Also, some non-lymphoid malignancies such as acute myeloid leukemia (AML) and histiocytic sarcoma were found.
  • Interestingly, composite lymphomas, including Hodgkin-like lymphomas, were also detected that had CD30(+) Hodgkin/Reed-Sternberg (H/RS)-like cells, representing a tumor type not previously described in mice.
  • Thus, this DR4 line is a useful model to investigate common molecular mechanisms that may contribute to important neoplastic diseases in man.
  • [MeSH-major] Chimerism. Hematologic Neoplasms / immunology. Hematologic Neoplasms / pathology. Histocompatibility Antigens Class II / immunology. Hodgkin Disease / immunology. Hodgkin Disease / pathology
  • [MeSH-minor] Animals. Antigens, CD30 / metabolism. Base Sequence. Lymphoma, B-Cell / pathology. Lymphoma, T-Cell / pathology. Mice. Mice, Transgenic. Molecular Sequence Data. Reed-Sternberg Cells / pathology. Survival Analysis. Transgenes / genetics

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  • (PMID = 20046882.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Histocompatibility Antigens Class II
  • [Other-IDs] NLM/ PMC2796171
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29. Calvo D, Cariddi LN, Grosso M, Demo MS, Maldonado AM: Achyrocline satureioides (LAM.) DC (Marcela): antimicrobial activity on Staphylococcus spp. and immunomodulating effects on human lymphocytes. Rev Latinoam Microbiol; 2006 Jul-Dec;48(3-4):247-55
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  • [Title] Achyrocline satureioides (LAM.) DC (Marcela): antimicrobial activity on Staphylococcus spp. and immunomodulating effects on human lymphocytes.
  • Achyrocline satureioides (LAM.
  • They were isolated from 18 patients with acne lesions and from 7 patients infected with Staphylococcus spp. (5 strains were taken from catheters and 2 from wounds).
  • On the other hand, cultures of lymphocytes were made from those patients who displayed infections caused by Staphylococcus spp. and from 12 control non-infected individuals.
  • The A. satureiodes decoction inhibited 95% of the isolated Staphylococcus spp. strains and stimulated the lymphocyte expansion, of which 40% were CD8+ T cells.
  • [MeSH-minor] Acne Vulgaris / microbiology. Adolescent. Adult. Bacteremia / microbiology. Catheterization. Cells, Cultured / drug effects. Drug Evaluation, Preclinical. Humans. Lymphocyte Activation / drug effects. Phytohemagglutinins / pharmacology. Plant Leaves / chemistry. Staphylococcal Infections / microbiology. Staphylococcal Skin Infections / microbiology. Wound Infection / microbiology

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  • (PMID = 18293658.001).
  • [ISSN] 0187-4640
  • [Journal-full-title] Revista latinoamericana de microbiología
  • [ISO-abbreviation] Rev. Latinoam. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Anti-Bacterial Agents; 0 / Phytohemagglutinins; 0 / Plant Extracts
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30. Senatore F, Arnold NA, Bruno M: Volatile components of Centaurea eryngiodes Lam. and Centaurea iberica Trev.var. hermonis Bois. Lam.,two Asteraceae growing wild in Lebanon. Nat Prod Res; 2005 Dec;19(8):749-54
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  • [Title] Volatile components of Centaurea eryngiodes Lam. and Centaurea iberica Trev.var. hermonis Bois. Lam.,two Asteraceae growing wild in Lebanon.
  • The volatile components of the flowerheads of Centaurea eryngioides Lam. and Centaurea iberica Trev. var. hermonis Boiss. Lam. were obtained by hydrodistillation and identified by GC and GC-MS.

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  • (PMID = 16317829.001).
  • [ISSN] 1478-6419
  • [Journal-full-title] Natural product research
  • [ISO-abbreviation] Nat. Prod. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oils, Volatile; 0 / Plant Oils
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31. Konoplev S, Huang X, Drabkin HA, Koeppen H, Jones D, Kantarjian HM, Garcia-Manero G, Chen W, Medeiros LJ, Bueso-Ramos CE: Cytoplasmic localization of nucleophosmin in bone marrow blasts of acute myeloid leukemia patients is not completely concordant with NPM1 mutation and is not predictive of prognosis. Cancer; 2009 Oct 15;115(20):4737-44
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  • [Title] Cytoplasmic localization of nucleophosmin in bone marrow blasts of acute myeloid leukemia patients is not completely concordant with NPM1 mutation and is not predictive of prognosis.
  • BACKGROUND: Nucleophosmin (NPM1) gene mutations are reported to predict a favorable prognosis in acute myeloid leukemia (AML) patients.
  • RESULTS: The study included 252 AML patients: 192 de novo AML, 33 AML preceded by either myelodysplastic syndrome or chronic myelomonocytic leukemia, and 27 therapy-related AML.
  • Cytoplasmic NPM was detected in 59 of 252 (23%) patients, including 48 of 192 (25%) de novo AML and 33 of 94 (35%) with a normal karyotype.
  • CONCLUSIONS: IHC assessment for NPM localization did not predict prognosis in this patient cohort.
  • [MeSH-major] Bone Marrow / metabolism. Cytoplasm / metabolism. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Nuclear Proteins / genetics. Nuclear Proteins / metabolism

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  • [Copyright] Copyright (c) 2009 American Cancer Society.
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  • (PMID = 19637342.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / U54 CA096300
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  • [Other-IDs] NLM/ NIHMS633932; NLM/ PMC4199225
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32. Kim HW, Choi SJ, Lee JH, Lee JH, Kim TS, Kim YG, Kang JM, Huh J, Park KM, Lee KH: Nonleukemic granulocytic sarcoma in the bile duct: a case report. J Korean Med Sci; 2006 Aug;21(4):745-8
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  • [Title] Nonleukemic granulocytic sarcoma in the bile duct: a case report.
  • Granulocytic sarcoma (GS) is an extramedullary tumor composed of immature myeloid cells, typically occurring during the course of acute myelogenous leukemia.
  • Non-leukemic GS, that is, GS with no evidence of overt leukemia and no previous history of leukemia, is very rare, and even more unusual is nonleukemic GS of the bile duct.
  • The patient was initially misdiagnosed as a bile duct carcinoma arising in the hilum of the liver (so-called Klatskin tumor), and received a right lobectomy of the liver.
  • Histological examination of the tumor yielded the diagnosis of GS, and the bone marrow biopsy did not show any evidence of leukemia.
  • Considering the risk of subsequent development of overt leukemia, the patient was treated with two cycles of combination chemotherapy as used in the cases of acute myelogenous leukemia.
  • To date, he has remained free of disease 15 months after treatment.
  • [MeSH-major] Bile Duct Neoplasms / chemically induced. Sarcoma, Myeloid / diagnosis
  • [MeSH-minor] Adult. Antigens, CD45 / analysis. Bile Ducts / chemistry. Bile Ducts / pathology. Diagnosis, Differential. Humans. Immunohistochemistry. Male. Peroxidase / analysis. Radiography, Abdominal. Tomography, X-Ray Computed / methods

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  • (PMID = 16891824.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] EC 1.11.1.7 / Peroxidase; EC 3.1.3.48 / Antigens, CD45
  • [Other-IDs] NLM/ PMC2729902
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33. Kuchenbauer F, Kern W, Schoch C, Kohlmann A, Hiddemann W, Haferlach T, Schnittger S: Detailed analysis of FLT3 expression levels in acute myeloid leukemia. Haematologica; 2005 Dec;90(12):1617-25
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  • [Title] Detailed analysis of FLT3 expression levels in acute myeloid leukemia.
  • BACKGROUND AND OBJECTIVES: FLT3 mutations are found in up to 30% of cases of acute myeloid leukemia (AML).
  • DESIGN AND METHODS: To further evaluate the role of FLT3 in AML we investigated FLT3 expression levels in 207 adult AML patients and 8 healthy donors by real-time polymerase chain reaction (PCR).
  • RESULTS: FLT3 expression levels were different in certain FAB types with increasing levels in the following order: M3<M3v<M6<M2<M4eo<M4<M0<M1<M5a<M5b.
  • Independent analysis of FLT3 expression in cytogenetic AML subgroups showed the lowest levels in t(15;17) and the highest in the t(11q23) positive AML.
  • On the molecular level, no differences in FLT3 expression levels were detected between AML with and without any FLT3 mutation as well as for FAB M5 with or without MLL abnormalities (p=0.495).
  • In patients with normal cytogenetics no impact or overall survival or event-free survival could be detected (p=0.128 and p=0.305, respectively) regardless of FLT3 muatation status, whereas investigating the group of patients with normal cytogenetics and wild-type FLT3, a clear tendency for a worse overall (p=0.059) and event free (p=0.087) survival was found.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Myeloid / enzymology. Neoplasm Proteins / biosynthesis. fms-Like Tyrosine Kinase 3 / biosynthesis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Antigens, CD34 / genetics. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Bone Marrow / pathology. Chromosome Aberrations. Disease-Free Survival. Enzyme Induction. Female. Gene Duplication. Humans. Karyotyping. Leukemia, Monocytic, Acute / genetics. Leukemia, Monocytic, Acute / pathology. Leukocyte Count. Life Tables. Male. Middle Aged. Polymerase Chain Reaction. Prognosis. Proportional Hazards Models. RNA, Messenger / biosynthesis. RNA, Messenger / metabolism. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / metabolism. Survival Analysis. Tandem Repeat Sequences

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  • [CommentIn] Haematologica. 2005 Dec;90(12):1586 [16330422.001]
  • (PMID = 16330434.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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34. Ohsaka A, Otsubo K, Yokota H, Hisa T, Saito H, Kozaki T: Spectral karyotyping and fluorescence in situ hybridization analyses identified a novel three-way translocation involving inversion 16 in therapy-related acute myeloid leukemia M4eo. Cancer Genet Cytogenet; 2008 Jul 15;184(2):113-8
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  • [Title] Spectral karyotyping and fluorescence in situ hybridization analyses identified a novel three-way translocation involving inversion 16 in therapy-related acute myeloid leukemia M4eo.
  • We report a novel three-way translocation involving inversion 16 and chromosome 12 at bands 16p13, 16q22, and 12q24 in a patient with therapy-related acute myeloid leukemia (AML)-M4eo.
  • Conventional G-banding of bone marrow cells at diagnosis was suggestive of inv(16)(p13q22) and a translocation of chromosomes 12 and 16.
  • Although we could not establish that this complex chromosomal aberration occurred either as a one-step, three-way event, or a sequential event with inv(16)(p13q22) followed by t(12;16)(q24;q22), SKY in combination with FISH and RT-PCR analyses successfully detected this complex chromosome abnormality in the patient.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 16. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics. Spectral Karyotyping. Translocation, Genetic

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  • (PMID = 18617061.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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35. Sahu GR, Mishra R, Nagpal JK, Das BR: Notice of retraction. Alteration of p73 in acute myelogenous leukemia. Am J Hematol; 2008 Aug;83(8):691
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  • [Title] Notice of retraction. Alteration of p73 in acute myelogenous leukemia.

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  • [RetractionOf] Sahu GR, Mishra R, Nagpal JK, Das BR. Am J Hematol. 2005 May;79(1):1-7 [15849769.001]
  • (PMID = 18615454.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Retraction of Publication
  • [Publication-country] United States
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36. Parikh SA, Kadia T, Jabbour E: Peripheral blasts on day 21 of induction chemotherapy in a patient with core binding factor acute myeloid leukemia: more than meets the eye. Clin Lymphoma Myeloma Leuk; 2010 Aug;10(4):301-2
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  • [Title] Peripheral blasts on day 21 of induction chemotherapy in a patient with core binding factor acute myeloid leukemia: more than meets the eye.
  • The combination of fludarabine, high-dose cytarabine, gemtuzumab ozogamicin, and granulocyte colony-stimulating factor (G-CSF), the FLAG-GO protocol, has resulted in excellent response rates and superior relapse-free survival as first-line therapy for patients with core binding factor acute myeloid leukemia (AML).
  • A side effect of administration of G-CSF is an increase in peripheral white blood cell count and blast cell percentage during the recovery phase of the bone marrow after induction chemotherapy.
  • A 60-year-old man with inversion 16 AML was admitted for induction chemotherapy with the FLAG-GO protocol at our institution.
  • Our case report underscores the importance of recognizing this phenomenon associated with the administration of G-CSF, and waiting for 5-7 days before administering re-induction therapy or classifying the disease as primary refractory AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 20709669.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factors; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; FLAG protocol
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37. Kessler T, Fehrmann F, Bieker R, Berdel WE, Mesters RM: Vascular endothelial growth factor and its receptor as drug targets in hematological malignancies. Curr Drug Targets; 2007 Feb;8(2):257-68
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  • With regard to hematological malignancies a stimulating effect of VEGF for proliferation, survival and migration of leukemia cells could be demonstrated.
  • Bone marrow of leukemia patients shows an increased microvessel density as well as VEGF expression.
  • Complete remissions in acute myeloid leukemia (AML) have been reported by targeting the receptor tyrosine kinase system of VEGF.
  • While the pathophysiology behind the contribution of VEGF to leukemia progression is not yet completely understood, VEGF and its receptors may provide promising targets not only in solid tumors but also hematological malignancies such as AML.
  • [MeSH-minor] Cell Proliferation. Cell Survival. Disease Progression. Humans

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  • (PMID = 17305503.001).
  • [ISSN] 1873-5592
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 226
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38. Rickerts V, Atta J, Herrmann S, Jacobi V, Lambrecht E, Bialek R, Just-Nübling G: Successful treatment of disseminated mucormycosis with a combination of liposomal amphotericin B and posaconazole in a patient with acute myeloid leukaemia. Mycoses; 2006;49 Suppl 1:27-30
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  • [Title] Successful treatment of disseminated mucormycosis with a combination of liposomal amphotericin B and posaconazole in a patient with acute myeloid leukaemia.
  • [MeSH-major] Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Leukemia, Myeloid, Acute / complications. Liposomes / therapeutic use. Mucormycosis / drug therapy. Rhizomucor / isolation & purification. Triazoles / therapeutic use

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  • (PMID = 16961579.001).
  • [ISSN] 0933-7407
  • [Journal-full-title] Mycoses
  • [ISO-abbreviation] Mycoses
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Liposomes; 0 / Triazoles; 0 / liposomal amphotericin B; 6TK1G07BHZ / posaconazole; 7XU7A7DROE / Amphotericin B
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39. Gong H, Liu WL, Zhou JF, Xu HZ: [Expression of mitosis checkpoint gene CHFR in acute leukemia]. Zhonghua Yi Xue Za Zhi; 2005 Apr 27;85(16):1085-8
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  • [Title] [Expression of mitosis checkpoint gene CHFR in acute leukemia].
  • OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with acute leukemia (AL) and its clinical significance.
  • METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with acute myelocytic leukemia (AML) and 22 with acute lymphocytic leukemia (ALL), 45 de novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.
  • The cell cycle was examined by flow cytometric analysis.
  • (1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent acute lymphoblastic leukemia (ALL) was 0.71, significantly higher than that of the de novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).
  • CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with acute leukemia.
  • Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of acute leukemia to chemotherapy.
  • [MeSH-major] Cell Cycle Proteins / biosynthesis. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / pharmacology. Cell Cycle. Child. Drug Resistance. Female. HL-60 Cells. Humans. Male. Middle Aged. Mitosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 16029562.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi 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 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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40. Zhou Q, Bucher C, Munger ME, Highfill SL, Tolar J, Munn DH, Levine BL, Riddle M, June CH, Vallera DA, Weigel BJ, Blazar BR: Depletion of endogenous tumor-associated regulatory T cells improves the efficacy of adoptive cytotoxic T-cell immunotherapy in murine acute myeloid leukemia. Blood; 2009 Oct 29;114(18):3793-802
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  • [Title] Depletion of endogenous tumor-associated regulatory T cells improves the efficacy of adoptive cytotoxic T-cell immunotherapy in murine acute myeloid leukemia.
  • To elucidate host factors contributing to the poor response of adoptively transferred tumor-reactive cytotoxic T lymphocytes (CTLs), we used a systemic model of murine acute myeloid leukemia (AML).
  • AML progression resulted in a progressive regulatory T-cell (Treg) accumulation in disease sites.
  • The adoptive transfer of in vitro-generated, potently lytic anti-AML-reactive CTLs failed to reduce disease burden or extend survival.
  • Compared with non-AML-bearing hosts, transferred CTLs had reduced proliferation in AML sites of metastases.
  • Treg depletion by a brief course of interleukin-2 diphtheria toxin (IL-2DT) transiently reduced AML disease burden but did not permit long-term survival.
  • In contrast, IL-2DT prevented anti-AML CTL hypoproliferation, increased the number of transferred CTLs at AML disease sites, reduced AML tumor burden, and resulted in long-term survivors that sustained an anti-AML memory response.
  • These data demonstrated that Tregs present at AML disease sites suppress adoptively transferred CTL proliferation, limiting their in vivo expansion, and Treg depletion before CTL transfer can result in therapeutic efficacy in settings of substantial pre-existing tumor burden in which antitumor reactive CTL infusion alone has proven ineffective.

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  • (PMID = 19724059.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120409-03; United States / NCI NIH HHS / CA / CA120409-03; United States / NCI NIH HHS / CA / R01 CA120409; United States / NCI NIH HHS / CA / R01 CA72669; United States / NHLBI NIH HHS / HL / R01 HL056067; United States / NCI NIH HHS / CA / R01 CA072669
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins; 0 / interleukin 2-diphtheria toxin
  • [Other-IDs] NLM/ PMC2773484
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41. Löwenberg B, Delwel HR, Valk PJ: [The diagnosis of acute myeloid leukaemia enhanced by using DNA microarrays]. Ned Tijdschr Geneeskd; 2005 Mar 19;149(12):623-5
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  • [Title] [The diagnosis of acute myeloid leukaemia enhanced by using DNA microarrays].
  • [Transliterated title] Diagnostiek van acute myeloïde leukemie in een stroomversnelling door toepassing van DNA-microarrays.
  • Recently, two studies have shown that the use ofgene-expression profiling using DNA microarrays or DNA chips may improve the classification of acute myeloid leukaemia (AML).
  • In both studies, cluster analyses based on the molecular signatures defined known subgroups as well as novel subgroups of AML.
  • Chromosomal lesions, mutations, and abnormal gene expression with prognostic value determined the clustering.
  • In fact, gene-expression profiling recognized leukaemias with certain chromosomal aberrations that had been missed by routine cytogenetics.
  • Thus, gene-expression profiling allows a comprehensive classification of AML that includes previously-identified genetically-defined as well as novel prognostically-relevant subgroups.
  • [MeSH-major] Chromosome Aberrations. Gene Expression Profiling / methods. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / genetics. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] Acute Disease. Cluster Analysis. Cytogenetic Analysis. Humans

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  • [CommentIn] Ned Tijdschr Geneeskd. 2005 Mar 19;149(12):618-22 [15813427.001]
  • (PMID = 15813428.001).
  • [ISSN] 0028-2162
  • [Journal-full-title] Nederlands tijdschrift voor geneeskunde
  • [ISO-abbreviation] Ned Tijdschr Geneeskd
  • [Language] dut
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Netherlands
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42. Sorror ML, Giralt S, Sandmaier BM, De Lima M, Shahjahan M, Maloney DG, Deeg HJ, Appelbaum FR, Storer B, Storb R: Hematopoietic cell transplantation specific comorbidity index as an outcome predictor for patients with acute myeloid leukemia in first remission: combined FHCRC and MDACC experiences. Blood; 2007 Dec 15;110(13):4606-13
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  • [Title] Hematopoietic cell transplantation specific comorbidity index as an outcome predictor for patients with acute myeloid leukemia in first remission: combined FHCRC and MDACC experiences.
  • A new hematopoietic cell transplantation-specific comorbidity index (HCT-CI) was effective in predicting outcomes among patients with hematologic malignancies who underwent HCT at Fred Hutchinson Cancer Research Center (FHCRC).
  • Here, we compared the performance of the HCT-CI to 2 other indices and then tested its capacity to predict outcomes among 2 cohorts of patients diagnosed with a single disease entity, acute myeloid leukemia in first complete remission, who underwent transplantation at either FHCRC or M. D.

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  • (PMID = 17873123.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA18029; 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 / NHLBI NIH HHS / HL / R00 HL088021; United States / NCI NIH HHS / CA / CA15704; United States / NCI NIH HHS / CA / P01 CA078902; United States / NHLBI NIH HHS / HL / K99 HL088021; United States / NHLBI NIH HHS / HL / HL088021
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2234788
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43. Jädersten M, Montgomery SM, Dybedal I, Porwit-MacDonald A, Hellström-Lindberg E: Long-term outcome of treatment of anemia in MDS with erythropoietin and G-CSF. Blood; 2005 Aug 1;106(3):803-11
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  • The International Prognostic Scoring System (IPSS) groups Low/Intermediate-1 (Low/Int-1) had longer response duration than Int-2/High (25 versus 7 months, P = .002).
  • The time until 25% developed acute myeloid leukemia (AML) was longer in the good and intermediate predictive groups for erythroid response compared with the poor predictive group (52 versus 13 months, P = .008).
  • Only 1 of 20 long-term responders developed AML.
  • There was no difference in survival (odds ratio [OR], 0.9; 95% confidence interval [CI], 0.7-1.2; P = .55) or risk of AML evolution (OR, 1.3; 95% CI, 0.7-2.2; P = .40) between treated and untreated patients.
  • Patients with high/intermediate probability of response and with IPSS Low/Int-1 show frequent and durable responses without adverse effects on outcome, while other patients should not be considered candidates for this treatment.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Analysis of Variance. Cell Transformation, Neoplastic. Female. Humans. Leukemia, Myeloid / etiology. Male. Middle Aged. Predictive Value of Tests. Prognosis. Survival Analysis. Treatment Outcome


44. van der Straaten HM, Fijnheer R, Nieuwenhuis HK, van de Winkel JG, Verdonck LF: The FcgammaRIIa-polymorphic site as a potential target for acute graft-versus-host disease in allogeneic stem cell transplantation. Biol Blood Marrow Transplant; 2005 Mar;11(3):206-12
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  • [Title] The FcgammaRIIa-polymorphic site as a potential target for acute graft-versus-host disease in allogeneic stem cell transplantation.
  • Graft-versus-host disease (GVHD) is a serious complication of allogeneic stem cell transplantation for hematologic diseases.
  • Polymorphisms are known for FcgammaRIIa, and this molecule is present on endothelial, dendritic, and Langerhans cells.
  • Donor cells reacting against the patient as GVHD can also react against the malignancy of the patient, and this is known as the graft-versus-leukemia (GVL) effect.
  • Because the FcgammaRIIa molecule is also present on acute myeloid leukemia (AML) cells, an FcgammaRIIa mismatch could be a target for both GVHD and GVL.
  • We retrospectively studied 73 AML patients and analyzed the differences in GVHD and relapse incidence between patients with and without a pro-GVHD/GVL FcgammaRIIa allotype mismatch.
  • Univariate and multivariate analyses demonstrated the pro-GVHD mismatch to be a significant risk factor for the development of acute GVHD.
  • The relapse incidence was not significantly different for patients with or without the pro-GVL mismatch, although there was a trend for fewer relapses in standard-risk AML patients with the pro-GVL mismatch.
  • We conclude that the polymorphism of the FcgammaRIIa receptor may be a candidate target for acute GVHD.
  • [MeSH-major] Antigens, CD / genetics. Graft vs Host Disease / genetics. Hematopoietic Stem Cell Transplantation / adverse effects. Polymorphism, Genetic. Receptors, IgG / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Analysis of Variance. Cohort Studies. Female. Graft vs Leukemia Effect / genetics. Graft vs Leukemia Effect / immunology. Humans. Incidence. Leukemia, Myeloid / complications. Leukemia, Myeloid / therapy. Male. Middle Aged. Recurrence. Retrospective Studies. Transplantation Immunology. Transplantation, Homologous

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  • (PMID = 15744239.001).
  • [ISSN] 1083-8791
  • [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] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Fc gamma receptor IIA; 0 / Receptors, IgG
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45. Dheda K, Davids V, Lenders L, Roberts T, Meldau R, Ling D, Brunet L, van Zyl Smit R, Peter J, Green C, Badri M, Sechi L, Sharma S, Hoelscher M, Dawson R, Whitelaw A, Blackburn J, Pai M, Zumla A: Clinical utility of a commercial LAM-ELISA assay for TB diagnosis in HIV-infected patients using urine and sputum samples. PLoS One; 2010 Mar 24;5(3):e9848
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  • [Title] Clinical utility of a commercial LAM-ELISA assay for TB diagnosis in HIV-infected patients using urine and sputum samples.
  • BACKGROUND: The accurate diagnosis of TB in HIV-infected patients, particularly with advanced immunosuppression, is difficult.
  • Recent studies indicate that a lipoarabinomannan (LAM) assay (Clearview-TB(R)-ELISA) may have some utility for the diagnosis of TB in HIV-infected patients; however, the precise subgroup that may benefit from this technology requires clarification.
  • The utility of LAM in sputum samples has, hitherto, not been evaluated.
  • METHODS: LAM was measured in sputum and urine samples obtained from 500 consecutively recruited ambulant patients, with suspected TB, from 2 primary care clinics in South Africa.
  • Culture positivity for M. tuberculosis was used as the reference standard for TB diagnosis.
  • Urine-LAM positivity was associated with HIV positivity (p = 0.007) and test sensitivity, although low, was significantly higher in HIV-infected compared to uninfected patients (21% versus 6%; p<0.001), and also in HIV-infected participants with a CD4 <200 versus >200 cells/mm(3) (37% versus 0%; p = 0.003).
  • Urine-LAM remained highly specific in all 3 subgroups (95%-100%).
  • 25% of smear-negative but culture-positive HIV-infected patients with a CD4 <200 cells/mm(3) were positive for urine-LAM.
  • Sputum-LAM had good sensitivity (86%) but poor specificity (15%) likely due to test cross-reactivity with several mouth-residing organisms including actinomycetes and nocardia species.
  • CONCLUSIONS: These preliminary data indicate that in a high burden primary care setting the diagnostic usefulness of urine-LAM is limited, as a rule-in test, to a specific patient subgroup i.e. smear-negative HIV-infected TB patients with a CD4 count <200 cells/mm(3), who would otherwise have required further investigation.

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  • (PMID = 20352098.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] None / None / / 89918; Canada / Canadian Institutes of Health Research / / 89918; Canada / Canadian Institutes of Health Research / / MOP-89918; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2844421
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51. Chowdhury T, Brady HJ: Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia. Blood Cells Mol Dis; 2008 Mar-Apr;40(2):192-9
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  • [Title] Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia.
  • Translocations involving the Mixed Lineage Leukemia (MLL) gene at 11q23 are found in both acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML), but have different prognostic implications depending on the phenotype of the leukemia in de novo pediatric cases.
  • Rearrangements of the MLL gene are found in most cases of infant AML and regardless of age confer an intermediate risk.
  • The treatment of MLL-rearranged ALL in children involves increased intensification of chemotherapy, and infants with ALL are treated with an intensive regimen of ALL- and AML-like chemotherapy, with the proportion of MLL-rearranged cases being responsible for the poor outcome in this age group.
  • The use of DNA microarray analysis to distinguish a particular gene signature for MLL-rearranged leukemias is shedding light on the molecular mechanisms and potential therapeutic targets of these leukemias.
  • It may also prove to have a useful role in both diagnosis and prognosis.
  • [MeSH-major] Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17905612.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Number-of-references] 82
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52. Czibere A, Grall F, Aivado M: Perspectives of proteomics in acute myeloid leukemia. Expert Rev Anticancer Ther; 2006 Nov;6(11):1663-75
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  • [Title] Perspectives of proteomics in acute myeloid leukemia.
  • Acute myeloid leukemia (AML) is a frequent hematological malignancy.
  • Despite enormous therapeutic efforts that range from various cytotoxic agents to allogeneic stem cell transplantation, overall survival of patients with AML remains unsatisfying.
  • There is hope that elucidation of the AML-specific proteome will prompt the discovery of novel therapeutic targets and biomarkers in AML.
  • Modern mass-spectrometry instrumentation has achieved excellent performance in terms of sensitivity, resolution and mass accuracy; however, so far, the contribution of proteomics to the care of patients with AML is virtually zero.
  • Since mass-spectrometry instruments are very intricate devices, their successful operation will hinge on the willingness and ability of mass-spectrometry experts and clinical researchers to adopt new views, learn from each other and cooperate in order to ultimately benefit the patient suffering from AML.
  • This review highlights some clinical problems circumventing the treatment of patients with AML.
  • Furthermore, it provides a brief overview of the technical background of standard proteomics approaches and describes opportunities, challenges and pitfalls of proteomic studies with regards to AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Proteomics

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  • (PMID = 17134369.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
  • [Number-of-references] 99
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53. Ayala F, Dewar R, Kieran M, Kalluri R: Contribution of bone microenvironment to leukemogenesis and leukemia progression. Leukemia; 2009 Dec;23(12):2233-41
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  • [Title] Contribution of bone microenvironment to leukemogenesis and leukemia progression.
  • Both BM stroma and leukemic blasts promote angiogenesis, which is increased in acute lymphoblastic leukemia and acute myeloid leukemia.
  • Growth factors like vascular endothelial growth factor (VEGF), basic fibroblast growth factor and angiopoietins are the main proangiogenic mediators in acute leukemia.
  • Interactions of stromal cells and extracellular matrix with leukemic blasts can also generate antiapoptotic signals that contribute to neoplastic progression and persistence of treatment-resistant minimal residual disease.
  • High expression of CXC chemokine ligand 4 (CXCR4) by leukemic blasts and activation of the CXCR4-CXCL12 axis is involved in leukemia progression and disruption of normal hematopoiesis.
  • Leukemia-associated bone microenvironment markers could be used as prognostic or predictive indicators of disease progression and/or treatment outcome.
  • Studies related to bone microenvironment would likely provide a better understanding of the treatment resistance associated with leukemia therapy and design of new treatments.

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  • (PMID = 19727127.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK61688; United States / NIDDK NIH HHS / DK / DK55001; United States / NIAAA NIH HHS / AA / R01 AA013913; United States / NIDDK NIH HHS / DK / R01 DK061688; United States / NIDDK NIH HHS / DK / R01 DK062987; United States / NCI NIH HHS / CA / R01 CA125550; United States / NCI NIH HHS / CA / CA125550; United States / NIDDK NIH HHS / DK / R01 DK055001; United States / NIDDK NIH HHS / DK / DK62987; United States / NIAAA NIH HHS / AA / AA13913
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 99
  • [Other-IDs] NLM/ NIHMS590537; NLM/ PMC4313556
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54. Schlenk RF, Döhner K, Kneba M, Götze K, Hartmann F, Del Valle F, Kirchen H, Koller E, Fischer JT, Bullinger L, Habdank M, Späth D, Groner S, Krebs B, Kayser S, Corbacioglu A, Anhalt A, Benner A, Fröhling S, Döhner H, German-Austrian AML Study Group (AMLSG): Gene mutations and response to treatment with all-trans retinoic acid in elderly patients with acute myeloid leukemia. Results from the AMLSG Trial AML HD98B. Haematologica; 2009 Jan;94(1):54-60
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  • [Title] Gene mutations and response to treatment with all-trans retinoic acid in elderly patients with acute myeloid leukemia. Results from the AMLSG Trial AML HD98B.
  • BACKGROUND: In a previous randomized trial, AML HD98B, we showed that administration of all-trans retinoic acid in addition to intensive chemotherapy improved the outcome of older patients with acute myeloid leukemia.
  • DESIGN AND METHODS: Data from mutation analyses of the NPM1, CEBPA, FLT3, and MLL genes were correlated with outcome in patients 61 years and older treated within the AML HD98B trial.
  • The genotype mutant NPM1 was positively and adverse cytogenetics as well as higher white blood cell count negatively correlated with achievement of complete remission.
  • Other significant factors for survival were age, adverse cytogenetics, and logarithm of white cell count.
  • CONCLUSIONS: In elderly patients with acute myeloid leukemia, NPM1 mutations are associated with achievement of complete remission, and the genotype 'mutant NPM1 without FLT3-ITD' appears to be a predictive marker for response to all-trans retinoic acid given as an adjunct to intensive chemotherapy (ClinicalTrials.gov Identifier: NCT00151242).
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Tretinoin / therapeutic use
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers / metabolism. Disease-Free Survival. Female. Humans. Male. Middle Aged. Pilot Projects. Survival Rate. Treatment Outcome


55. Griessinger E, Imbert V, Lagadec P, Gonthier N, Dubreuil P, Romanelli A, Dreano M, Peyron JF: AS602868, a dual inhibitor of IKK2 and FLT3 to target AML cells. Leukemia; 2007 May;21(5):877-85
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  • [Title] AS602868, a dual inhibitor of IKK2 and FLT3 to target AML cells.
  • Acute myeloid leukemia (AML) cells carry molecular defects that promote their leukemic proliferation, resistance to apoptosis and defect in differentiation.
  • Pharmacological targeting of the nuclear factor kappaB (NF-kappaB) pathway has been shown to promote apoptosis of primary AML cells and to sensitize blasts to neoplastic drugs (Frelin, Blood 2005, 105, 804).
  • The Fms-like tyrosine kinase 3 (FLT3), which sustains proliferation of normal hematopoietic progenitors is frequently overexpressed or mutated in AML patients.
  • Using Ba/F3 murine pre-B cells transfected with various mutants of FLT3 (ITD, D835V, D835Y) and the MV4-11 human AML line, we show that normal or oncogenic stimulation of FLT3 led to activation of NF-kappaB.
  • Pharmacological inhibition of either FLT3 with AG1296 or NF-kappaB with the small molecule inhibitor of IkappaB kinase-2 AS602868 reduced viability and triggered cell death.
  • AS602868 thus appears to target two different kinases that play a crucial role in the pathogenesis of AML, making it particularly attractive as a new therapeutical approach for AML.
  • [MeSH-major] I-kappa B Kinase / antagonists & inhibitors. Leukemia, Myeloid, Acute / drug therapy. Protein Kinase Inhibitors / pharmacology. Pyrimidines / pharmacology. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors
  • [MeSH-minor] Animals. Annexin A5 / analysis. Caspase 3 / metabolism. Cell Line. Cell Proliferation. Child. Humans. Male. Mice. NF-kappa B / metabolism. Poly(ADP-ribose) Polymerases / metabolism. bcl-X Protein / analysis

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  • (PMID = 17330097.001).
  • [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 / AS602868; 0 / Annexin A5; 0 / NF-kappa B; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / bcl-X Protein; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.10 / I-kappa B Kinase; EC 3.4.22.- / Caspase 3
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56. Siegler U, Meyer-Monard S, Jörger S, Stern M, Tichelli A, Gratwohl A, Wodnar-Filipowicz A, Kalberer CP: Good manufacturing practice-compliant cell sorting and large-scale expansion of single KIR-positive alloreactive human natural killer cells for multiple infusions to leukemia patients. Cytotherapy; 2010 Oct;12(6):750-63
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  • [Title] Good manufacturing practice-compliant cell sorting and large-scale expansion of single KIR-positive alloreactive human natural killer cells for multiple infusions to leukemia patients.
  • The introduction of NK cell-based immunotherapy to current treatment options in acute myeloid leukemia (AML) requires NK cell products with high anti-leukemic efficacy optimized for clinical use.
  • METHODS: We describe a good manufacturing practice (GMP)-compliant protocol of large-scale ex vivo expansion of alloreactive NK cells suitable for multiple donor lymphocyte infusions (NK-DLI) in AML.
  • NK cell numbers increased 117.0 ± 20.0-fold in 19 days.
  • To reduce the culture volume associated with expansion of bulk NK cells and to expand selectively the alloreactive NK cell subsets, GMP-certified cell sorting was introduced to obtain cells with single killer immunoglobulin-like receptor (KIR) specificities.
  • The subsequent GMP-compliant expansion of single KIR+ cells was 268.3 ± 66.8-fold, with a contaminating T-cell content of only 0.006 ± 0.002%.
  • The single KIR-expressing NK cells were cytotoxic against HLA-mismatched primary AML blasts in vitro and effectively reduced tumor cell load in vivo in NOD/SCID mice transplanted with human AML.
  • CONCLUSIONS: The approach to generating large numbers of GMP-grade alloreactive NK cells described here provides the basis for clinical efficacy trials of NK-DLI to complement and advance therapeutic strategies against human AML.
  • [MeSH-major] Cell Culture Techniques / methods. Cell Proliferation. Immunotherapy, Adoptive. Killer Cells, Natural / metabolism. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Animals. Antineoplastic Protocols. Cell Line, Tumor. Cytotoxicity, Immunologic. Guideline Adherence. Humans. Infusions, Intravenous. Isoantigens / immunology. Mice. Mice, SCID. Neoplasm Transplantation. Receptors, KIR / metabolism. Tumor Burden

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  • (PMID = 20491532.001).
  • [ISSN] 1477-2566
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Isoantigens; 0 / Receptors, KIR
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57. Liu XM, Chen YZ, Huang MJ, Liu X, Guo JR: [The potential prognostic influence of granulocyte-colony stimulating factor in acute leukemia]. Zhonghua Nei Ke Za Zhi; 2005 Jul;44(7):518-21
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  • [Title] [The potential prognostic influence of granulocyte-colony stimulating factor in acute leukemia].
  • OBJECTIVE: To investigate the potential influence of granulocyte-colony stimulating factor (G-CSF) on the prognosis of patients with acute leukemia(AL).
  • METHODS: In 171 evaluable cases with AL, the complete remission (CR) rate post first course of chemotherapy, CR rate, effective rate, duration of leucopenia post chemotherapy, CR duration, lifespan and the relationship between the dosage of G-CSF and CR duration or lifespan were retrospectively analyzed with Chi-square test, paired t-test, Cox regression, Kaplan-Meier and rank correlation method.
  • For remission induction and postremission therapy, the cases with acute myeloid leukemia (AML) received chemotherapy regimes based on daunorubicin + ara-C (DA), homoharringtonine + ara-C (HA) or mitoxantrone + ara-C (MA).
  • The patients with acute lymphocyte leukemia (ALL) were treated with regimes based on vinblastine + daunorubicin + prednisone (VDP), vinblastine + adriamycin + prednisone (VAP), vinblastine + mitoxantrone + prednisone (VMP) or cyclophosphamide + vinblastine + daunorubicin + prednisone(CODP).
  • However, there was no statistical difference between the two groups in the CR rate post first course of chemotherapy, CR rate and the effective rate of treatment. (2) Use of G-CSF did not affect CR durations of ALL patients, but shortened that of AML patients. (3) The application of G-CSF had little effect on the lifespan of ALL patients.
  • By contrast, it showed clearly negative effects on that of AML patients. (4) No relationship between the dosage of G-CSF and CR duration or lifespan in AML patients.
  • CONCLUSION: With AML patients, the administration of G-CSF must be very cautious.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Granulocyte Colony-Stimulating Factor / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16080844.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
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58. Cilloni D, Messa E, Messa F, Carturan S, Defilippi I, Arruga F, Rosso V, Catalano R, Bracco E, Nicoli P, Saglio G: Genetic abnormalities as targets for molecular therapies in myelodysplastic syndromes. Ann N Y Acad Sci; 2006 Nov;1089:411-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent advances in molecular genetics have increased knowledge regarding the mechanisms leading to myelodysplastic syndrome (MDS), secondary acute myeloid leukemia (AML), and therapy-induced MDS.
  • Many genetic defects underlying MDS and AML have been identified thereby allowing the development of new molecular-targeted therapies.
  • These agents have been tested in patients with solid tumors and hematologic malignancies such as AML and MDS.
  • The DNA hypomethylating compounds azacytidine and decitabine may reduce hypermethylation and induce re-expression of key tumor suppressor genes in MDS.
  • Future therapies will attempt to resolve cytopenias in MDS, eliminate malignant clones, and allow differentiation by attacking specific mechanisms of the disease.

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  • (PMID = 17261784.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / MECOM protein, human; 0 / Transcription Factors; 0 / WT1 Proteins; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Number-of-references] 76
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59. Yang L, Dong ZR, Wen SP, Pan L, Zhang XJ, Luo JM, Xu SR: [Relationship between VEGF and MMP-2, MMP-9 in 82 patients with acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Feb;14(1):15-20
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  • [Title] [Relationship between VEGF and MMP-2, MMP-9 in 82 patients with acute myeloid leukemia].
  • In order to investigate the relationship between VEGF and matrix metalloproteinase (MMP)-2, -9 in acute myeloid leukemia patients, and evaluate the significance of them in extramedullary leukemic invasion, the expressions of MMP-2 mRNA, MMP-9 mRNA, VEGF mRNA in bone marrow from 86 patients with acute myeloid leukemia (AML), as well as human hematopoietic cell lines were analyzed by reverse transcription-polymerase chain reaction (RT-PCR).
  • But no such correlation was demonstrated in the AML (CR) and normal control (NC) groups.
  • More extramedullary infiltration occurred in VEGF positive groups than that in VEGF negative groups of AML.
  • It is concluded that there are significantly positive correlations between the expression of MMP-2 and MMP-9 with VEGF mRNA or protein levels in AML patients.
  • VEGF and MMP-2, MMP-9 may participate in the extramedullary leukemic invasion of AML patients.

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  • (PMID = 16584583.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
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60. Racay P, Hatok J, Hudecek J, Chudej J, Jurecekova J, Dobrota D: Transcription of genes of p53-dependent apoptosis in acute leukaemia. Int J Mol Med; 2008 Dec;22(6):833-9
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  • [Title] Transcription of genes of p53-dependent apoptosis in acute leukaemia.
  • We demonstrated that acute leukaemia, myeloblastic (AML) and lymphoblastic (ALL), is associated with significantly elevated levels of p53 and Bax mRNA in leukaemic cells.
  • Altered alternative processing of Bcl-x and myeloid cell leukaemia-1 (MCL1) primary transcripts were observed in the case of AML and AML and ALL, respectively.
  • We assumed that increased glyceraldehyde-3-phosphate dehydrogenase (gapdh) transcription and decreased MCL1s mRNA were not fully responsible for the dysregulation of p53-dependent apoptosis in the case of AML.
  • In addition, transcription of hsp70.1 and Bcl-2 producing anti-apoptotic proteins was not affected in acute leukaemia.
  • [MeSH-major] Apoptosis. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription, Genetic. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Actins / genetics. Actins / metabolism. Glyceraldehyde-3-Phosphate Dehydrogenases / genetics. Glyceraldehyde-3-Phosphate Dehydrogenases / metabolism. HSP70 Heat-Shock Proteins / genetics. HSP70 Heat-Shock Proteins / metabolism. Humans. Leukocytes, Mononuclear / metabolism. Myeloid Cell Leukemia Sequence 1 Protein. Polymorphism, Single-Stranded Conformational. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. bcl-2-Associated X Protein / genetics. bcl-2-Associated X Protein / metabolism. bcl-X Protein / genetics. bcl-X Protein / metabolism

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  • (PMID = 19020783.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Actins; 0 / BCL2L1 protein, human; 0 / HSP70 Heat-Shock Proteins; 0 / MCL1 protein, human; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases
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61. Crapanzano JP: Fine-needle aspiration of renal angiomyolipoma: cytological findings and diagnostic pitfalls in a series of five cases. Diagn Cytopathol; 2005 Jan;32(1):53-7
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  • Diagnosis of renal angiomyolipoma (AML) by fine-needle aspiration (FNA) may be difficult because cytological and radiological findings sometimes overlap with renal cell carcinoma (RCC) and liposarcoma.
  • Five FNAs of AMLs were studied.
  • Corresponding surgical material showed typical features of AML.
  • In FNA, bland chromatin and inconspicuous nucleoli distinguish renal AML from RCC and liposarcoma.
  • Adipose tissue is not universally present.
  • Immunocytochemical (ICC) stains may elucidate the correct diagnosis.
  • [MeSH-minor] Adenoma, Oxyphilic / diagnosis. Adult. Aged. Carcinoma, Renal Cell / diagnosis. Diagnosis, Differential. Epithelioid Cells / pathology. Female. Humans. Liposarcoma / diagnosis. Male. Middle Aged. Retroperitoneal Neoplasms / diagnosis. Stromal Cells / pathology

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15584043.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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62. Wang Z, Xu HX, Xie XY, Xie XH, Kuang M, Xu ZF, Liu GJ, Chen LD, Lin MX, Lu MD: Imaging features of hepatic angiomyolipomas on real-time contrast-enhanced ultrasound. Br J Radiol; 2010 May;83(989):411-8
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  • The aim of this study was to evaluate the imaging features of hepatic angiomyolipoma (AML) on contrast-enhanced ultrasound (CEUS).
  • The imaging features of 12 pathologically proven hepatic AML lesions in 10 patients who had undergone baseline ultrasound (BUS) and CEUS examinations were evaluated retrospectively.
  • The results showed that 75% (9/12) of the AML lesions exhibited mixed echogenicity on BUS and most showed remarkable hyperechogenicity in combination with a hypoechoic or anechoic portion.
  • Arterial flow signals were detected in 75% (9/12) of the lesions on colour Doppler imaging.
  • On CEUS, 66.7% (n = 8) of the 12 lesions exhibited hyperenhancement in the arterial phase, slight hyperenhancement (n = 2) or isoenhancement (n = 6) in the portal phase, and slight hyperenhancement (n = 1) or isoenhancement (n = 7) in the late phase.
  • Three (25%) lesions exhibited hyperenhancement in the arterial phase and hypoenhancement in both portal and late phases.
  • One (8.3%) lesion exhibited hypoenhancement throughout the CEUS process.
  • Before pathological examination with BUS, only 3 (25%) lesions were correctly diagnosed as hepatic AML.
  • Conversely, on CEUS, correct diagnoses were made for 66.8% (8/12) of hepatic AMLs.
  • Therefore, arterial hyperenhancement and subsequent sustained enhancement on CEUS were found in the majority of hepatic AMLs.
  • The combination of BUS and CEUS leads to the correct diagnosis in the majority of hepatic AMLs, and is higher than the success rate achieved by BUS alone.
  • [MeSH-major] Angiomyolipoma / ultrasonography. Liver Neoplasms / ultrasonography

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  • [ISSN] 1748-880X
  • [Journal-full-title] The British journal of radiology
  • [ISO-abbreviation] Br J Radiol
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  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
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63. Wihlidal P, Varga F, Pfeilstöcker M, Karlic H: Expression and functional significance of osteocalcin splicing in disease progression of hematological malignancies. Leuk Res; 2006 Oct;30(10):1241-8
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  • [Title] Expression and functional significance of osteocalcin splicing in disease progression of hematological malignancies.
  • We analysed bone marrow obtained from two patients with chronic myeloid leukemia (CML), seven patients with other myeloproliferative diseases (MPD) and four patients with acute myeloid leukemia (AML).
  • [MeSH-minor] Bone Marrow Cells / pathology. DNA Primers. Disease Progression. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Myeloproliferative Disorders / genetics. Protein Biosynthesis. Proto-Oncogene Proteins c-kit / genetics. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Stem Cells / pathology. Transcription, Genetic

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  • (PMID = 16387359.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 104982-03-8 / Osteocalcin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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64. Fernandes MS, Reddy MM, Croteau NJ, Walz C, Weisbach H, Podar K, Band H, Carroll M, Reiter A, Larson RA, Salgia R, Griffin JD, Sattler M: Novel oncogenic mutations of CBL in human acute myeloid leukemia that activate growth and survival pathways depend on increased metabolism. J Biol Chem; 2010 Oct 15;285(42):32596-605
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  • [Title] Novel oncogenic mutations of CBL in human acute myeloid leukemia that activate growth and survival pathways depend on increased metabolism.
  • Acute myeloid leukemia (AML) is characterized by multiple mutagenic events that affect proliferation, survival, as well as differentiation.
  • Recently, gain-of-function mutations in the α helical structure within the linker sequence of the E3 ubiquitin ligase CBL have been associated with AML.
  • We identified four novel CBL mutations, including a point mutation (Y371H) and a putative splice site mutation in AML specimens.
  • Overall, our data demonstrate that mutations of CBL alter cellular biology at multiple levels and require not only the activation of receptor proximal signaling events but also an increase in cellular glucose metabolism.
  • Pathways that are activated by CBL gain-of-function mutations can be efficiently targeted by small molecule drugs.

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  • (PMID = 20622007.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA087986; United States / NCI NIH HHS / CA / 5R01CA134660-02; United States / NCI NIH HHS / CA / CA099163-11; United States / NCI NIH HHS / CA / 5R01CA87986-12; United States / NCI NIH HHS / CA / R01 CA099163-09; United States / NCI NIH HHS / CA / 5R01CA105489-06; United States / NCI NIH HHS / CA / CA099163-10; United States / NCI NIH HHS / CA / 5R01CA125541-04; United States / NCI NIH HHS / CA / 5R01CA129501-02; United States / NCI NIH HHS / CA / R01 CA125541; United States / NCI NIH HHS / CA / 5R01CA116552-04; United States / NCI NIH HHS / CA / R01 CA116552; United States / NCI NIH HHS / CA / CA099163-09; United States / NCI NIH HHS / CA / R01 CA105489; United States / NCI NIH HHS / CA / 5R01CA99163-09; United States / NCI NIH HHS / CA / R01 CA099163-11; United States / NCI NIH HHS / CA / 5R01CA100750-06; United States / NCI NIH HHS / CA / R01 CA129501; United States / NCI NIH HHS / CA / R01 CA099163-10; United States / NCI NIH HHS / CA / R01 CA061593; United States / NCI NIH HHS / CA / R01 CA099163; United States / NCI NIH HHS / CA / R01 CA100750; United States / NCI NIH HHS / CA / R01 CA134660
  • [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 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 0 / STAT5 Transcription Factor; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.6.1.- / GTP-Binding Proteins; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ PMC2952262
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65. Ngo N, Lampert IA, Naresh KN: Bone marrow trephine findings in acute myeloid leukaemia with multilineage dysplasia. Br J Haematol; 2008 Feb;140(3):279-86
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  • [Title] Bone marrow trephine findings in acute myeloid leukaemia with multilineage dysplasia.
  • Acute myeloid leukaemia (AML) with multilineage dysplasia (MD) is one of the four main categories of AML in the World Health Organization (WHO) classification.
  • The role of bone marrow trephine biopsy (BMTB) histology and immunohistochemistry in the diagnosis of AML-MD is currently unclear.
  • BMTBs were studied in 11 cases of AML-MD and two cases of myelodysplasia that subsequently transformed to AML.
  • With respect to conforming to the WHO definition of AML, documentation of an increased proportion of immature myeloid cells was possible on morphology and counting of immature cells following immunostaining with CD34, CD117 or HLA-DR antibodies.
  • Based on this relatively small series of cases we show the utility of BMTB and immunohistochemistry as an aid to the diagnosis of AML-MD.
  • This has to be seen not just in light of its utility at diagnosis, but also the role the diagnostic BMTB would play for purposes of comparison when follow-up BMTBs are submitted in this group of patients.
  • [MeSH-major] Bone Marrow Cells / pathology. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD34 / analysis. Biomarkers / analysis. Biopsy / methods. Bone Marrow Examination / methods. Cytogenetics. Disease Progression. Erythroblasts / pathology. Female. Humans. Immunohistochemistry. Immunophenotyping. Male. Megakaryocytes / pathology. Middle Aged. Myeloid Cells / pathology. Proto-Oncogene Proteins c-kit / analysis

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  • (PMID = 17973948.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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66. Huang XF, Luo SK, Xu J, Li J, Xu DR, Wang LH, Yan M, Wang XR, Wan XB, Zheng FM, Zeng YX, Liu Q: Aurora kinase inhibitory VX-680 increases Bax/Bcl-2 ratio and induces apoptosis in Aurora-A-high acute myeloid leukemia. Blood; 2008 Mar 1;111(5):2854-65
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  • [Title] Aurora kinase inhibitory VX-680 increases Bax/Bcl-2 ratio and induces apoptosis in Aurora-A-high acute myeloid leukemia.
  • In this study, we found that expression of Aur-A was markedly elevated in bone marrow mononuclear cells (BMMCs) obtained from a significant portion of de novo acute myeloid leukemia (AML) patients.
  • Targeting human primary AML cells with Aur-A kinase inhibitory VX-680 led to apoptotic cell death in a dose-dependent manner.
  • Importantly, VX-680-induced cell death was preferentially higher in Aur-A-high primary leukemic blasts compared with Aur-A-low AML (P < .001) or normal BMMCs (P < .001), suggesting the possible pharmacologic window in targeting Aurora kinase among Aur-A-high VX-680-sensitive leukemia patients.
  • VX-680-induced cell death in AML cell lines was accompanied by formation of monopolar mitotic spindles, G(2)/M phase arrest, decreased phosphorylated(p)-Akt-1, and increased proteolytic cleavage of procaspase-3 and poly(ADP)ribose polymerase.
  • Notably, VX-680 increased Bax/Bcl-2 expression ratio, a favorable proapoptotic predictor for drug response and survival in AML.
  • Lastly, VX-680 enhanced the cytotoxic effect of the chemotherapeutic agent etoposide (VP16) on AML cells.
  • Together, we concluded that Aurora kinases were potentially therapeutic targets for AML and that Aur-A-high expression may serve as a differential marker for selective treatment.
  • [MeSH-major] Apoptosis / drug effects. Leukemia, Myeloid, Acute / enzymology. Leukemia, Myeloid, Acute / pathology. Piperazines / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. bcl-2-Associated X Protein / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / pharmacology. Aurora Kinases. Bone Marrow Cells / drug effects. Bone Marrow Cells / enzymology. Bone Marrow Cells / pathology. Caspases / metabolism. Cell Division / drug effects. Cell Line, Tumor. Child. Drug Screening Assays, Antitumor. Drug Synergism. Enzyme Activation / drug effects. Etoposide / pharmacology. Female. G2 Phase / drug effects. Humans. Male. Middle Aged. Mutation / genetics. fms-Like Tyrosine Kinase 3 / metabolism

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  • (PMID = 18160664.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Piperazines; 0 / bcl-2-Associated X Protein; 639089-54-6 / VX680; 6PLQ3CP4P3 / Etoposide; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.4.22.- / Caspases
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67. 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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68. Andersen MH, Svane IM, Kvistborg P, Nielsen OJ, Balslev E, Reker S, Becker JC, Straten PT: Immunogenicity of Bcl-2 in patients with cancer. Blood; 2005 Jan 15;105(2):728-34
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  • B-cell lymphoma 2 (Bcl-2) is a pivotal regulator of apoptotic cell death and it is overexpressed in many cancers.
  • Consequently, the Bcl-2 protein is an attractive target for drug design, and Bcl-2-specific antisense oligonucleotides or small-molecule Bcl-2 inhibitors have shown broad anticancer activities in preclinical models and are currently in several clinical trials.
  • The clinical application of immunotherapy against cancer is rapidly moving forward in multiple areas, including the adoptive transfer of anti-tumor-reactive T cells and the use of "therapeutic" vaccines.
  • Herein, we describe spontaneous T-cell reactivity against Bcl-2 in peripheral blood from patients suffering from unrelated tumor types (ie, pancreatic cancer, breast cancer, acute myeloid leukemia [AML], and chronic lymphocytic leukemia [CLL]).
  • [MeSH-minor] Acute Disease. Breast Neoplasms / immunology. Granzymes. HLA-A2 Antigen / metabolism. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Leukemia, Myeloid / immunology. Peptide Fragments / metabolism. Protein Binding. Serine Endopeptidases. T-Lymphocytes, Cytotoxic / immunology. Tumor Cells, Cultured

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  • (PMID = 15367432.001).
  • [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 / Antigens, Neoplasm; 0 / HLA-A2 Antigen; 0 / Peptide Fragments; 0 / Proto-Oncogene Proteins c-bcl-2; EC 3.4.21.- / GZMB protein, human; EC 3.4.21.- / Granzymes; EC 3.4.21.- / Serine Endopeptidases
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69. Petrovici K, Graf M, Hecht K, Reif S, Pfister K, Schmetzer H: Use of NG2 (7.1) in AML as a tumor marker and its association with a poor prognosis. Cancer Genomics Proteomics; 2010 Jul-Aug;7(4):173-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Use of NG2 (7.1) in AML as a tumor marker and its association with a poor prognosis.
  • We analyzed 70 bone marrow (BM) samples from acute myeloid leukemia (AML) patients for 11q23 aberrations and reactivity with the monoclonal antibody NG2.
  • We detected NG2(+) cells in AML cases with normal karyotype, however, not in healthy BM cells.
  • This means that NG2 qualifies as a reliable AML blast tumor marker, enabling monitoring of the course of AML independently of, although often associated with, 11q23-aberrations.
  • While 31% of the patients with NG2(+) cells responded to chemotherapy, 58% of the group with NG2(+) cells did not respond (p=0.047).
  • In conclusion, NG2 detects many, but not all 11q23 aberrations and other cases without 11q23 aberrations.
  • However, it does not react with healthy BM cells, thereby contributing to the detection of patients with poor prognosis.
  • [MeSH-major] Antigens / analysis. Biomarkers, Tumor / analysis. Leukemia, Myeloid, Acute / metabolism. Proteoglycans / analysis

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  • (PMID = 20656983.001).
  • [ISSN] 1790-6245
  • [Journal-full-title] Cancer genomics & proteomics
  • [ISO-abbreviation] Cancer Genomics Proteomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens; 0 / Biomarkers, Tumor; 0 / Proteoglycans; 0 / chondroitin sulfate proteoglycan 4
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70. Hoshino T, Matsushima T, Saitoh Y, Yamane A, Takizawa M, Irisawa H, Saitoh T, Handa H, Tsukamoto N, Karasawa M, Murakami H, Nojima Y: Sacroiliitis as an initial manifestation of acute myelogenous leukemia. Int J Hematol; 2006 Dec;84(5):421-4
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  • [Title] Sacroiliitis as an initial manifestation of acute myelogenous leukemia.
  • We herein report a 28-year-old female patient who presented with sacroiliitis as an initial manifestation of acute myelogenous leukemia (AML).
  • Although she was initially diagnosed with myelodysplastic syndrome (MDS), blasts rapidly increased and AML developed 1 month after the diagnosis of MDS with Sacroiliitis.
  • Induction chemotherapy failed to induce a complete remission of AML, but it did effectively treat the sacroiliitis.
  • However, the sacroiliitis relapsed when the leukemia cells progressed thereafter.
  • The close relationship between the occurrence of sacroiliitis and AML suggested that autoimmune sacroiliitis was a paraneoplastic phenomenon of AML in this patient.
  • Although autoimmune disorders develop in a substantial number of MDS patients, they are rarely observed in de novo AML.
  • No previous report has described sacroiliitis as the initial manifestation of de novo AML.
  • [MeSH-major] Leukemia, Myeloid, Acute. Sacroiliac Joint. Spondylitis, Ankylosing
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Blast Crisis / diagnosis. Blast Crisis / diagnostic imaging. Blast Crisis / therapy. Bone Marrow Transplantation. Fatal Outcome. Female. Humans. Radiography. Recurrence. Transplantation, Homologous


71. McGrath P, Suppiah R, Patton MA: Re-entering life: paediatric acute myeloid leukaemia at one year post treatment. Aust J Holist Nurs; 2005 Oct;12(2):23-34
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  • [Title] Re-entering life: paediatric acute myeloid leukaemia at one year post treatment.
  • To date, there is scant psychosocial research on the experience of childhood AML.
  • The findings highlight challenges associated with re-entering life post-treatment with an emphasis on the ongoing sense of uncertainty, the changed sense of normalcy, and the difficulty of returning to the hospital for check-ups.
  • A number of recommendations are made including the desirability of providing hospital space for check-ups away from the treatment area and the need for ongoing reassurance and support.
  • [MeSH-major] Attitude to Health. Holistic Health. Leukemia, Myelomonocytic, Acute / psychology. Parent-Child Relations. Parenting / psychology

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  • (PMID = 19175261.001).
  • [ISSN] 1322-8803
  • [Journal-full-title] The Australian journal of holistic nursing
  • [ISO-abbreviation] Aust J Holist Nurs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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72. Liu Z, Liu S, Xie Z, Blum W, Perrotti D, Paschka P, Klisovic R, Byrd J, Chan KK, Marcucci G: Characterization of in vitro and in vivo hypomethylating effects of decitabine in acute myeloid leukemia by a rapid, specific and sensitive LC-MS/MS method. Nucleic Acids Res; 2007;35(5):e31
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  • [Title] Characterization of in vitro and in vivo hypomethylating effects of decitabine in acute myeloid leukemia by a rapid, specific and sensitive LC-MS/MS method.
  • DNA hypermethylation is a common finding in malignant cells and has been explored as a therapeutic target for hypomethylating agents (e.g., decitabine).
  • The assay was validated in a linear range from 40 fmol to 200 pmol 5mdC.
  • This method was initially applied for characterization of decitabine-induced GDM changes in in-vitro-treated leukemia cells.
  • The clinical applicability of this method was then demonstrated in bone marrow samples from patients with acute myeloid leukemia treated with decitabine.

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  • (PMID = 17264127.001).
  • [ISSN] 1362-4962
  • [Journal-full-title] Nucleic acids research
  • [ISO-abbreviation] Nucleic Acids Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / R01 CA102031; United States / NCI NIH HHS / CA / CA102031
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; 776B62CQ27 / decitabine; B200GV71QM / 5-methyldeoxycytidine; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA (cytosine-5-)-methyltransferase 1; G9481N71RO / Deoxyguanosine; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC1865075
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73. Bao L, Wang X, Ryder J, Ji M, Chen Y, Chen H, Sun H, Yang Y, Du X, Kerzic P, Gross SA, Yao L, Lv L, Fu H, Lin G, Irons RD: Prospective study of 174 de novo acute myelogenous leukemias according to the WHO classification: subtypes, cytogenetic features and FLT3 mutations. Eur J Haematol; 2006 Jul;77(1):35-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prospective study of 174 de novo acute myelogenous leukemias according to the WHO classification: subtypes, cytogenetic features and FLT3 mutations.
  • We report a prospective study of 174 unselected adult de novo acute myeloid leukemia (AML) cases diagnosed using the WHO classification.
  • Of those, 57 (33%) were AML with recurrent cytogenetic abnormalities, 41 were (24%) AML with multilineage dysplasia, 74 (42%) were AML not otherwise categorized, and two were acute leukemias of ambiguous lineage.
  • Clonal cytogenetic abnormalities were detected in 64% of the WHO AML cases with t(15;17) (15%), t(8;21) (12%), +8 (11%), -7/del7q (8%) and del9q (5%) being the most common ones.
  • The FLT3/ITD mutations (FMS-like tyrosine kinase 3/internal tandem duplication) were observed in 12% of the WHO AML cases, which is much lower than ones in the literature, while the 6% incidence of the FLT3-activating loop mutations (either FLT3/D835 or FLT3/I836) was comparable with others.
  • [MeSH-major] Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics. Mutation. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Classification. Cytogenetic Analysis. Female. Humans. Leukocytosis / genetics. Male. Middle Aged. Prospective Studies. World Health Organization

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  • (PMID = 16573742.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [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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74. ZHANG LW, WANG Y, ZHANG CH: [A case with severity stenosis of left main artery manifested with recurrent syncope]. Zhonghua Xin Xue Guan Bing Za Zhi; 2010 Sep;38(9):844-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Aortic Valve Stenosis / diagnosis. Syncope / diagnosis

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  • (PMID = 21092658.001).
  • [ISSN] 0253-3758
  • [Journal-full-title] Zhonghua xin xue guan bing za zhi
  • [ISO-abbreviation] Zhonghua Xin Xue Guan Bing Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
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75. Glienke W, Chow KU, Bauer N, Bergmann L: Down-regulation of wt1 expression in leukemia cell lines as part of apoptotic effect in arsenic treatment using two compounds. Leuk Lymphoma; 2006 Aug;47(8):1629-38
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  • [Title] Down-regulation of wt1 expression in leukemia cell lines as part of apoptotic effect in arsenic treatment using two compounds.
  • Arsenic trioxide (As2O3) induces remission in patients with acute promyelocytic leukemia (APL).
  • The Wilms' tumor gene (wt1) is up-regulated in acute myeloid leukemia (AML) and a variety of leukemia cell lines.
  • Low concentrations of 0.1 microM arsenic induced expression of the anti-apoptotic bcl-2 gene in both cell lines HL-60 and K562.
  • After arsenic treatment of the leukemia cell lines HL-60 and K562 the up-regulation of par-4 may contribute to the induction of apoptosis rather than down-regulation of bcl-2.
  • [MeSH-major] Apoptosis / drug effects. Arsenicals / pharmacology. Carrier Proteins / genetics. Leukemia / drug therapy. WT1 Proteins / genetics

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  • (PMID = 16966277.001).
  • [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 / Apoptosis Regulatory Proteins; 0 / Arsenicals; 0 / Arsenites; 0 / Carrier Proteins; 0 / Oxides; 0 / Sodium Compounds; 0 / WT1 Proteins; 0 / WTIP protein, human; 48OVY2OC72 / sodium arsenite; S7V92P67HO / arsenic trioxide
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76. Shen Q, Chen Z, Liu XP, Xing HY, Wang M, Wang JX: [Expression of PTEN mRNA in acute leukemia and its clinical significance]. Zhonghua Xue Ye Xue Za Zhi; 2005 Aug;26(8):493-6
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  • [Title] [Expression of PTEN mRNA in acute leukemia and its clinical significance].
  • OBJECTIVE: To explore PTEN gene expression and its clinical significance in acute leukemia.
  • METHODS: The expression levels of PTEN mRNA in 5 leukemia cell lines, 87 patients with acute leukemias (AL), including 59 acute myeloid leukemia (AML), 26 acute lymphoblastic leukemia (ALL), and 2 acute hybrid leukemia, 21 AL in complete remission (AL-CR), 31 chronic myelogenous leukemia (CML) and 14 normal controls were assayed by RT-PCR.
  • RESULTS: PTEN mRNA was detected in K562 cell line, but not in Kasumi-1, HL-60, U937, Nalm-6 cell lines.
  • The decreased level of PTEN mRNA had a positive correlation with poor-prognostic factors (high white blood cell count of > or = 20 x 10(9)/L and chromosome abnormality).
  • [MeSH-major] Leukemia / metabolism. PTEN Phosphohydrolase / metabolism
  • [MeSH-minor] Cell Line, Tumor. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16383243.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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77. Rahmani M, Anderson A, Habibi JR, Crabtree TR, Mayo M, Harada H, Ferreira-Gonzalez A, Dent P, Grant S: The BH3-only protein Bim plays a critical role in leukemia cell death triggered by concomitant inhibition of the PI3K/Akt and MEK/ERK1/2 pathways. Blood; 2009 Nov 12;114(20):4507-16
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  • [Title] The BH3-only protein Bim plays a critical role in leukemia cell death triggered by concomitant inhibition of the PI3K/Akt and MEK/ERK1/2 pathways.
  • Mechanisms underlying apoptosis induced by concomitant interruption of the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase 1/2 (MEK/ERK1/2) and phosphatidylinositol 3-kinase (PI3K)/Akt pathways were investigated in human leukemia cells.
  • Inhibition of these pathways using the MEK inhibitor PD184352 or U0126 and the PI3K/Akt inhibitor perifosine strikingly induced apoptosis in multiple malignant human hematopoietic cells, and substantially reduced the colony-forming capacity of primary acute myeloblastic leukemia, but not normal CD34+ cells.
  • These events were associated with pronounced Bim up-regulation, Mcl-1 down-regulation, marked Bak/Bax conformational change accompanied by Bax membrane translocation, and a pronounced increase in Bax/Bak association.
  • Notably, knockdown of Bim, but not Bad, blocked Bak and Bax conformational change, inhibited Bax membrane translocation, diminished Bax/Bak binding, and sharply attenuated perifosine/PD184352-induced apoptosis.
  • Collectively, these findings suggest that Bim, and Mcl-1, but not Bad, integrate death signaling triggered by concomitant disruption of the PI3K/Akt and MEK1/2/ERK1/2 pathways in human leukemia cells.

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  • (PMID = 19773546.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA63753; United States / NCI NIH HHS / CA / R01 CA100866; United States / NCI NIH HHS / CA / R01 CA063753; United States / NCI NIH HHS / CA / P50CA130805; United States / NCI NIH HHS / CA / R01 CA093738; United States / NCI NIH HHS / CA / CA100866; United States / NCI NIH HHS / CA / P50 CA130805; United States / NCI NIH HHS / CA / R01 CA141703; United States / NCI NIH HHS / CA / CA93738; United States / NIDDK NIH HHS / DK / R01 DK052825; United States / NCI NIH HHS / CA / R01 CA150214
  • [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 / Apoptosis Regulatory Proteins; 0 / BAD protein, human; 0 / Bcl-2-like protein 11; 0 / Enzyme Inhibitors; 0 / Membrane Proteins; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-Associated Death Protein; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases
  • [Other-IDs] NLM/ PMC2777129
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78. Vrbanus L, Sucić M, Marković-Glamocak M, Ries S, Gjadrov-Kuvezdić K, Fabijanić I, Antulov J, Petrik J, Labar B: Apoptosis of leukemic cells: a case report. Coll Antropol; 2010 Jun;34(2):705-11
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  • However, some studies have revealed that Fas (CD95/APO1) which mediates apoptotic signal and decrease of anti-apoptotic Bcl-2 are frequently observed in acute myeloid leukemia (AML) M4/M5 leukemic cells.
  • The aim of the study was to compare cytomorphology and cytochemistry of bone marrow (BM) apoptotic leukemic cells to preserved peripheral blood (PB) leukemic cells in our patient, a 76-year-old man with AML-M5b treated at Zagreb University Hospital Center.
  • BM and PB of the AL patient were analyzed after Pappenheim and cytochemical stainings, and leukemic cells were classified according to FAB and WHO classification.
  • Thus, cytomorphology of PB leukemic cells pointed to proliferation of immature monocytic cells, and cytomorphology of BM to cell apoptosis.
  • Cytochemistry of PB monocytic cells and BM apoptotic cells confirmed monocytic cell lineage because esterase was strongly positive in almost all BM apoptotic leukemic cells and PB leukemic cells, and esterase was completely inhibited with sodium fluoride.
  • On the basis of these findings, AML-M5b was diagnosed in our patient.
  • There are many possible explanations for our observation of BM leukemic cell apoptosis in a patient with AML-M5.
  • Mass BM leukemic cell apoptosis that was recorded in contrast to numerous preserved leukemic cells in PK could be probably connected to unfavorable ratio of relatively low concentration of cytokines in relation to high leukemic cell number in BM aspirated cytologic specimen.
  • [MeSH-major] Apoptosis. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Aged. Antigens, CD95 / analysis. Blood Cells / pathology. Bone Marrow / pathology. Cell Nucleus / pathology. Cell Size. Humans. Male. Megakaryocytes / pathology. Monocytes / pathology

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  • (PMID = 20698159.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / Antigens, CD95
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79. Tang HR, Wang FC, Jiang YW, Fei X, Jiang Q, Xu WL, Lin J: [CD36 expression in leukemia cells checked with multi-parameter flow cytometry and its significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Feb;15(1):29-34
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  • [Title] [CD36 expression in leukemia cells checked with multi-parameter flow cytometry and its significance].
  • The aim of study was to investigate the expression of CD36 in leukemia cells and to explore its significance in diagnosis and differential diagnosis for leukemia in patients.
  • Blood samples from 133 cases of leukemias were analyzed by CD45/SSC double parameters and multi-color flow cytometry in order to determine the CD36 and other leukocyte differentiation antigens.
  • The results show that the CD36 positive rate was 21.8% (29/133) in 133 cases of leukemia, 41.9% (26/62) in 62 cases of AML (acute myeloid leukemia), and none of the 54 cases of lymphocytic leukemia was positive for this antigen.
  • A significantly negative regression was found between CD36 and CD117 in AML (r = -0.751, P = 0.005).
  • In monocyte lineage involved leukemia (MLIL), the positive rate of CD36 (92.6%, 25/27) was significantly higher than that of CD14 (48.1%, 13/27)(P = 0.001).
  • None of the 7 cases with M(5a) was positive for CD14, but 4 of 5 cases of M(5b) were positive.
  • It is concluded that the combination of CD36 with lymphoid and myeloid antigens is helpful to the diagnosis and differential diagnosis of lymphoid, myeloid and MLIL.

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  • (PMID = 17490515.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Antigens, CD36; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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80. Bhagwat N, Levine RL: Metabolic syndromes and malignant transformation: where the twain shall meet. Sci Transl Med; 2010 Oct 20;2(54):54ps50
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  • Recurrent somatic mutations in the isocitrate dehydrogenase 1 (IDH1) and IDH2 genes that result in the accumulation of D-2-hydroxyglutarate (D-2-HG) have been identified in malignant gliomas and in acute myeloid leukemia (AML).
  • A report in the current issue of Science describes a germline IDH2 mutation in a subset of patients with a rare metabolic disorder--D-2-hydroxyglutaric aciduria-that is similar to mutations seen in cancer patients.
  • [MeSH-major] Cell Transformation, Neoplastic. Glioma / complications. Glutarates / metabolism. Leukemia, Myeloid, Acute / complications. Metabolism, Inborn Errors / complications

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  • (PMID = 20962328.001).
  • [ISSN] 1946-6242
  • [Journal-full-title] Science translational medicine
  • [ISO-abbreviation] Sci Transl Med
  • [Language] eng
  • [Grant] United States / Howard Hughes Medical Institute / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glutarates; 2889-31-8 / alpha-hydroxyglutarate; EC 1.1.1.41 / Isocitrate Dehydrogenase
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81. Hiramatsu A, Miwa H, Shikami M, Ikai T, Tajima E, Yamamoto H, Imai N, Hattori A, Kyo T, Watarai M, Miura K, Satoh A, Itoh M, Imamura A, Mihara H, Katoh Y, Nitta M: Disease-specific expression of VEGF and its receptors in AML cells: possible autocrine pathway of VEGF/type1 receptor of VEGF in t(15;17) AML and VEGF/type2 receptor of VEGF in t(8;21) AML. Leuk Lymphoma; 2006 Jan;47(1):89-95
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  • [Title] Disease-specific expression of VEGF and its receptors in AML cells: possible autocrine pathway of VEGF/type1 receptor of VEGF in t(15;17) AML and VEGF/type2 receptor of VEGF in t(8;21) AML.
  • Various angiogenic factors, such as vascular endothelial growth factor (VEGF) and an associated molecule, placenta growth factor (PlGF), are thought to be important for normal and malignant hematopoiesis.
  • This study examined mRNA expression of VEGF, PlGF and receptors for these molecules in AML cells and identified the disease-specific patterns of expression.
  • AML M3 having t(15;17) abnormality showed highest expression of VEGF and VEGF receptor type 1 (VEGFR1), suggesting the autocrine pathway of VEGF-VEGFR1.
  • Then, t(8;21) AML demonstrated augmented expression of VEGF and VEGF receptor type 2 (VEGFR2), suggesting VEGF-VEGFR2 autocrine pathway.
  • Then, addition of VEGFR2 kinase inhibitor in Kasumi-1, a t(8;21) AML cell line, resulted in marked inhibition of cell growth, although growth inhibitory effect of R2 kinase inhibitor to HL-60 was marginal.
  • In addition, cell cycle analysis study showed S-phase cell population reduction by R2 kinase inhibitor in Kasumi-1, but not in HL-60.
  • This observation is thought to be the rationale for novel molecular target therapy directed to angiogenic molecules.
  • [MeSH-major] Autocrine Communication / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor Receptor-1 / genetics. Vascular Endothelial Growth Factor Receptor-2 / genetics
  • [MeSH-minor] Adult. Aged. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. Cell Proliferation / drug effects. Chromosome Aberrations. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Disease. Enzyme Inhibitors / pharmacology. Gene Expression Regulation, Leukemic / genetics. HL-60 Cells. Humans. Middle Aged. Pregnancy Proteins / biosynthesis. Pregnancy Proteins / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 16465716.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Pregnancy Proteins; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; 144589-93-5 / placenta growth factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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82. Piloto O, Wright M, Brown P, Kim KT, Levis M, Small D: Prolonged exposure to FLT3 inhibitors leads to resistance via activation of parallel signaling pathways. Blood; 2007 Feb 15;109(4):1643-52
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  • To study resistance to TKIs targeting FLT3, a receptor tyrosine kinase that is frequently mutated in acute myelogenous leukemia (AML), we developed resistant human cell lines through prolonged coculture with FLT3 TKIs.
  • FLT3 TKI-resistant cell lines and primary samples still exhibit inhibition of FLT3 phosphorylation on FLT3 TKI treatment.
  • However, FLT3 TKI-resistant cell lines and primary samples often show continued activation of downstream PI3K/Akt and/or Ras/MEK/MAPK signaling pathways as well as continued expression of genes involved in FLT3-mediated cellular transformation.
  • Mutational screening of FLT3 TKI-resistant cell lines revealed activating N-Ras mutations in 2 cell lines that were not present in the parental FLT3 TKI-sensitive cell line.

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  • (PMID = 17047150.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090668; United States / NCI NIH HHS / CA / P01 CA070970; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / CA70970; United States / NCI NIH HHS / CA / K23 CA111728; United States / NCI NIH HHS / CA / CA111728; United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / CA90668; United States / NCI NIH HHS / CA / CA95600-03; United States / NCI NIH HHS / CA / K08 CA095600
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ PMC1794049
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83. Chang PH, Lai YH, Shun SC, Lin LY, Chen ML, Yang Y, Tsai JC, Huang GS, Cheng SY: Effects of a walking intervention on fatigue-related experiences of hospitalized acute myelogenous leukemia patients undergoing chemotherapy: a randomized controlled trial. J Pain Symptom Manage; 2008 May;35(5):524-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of a walking intervention on fatigue-related experiences of hospitalized acute myelogenous leukemia patients undergoing chemotherapy: a randomized controlled trial.
  • The purpose of this randomized, controlled clinical trial was to preliminarily examine the effects of a three-week walking exercise program (WEP) on fatigue-related experiences of acute myelogenous leukemia (AML) patients receiving chemotherapy.
  • Eligible AML patients were randomly assigned to either an experimental group (n=11), which received 12 minutes of WEP per day, five days per week for three consecutive weeks, or to a control group (n=11), which received standard ward care.
  • Data were analyzed by Generalized Estimating Equation and revealed that AML patients in the three-week WEP group had a significantly greater increase in 12-minute walking distance than the control group.
  • Although preliminary, our results strongly suggest that three weeks of systematic walking exercise is clinically feasible for AML patients undergoing chemotherapy and can effectively improve their fatigue-related experiences.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Exercise Therapy. Fatigue / etiology. Fatigue / therapy. Leukemia, Myeloid, Acute / complications. Walking / physiology


84. Forestier E, Izraeli S, Beverloo B, Haas O, Pession A, Michalová K, Stark B, Harrison CJ, Teigler-Schlegel A, Johansson B: Cytogenetic features of acute lymphoblastic and myeloid leukemias in pediatric patients with Down syndrome: an iBFM-SG study. Blood; 2008 Feb 1;111(3):1575-83
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  • [Title] Cytogenetic features of acute lymphoblastic and myeloid leukemias in pediatric patients with Down syndrome: an iBFM-SG study.
  • Children with Down syndrome (DS) have a markedly increased risk of acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).
  • To identify chromosomal changes cooperating with +21 that may provide information on the pathogenesis of these leukemias, we analyzed 215 DS-ALLs and 189 DS-AMLs.
  • Unlike previous smaller series, a significant proportion of DS-ALLs had the typical B-cell precursor ALL abnormalities high hyperdiploidy (HeH; 11%) and t(12;21)(p13;q22) (10%).
  • The HeH DS-ALLs were characterized by gains of the same chromosomes as non-DS-HeH, suggesting the same etiology/pathogenesis.
  • Unlike DS-ALL, the common translocations associated with non-DS-AML were rare in DS-AML, which instead were characterized by the frequent presence of dup(1q), del(6q), del(7p), dup(7q), +8, +11, del(16q), and +21.
  • This series of DS leukemias-the largest to date-reveals that DS-ALL is a heterogeneous disorder that comprises both t(12;21) and HeH as well as DS-related abnormalities.
  • Furthermore, this analysis confirms that DS-AML is a distinct entity, originating through other genetic pathways than do non-DS-AMLs, and suggests that unbalanced changes such as dup(1q), +8, and +21 are involved in the leukemogenic process.
  • [MeSH-major] Down Syndrome / complications. Down Syndrome / genetics. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Chromosome Aberrations / classification. Chromosomes, Human / genetics. Cytogenetics. Female. Genome, Human / genetics. Humans. Infant. Infant, Newborn. Karyotyping. Male


85. Chehensse C, Braun T, Morin AS, Stirnemann J, Agranat P, Boukari L, Aras N, Kiladjian JJ, Ziol M, Fenaux P, Fain O: [Extramedullary blastic transformation revealed by a prolonged fever during the course of a 5q- syndrome]. Rev Med Interne; 2009 Oct;30(10):886-9
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  • [Title] [Extramedullary blastic transformation revealed by a prolonged fever during the course of a 5q- syndrome].
  • INTRODUCTION: Fever during a myelodysplastic syndrome can be due to infectious complications, systemic disease or acute transformation with clonal evolution.
  • Neither bone marrow nor blood blasts were detected, but liver biopsy demonstrated significant blast infiltration compatible with the diagnosis of acute myeloid leukaemia (AML).
  • CONCLUSION: The absence of blasts in blood or bone marrow does not exclude the malignant transformation of a myelodysplastic syndrome to AML.


86. Unal S, Cakir M, Kuşkonmaz B, Cetin M, Tuncer AM: Successful treatment with gemtuzumab ozogamicin monotherapy in a pediatric patient with resistant relapse of acute myeloid leukemia. Turk J Pediatr; 2009 Jan-Feb;51(1):69-71
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  • [Title] Successful treatment with gemtuzumab ozogamicin monotherapy in a pediatric patient with resistant relapse of acute myeloid leukemia.
  • There are few therapeutic options in relapsed or refractory acute myeloid leukemia patients.
  • Herein, we present a 15-year-old acute myeloid leukemia patient who was resistant at relapse and could achieve remission with gemtuzumab ozogamicin at a total dose of 9 mg/m2, divided into three doses and delivered to hematopoietic stem-cell transplantation; however, the patient relapsed in a short time without application of transplantation.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adolescent. Antibodies, Monoclonal, Humanized. Antigens, CD / blood. Antigens, Differentiation, Myelomonocytic / blood. Hematopoietic Stem Cell Transplantation. Humans. Leukocyte Count. Male. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 19378895.001).
  • [ISSN] 0041-4301
  • [Journal-full-title] The Turkish journal of pediatrics
  • [ISO-abbreviation] Turk. J. Pediatr.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
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87. Walter K, Cockerill PN, Barlow R, Clarke D, Hoogenkamp M, Follows GA, Richards SJ, Cullen MJ, Bonifer C, Tagoh H: Aberrant expression of CD19 in AML with t(8;21) involves a poised chromatin structure and PAX5. Oncogene; 2010 May 20;29(20):2927-37
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  • [Title] Aberrant expression of CD19 in AML with t(8;21) involves a poised chromatin structure and PAX5.
  • Co-expression of lymphoid and myeloid molecules is a well-known feature of acute myeloblastic leukemia (AML) with t(8;21).
  • These cells consistently express the B-cell-specific transcription factor PAX5, and the B-cell-specific cell surface protein CD19.
  • We show that CD19 chromatin exists in a poised configuration in myeloid progenitors and that this poised chromatin structure facilitates PAX5-dependent CD19 activation.
  • Our results also show a positive correlation between PAX5 and CD19 expression in t(8;21)-positive AML cells and demonstrate that PAX5 binds to the promoter and enhancer of CD19 gene and remodels chromatin structure at the promoter.
  • This study shows that expression of PAX5 in leukemic cells has functional consequences and points to an important role of a progenitor-specific chromatin configuration in myeloid leukemia.
  • [MeSH-major] Antigens, CD19 / genetics. B-Cell-Specific Activator Protein / genetics. Chromatin / chemistry. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 20208555.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / B-Cell-Specific Activator Protein; 0 / Chromatin; 0 / PAX5 protein, human
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88. Scholl S, Theuer C, Scheble V, Kunert C, Heller A, Mügge LO, Fricke HJ, Höffken K, Wedding U: Clinical impact of nucleophosmin mutations and Flt3 internal tandem duplications in patients older than 60 yr with acute myeloid leukaemia. Eur J Haematol; 2008 Mar;80(3):208-15
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  • [Title] Clinical impact of nucleophosmin mutations and Flt3 internal tandem duplications in patients older than 60 yr with acute myeloid leukaemia.
  • BACKGROUND: Nucleophosmin (NPM1) and Flt3 internal tandem duplications (Flt3-ITD mutations) represent the most frequent molecular aberrations in patients with acute myeloid leukemia (AML).
  • While NPM1 mutations are associated with favourable prognosis in younger AML patients, Flt3-ITD mutations reflect an unfavourable prognostic factor in these patients.
  • So far, especially NPM1 mutations have not yet been evaluated exclusively in older patients.
  • PATIENTS AND METHODS: We retrospectively analysed the prevalence of NPM1 and Flt3-ITD mutations and its association with complete remission (CR), and survival in 99 elderly patients (median age 71 yr, range 60-85 yr) newly diagnosed for AML.
  • Interestingly, there is no significant difference in overall survival between group 1 and group 2 (Log-rank test P = 0.22, median 440 d vs. 1125 d).
  • In contrast, patients carrying a Flt3-ITD mutation had a significant worse overall survival compared to wildtype patients (P = 0.03, median 210 d for group 3 + 4 vs. 634 d for group 1 + 2) while no difference of CR rate could be observed (42.8% vs. 48.9%, P = 0.91).
  • CONCLUSION: As elderly but medically fit patients with AML carrying a NPM1 mutation have a high CR rate, age itself should not be a barrier for induction treatment.
  • However, new therapeutic concepts of postremission therapy (e.g. allogeneic stem cell transplantation after dose-reduced conditioning) should be considered for these patients in first CR.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Aged. Aged, 80 and over. Cohort Studies. Disease-Free Survival. Female. Gene Frequency. Humans. Male. Middle Aged. Prognosis. Remission Induction. Retrospective Studies

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  • (PMID = 18081718.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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89. Di Cataldo A, La Spina M, Bertuna G, Lo Nigro L, Branciforte F, Castagnola E: Spleen and lung involvement by Acinetobacter calcoaceticus bacteremia mimicking deep fungal infection in a child with acute non-lymphoblastic leukemia. Pediatr Blood Cancer; 2006 Feb;46(2):266
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  • [Title] Spleen and lung involvement by Acinetobacter calcoaceticus bacteremia mimicking deep fungal infection in a child with acute non-lymphoblastic leukemia.
  • [MeSH-major] Acinetobacter Infections / drug therapy. Acinetobacter calcoaceticus. Anti-Infective Agents / administration & dosage. Ciprofloxacin / administration & dosage. Leukemia, Myeloid, Acute / complications


90. Ishikawa T, Kakumu S: Combination therapy with lamivudine and HB vaccine on chronic hepatitis B. Hepatol Res; 2007 Jul;37(s1):S62-6
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  • BACKGROUND AND AIM: Lamivudine (LAM) has problems of breakthrough hepatitis (BTH) and post-treatment relapse despite its significant effect for suppressing hepatitis B virus (HBV) replication.
  • In order to find solutions for the problems, the efficacy of combination therapy of LAM plus hepatitis B (HB) vaccine in patients with chronic HBV infection was assessed.
  • PATIENTS AND METHODS: Fifty-three patients with chronic hepatitis B, 33 hepatitis B e-antigen positive (HBeAg+), and 20 HBeAg negative (HBeAg-) patients, were enrolled in the study, and randomized to receive either LAM monotherapy or combination therapy of LAM and HB vaccine.
  • In the combination therapy group, 100 mg/day of LAM was administered as a baseline therapy, and 10 mug of HB vaccine was injected subcutaneously every month starting at 2 months after LAM administration, six times in total.
  • RESULTS: HBeAg negative patients responded well to LAM therapy, and there were no significant differences in short-term effects between the two therapy groups.
  • Regardless of HBeAg serologic status or therapy protocols, post-treatment relapse was seen in most patients when the administrations of LAM were discontinued.
  • CONCLUSION: Combination therapy of LAM and HB vaccine is a safe and effective way to control HBV replication and prevent the development of BTH especially in patients with high viral load.
  • However, further study is required in order to achieve the continuous suppression of HBV replication even after cessation of LAM.

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  • (PMID = 17627638.001).
  • [ISSN] 1386-6346
  • [Journal-full-title] Hepatology research : the official journal of the Japan Society of Hepatology
  • [ISO-abbreviation] Hepatol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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91. Seyama K, Kumasaka T, Souma S, Sato T, Kurihara M, Mitani K, Tominaga S, Fukuchi Y: Vascular endothelial growth factor-D is increased in serum of patients with lymphangioleiomyomatosis. Lymphat Res Biol; 2006;4(3):143-52
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  • BACKGROUND: Lymphangioleiomyomatosis (LAM) is a rare destructive lung disease characterized by an abnormal proliferation of smooth muscle-like cells (LAM cells) in the lung and along the axial lymphatics.
  • LAM demonstrates a heterogeneous clinical course, but there is no serum surrogate marker available for assessing the disease severity or predicting the disease progression.
  • Since the authors have recently demonstrated the extensive LAM-associated lymphangiogenesis and its potential role in progression and metastasis of LAM cells, they hypothesized that serum levels of lymphangiogenic growth factors might be increased in LAM and become a surrogate marker for disease severity.
  • METHODS AND RESULTS: VEGF-A, VEGF-C, and VEGF-D in serum of 44 patients with LAM were measured by enzyme-linked immunosorbant assay.
  • Only VEGF-D was significantly increased in LAM patients as compared with age- and gender-matched healthy volunteers (n=24) (LAM vs. control, geometric mean 95% CI; 1069.3 pg/mL (809.4 approximately 1412.6) vs. 295.9 pg/mL (262.6 approximately 333.5), p<0.0001).
  • Immunohistochemical examination of lung specimens demonstrated the positive immunoreactivity of LAM cells for VEGF-D.
  • CONCLUSION: Serum VEGF-D levels may be a valuable surrogate marker for evaluating the disease severity in LAM.

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  • (PMID = 17034294.001).
  • [ISSN] 1539-6851
  • [Journal-full-title] Lymphatic research and biology
  • [ISO-abbreviation] Lymphat Res Biol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hormones; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C; 0 / Vascular Endothelial Growth Factor D
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92. 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


93. Rheingold SR: Acute myeloid leukemia in a child with hereditary thrombocytopenia. Pediatr Blood Cancer; 2007 Jan;48(1):105-7
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  • [Title] Acute myeloid leukemia in a child with hereditary thrombocytopenia.
  • A child with a known diagnosis of an autosomal dominant macrothrombocytopenia, Fechtner Syndrome, developed acute myeloid leukemia (AML).
  • Recently the disease gene for the inherited macrothrombocytopenias has been identified as MYH9, encoding for non-muscle myosin heavy chain-A.
  • MYH9 has never been associated with the development of acute leukemia, but MYH11 is disrupted in the M4 eosinophilia sub-type of AML (inv16).
  • The patients leukemic blasts did carry the common t(8;21) which yields an AML1-ETO fusion protein that inhibits AML-1.
  • [MeSH-major] Blood Coagulation Disorders, Inherited / genetics. Chromosome Disorders / genetics. Leukemia, Myeloid, Acute / genetics. Thrombocytopenia / genetics

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16276527.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / MYH9 protein, human; 0 / Molecular Motor Proteins; 0 / Oncogene Proteins, Fusion; EC 3.6.4.1 / Myosin Heavy Chains
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94. Shimoyama M, Yamamoto K, Nishikawa S, Minagawa K, Katayama Y, Matsui T: Duplication of isodicentric chromosome 21, idic(21)(p11.2), leading to pentasomy 21q in acute myeloid leukemia with multilineage dysplasia. Cancer Genet Cytogenet; 2009 Oct;194(1):38-43
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  • [Title] Duplication of isodicentric chromosome 21, idic(21)(p11.2), leading to pentasomy 21q in acute myeloid leukemia with multilineage dysplasia.
  • Isodicentric chromosome 21, idic(21)(p11.2), is a rare but recurrent cytogenetic aberration in acute lymphoblastic leukemia.
  • We describe here a novel case of acute myeloid leukemia (AML) with double idic(21)(p11.2).
  • A 35-year-old man was diagnosed as having de novo AML with multilineage dysplasia because of 30% myeloperoxidase-positive blasts and trilineage dysplasia in the bone marrow.
  • These results suggest that the idic(21)(p11.2) could be implicated also in the pathogenesis of AML through amplification of genes including RUNX1 located on 21q.
  • [MeSH-major] Aneuploidy. Chromosomes, Human, Pair 21 / genetics. Gene Duplication. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / blood. Antigens, CD13 / blood. Antigens, CD34 / blood. Antigens, CD7 / blood. Antigens, Differentiation, Myelomonocytic / blood. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. HLA-DR Antigens / blood. Humans. In Situ Hybridization, Fluorescence. Male. Sialic Acid Binding Ig-like Lectin 3. Spectral Karyotyping

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  • (PMID = 19737652.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, CD7; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / HLA-DR Antigens; 0 / RUNX1 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
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95. Abdel Alim A, Youssef SR, Farouk HM: The prognostic potential of bone marrow cyclin E and P27, in Egyptian patients with acute myeloid leukemia. Egypt J Immunol; 2010;17(1):9-18
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  • [Title] The prognostic potential of bone marrow cyclin E and P27, in Egyptian patients with acute myeloid leukemia.
  • Aberrations in the cell cycle control are often observed in tumors and might even be mandatory in tumor development.
  • There are few molecular biologic determinants that may be prognostic for patients with acute myeloid leukemia (AML).
  • To investigate the importance of cell cycle defects in AML, the cellular levels of cyclin E and the cyclin-dependent kinase inhibitor P27 (Kip 1) were evaluated in thirty AML patients (11 males and 19 females) diagnosed by standard clinical, morphological and immunophenotypic criteria and staged according to the FAB classification.
  • Using immunoblot analysis, cyclin E and P27 were detected in blast cells of AML patients who were then treated by the standard AML chemotherapeutic protocol and were followed up.
  • With respect to cyclin E, it was detected in 9/30(30%) AML cases among them 13.3% (4/30 cases) exhibited very strong bands while 16.6% (5/30 cases) showed faint bands.
  • Cyclin E was high among M4/M5 cases and low among M3 cases and showed a statistically significant positive correlation with percentage of blast cells, aberrant phenotype and abnormal karyotype at diagnosis.
  • All our AML cases exhibited P27 at low and high levels as seen in 19/30 (63.4%) and 11/30 (36.6%) cases, respectively.
  • P27 showed a statistically significant negative correlation to the percentage of blasts at diagnosis and a significant positive correlation with achievement of CR.
  • The present study suggested that levels of cell cycle regulators cyclin E and P27 can be used as a useful prognostic molecular markers in AML patients.

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  • (PMID = 22053605.001).
  • [ISSN] 1110-4902
  • [Journal-full-title] The Egyptian journal of immunology
  • [ISO-abbreviation] Egypt J Immunol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cyclin E; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
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96. Rytting M, Ravandi F, Estey E, Cortes J, Faderl S, Garcia-Manero G, Jeha S, Ouzounian S, Pierce S, Kantarjian H: Intensively timed combination chemotherapy for the induction of adult patients with acute myeloid leukemia: long-term follow-up of a phase 2 study. Cancer; 2010 Nov 15;116(22):5272-8
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  • [Title] Intensively timed combination chemotherapy for the induction of adult patients with acute myeloid leukemia: long-term follow-up of a phase 2 study.
  • BACKGROUND: Despite advances in therapy, the majority of adult patients diagnosed with acute myeloid leukemia (AML) develop disease recurrence and die of their disease.
  • Early intensification of treatment for AML using timed sequential therapy (TST) has been proposed as a means of improving the survival outcome in children.
  • The Children's Cancer Group demonstrated that children with AML who were randomized to receive 2 courses of daunorubicin, cytarabine, thioguanine, etoposide, and dexamethasone (the DCTER regimen) given 10 days apart had an improved event-free survival (EFS) and disease-free survival (DFS) (42% ± 7% and 55% ± 9%, respectively, at 2 years).
  • Reports have suggested an improved outcome in adult patients with AML using TST (at the cost of increased toxicity).
  • The current study was conducted to evaluate the feasibility and effectiveness of the intensively timed DCTER regimen for non-core-binding factor AML in adult patients aged <50 years.
  • The timed sequential DCTER regimen had a lower complete remission (CR) rate when compared with the IA combination,, (71% vs 80%, respectively), but this appeared to be counterbalanced by a higher long-term leukemia-free survival rate using the intensified regimen (48% vs 30%, respectively) in patients who achieved a CR (P = .06).
  • CONCLUSIONS: The intensively timed regimen of DCTER was found to induce durable remissions in adult patients with AML, including those patients with high-risk disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Myeloid, Acute / drug therapy

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  • [Copyright] Copyright © 2010 American Cancer Society.
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  • (PMID = 20665501.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; FTK8U1GZNX / Thioguanine; ZS7284E0ZP / Daunorubicin; DCTER protocol
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97. Bullinger L, Krönke J, Schön C, Radtke I, Urlbauer K, Botzenhardt U, Gaidzik V, Carió A, Senger C, Schlenk RF, Downing JR, Holzmann K, Döhner K, Döhner H: Identification of acquired copy number alterations and uniparental disomies in cytogenetically normal acute myeloid leukemia using high-resolution single-nucleotide polymorphism analysis. Leukemia; 2010 Feb;24(2):438-49
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of acquired copy number alterations and uniparental disomies in cytogenetically normal acute myeloid leukemia using high-resolution single-nucleotide polymorphism analysis.
  • As acute myeloid leukemia (AML) represents a genetically heterogeneous disease, this technology might prove helpful, especially for cytogenetically normal AML (CN-AML) cases.
  • Thus, we performed high-resolution SNP analyses in 157 adult cases of CN-AML.
  • Furthermore, we identified two cases with a cryptic t(6;11) as well as several non-recurrent aberrations pointing to leukemia-relevant regions.
  • These data show the potential of high-resolution SNP analysis for identifying genomic regions of potential pathogenic and clinical relevance in AML.
  • [MeSH-major] Gene Dosage. Leukemia, Myeloid, Acute / genetics. Polymorphism, Single Nucleotide / genetics. Uniparental Disomy / genetics

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  • (PMID = 20016533.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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98. Fischbach NA, Rozenfeld S, Shen W, Fong S, Chrobak D, Ginzinger D, Kogan SC, Radhakrishnan A, Le Beau MM, Largman C, Lawrence HJ: HOXB6 overexpression in murine bone marrow immortalizes a myelomonocytic precursor in vitro and causes hematopoietic stem cell expansion and acute myeloid leukemia in vivo. Blood; 2005 Feb 15;105(4):1456-66
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  • [Title] HOXB6 overexpression in murine bone marrow immortalizes a myelomonocytic precursor in vitro and causes hematopoietic stem cell expansion and acute myeloid leukemia in vivo.
  • Dysregulated HOX gene expression profoundly effects the proliferation and differentiation of hematopoietic stem cells (HSCs) and committed progenitors, and aberrant activation of HOX genes is a common event in human myeloid leukemia.
  • HOXB6 is frequently overexpressed in human acute myeloid leukemia (AML).
  • We also explored structure-function relationships using mutant HOXB6 proteins unable to bind to DNA or a key HOX-binding partner, pre-B-cell leukemia transcription factor-1 (PBX1).
  • Additionally, we investigated the potential cooperative interaction with myeloid ecotropic viral integration site 1 homolog (MEIS1).
  • In vivo, HOXB6 expanded HSCs and myeloid precursors while inhibiting erythropoiesis and lymphopoiesis.
  • Overexpression of HOXB6 resulted in AML with a median latency of 223 days.
  • Coexpression of MEIS1 dramatically shortened the onset of AML.
  • Cytogenetic analysis of a subset of HOXB6-induced AMLs revealed recurrent deletions of chromosome bands 2D-E4, a region frequently deleted in HOXA9-induced AMLs.
  • In vitro, HOXB6 immortalized a factor-dependent myelomonocytic precursor capable of granulocytic and monocytic differentiation.
  • [MeSH-major] Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Cell Transformation, Neoplastic / pathology. Homeodomain Proteins / biosynthesis. Homeodomain Proteins / genetics. Leukemia, Myeloid / blood. Myeloid Progenitor Cells / metabolism. Myeloid Progenitor Cells / pathology
  • [MeSH-minor] Acute Disease. Animals. Cell Differentiation / genetics. Cell Line, Transformed. Cell Proliferation. Erythropoiesis / genetics. Female. Karyotyping. Lymphopoiesis / genetics. Mice. Mice, Congenic. Mice, Inbred C57BL. Neoplasm Proteins / physiology. Phenotype. Time Factors

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  • (PMID = 15522959.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK48642
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Hoxb6 protein, mouse; 0 / Neoplasm Proteins; 0 / myeloid ecotropic viral integration site 1 protein
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99. Ferrara F, D'Arco AM, De Simone M, Mele G, Califano C, Pocali B, Danise P, Palmieri S: Fludarabine and cytarabine as continuous sequential infusion for elderly patients with acute myeloid leukemia. Haematologica; 2005 Jun;90(6):776-84
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  • [Title] Fludarabine and cytarabine as continuous sequential infusion for elderly patients with acute myeloid leukemia.
  • BACKGROUND AND OBJECTIVES: A phase II study was conducted to investigate the effects of a therapeutic program based on the combination of fludarabine and cytarabine (ARA-C) administered as a sequential continuous infusion in untreated elderly patients with acute myeloid leukemia (AML).
  • DESIGN AND METHODS: Sixty-three patients with non-M3 AML, median age 69 years (range 61-81), were accrued.
  • Twenty-four patients (38%) had AML secondary to myelodysplastic syndrome.
  • Patients achieving complete remission (CR) were intended to receive an additional course, followed by autologous stem cell transplantation (ASCT).
  • The median overall and disease-free survival were both 10 months.
  • Results in terms of CR achievement, CD34+ cell collection and ASCT feasibility.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Vidarabine / analogs & derivatives
  • [MeSH-minor] Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Disease-Free Survival. Female. Humans. Male. Middle Aged. Myelodysplastic Syndromes / complications. Stem Cell Transplantation. Treatment Outcome

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  • (PMID = 15951290.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD34; 04079A1RDZ / Cytarabine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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100. Balaian L, Ball ED: Cytotoxic activity of gemtuzumab ozogamicin (Mylotarg) in acute myeloid leukemia correlates with the expression of protein kinase Syk. Leukemia; 2006 Dec;20(12):2093-101
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  • [Title] Cytotoxic activity of gemtuzumab ozogamicin (Mylotarg) in acute myeloid leukemia correlates with the expression of protein kinase Syk.
  • Acute myeloid leukemia (AML) cells express the cell surface antigen CD33 that, upon ligation with a monoclonal antibody (mAb), is a downregulator of cell growth in a Syk-dependent manner.
  • An anti-CD33 mAb coupled to a toxin, gemtuzumab ozogamicin (GO), is used for the treatment of AML (Mylotarg).
  • Therefore, we investigated whether the response of AML cells to GO treatment also depends on Syk expression.
  • Forty primary AML samples (25 Syk-positive and 15 Syk-negative) were tested for their response to the anti-proliferative effects of GO and unmodified anti-CD33 mAb.
  • A correlation between Syk expression and the response of leukemia cells to GO and anti-CD33 mAb was found.
  • 'Blocking' of Syk by small interfering RNA resulted in unresponsiveness of AML cells to both GO and anti-CD33 mAb-mediated cytotoxicity.
  • Syk upregulation by the de-methylating agent 5-azacytidine (5-aza) induced re-expression of Syk in some cases, resulting in enhanced GO and anti-CD33-mediated inhibition of leukemia cell growth.
  • Thus, the cytotoxicity of both GO and anti-CD33 in primary AML samples was associated with Syk expression.
  • 5-Aza restored Syk and increased the sensitivity of originally Syk-negative, non-responsive cells to CD33 ligation to levels of Syk-positive cells.
  • [MeSH-major] Aminoglycosides / pharmacology. Antibodies, Monoclonal / pharmacology. Antineoplastic Agents / pharmacology. Immunotoxins / pharmacology. Intracellular Signaling Peptides and Proteins / analysis. Leukemia, Myeloid, Acute / drug therapy. Protein-Tyrosine Kinases / analysis
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Azacitidine / pharmacology. Cell Line, Tumor. Humans. RNA, Small Interfering. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 17051243.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Immunotoxins; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Syk kinase; M801H13NRU / Azacitidine
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