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1. Villiers E, Baines S, Law AM, Mallows V: Identification of acute myeloid leukemia in dogs using flow cytometry with myeloperoxidase, MAC387, and a canine neutrophil-specific antibody. Vet Clin Pathol; 2006 Mar;35(1):55-71
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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 acute myeloid leukemia in dogs using flow cytometry with myeloperoxidase, MAC387, and a canine neutrophil-specific antibody.
  • BACKGROUND: Flow cytometry may be used to determine immunophenotype or lineage of leukemic cells, but few antibodies are available that are specific for cells of monocytic and granulocytic lineage.
  • OBJECTIVE: The purpose of this study was to evaluate the flow cytometric staining patterns of 3 commercial monoclonal antibodies for monocytes and granulocytes in clinically healthy dogs and in dogs with acute myeloid leukemia (AML).
  • METHODS: Mouse antihuman macrophage antibody (MAC387), mouse anti-human myeloperoxidase (MPO), and a canine neutrophil-specific antibody (NSA) were evaluated using flow cytometry on blood from 6 clinically healthy control dogs, and on blood (n = 7) and/or bone marrow (n = 2) from 8 dogs with AML.
  • A diagnosis of acute leukemia was confirmed by >30% blasts in bone marrow or >30% blasts in peripheral blood, together with bi- or pancytopenia, circulating CD34-positive blast cells, and clinical signs of disease.
  • One case was classified as AML of granulocytic lineage (AML-M1), 6 cases were classified as acute monocytic leukemia (AML-M5), and 1 case was classified as acute myelomonocytic leukemia (AML-M4).
  • Neoplastic myeloblasts in the dog with granulocytic AML were positive for MPO, NSA, MAC387, and CD4.
  • All monoblasts from the dogs with AML-M5 were positive for CD14, 5 of 6 were positive for MAC387, and 2 were positive for MPO.
  • NSA staining was negative in the 2 dogs with AML-M5 in which it was evaluated.
  • In the dog with AML-M4 variable percentages of blast cells were positive for CD14, MPO, MAC387, CD4, and NSA.
  • These 3 antibodies may be useful as part of a wider panel for immunophenotyping AML in dogs.

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  • (PMID = 16511792.001).
  • [ISSN] 0275-6382
  • [Journal-full-title] Veterinary clinical pathology
  • [ISO-abbreviation] Vet Clin Pathol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; EC 1.11.1.7 / Peroxidase
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2. Abdel Rahman H, Farrag SA, El-Attar IA: AML1/ETO Fusion Gene in de novo Pediatric Acute Myeloid Leukemia: Clinical Significance and Prognostic Implications. J Egypt Natl Canc Inst; 2007 Mar;19(1):39-47
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  • [Title] AML1/ETO Fusion Gene in de novo Pediatric Acute Myeloid Leukemia: Clinical Significance and Prognostic Implications.
  • The characterization of leukemia-associated chromosome translocations has contributed relevant insights into our understanding of leukemia pathogenesis and has provided new specific tumor markers essential in prognostic assessment and minimal residual disease studies.
  • The aim of this work is to study the frequency of AML1/ETO fusion gene in a series of Egyptian childhood AML cases.
  • The clinical significance and prognostic implications of this aberration, including CR rate, duration of first CR, extramedullary leukemia (EML), and survival are investigated as well.
  • Peripheral blood and/or bone marrow mononuclear cells were available for analysis from 78 children, all newly diagnosed with AML.
  • Patients with de novo AML were treated by 2 courses of induction chemotherapy, followed by 4 courses of consolidation treatment if the patient achieved complete remission (CR).
  • Seven cases (46.67%) belonged to FAB subtype M1, 7 (46.67%) M2, while only one case (6.67%) belonged to M5a subtype.
  • Lymph nodes were enlarged in 8/15 cases (53.34%), hepatomegly was observed in 4/15 cases (26.67%), splenomegaly in 8/15 cases (53.34%), purpura in 6/15 cases (40%), while pallor was observed in all fifteen cases.Extramedullary leukemia occurred in 4/15 cases (26.67%).
  • In conclusion, we report a frequency of 19.2% of AML1/ETO fusion gene in our newly diagnosed pediatric AML cases.
  • Key Words: Pediatric acute myeloid leukemia , AML1/ETO fusion gene , RT-PCR , Clinical outcome , Prognostic significance.

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  • (PMID = 18839034.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
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3. Mukaiyama Y, Hashino S, Onozawa M, Okada K, Takahata M, Kahata K, Asaka M: [Pyogenic spondylitis following unrelated hematopoietic stem cell transplantation]. Rinsho Ketsueki; 2009 Dec;50(12):1706-10
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  • The patient was a 56-year-old female with AML-M1 who underwent allogeneic HSCT in our hospital.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / adverse effects. Immunocompromised Host. Spondylitis / diagnosis. Spondylitis / etiology
  • [MeSH-minor] Anti-Bacterial Agents / administration & dosage. Back Pain / etiology. Diagnosis, Differential. Female. Humans. Leukemia, Myeloid, Acute / therapy. Magnetic Resonance Imaging. Middle Aged. Suppuration. Thienamycins / administration & dosage. Time Factors. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 20068278.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Thienamycins; FV9J3JU8B1 / meropenem
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4. Mardis ER, Ding L, Dooling DJ, Larson DE, McLellan MD, Chen K, Koboldt DC, Fulton RS, Delehaunty KD, McGrath SD, Fulton LA, Locke DP, Magrini VJ, Abbott RM, Vickery TL, Reed JS, Robinson JS, Wylie T, Smith SM, Carmichael L, Eldred JM, Harris CC, Walker J, Peck JB, Du F, Dukes AF, Sanderson GE, Brummett AM, Clark E, McMichael JF, Meyer RJ, Schindler JK, Pohl CS, Wallis JW, Shi X, Lin L, Schmidt H, Tang Y, Haipek C, Wiechert ME, Ivy JV, Kalicki J, Elliott G, Ries RE, Payton JE, Westervelt P, Tomasson MH, Watson MA, Baty J, Heath S, Shannon WD, Nagarajan R, Link DC, Walter MJ, Graubert TA, DiPersio JF, Wilson RK, Ley TJ: Recurring mutations found by sequencing an acute myeloid leukemia genome. N Engl J Med; 2009 Sep 10;361(11):1058-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurring mutations found by sequencing an acute myeloid leukemia genome.
  • BACKGROUND: The full complement of DNA mutations that are responsible for the pathogenesis of acute myeloid leukemia (AML) is not yet known.
  • METHODS: We used massively parallel DNA sequencing to obtain a very high level of coverage (approximately 98%) of a primary, cytogenetically normal, de novo genome for AML with minimal maturation (AML-M1) and a matched normal skin genome.
  • Four of the 64 mutations occurred in at least 1 additional AML sample in 188 samples that were tested.
  • Mutations in NRAS and NPM1 had been identified previously in patients with AML, but two other mutations had not been identified.
  • One of these mutations, in the IDH1 gene, was present in 15 of 187 additional AML genomes tested and was strongly associated with normal cytogenetic status; it was present in 13 of 80 cytogenetically normal samples (16%).
  • The other was a nongenic mutation in a genomic region with regulatory potential and conservation in higher mammals; we detected it in one additional AML tumor.
  • The AML genome that we sequenced contains approximately 750 point mutations, of which only a small fraction are likely to be relevant to pathogenesis.
  • CONCLUSIONS: By comparing the sequences of tumor and skin genomes of a patient with AML-M1, we have identified recurring mutations that may be relevant for pathogenesis.


5. Skladanowski A, Bozko P, Sabisz M, Larsen AK: Dual inhibition of PI3K/Akt signaling and the DNA damage checkpoint in p53-deficient cells with strong survival signaling: implications for cancer therapy. Cell Cycle; 2007 Sep 15;6(18):2268-75
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  • We compared the influence of UCN-01, which affects both the DNA damage checkpoint and PI3K/Akt-mediated survival signaling, with the PI3K inhibitors wortmannin and LY294002 in p53-deficient M1 acute myeloid leukemia cells treated with the DNA damaging agent cisplatin.
  • Unexpectedly, dual inhibition of both survival and checkpoint signaling by UCN-01, also increased the cytotoxicity of cisplatin, but to a lesser degree than wortmannin or LY294002.

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  • (PMID = 17890906.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tumor Suppressor Protein p53; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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6. Liang DC, Shih LY, Huang CF, Hung IJ, Yang CP, Liu HC, Jaing TH, Wang LY, Chang WH: CEBPalpha mutations in childhood acute myeloid leukemia. Leukemia; 2005 Mar;19(3):410-4
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  • [Title] CEBPalpha mutations in childhood acute myeloid leukemia.
  • CEBPalpha: mutations have been described in adult acute myeloid leukemia (AML) and conferred a favorable prognosis.
  • We investigated 117 children with de novo AML using DNA PCR assay followed by sequencing for each PCR product.
  • CEBPalpha mutations were detected in seven patients, four had FAB M2, two M1 and one M4.
  • Our results showed that CEBPalpha mutations occurred in 6% of childhood AML and most exhibited combined mutations in both N-terminal part and bZIP domain.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Leukemia, Myeloid, Acute / genetics. Mutation


7. Nakamura S, Hirano I, Okinaka K, Takemura T, Yokota D, Ono T, Shigeno K, Shibata K, Fujisawa S, Ohnishi K: The FOXM1 transcriptional factor promotes the proliferation of leukemia cells through modulation of cell cycle progression in acute myeloid leukemia. Carcinogenesis; 2010 Nov;31(11):2012-21
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  • [Title] The FOXM1 transcriptional factor promotes the proliferation of leukemia cells through modulation of cell cycle progression in acute myeloid leukemia.
  • However, it is not clearly understood how FOXM1 contributes to acute myeloid leukemia (AML) cell proliferation.
  • In this study, we investigated the cellular and molecular function of FOXM1 in AML cells.
  • The FOXM1 messenger RNA (mRNA) expressed in AML cell lines was predominantly the FOXM1B isoform, and its levels were significantly higher than in normal high aldehyde dehydrogenase activity (ALDH(hi)) cells.
  • Reduction of FOXM1 expression in AML cells inhibited cell proliferation compared with control cells, through induction of G(2)/M cell cycle arrest, a decrease in the protein expression of Aurora kinase B, Survivin, Cyclin B1, S-phase kinase-associated protein 2 and Cdc25B and an increase in the protein expression of p21(Cip1) and p27(Kip1).
  • FOXM1 messenger RNA (mRNA) was overexpressed in all 127 AML clinical specimens tested (n = 21, 56, 32 and 18 for M1, M2, M4 and M5 subtypes, respectively).
  • Compared with normal ALDH(hi) cells, FOXM1 gene expression was 1.65- to 2.26-fold higher in AML cells.
  • Moreover, the FOXM1 protein was more strongly expressed in AML-derived ALDH(hi) cells compared with normal ALDH(hi) cells.
  • In addition, depletion of FOXM1 reduced colony formation of AML-derived ALDH(hi) cells due to inhibition of Cdc25B and Cyclin B1 expression.
  • In summary, we found that FOXM1B mRNA is predominantly expressed in AML cells and that aberrant expression of FOXM1 induces AML cell proliferation through modulation of cell cycle progression.
  • Thus, inhibition of FOXM1 expression represents an attractive target for AML therapy.
  • [MeSH-major] Cell Cycle. Cell Cycle Proteins / metabolism. Cell Proliferation. Forkhead Transcription Factors / physiology. Leukemia, Myeloid, Acute / pathology

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  • (PMID = 20823107.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / CCNB1 protein, human; 0 / CDKN1A protein, human; 0 / CDKN1B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin B1; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / FOXM1 protein, human; 0 / Forkhead Transcription Factors; 0 / Inhibitor of Apoptosis Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Microtubule-Associated Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / S-Phase Kinase-Associated Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 1.2.1.3 / Aldehyde Dehydrogenase; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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8. Mori H, Sakai H, Sanada M, Shimamoto K, Sasaki S, Azuma R, Higuchi T, Harada H, Niikura H, Omine M, Fujita K, Takahashi N: [Clinical analysis of HLA-DR-negative non-M3 AML]. Rinsho Ketsueki; 2007 Jul;48(7):547-53
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  • [Title] [Clinical analysis of HLA-DR-negative non-M3 AML].
  • The type of leukemia was defined as HLA-DR(-) non-M3-AML, when HLA antigens were detected by flow cytometry at an incidence of < 20% of the blast population excluding M3-AML.
  • Out of 109 patients with de novo acute myeloid leukemia, 8 patients had HLA-DR(-) non-AML-M3.
  • According to the French-American-British criteria, 7 patients could be subdivided into 3 patients with M1, 4 patients with M2 and 1 patient with M4.
  • Overall survival and disease-free survival showed no significant differences between the HLA-DR(-) non- M3-AML group and the HLA-DR(+) AML group.
  • [MeSH-major] HLA-DR Antigens / analysis. Leukemia, Myeloid, Acute / immunology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Flow Cytometry. Humans. Leukemia, Promyelocytic, Acute / immunology. Leukemia, Promyelocytic, Acute / mortality. Male. Middle Aged. Remission Induction

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  • (PMID = 17695303.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / HLA-DR Antigens
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9. Sino US Leukemia Cooperative Group of Shanghai: [Clinical study of 572 adult acute leukemia patients in Shanghai according to WHO classification]. Zhonghua Xue Ye Xue Za Zhi; 2007 Jul;28(7):444-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical study of 572 adult acute leukemia patients in Shanghai according to WHO classification].
  • OBJECTIVE: To evaluate WHO classification of acute leukemia (AL) in Shanghai and compare the difference between WHO and FAB classification.
  • METHODS: Successive and unselected leukemia patients were referred to Sino-US Leukemia Cooperative Group of Shanghai from 2003 to 2006.
  • A total of 572 adult AL cases were diagnosed and classified according to WHO and FAB classification.
  • RESULTS: Of the 572 AL patients, 436 (76.2%) were diagnosed as acute myeloid leukemia (AML), 119 (20.8%) acute lymphoblastic leukemia (ALL).
  • The AML and ALL percentage ratio was 3.66: 1.
  • AML with recurrent cytogenetic abnormalities accounted for 35.3%, and with multilineage dysplasia for 13.1%, therapy-related AML accounted for 0.9%, and AML not otherwise categorized for 50.7%.
  • The percentage of therapy-related AML in Shanghai was lower than that in the Western.
  • According to FAB classification, AML-M4 was the most (38.5%) common subtype.
  • The percentage of AML-M3 and M4 in Shanghai were higher than that in the Western, but that of AML-M, was lower.
  • The incidence of karyotypic abnormalities in AML was 60.8%.
  • The incidence of AML with t (15;17) was higher than that in the Western.
  • Favorable cytogenetic risk group accounted for 30.6%, intermediate group for 51.5%, unfavorable group for 17.9% of AML.
  • CONCLUSIONS: The percentages of AML with t (15;17) and AML-M4 in Shanghai and the incidence of cytogenetic favorable group were higher than that in the Western.
  • It was different in WHO classification and karyotypic abnormalities of AML between Shanghai and the Western.
  • Comparing to the AL data of Shanghai Leukemia Group between 1984 and 1994, the percentage of AML-M4 was increased, but that of AML-M1 and M5 were decreased.
  • [MeSH-major] Leukemia / classification
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. China. Female. Humans. Karyotyping. Male. Middle Aged

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  • (PMID = 18072625.001).
  • [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
  • [Publication-country] China
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10. Poggi A, Catellani S, Garuti A, Pierri I, Gobbi M, Zocchi MR: Effective in vivo induction of NKG2D ligands in acute myeloid leukaemias by all-trans-retinoic acid or sodium valproate. Leukemia; 2009 Apr;23(4):641-8
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  • [Title] Effective in vivo induction of NKG2D ligands in acute myeloid leukaemias by all-trans-retinoic acid or sodium valproate.
  • Herein, we show that in vivo administration of all-trans-retinoic acid (ATRA) or the histone deacetylase inhibitor sodium valproate (VPA) to patients affected with acute myeloid leukaemia (AML) M3 or M1 respectively, leads to the induction of transcription and expression of NKG2D-L at the surface of leukaemic cells.
  • Conversely, AML blasts from patients treated with chemotherapy not including ATRA or VPA did not show any induction of NKG2D-L transcription.
  • [MeSH-major] Intercellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid, Acute / drug therapy. NK Cell Lectin-Like Receptor Subfamily K / metabolism. Transcriptional Activation / drug effects. Tretinoin / administration & dosage. Valproic Acid / administration & dosage

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  • (PMID = 19151770.001).
  • [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 / GPI-Linked Proteins; 0 / Histone Deacetylase Inhibitors; 0 / Intercellular Signaling Peptides and Proteins; 0 / Ligands; 0 / NK Cell Lectin-Like Receptor Subfamily K; 0 / ULBP2 protein, human; 5688UTC01R / Tretinoin; 614OI1Z5WI / Valproic Acid
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11. Seckin D, Senol A, Gurbuz O, Demirkesen C: Leukemic vasculitis: an unusual manifestation of leukemia cutis. J Am Acad Dermatol; 2009 Sep;61(3):519-21
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  • [Title] Leukemic vasculitis: an unusual manifestation of leukemia cutis.
  • Leukemia cutis is frequently observed as papules, nodules, and plaques, but unusual clinical manifestations rarely occur.
  • We report a 64-year-old woman with acute myeloid leukemia M1 who presented with erythematous papules and vesiculobullous lesions limited to the arms, hands, and neck in addition to purpuric papules on the legs.
  • Because of the symmetric distal involvement and vesiculobullous nature of the skin lesions, the differential diagnosis included erythema multiforme and vasculitis.
  • Leukemia cutis associated with vasculitis was diagnosed.
  • A few blast cells can be observed in many reactive dermatoses in patients with leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Leukemic Infiltration. Skin / pathology. Vasculitis / etiology. Vasculitis / pathology

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  • (PMID = 19481293.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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12. Jiang SH, Shi WY, Liu H, Song GQ, Sun GX, Lu W, Liu DF: [Cytogenetic and clinical study of myeloid leukemia]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2007 Oct;24(5):571-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Cytogenetic and clinical study of myeloid leukemia].
  • OBJECTIVE: To explore the clinical cytogenetic features and prognosis of myeloid leukemia patients.
  • RESULTS: Among 420 patients with acute myeloid leukemia (AML), 223 cases were found to exhibit clonal chromosome abnormalities, accounted for 53.1%.
  • Out of 158 patients with chronic myeloid leukemia (CML), 96.8% (153/158) were found to exhibit clonal chromosome abnormalities.
  • T(9;22) was specifically associated with CML and some cases of M0, M1 and M2.
  • In these myeloid leukemia cases, there were 18 cases (AML 13 cases, CML 15 cases) without clonal chromosome abnormalities, accounted for 3.1% (18/578) and this phenomenon agreed with the diagnose of clinical signs, marrow morphology and immunology incompletely.
  • CONCLUSION: Karyotype analysis was not only helpful to the diagnose and differential diagnose of myeloid leukemia, but also an important standard of the remission, relapse and therapeutic effect of myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology

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  • (PMID = 17922430.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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13. Schuch G, Oliveira-Ferrer L, Loges S, Laack E, Bokemeyer C, Hossfeld DK, Fiedler W, Ergun S: Antiangiogenic treatment with endostatin inhibits progression of AML in vivo. Leukemia; 2005 Aug;19(8):1312-7
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  • [Title] Antiangiogenic treatment with endostatin inhibits progression of AML in vivo.
  • Increased vessel density in the bone marrow of patients with acute myeloid leukemia as well as elevated expression of proangiogenic factors by leukemic cells implies a central role of angiogenesis in hematological malignancies.
  • Using microencapsulation technology, we studied the therapeutic effect of ES in AML.
  • While ES had no effect on proliferation of M1 murine leukemic cells in vitro, ES producing microbeads significantly inhibited growth of subcutaneous chloromas in SCID mice as compared to controls.
  • In a leukemia model using M1 cells the concomitant treatment of mice with ES microbeads prolonged median survival significantly.
  • Taken together, ES has inhibitory effects on neo-angiogenesis in the bone marrow and on progression of leukemia in vivo.
  • These experiments suggest a possible therapeutic role of antiangiogenic gene therapy with ES in AML.
  • [MeSH-minor] Acute Disease. Animals. Antigens, CD31 / analysis. Bone Marrow Examination. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Compounding. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / pathology. Mice. Mice, SCID. Neoplasms, Experimental. Neovascularization, Pathologic / drug therapy. Survival Rate

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  • [Copyright] Leukemia (2005) 19, 1312-1317.
  • (PMID = 15931265.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD31; 0 / Endostatins
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14. Orazi A, Chiu R, O'Malley DP, Czader M, Allen SL, An C, Vance GH: Chronic myelomonocytic leukemia: The role of bone marrow biopsy immunohistology. Mod Pathol; 2006 Dec;19(12):1536-45
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  • [Title] Chronic myelomonocytic leukemia: The role of bone marrow biopsy immunohistology.
  • The World Health Organization criteria for diagnosing chronic myelomonocytic leukemia (CMML) are largely based on findings observed in the peripheral blood and bone marrow aspirate.
  • We examined whether bone marrow biopsy supplemented by immunohistochemistry may be helpful in distinguishing CMML from cases of chronic myelogenous leukemia and atypical chronic myeloid leukemia (aCML).
  • We immunostained 25 cases of CMML with paraffin reactive antibodies which included CD68 (KP1), CD68R (PG-M1), and CD163, and compared the results with those observed in six cases of chronic myelogenous leukemia and in three cases of atypical CML.
  • In addition, we examined whether CD34 immunohistochemistry could be useful in separating cases of CMML with less than 10% blasts (type-1) from cases of CMML with blasts accounting for 10-19% (type-2), and cases of CMML in acute transformation to acute myeloid leukemia (blasts > or = 20%).
  • CD34 analysis allowed separating CMML type-1 from type-2 and the former from CMML in acute transformation.
  • CD68R was more restricted to bone marrow macrophages and monocytes than CD68, but the differences between CMML and chronic myelogenous leukemia or atypical CML were still not significant.
  • Although CD42b immunostaining facilitated the detection of dwarf megakaryocytes often present in CMML, the distinction between those and the small forms seen in chronic myelogenous leukemia was still problematic.
  • [MeSH-major] Biopsy, Needle. Bone Marrow / pathology. Immunoenzyme Techniques / methods. Leukemia, Myelomonocytic, Chronic / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD / metabolism. Biomarkers, Tumor / metabolism. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Diagnosis, Differential. Female. Humans. Karyotyping. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Male. Megakaryocytes / metabolism. Megakaryocytes / pathology. Middle Aged

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  • (PMID = 17041567.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor
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15. Matsuno N, Hoshino K, Nanri T, Kawakita T, Suzushima H, Kawano F, Mitsuya H, Asou N: p15 mRNA expression detected by real-time quantitative reverse transcriptase-polymerase chain reaction correlates with the methylation density of the gene in adult acute leukemia. Leuk Res; 2005 May;29(5):557-64
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  • [Title] p15 mRNA expression detected by real-time quantitative reverse transcriptase-polymerase chain reaction correlates with the methylation density of the gene in adult acute leukemia.
  • Cyclin-dependent kinase inhibitor p15 is frequently inactivated by either methylation or deletion in patients with acute leukemia.
  • To examine pathologic and clinical significance of the p15 gene inactivation, we established a quantitative assay of p15 mRNA expression in the bone marrow cells by real-time quantitative reverse transcriptase-polymerase chain reaction. p15 mRNA expression in 14 patients with precursor B-cell acute lymphoblastic leukemia (PBC-ALL) well correlated with status of deletion and methylation in the p15 gene analyzed by Southern blotting.
  • Furthermore, two patients with PBC-ALL and 11 acute myeloblastic leukemia (AML) were quantitatively examined for p15 gene methylation using bisulfite genomic sequencing.
  • Among 108 AML patients, p15 mRNA expression was significantly lower in the myeloid lineage (M1, M2, M3) than the monocytic lineage (M4, M5) (P = 0.0019).
  • Above all, the majority of M3 patients showed low p15 expression compared with M1 and M2 patients (P = 0.029).
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Cycle Proteins / genetics. DNA Methylation. Gene Expression Regulation, Leukemic. Leukemia, Myeloid / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Messenger / metabolism. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Acute Disease. Adult. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Cell Lineage. CpG Islands. Cyclin-Dependent Kinase Inhibitor p15. Humans. Reverse Transcriptase Polymerase Chain Reaction. Sequence Deletion. Tumor Cells, Cultured

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  • (PMID = 15755508.001).
  • [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 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins
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16. Chou WC, Hou HA, Chen CY, Tang JL, Yao M, Tsay W, Ko BS, Wu SJ, Huang SY, Hsu SC, Chen YC, Huang YN, Chang YC, Lee FY, Liu MC, Liu CW, Tseng MH, Huang CF, Tien HF: Distinct clinical and biologic characteristics in adult acute myeloid leukemia bearing the isocitrate dehydrogenase 1 mutation. Blood; 2010 Apr 8;115(14):2749-54
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  • [Title] Distinct clinical and biologic characteristics in adult acute myeloid leukemia bearing the isocitrate dehydrogenase 1 mutation.
  • Recent genome-wide screening also revealed IDH1 mutation as a recurrent event in acute myeloid leukemia (AML), but its clinical implications in AML are largely unknown.
  • We analyzed 493 adult Chinese AML patients in Taiwan and found 27 patients (5.5%) harboring this mutation.
  • IDH1 mutation was strongly associated with normal karyotype (8.4%, P = .002), isolated monosomy 8 (P = .043), NPM1 mutation (P < .001), and French-American-British M1 subtype (P < .001), but inversely associated with French-American-British M4 subtype (P = .030) and expression of HLA-DR, CD13, and CD14 (P = .002, .003, and .038, respectively).
  • None of the 112 patients without IDH1 mutation at diagnosis acquired this mutation at relapse.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Monosomy. Neoplasm Proteins / genetics

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  • [CommentIn] Blood. 2010 Jul 22;116(3):495-6 [20651083.001]
  • (PMID = 20097881.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / HLA-DR Antigens; 0 / Neoplasm Proteins; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 3.4.11.2 / Antigens, CD13
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17. Al-Tonbary Y, Mansour AK, Ghazy H, Elghannam DM, Abd-Elghaffar HA: Prognostic significance of foetal-like tyrosine kinase 3 mutation in Egyptian children with acute leukaemia. Int J Lab Hematol; 2009 Jun;31(3):320-6
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  • [Title] Prognostic significance of foetal-like tyrosine kinase 3 mutation in Egyptian children with acute leukaemia.
  • In children with acute myelogenous leukaemia (AML), internal tandem duplication of the Flt3 gene (Flt3/ITD) was previously reported and correlated to poor prognosis.
  • Limited data are available about childhood acute lymphoblastic leukaemia (ALL).
  • We analysed bone marrow specimens from 55 newly diagnosed acute leukaemia cases including 30 AML and 25 ALL by genomic PCR for the presence of Flt3/ITD and correlated its presence with clinical outcome.
  • Tandem duplication was found in 6/30(20%) AML cases: 2/8 M1, 1/8 M2, 2/6 M3, 1/6 M4 with loss of heterozygosity (LOH) in two cases.
  • Patients with Flt3/ITD appear to be refractory to primary induction therapy, and for those who achieve remission, there is a high rate of relapse and death so there may be an association between this type of mutation and patient outcome.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 18336585.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [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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18. Pelloso LA, Da Silva ID, De Souza NC, Yamamoto M, Botelho CA, Chauffaille Mde L: CYP1A1 polymorphisms modify overall survival in acute myeloid leukemia patients. Leuk Lymphoma; 2007 Jun;48(6):1211-5
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  • [Title] CYP1A1 polymorphisms modify overall survival in acute myeloid leukemia patients.
  • [MeSH-major] Cytochrome P-450 CYP1A1 / genetics. Leukemia, Myeloid / genetics. Leukemia, Myeloid / mortality. Polymorphism, Genetic
  • [MeSH-minor] Acute Disease. Female. Glutathione Transferase / genetics. Humans. Male. Middle Aged. Multivariate Analysis. Survival Analysis

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  • [CommentIn] Leuk Lymphoma. 2007 Jun;48(6):1070-1 [17577768.001]
  • (PMID = 17577786.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.14.14.1 / Cytochrome P-450 CYP1A1; 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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19. Shman TV, Belevtsev MV, Buglova SE: [Drug sensitivity of tumor cells in varieties of acute childhood leukemia]. Vopr Onkol; 2005;51(5):558-62
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  • [Title] [Drug sensitivity of tumor cells in varieties of acute childhood leukemia].
  • Drug sensitivity of tumor cells was studied in 154 children diagnosed with acute leukemia.
  • Cellular sensitivity in acute lymphoblastic leukemia (ALL) was higher than in acute myeloid one (AML), while T-line ALL cells were more sensitive to dexamethasone than those of B-line.
  • Among AML cells, M3 variant was less sensitive to cytozar while M4 - to vepeside.
  • Reduced sensitivity to vincristine was found in series M3 > M1 - M2 > M4 while that to L-asparaginase was in M1- M2 > M4 > M3.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16756010.001).
  • [ISSN] 0507-3758
  • [Journal-full-title] Voprosy onkologii
  • [ISO-abbreviation] Vopr Onkol
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7006-34-0 / Asparagine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone
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20. Zhao F, Chen Y: [Immunologic characteristics and prognosis of acute myeloid leukemia M1]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):687-91
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  • [Title] [Immunologic characteristics and prognosis of acute myeloid leukemia M1].
  • The study was aimed to investigate the immunological characteristics and prognosis of acute myeloid leukemia (AML) M(1) and to find the main points in immunology to differentiate AML M(1) from M(2), and M(1) from ALL (proB, preB, T).
  • Immunophenotyping was performed in 41 AML M(1) patients by three-color flow cytometry analysis using CD45/SSC gating, meanwhile the cytogenetic analysis was performed in 17 patients.
  • 51 newly diagnosed AML M(2) patients and 58 newly diagnosed ALL patients were used as control at the same time.
  • The results showed that the positive rate of CD33 in M(1) was 100%, which was high in sensitivity, but low in specificity; the positive rate of CD11b, CD15, MPO, CD117 in M(1) were significantly lower than that in M(2) (p < 0.05); the positive rate of T-lineage antigen in Ly + AML M(1) was higher than that in M(2) (p < 0.05); compared with ALL ProB, M(1) had high expression of HLA-DR, simultaneously myeloid antigen CD13, CD15, CD33, CD117, MPO and T-lineage antigen CD4, CD7 were all highly expressed (p < 0.05); compared with ALL PreB, M(1) had high expression of HLA-DR, CD34, meanwhile myeloid antigen CD13, CD15, CD33, CD117, MPO and T-lineage antigen CD4, CD5 were all highly expressed (p < 0.05); as compared with T-ALL, the early-phase antigen HLA-DR, CD34, myeloid antigen CD13, CD15, CD33, CD117, MPO of M(1) were all significantly highly expressed (p < 0.05).
  • In M(1), the complete remission (CR) rate in patients with CD7 positive had no statistical difference from that in patients with CD7 negative (p > 0.05); the CR rate of patients with CD34 positive had no statistical difference from that of patients with CD34 negative (p > 0.05); CR rate in M(1) was lower than that in M(2) (p < 0.05), time to reach CR was longer, the incidence of hyperleukocytic acute leukemia was higher (p < 0.05), CR rate in hyperleukocytic acute leukemia was lower (p < 0.05).
  • It is concluded that the myeloid antigen CD33, CD13 in M(1) are highly expressed, early-phase antigen HLA-DR in M(1) is also highly expressed, but the myeloid antigen CD11b, CD15, MPO, CD117 in M(1) are lowly expressed, T-lineage antigen CD4, CD7 in M(1) are highly expressed in the meantime.
  • AML M(1), ALL ProB, ALL PreB and T-ALL, which are difficult to differentiate in morphology can be well seperated through the analysis of immunological phenotype.
  • CD117 is mainly expressed in AML, which is useful for the differentiation diagnosis between AML and ALL.

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  • (PMID = 17708783.001).
  • [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, CD; 0 / Antigens, CD4; 0 / Antigens, CD7; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / HLA-DR Antigens; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
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21. Manola KN, Georgakakos VN, Stavropoulou C, Spyridonidis A, Angelopoulou MK, Vlachadami I, Katsigiannis A, Roussou P, Pantelias GE, Sambani C: Jumping translocations in hematological malignancies: a cytogenetic study of five cases. Cancer Genet Cytogenet; 2008 Dec;187(2):85-94
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  • These cases involve JT of 1q in a case of acute myeloblastic leukemia (AML)-M1, a case of Burkitt lymphoma, and a case of BCR/ABL-positive acute lymphoblastic leukemia, as well as a JT of 13q in a case of AML-M5, and a JT of 11q segment in a case of undifferentiated leukemia.
  • To our knowledge, with regard to hematologic malignancies, this study presents the first case of JT associated with AML-M1, the first case of JT involving 13q as a donor chromosome, and the first report of JT involving a segment of 11q containing two copies of the MLL gene, jumping on to two recipient chromosomes in each cell line and resulting in six copies of the MLL gene.
  • Our investigation suggests that JT may not contribute to the pathogenesis but rather to the progression of the disease, and it demonstrates that chromosome band 1q10 as a breakpoint of the donor chromosome 1q is also implicated in AML, not only in multiple myeloma as it has been known until now.
  • [MeSH-minor] Adult. Aged. Burkitt Lymphoma / diagnosis. Burkitt Lymphoma / genetics. Cytogenetic Analysis. Female. Humans. Karyotyping. Leukemia / diagnosis. Leukemia / genetics. Leukemia, Monocytic, Acute / diagnosis. Leukemia, Monocytic, Acute / genetics. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Young Adult

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  • (PMID = 19027489.001).
  • [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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22. Lau LC, Koh LP, Lim TH, Loo LE, Tien SL: A cryptic three-way translocation involving chromosomes 8, 14, and 21 in a case of acute myeloid leukemia subtype M1. Cancer Genet Cytogenet; 2005 Nov;163(1):86-90
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  • [Title] A cryptic three-way translocation involving chromosomes 8, 14, and 21 in a case of acute myeloid leukemia subtype M1.
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 16271963.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains
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23. Ohnishi H, Yoshino H, Yoneyama R, Ishii M, Watanabe T, Bessho F: Faggot formation in mature neutrophils and metamyelocytes in acute myeloid leukemia without maturation. Pediatr Hematol Oncol; 2008 Apr-May;25(3):165-70
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  • [Title] Faggot formation in mature neutrophils and metamyelocytes in acute myeloid leukemia without maturation.
  • The authors report a rare case of acute myeloid leukemia (AML) M1 with faggot formation in mature neutrophils and metamyelocytes.
  • Although Auer rods in mature neutrophils are occasionally experienced, they are usually found in AML M2, M3, or M4 cases, but not in M1 cases.
  • In addition, faggot formation in mature neutrophils, as seen in this case, is considered to be particularly unusual because most previously reported cases tended to show simple Auer rods except for AML M3 cases.
  • [MeSH-major] Granulocyte Precursor Cells / pathology. Leukemia, Myeloid, Acute / pathology. Neutrophils / pathology. Trisomy / pathology

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  • (PMID = 18432498.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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24. Niparuck P, Chuncharunee S, Ungkanont A, Udomtrupayakul U, Aungchaisuksiri P, Rerkamnuatchoke B, Jootar S, Atichartakarn V: Long-term outcomes of de novo acute myeloid leukemia in Thai patients. J Med Assoc Thai; 2009 Sep;92(9):1143-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcomes of de novo acute myeloid leukemia in Thai patients.
  • BACKGROUND: Acute myeloid leukemia (AML) is the heterogeneous disease.
  • As per previous reports, there are some differences in clinical features and cytogenetic biomarkers of AML among different ethnic backgrounds.
  • Therefore, we conducted a retrospective study to analyze clinical outcomes and predictive factors of Thai AML patients receiving chemotherapy treatment.
  • MATERIAL AND METHOD: The authors performed a retrospective analysis of 106 adults with newly diagnosed de novo AML at Ramathibodi Hospital between 2003 and 2007.
  • Common subtypes were M4 (28.3%), M1 (26.4%) and M2 (20.8%).
  • AML with recurrent cytogenetic translocations, complex chromosome, trisomy 8, polyploidy, del 5q and del 7q were found in 16.8, 6.3, 5.3, 5.3, 2.1 and 3.2%, respectively.
  • CONCLUSION: The overall complete remission rate of Thai AML patients is in 60%.
  • Only a small proportion of the presented patients have long-term DFS and OS, the significant factor for predicting survival of Thai AML patients is the complete remission status.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 19772172.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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25. Leroy H, Roumier C, Huyghe P, Biggio V, Fenaux P, Preudhomme C: CEBPA point mutations in hematological malignancies. Leukemia; 2005 Mar;19(3):329-34
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  • The CCAAT/enhancer-binding protein-alpha (CEBPA) is a transcription factor strongly implicated in myelopoiesis through control of proliferation and differentiation of myeloid progenitors.
  • CEBPA mutations were reported exclusively in acute myeloid leukemia (AML) (according to WHO classification criteria) and mutated patients preferentially belonged to M1, M2 and M4 FAB subtypes.
  • Systematic analysis of CEBPA mutations, in addition to that of alterations in master genes of hematopoiesis, may be useful to assess the prognosis of AML particularly in patients belonging to the 'intermediate' prognostic subgroup.

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  • (PMID = 15674366.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha
  • [Number-of-references] 39
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26. Zatkova A, Fonatsch C, Sperr WR, Valent P: A patient with de novo AML M1 and t(16;21) with karyotype evolution. Leuk Res; 2007 Sep;31(9):1319-21
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  • [Title] A patient with de novo AML M1 and t(16;21) with karyotype evolution.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 21 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 17126398.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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27. Hentschel N, Krusch M, Kiener PA, Kolb HJ, Salih HR, Schmetzer HM: Serum levels of sCD137 (4-1BB) ligand are prognostic factors for progression in acute myeloid leukemia but not in non-Hodgkin's lymphoma. Eur J Haematol; 2006 Aug;77(2):91-101
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  • [Title] Serum levels of sCD137 (4-1BB) ligand are prognostic factors for progression in acute myeloid leukemia but not in non-Hodgkin's lymphoma.
  • In this study, we correlated sCD137L and sCD178 levels in sera of 42 samples of patients with acute myeloid leukemia (AML) and 46 samples of patients with non-Hodgkin's lymphoma (NHL) with stages, subtypes, and the clinical course of the diseases and determined cut-off values with maximum probability for significant differentiation between cases with higher/lower probability for progress free survival.
  • In contrast to patients with MDS, surprisingly no correlation between sCD178 levels and different subtypes and stages or with prognosis in AML or NHL were observed.
  • Regarding sCD137L, NHL-patients displayed lower levels compared with AML.
  • Statistically significant higher median levels of sCD137L are present in patients with undifferentiated AML (M1/M2, 1,470 pg/mL), poor cytogenetic risk (288 pg/mL) and higher levels of BM-blasts (186 pg/mL) compared with patients with monocytoid AML (M4/M5, 89 pg/mL), intermediate cytogenetic risk (59 pg/mL) and lower levels of BM-blasts (14 pg/mL) respectively.
  • Furthermore, in AML patients sCD137L levels correlate significantly with the probabilities to achieve complete remission (CR), stay in CR or with progress of the disease.
  • Taken together, our data demonstrate that sCD137L can be used as a prognostic factor not only in MDS but also in AML.
  • [MeSH-major] Biomarkers, Tumor / blood. Leukemia, Myeloid / blood. Lymphoma, Non-Hodgkin / blood. Membrane Glycoproteins / blood. Neoplasm Proteins / blood. Tumor Necrosis Factors / blood
  • [MeSH-minor] 4-1BB Ligand. Acute Disease. Adult. Aged. Aged, 80 and over. Blast Crisis / blood. Child, Preschool. Disease Progression. Disease-Free Survival. Fas Ligand Protein. Female. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / blood. Lymphoma, B-Cell / blood. Lymphoma, T-Cell / blood. Male. Middle Aged. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / blood. Prognosis. Retrospective Studies. Solubility. Survival Analysis

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  • (PMID = 16800841.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / 4-1BB Ligand; 0 / Biomarkers, Tumor; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / TNFSF9 protein, human; 0 / Tumor Necrosis Factors
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28. Olcay L, Dingil G, Yildirim E, Dilek G, Dirim E: Splenic abscesses in therapy-resistant acute myeloblastic leukemia presenting as recurrent febrile neutropenia and unresolved splenomegaly. Turk J Pediatr; 2007 Jul-Sep;49(3):315-8
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  • [Title] Splenic abscesses in therapy-resistant acute myeloblastic leukemia presenting as recurrent febrile neutropenia and unresolved splenomegaly.
  • A 14 7/12-year-old boy with acute myeloblastic leukemia M3v was admitted with disseminated intravascular coagulation, otitis media, lobar pneumonia, and splenomegaly.
  • The lesions persisted after M1 bone marrow was attained.
  • He developed acute appendicitis and was operated.
  • The pathologic examination confirmed the diagnosis.
  • [MeSH-major] Abscess / complications. Leukemia, Myeloid, Acute / complications. Neutropenia / diagnosis. Splenic Diseases / complications
  • [MeSH-minor] Adolescent. Diagnosis, Differential. Fatal Outcome. Humans. Male. Splenomegaly


29. Chen W, Konoplev S, Medeiros LJ, Koeppen H, Leventaki V, Vadhan-Raj S, Jones D, Kantarjian HM, Falini B, Bueso-Ramos CE: Cuplike nuclei (prominent nuclear invaginations) in acute myeloid leukemia are highly associated with FLT3 internal tandem duplication and NPM1 mutation. Cancer; 2009 Dec 1;115(23):5481-9
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  • [Title] Cuplike nuclei (prominent nuclear invaginations) in acute myeloid leukemia are highly associated with FLT3 internal tandem duplication and NPM1 mutation.
  • BACKGROUND: A small subset of patients with acute myeloid leukemia (AML) have cuplike nuclei.
  • METHODS: The authors searched for patients who had AML with cuplike nuclei at their institution over a 10-year interval.
  • The relevant data were reviewed, and the results were compared with a control group of patients who had AML without cuplike nuclei.
  • RESULTS: In total, 22 patients who had AML with cuplike nuclei were identified and were classified as AML without maturation (French-American-British classification M1) (AML M1).
  • Compared with the control group (AML M1), patients who had AML with cuplike nuclei were associated significantly with fms-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD) (86% vs 38%, respectively; P = .002); nucleophosmin 1 (NPM1) mutations (86% vs 19%; P < .0001); both mutations (77% vs 14%; P < .0001); normal karyotype (86% vs 40%; P = .003); bone marrow blast count (90% vs 84%; P = .016); myeloperoxidase positivity (95% vs 30% blasts; P = .001); higher D-dimer levels (>5000 ng/mL vs 569 ng/mL; P = .001); and the absence of CD7 (91% vs 52%; P = .007), CD34 (82% vs 5%; P < .0001), and human leukocyte antigen, D-related (59% vs 10%; P = .001).
  • The positive predictive value of recognizing AML with cuplike nuclei for FLT3-ITD, NPM1, and both mutations was 81%, 86%, and 77%, respectively.
  • CONCLUSIONS: Cuplike nuclei in AML were highly associated with the presence of NPM1 and FLT3-ITD mutations and with several clinicopathologic and immunophenotypic features.
  • Recognition of the distinctive morphologic features of AML with cuplike nuclei may be helpful in streamlining the workup of these neoplasms.

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  • [Copyright] (c) 2009 American Cancer Society.
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  • (PMID = 19672946.001).
  • [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 / P50 CA100632; United States / NCI NIH HHS / CA / P50 CA 100632-04
  • [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 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ NIHMS140671; NLM/ PMC3378048
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30. El-Sissy AH, El-Mashari MA, Bassuni WY, El-Swaayed AF: Aberrant lymphoid antigen expression in acute myeloid leukemia in Saudi Arabia. J Egypt Natl Canc Inst; 2006 Sep;18(3):244-9
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  • [Title] Aberrant lymphoid antigen expression in acute myeloid leukemia in Saudi Arabia.
  • BACKGROUND: Immunophenotyping improves both accuracy and reproducibility of acute leukemia classification and is considered particularly useful for identifying aberrant lineage association of acute leukemia, biphenotypic and bilineal acute leukemia, as well as monitoring minimal residual disease.
  • THE AIM OF OUR STUDY: Is to determine aberrant lymphoid antigen expression in Saudi acute myeloid leukemia (AML), correlate them with FAB subtypes, evaluate early surface markers CD7 and CD56, and to investigate the role of cytoplasmic CD79a (a B cell marker that is assigned a high score of 2.0 in the WHO classification).
  • PATIENTS AND METHODS: Thirty four newly diagnosed AML cases were included in this study, 47% showed aberrant lymphoid antigen expression.
  • CD9 was expressed in 3/6 (50%) of M3 cases, CD7 was expressed in 11.8% and was mostly confined to FAB M1 and M2 and associated with immature antigens CD34, HLA-DR and TdT.
  • CD79a was expressed in one case together with CD19, diagnosed as acute biphenotypic leukemia, and was associated with t(8;21) (q22;q22).
  • CONCLUSION: Minimal residual disease in AML is very difficult to trace, detection of aberrant expression of lymphoid antigens will make it easier.
  • [MeSH-major] Antigens, CD56 / analysis. Antigens, CD7 / analysis. Antigens, CD79 / analysis. Antigens, Neoplasm / analysis. Biomarkers, Tumor / analysis. Leukemia, Myeloid, Acute / diagnosis


31. Tang JL, Hou HA, Chen CY, Liu CY, Chou WC, Tseng MH, Huang CF, Lee FY, Liu MC, Yao M, Huang SY, Ko BS, Hsu SC, Wu SJ, Tsay W, Chen YC, Lin LI, Tien HF: AML1/RUNX1 mutations in 470 adult patients with de novo acute myeloid leukemia: prognostic implication and interaction with other gene alterations. Blood; 2009 Dec 17;114(26):5352-61
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  • [Title] AML1/RUNX1 mutations in 470 adult patients with de novo acute myeloid leukemia: prognostic implication and interaction with other gene alterations.
  • Somatic mutation of the AML1/RUNX1(RUNX1) gene is seen in acute myeloid leukemia (AML) M0 subtype and in AML transformed from myelodysplastic syndrome, but the impact of this gene mutation on survival in AML patients remains unclear.
  • In this study, we sought to determine the clinical implications of RUNX1 mutations in 470 adult patients with de novo non-M3 AML.
  • The RUNX1 mutation was closely associated with male sex, older age, lower lactic dehydrogenase value, French-American-British M0/M1 subtypes, and expression of HLA-DR and CD34, but inversely correlated with CD33, CD15, CD19, and CD56 expression.
  • AML patients with RUNX1 mutations had a significantly lower complete remission rate and shorter disease-free and overall survival than those without the mutation.
  • Our findings provide evidence that RUNX1 mutations are associated with distinct biologic and clinical characteristics and poor prognosis in patients with de novo AML.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality


32. Chang WR, Park IJ, Lee HW, Park JS, Kim HC, Kim HJ, Han JH, Cho SR: [Two cases of acute myeloid leukemia with t(16;21)(p11;q22) and TLS/FUS-ERG fusion transcripts]. Korean J Lab Med; 2009 Oct;29(5):390-5
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  • [Title] [Two cases of acute myeloid leukemia with t(16;21)(p11;q22) and TLS/FUS-ERG fusion transcripts].
  • Many AML-associated chromosomal abnormalities, such as t(8;21), t(15;17), inv(16), t(9;11), t(9;22) and t(6;9) are well known.
  • The chromosomal aberration of t(16;21)(p11;q22) in AML is rare and it is known to be associated with poor prognosis, young age (median age, 22 yr), and involvement of various subtypes of the French-American-British classification.
  • We report here 2 AML patients with t(16;21)(p11;q22), proved by conventional cytogenetics and/or reverse transcription (RT)-PCR.
  • One patient was a 24 yr-old male with acute myelomonocytic leukemia.
  • Although he received allogeneic peripheral blood stem cell transplantation after the first remission, he died 9 months after the initial diagnosis due to relapse of the disease and graft-versus-host disease.
  • The other patient was a 72 yr-old male with acute myeloid leukemia without maturation.
  • We suggest that the presence of t(16;21)(p11;q22) and/or TLS/FUS-ERG fusion transcripts has to be considered in cases of AML with erythrophagocytosis.
  • [MeSH-major] Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 22 / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic
  • [MeSH-minor] Aged. Graft vs Host Disease / diagnosis. Humans. Karyotyping. Male. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • (PMID = 19893346.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human
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33. Hiçsönmez G: A novel approach to treatment in childhood acute myeloblastic leukemia and myelodysplastic syndrome with high-dose methylprednisolone as a differentiation- and apoptosis-inducing agent of myeloid leukemic cells. Turk J Haematol; 2010 Mar 5;27(1):1-7
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  • [Title] A novel approach to treatment in childhood acute myeloblastic leukemia and myelodysplastic syndrome with high-dose methylprednisolone as a differentiation- and apoptosis-inducing agent of myeloid leukemic cells.
  • [Transliterated title] Çocukluk yaşı akut myeloblastik lösemi ve myelodisplastik sendromunda myeloid lösemik hücrelerde farklılaşma ve apoptosisi sağlayan yüksek doz metilprednizolon ile yeni bir tedavi yaklaşımı.
  • Differentiation-inducing therapy with all-trans retinoic acid significantly improved the outcome in children with acute promyelocytic leukemia (APL).
  • Based on the experimental studies in mice, we have shown that short-course high-dose methylprednisolone (HDMP) treatment can induce terminal differentiation of leukemic cells in children with various subtypes of acute myeloblastic leukemia (AML-M1,-M2,-M3,-M4,-M7).
  • It has also been shown to induce apoptosis of myeloid leukemic cells with or without differentiation.
  • Administration of HDMP as a single agent resulted in a rapid clinical improvement, a marked decrease in blast cells in both peripheral blood and bone marrow and dramatic decreases in the size of extramedullary leukemic mass in children with AML and myelodysplastic syndrome (MDS).

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  • (PMID = 27265790.001).
  • [ISSN] 1300-7777
  • [Journal-full-title] Turkish journal of haematology : official journal of Turkish Society of Haematology
  • [ISO-abbreviation] Turk J Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
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34. Yan LZ, Chen SN, Liang JY, Feng YF, Cen JN, He J, Chang WR, Zhu ZL, Pan JL, Wu YF, Xue YQ, Wu DP: [Analysis of NPM1 gene mutations in acute myeloid leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2007 May;28(5):289-93
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  • [Title] [Analysis of NPM1 gene mutations in acute myeloid leukemia].
  • OBJECTIVE: To evaluate the prevalence of nucleophosmin (NPM1) gene exon 12 mutations in adults with acute myeloid leukemia (AML) and its clinical characteristics.
  • METHODS: Genomic DNAs from 101 AML adults were screened by PCR and sequencing or capillary electrophoresis (CE) for NPMI mutations.
  • RESULTS: NPM1 exon 12 mutations were present in 31.7% of the overall cohort, including 1/1 (100%) of M0, 9/17(52.9%) of M1 , 7/25 (28.0%) of M2, 0/23(0%) of M3, 2/7 (28.6%) of M4 and 13/25 (52.0% ) of M5.
  • Sequence analysis of these NPM1 mutant cases revealed 5 known mutations (type A, B, D, N(M), and P(M)) and 1 novel variant (named as type S).
  • CONCLUSIONS: NPM1 exon 12 mutations occur with a considerable percentage in AML patients with normal karyotype, M1/M5 subtype and older age, and are associated with higher peripheral white cell count and lower expression of CD34 and CD117.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics

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  • (PMID = 17877154.001).
  • [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 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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35. Malissein E, Reynaud S, Bordessoule D, Faucher JL, Turlure P, Trimoreau F, Denizot Y: PGE(2) receptor subtype functionality on immature forms of human leukemic blasts. Leuk Res; 2006 Oct;30(10):1309-13
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  • We investigated, for the first time, the functionality of EP receptors on immature forms of blast cells of acute myeloid leukemic (AML) and acute lymphoid leukemic (ALL) patients.
  • RT-PCR experiments documented the presence of the four EP receptor subtype transcripts in leukemic blasts of AML M0, AML M1, AML M2 and ALL patients.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Prostaglandin E / classification. Receptors, Prostaglandin E / genetics

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  • (PMID = 16460799.001).
  • [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 / Receptors, Prostaglandin E; SY7Q814VUP / Calcium
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36. Dăscălescu A, Zlei M, Grigore G, Dănăila C, Jitaru D, Carasevici E: [Prognostic significance of leukemia-associated phenotype in correlation with other biologic markers in acute myeloid leukemia patients]. Rev Med Chir Soc Med Nat Iasi; 2009 Oct-Dec;113(4):1176-81
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  • [Title] [Prognostic significance of leukemia-associated phenotype in correlation with other biologic markers in acute myeloid leukemia patients].
  • The main aim of the current study is to identify correlation between recognized prognostic factors in acute myeloid leukemia (AML) patients and other phenotypic markers.
  • MATERIAL AND METHOD: Imunophenotypic analysis (BDFACS CantoII, FACSDiva Software) was performed on peripheral blood/bone marrow aspirate samples of 56 patients diagnosed with AML (9 M0, 3 M1, 10 M2, 4 M3, 28 M4/M5, 1 M6, 1 M7) between 2007-2009 in Hematology Department of "Sf.
  • RESULTS: In our study, IL7R expression on AML blasts was significant correlate with low WBC count at diagnosis (p = 0.04) and with multilinear displasia (p = 0.01), high CXCR4 expression was correlate (p = 0.05) with lack of response at first induction therapy and CD123 (IL3Ra) expression was correlate with M4 FAB phenotype.
  • Survival was negative influenced by presence of IL3R on AML blasts, but flt3 mutations, CXCR4, IL7R expression on leukemic cells, other phenotypic aberrancies did not influenced treatment response and survival in our patients population.
  • [MeSH-major] Biomarkers, Tumor / blood. Leukemia, Myeloid, Acute / immunology. Receptors, Chemokine / blood. Receptors, Cytokine / blood

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  • (PMID = 20191895.001).
  • [ISSN] 0048-7848
  • [Journal-full-title] Revista medico-chirurgicală̆ a Societă̆ţ̜ii de Medici ş̧i Naturaliş̧ti din Iaş̧i
  • [ISO-abbreviation] Rev Med Chir Soc Med Nat Iasi
  • [Language] rum
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, CCR5; 0 / Receptors, CXCR4; 0 / Receptors, Chemokine; 0 / Receptors, Cytokine; 0 / Receptors, Interleukin-3; 0 / Receptors, Interleukin-7
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37. Vasilatou D, Papageorgiou S, Pappa V, Papageorgiou E, Dervenoulas J: The role of microRNAs in normal and malignant hematopoiesis. Eur J Haematol; 2010 Jan 1;84(1):1-16
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  • Several lines of evidence suggest that they have an important role in normal hematopoiesis as exemplified by the role of mir-155 and mir-150 in the differentiation of B and T lymphocytes, the suppressive role of mir-221 and mir-222 in erythroid differentiation, the inhibitory effect of mir-181 on hematopoietic differentiation and the induction of myeloid differentiation by mir-223.
  • Their aberrant expression has been associated with solid tumors and hematopoietic malignancies as suggested by the frequent deletion of mir-15a and mir-16-1 in chronic lymphocytic leukemia, the increased levels of mir-155 in diffuse large B-cell lymphomas and the increased levels of mir-181 in acute myeloid leukemia M1 and M2.
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / genetics. Down-Regulation. Erythroid Precursor Cells / cytology. Gene Expression Regulation, Neoplastic / genetics. Genes, Tumor Suppressor. Humans. Invertebrates / genetics. Lymphocytes / cytology. Mice. Myeloid Cells / cytology. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Oncogenes. RNA, Neoplasm / antagonists & inhibitors. RNA, Neoplasm / genetics

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  • (PMID = 19744129.001).
  • [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; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / Neoplasm Proteins; 0 / RNA, Neoplasm
  • [Number-of-references] 110
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38. Majumdar S, Mondal BC, Ghosh M, Dey S, Mukhopadhyay A, Chandra S, Dasgupta UB: Association of cytochrome P450, glutathione S-transferase and N-acetyl transferase 2 gene polymorphisms with incidence of acute myeloid leukemia. Eur J Cancer Prev; 2008 Apr;17(2):125-32
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  • [Title] Association of cytochrome P450, glutathione S-transferase and N-acetyl transferase 2 gene polymorphisms with incidence of acute myeloid leukemia.
  • The objective of the paper was to study the association of polymorphisms of phases I and II xenobiotic metabolizing enzyme genes cytochrome P450 (CYP-4501A1*2A, *2B, *2C and *4 alleles, CYP-4502D6*4 allele), glutathione-S-transferase (GSTM1 and GSTT1 null genotypes) and N-acetyl transferase 2 (NAT2*6B and *7A alleles) with the incidence of acute myeloid leukemia (AML) in an eastern Indian population.
  • Polymerase chain reaction and restriction fragment length polymorphism of genomic DNA from peripheral blood cells were used to detect CYP-450 and NAT2 gene polymorphisms in 110 AML patients and 144 racially and geographically matched normal controls.
  • A statistically significant difference between the AML group and the normal group was observed in the case of glutathione-S-transferase M1 null (odds ratio 3.25, 95% confidence interval 1.9-5.58, P<0.001) and N-acetyl transferase 2*6B (odds ratio 3.04, 95% confidence interval 1.79-5.16, P<0.001) genotypes.
  • Combined deficiency of N-acetyl transferase 2 and glutathione-S-transferase M1 genes produced an odds ratio of 11.91 (95% confidence interval 4.06-34.96, P<0.001).
  • In the population studied, persons with glutathione-S-transferase M1 null genotype and N-acetyl transferase 2*6B allele are at increased risk of developing AML, and the risk is considerably enhanced in persons with both glutathione-S-transferase M1 and N-acetyl transferase 2 deficiency.
  • [MeSH-major] Arylamine N-Acetyltransferase / genetics. Glutathione Transferase / genetics. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Cytochrome P-450 CYP1A1 / genetics. Cytochrome P-450 CYP2D6 / genetics. Female. Humans. Incidence. India / epidemiology. Male. Middle Aged. Polymorphism, Genetic

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  • (PMID = 18287869.001).
  • [ISSN] 1473-5709
  • [Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
  • [ISO-abbreviation] Eur. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 1.14.14.1 / Cytochrome P-450 CYP2D6; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / NAT2 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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39. Hubeek I, Peters GJ, Broekhuizen R, Zwaan CM, Kaaijk P, van Wering ES, Gibson BE, Creutzig U, Janka-Schaub GE, den Boer ML, Pieters R, Kaspers GJ: In vitro sensitivity and cross-resistance to deoxynucleoside analogs in childhood acute leukemia. Haematologica; 2006 Jan;91(1):17-23
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  • [Title] In vitro sensitivity and cross-resistance to deoxynucleoside analogs in childhood acute leukemia.
  • BACKGROUND AND OBJECTIVES: Cytarabine (ara-C) is a key drug in the treatment of acute leukemia.
  • DESIGN AND METHODS: Using the MTT assay, we determined in vitro sensitivity and cross-resistance to deoxynucleoside analogs in 362 acute leukemia samples from untreated children and 32 normal bone marrow mononuclear cell samples.
  • RESULTS: Normal bone marrow samples were significantly more resistant to ara-C, cladribine and fludarabine than were acute myeloid leukemia (AML) samples and significantly more resistant to ara-C and fludarabine than were acute lymphoblastic leukemia (ALL) samples.
  • The only drug to which AML samples were more sensitive in vitro than ALL was cladribine.
  • AML FAB M5 was significantly more sensitive in vitro to ara-C and cladribine than FAB M1/2 or FAB M4.
  • A paired analysis of 60 AML and 99 ALL samples demonstrated significant cross-resistance between all four deoxynucleoside analogs.
  • Cross-resistance was also observed between ara-C and etoposide (Rp=0.54, p<0.0001), and ara-C and daunorubicin (Rp=0.48, p<0.0001) in AML.
  • In ALL blasts, cross-resistance was observed between ara-C and vincristine (Rp=0.50; p<0.0001), and between ara-C and daunorubicin and L-asparaginase (Rp=0.25; p=0.01; Rp=0.28; p=0.005).
  • INTERPRETATION AND CONCLUSIONS: Cladribine appears to be a useful drug in AML, particularly in FAB M5.
  • We observed cross-resistance between ara-C and other deoxynucleoside analogs, as well as between ara-C and drugs with different modes of action in childhood acute leukemia.
  • [MeSH-major] Drug Resistance, Multiple. Leukemia / drug therapy. Nucleosides / therapeutic use
  • [MeSH-minor] Acute Disease. Child. Cytarabine / therapeutic use. Drug Screening Assays, Antitumor. Humans

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  • (PMID = 16434366.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nucleosides; 04079A1RDZ / Cytarabine
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40. Herry A, Douet-Guilbert N, Guéganic N, Morel F, Le Bris MJ, Berthou C, De Braekeleer M: Del(5q) and MLL amplification in homogeneously staining region in acute myeloblastic leukemia: a recurrent cytogenetic association. Ann Hematol; 2006 Apr;85(4):244-9
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  • [Title] Del(5q) and MLL amplification in homogeneously staining region in acute myeloblastic leukemia: a recurrent cytogenetic association.
  • We report here a 71 year-old female presenting with acute myeloblastic leukemia (FAB-M1) after treatment of essential thrombocythemia with Vercyte.
  • Twenty-one cases, including ours, of myelodysplastic syndromes and acute myelogenous leukemia with MLL amplification present in hsr or dmin were found in the literature.
  • Most of these patients shared some characteristics: they were old, they had de novo acute myeloid leukemia (AML) with a complex karyotype and a short survival, 90% of them having also a del(5q).
  • Therefore, the simultaneous presence of MLL amplification and del(5q) appears to be a nonrandom association that could be the signature of AML in elderly patients with a poor prognosis.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 7 / genetics. Gene Amplification. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] 6-Mercaptopurine / therapeutic use. Aged. Cytogenetic Analysis. Fatal Outcome. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence / methods. Karyotyping. Pipobroman / therapeutic use. Prognosis. Sensitivity and Specificity. Thrombocytosis / diagnosis. Thrombocytosis / drug therapy

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  • (PMID = 16425025.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6Q99RDT97R / Pipobroman; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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41. Shahin D, Aly R, Ebrahim MA: Prognostic significance of FLT3 internal tandem duplication in egyptian patients with acute myeloid leukemia with normal or favorable risk cytogenetics. Egypt J Immunol; 2010;17(2):23-32
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  • [Title] Prognostic significance of FLT3 internal tandem duplication in egyptian patients with acute myeloid leukemia with normal or favorable risk cytogenetics.
  • Internal tandem duplication (ITD) of the FLT3 gene (FLT3/ITD) has been linked to poor outcome in acute myeloid leukemia (AML).
  • The aim of this study was to evaluate the prognostic significance of FLT3/ITD in patients with de novo AML and normal or favorable risk cytogenetics (NFC-AML).
  • Blood samples from 39 patients with AML were subjected to PCR of exons 14 and 15 of the FLT3 gene.
  • Patients were M1 3/13, M2 2/12, M3 1/9, M4 0/4 and M5 0/1.

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  • (PMID = 23082484.001).
  • [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] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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42. Yan L, Chen S, Liang J, Feng Y, Cen J, He J, Chang W, Zhu Z, Pan J, Wu Y, Xue Y, Wu D: Analysis of NPM1 gene mutations in Chinese adults with acute myeloid leukemia. Int J Hematol; 2007 Aug;86(2):143-6
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  • [Title] Analysis of NPM1 gene mutations in Chinese adults with acute myeloid leukemia.
  • Many European groups have recently described that mutations at exon-12 of the nucleophosmin (NPM1) gene are the most frequent genetic lesion in patients with acute myeloid leukemia (AML), especially in the presence of a normal karyotype.
  • This study explored the prevalence and clinical profile of NPM1 mutations in a cohort of 156 Chinese adults with AML.
  • NPM1 mutations were present in 28.2% of the overall population, including 1/1 (100%) of M0, 11/27 (40.7%) of M1, 11/46 (23.9%) of M2, 0/29 (0%) of M3, 2/9 (22.2%) of M4, 18/39 (46.2%) of M5, and 1/5 (20.0%) of M6.
  • Sequence analysis of 25 NPM1-mutated cases revealed known mutations (type A, D, N(M), and P(M)) as well as one novel sequence variation (here named as type S).
  • NPM1 mutations were significantly associated with old age (P < .05), high peripheral white blood cell count (P < .05), and the subtypes of French-American-British categories M1/M5, but negatively associated with expression of CD34 (P < .05) and CD117 (P < .05).
  • [MeSH-major] Leukemia, Myeloid / genetics. Mutation. Nuclear Proteins / genetics

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  • [Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]
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  • (PMID = 17875528.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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43. David S, Ribeiro DR, Antunes A, Portugal C, Sancho L, de Sousa JG: Contribution of spoligotyping to the characterization of the population structure of Mycobacterium tuberculosis isolates in Portugal. Infect Genet Evol; 2007 Sep;7(5):609-17
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  • Distribution amongst major spoligotype families, including the Latin American Mediterranean (LAM), T, Haarlem and Beijing, was compared to that of the international spoligotype database SpolDB4 and to the European countries of traditional Portuguese immigration represented in SpolDB4.
  • The importance of the LAM family, and especially of LAM1 and LAM9 sub-families that alone represented 38% of all the isolates in this study as compared to 8% relative to the European sub group, led us to believe that at least in this respect the population structure was closer to that of Africa and South America than to Europe.
  • These included SIT244 a T1 sub-family predominant in Portugal and Bangladesh, SIT64 a LAM 6 sub-family common to Portugal and Brazil, and SIT1106 a LAM 9 sub-family.

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  • (PMID = 17625987.001).
  • [ISSN] 1567-1348
  • [Journal-full-title] Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases
  • [ISO-abbreviation] Infect. Genet. Evol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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44. Carnicer MJ, Lasa A, Buschbeck M, Serrano E, Carricondo M, Brunet S, Aventin A, Sierra J, Di Croce L, Nomdedeu JF: K313dup is a recurrent CEBPA mutation in de novo acute myeloid leukemia (AML). Ann Hematol; 2008 Oct;87(10):819-27
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  • [Title] K313dup is a recurrent CEBPA mutation in de novo acute myeloid leukemia (AML).
  • The CEBPA gene codes for a transcription factor that has a pivotal role in controlling proliferation and differentiation of myeloid progenitors.
  • Acquired CEBPA mutations have been found in acute myeloid leukemias (AML) with a good prognosis, and most of these patients have a normal karyotype.
  • All four had an AML-M1 with CD7 positivity and T-cell receptor gamma chain (TCR-gamma) rearrangement.
  • In transfected cells, the K313dup mutant had reduced protein stability with respect to the wild-type protein.
  • K313dup seems to be selected in leukemic cells, and its frequency in other AML series could be determined using the screening method reported in this paper.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Mutation

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  • (PMID = 18587575.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Receptors, Antigen, T-Cell, gamma-delta
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45. Auewarakul CU, Lauhakirti D, Tocharoentanaphol C: Frequency of RAS gene mutation and its cooperative genetic events in Southeast Asian adult acute myeloid leukemia. Eur J Haematol; 2006 Jul;77(1):51-6
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  • [Title] Frequency of RAS gene mutation and its cooperative genetic events in Southeast Asian adult acute myeloid leukemia.
  • RAS gene as one of the most frequently mutated genes in acute myeloid leukemia (AML) has become an attractive target for molecular therapy.
  • The role of oncogenic RAS and its associated genetic events in AML are not yet defined.
  • We examined the frequency of RAS mutation in 239 Thai de novo adult AML patients using polymerase chain reaction-single-strand conformational polymorphism analysis.
  • Thirty-five RAS mutations were found in 32 cases (13%) predominantly classified as M1/M2 (53%) followed by M4/M5 subtype (38%).
  • Most M1/M2 cases had mutations at codon 12 or 13, whereas M4/M5 cases preferentially affected codon 61.
  • Four patients had core-binding factor leukemia and four additional patients had coexisting FLT3 or AML1 mutation.
  • Future molecular-targeting approaches should take into account the multiple genetic events that coexist with RAS mutations in AML patients.
  • [MeSH-major] Leukemia, Myeloid / classification. Leukemia, Myeloid / genetics. Mutation. ras Proteins / genetics
  • [MeSH-minor] Acute Disease. Adult. Asia, Southeastern / epidemiology. Codon. Core Binding Factor Alpha 2 Subunit / genetics. DNA Mutational Analysis. Female. Gene Frequency. Humans. Male. Molecular Epidemiology. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16573741.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Codon; 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.5.2 / ras Proteins
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46. Liu M, Wei XD, Lü XD, Fan RH, Yin QS, Zhou J: [Expression of NF-kappaB mRNA in acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Apr;18(2):359-62
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  • [Title] [Expression of NF-kappaB mRNA in acute myeloid leukemia].
  • This study was aimed to investigate the expression level of NF-kappaB mRNA in acute myeloid leukemia (AML) using real time fluorescence quantitative polymerase chain reduction (qPCR) detection and to explore the effect of NF-kappaB mRNA in pathogenesis of AML.
  • The fresh bone marrow was collected from 60 newly diagnosed patients with AML, the total RNA was extracted by means of RTIzoL, the cDNA was synthesized, the expression of NF-kappaB mRNA was detected by qPCR using GAPDH as internal reference.
  • The results showed that the expression of NF-kappaB mRNA in patients with AML was higher than that in normal healthy persons with significant difference (p<0.05), the expression of NF-kappaB mRNA in patients with AML-M4 and -M5 were higher than that in patients with AML-M1, -M2 and -M3.
  • It is concluded that the expression of NF-kappaB mRNA is higher in patients with AML.
  • The up-regulation of NF-kappaB expression in patients with AML may play an important role in pathogenesis of AML.

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  • (PMID = 20416168.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / RNA, Messenger
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47. Corveleyn A, Wlodarska I, Mecucci C, Marynen P: The der(12)t(12;16) breakpoint in an acute leukaemia case targets a Sec7 domain containing protein. Int J Oncol; 2005 Apr;26(4):1111-20
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  • [Title] The der(12)t(12;16) breakpoint in an acute leukaemia case targets a Sec7 domain containing protein.
  • A balanced translocation t(12;16)(p13;p13) in a patient with AML-M1 and bone marrow eosinophilia was previously analysed by FISH.
  • The 16p13 breakpoint was shown to occur in the MYH11 gene, the fusion partner of CBFbeta in leukaemia patients with an inv(16) or a t(16;16), whereas the 12p13 breakpoint was shown to be present in cosmid c4H9.
  • The FISH data led to the hypothesis that rearrangement of SLAG might be involved in the pathogenesis of AML through the generation of a new fusion gene with MYH11.
  • [MeSH-major] Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 16 / genetics. Guanine Nucleotide Exchange Factors / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 15754009.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Guanine Nucleotide Exchange Factors; 0 / Nerve Tissue Proteins; 0 / Recombinant Fusion Proteins; 0 / SLAG protein, human; 0 / Sec7 guanine nucleotide exchange factors
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48. Mashita T, Shimoda T, Yoshioka H, Takahashi Y, Mitsuda M: A cat with acute myeloblastic leukemia without maturation (M1) treated with combination chemotherapy. J Vet Med Sci; 2006 Jan;68(1):97-101
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  • [Title] A cat with acute myeloblastic leukemia without maturation (M1) treated with combination chemotherapy.
  • Acute myeloblastic leukemia without maturation (M1) was diagnosed according to the FAB classification.

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  • (PMID = 16462128.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; EC 1.11.1.7 / Peroxidase
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49. Voso MT, Hohaus S, Guidi F, Fabiani E, D'Alò F, Groner S, Späth D, Doehner K, Leone G, Doehner H, Schlenk RF: Prognostic role of glutathione S-transferase polymorphisms in acute myeloid leukemia. Leukemia; 2008 Sep;22(9):1685-91
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  • [Title] Prognostic role of glutathione S-transferase polymorphisms in acute myeloid leukemia.
  • We were interested whether their polymorphic variants may account for differences in outcome of patients with acute myeloid leukemia (AML) following chemotherapy.
  • We studied the prognostic role of polymorphisms in three GST genes (GSTP1/M1/T1) in a large patient cohort of the German Austrian Acute Myeloid Leukemia Study Group, treated according to prospective multicenter clinical trials (AML HD98A: 254 patients; AML HD98-B: 100 patients), with a median follow-up of 46 months.
  • Looking at short-term adverse drug reactions, homozygous carriers of the GSTP1*105 Val allele had a faster neutrophil and platelet recovery (P=0.002 and 0.02, respectively) and a reduced need of red cell and platelet transfusions (P=0.01 and 0.03, respectively).
  • [MeSH-major] Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics. Polymorphism, Genetic


50. Ho PA, Alonzo TA, Gerbing RB, Pollard J, Stirewalt DL, Hurwitz C, Heerema NA, Hirsch B, Raimondi SC, Lange B, Franklin JL, Radich JP, Meshinchi S: Prevalence and prognostic implications of CEBPA mutations in pediatric acute myeloid leukemia (AML): a report from the Children's Oncology Group. Blood; 2009 Jun 25;113(26):6558-66
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  • [Title] Prevalence and prognostic implications of CEBPA mutations in pediatric acute myeloid leukemia (AML): a report from the Children's Oncology Group.
  • CEBPA mutations have been associated with improved outcome in adult acute myeloid leukemia (AML).
  • We evaluated the prevalence and prognostic significance of CEBPA mutations in 847 children with AML treated on 3 consecutive pediatric trials.
  • CEBPA mutations were significantly more common in older patients, patients with FAB M1 or M2, and patients with normal karyotype.
  • As CEBPA mutations are associated with lower relapse rate and improved survival, CEBPA mutation analysis needs to be incorporated into initial screening for risk identification and therapy allocation at diagnosis.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Neoplasm Proteins / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Clinical Trials as Topic / statistics & numerical data. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease-Free Survival. Female. Humans. Infant. Kaplan-Meier Estimate. Male. Polymorphism, Genetic. Prevalence. Prognosis. Protein Structure, Tertiary. Retrospective Studies. Treatment Outcome. Young Adult

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  • (PMID = 19304957.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00002798/ NCT00070174
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009351; United States / NCI NIH HHS / CA / R21 CA10262-01; United States / NCI NIH HHS / CA / R01 CA114563-01; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / U10 CA98543
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC2943755
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51. Ullah K, Ahmed P, Raza S, Satti TM, Chaudhry QU, Akhtar F, Kamal MK, Akhtar FM, Khan B: Management of acute myeloid leukaemia--5 years experience at Armed Forces Bone Marrow Transplant Centre, Rawalpindi. J Pak Med Assoc; 2007 Sep;57(9):434-9
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  • [Title] Management of acute myeloid leukaemia--5 years experience at Armed Forces Bone Marrow Transplant Centre, Rawalpindi.
  • OBJECTIVE: To evaluate the outcome in denovo AML patients treated with different remission induction and consolidation chemotherapy regimens in our population.
  • METHODS: A retrospective study on acute myeloid leukaemia (AML) patients was carried out at Armed Forces Bone Marrow Transplant Centre Rawalpindi Pakistan between July 2001 and June 2006.
  • During 5 years period 46 patients received treatment for AML at our centre.
  • These 46 patients were categorized into two groups on the basis of type of leukaemia and chemotherapy given.
  • In group-I 40 patients (group Ia: 23 patients of M1-M6, less M3 group Ib: 17 patients of AML M3) received anthracycline and cytarabin based chemotherapy.
  • In group-II, six patients (AML- M3) received all trans retinoic acid (ATRA) based chemotherapy.
  • Survival in AML-M3 patients treated with ATRA based chemotherapy is significantly superior than anthracycline based chemotherapy (66.6% vs. 29.4%).
  • [MeSH-major] Anthracyclines / therapeutic use. Antineoplastic Agents / therapeutic use. Cytarabine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Military Medicine. Military Personnel. Treatment Outcome. Tretinoin / therapeutic use


52. Braham Jmili N, Omri H, Senana Sendi H, Fekih S, Hizem S, Sriha B, Khelif A, Saad A, Kortas M: Identification of the translocation t(15;17) in acute myeloid leukemia (AML) initially classified as FAB M1: case report and review of the literature. Clin Lab; 2006;52(3-4):125-30
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  • [Title] Identification of the translocation t(15;17) in acute myeloid leukemia (AML) initially classified as FAB M1: case report and review of the literature.
  • Immunophenotyping showed myeloid typical markers of granulocytic lineage (MP0+, CD13+, CD33+, CD117+, CD34-).
  • The diagnosis of acute myeloid leukaemia (AML) was then evoked initially.
  • The cytological features corresponded closely to the M1 subtype as defined in the FAB classification.
  • From the biological findings the patient was retrospectively diagnosed as having promyelocytic leukemia (hyperbasophilic form).
  • [MeSH-major] Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Leukemia, Myeloid, Acute / genetics. Leukemia, Promyelocytic, Acute / genetics. Neoplasms, Second Primary / genetics. Translocation, Genetic


53. Abolfazl M, Fatemeh I, Hamid A, Mojtaba G, Alireza MJ, Ali MM: Specific chromosomal abnormalities in patients with acute nonlymphocytic leukemia from the Islamic Republic of Iran. Asian Pac J Cancer Prev; 2006 Jul-Sep;7(3):447-50
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  • [Title] Specific chromosomal abnormalities in patients with acute nonlymphocytic leukemia from the Islamic Republic of Iran.
  • Cytogenetic analysis performed at diagnosis is considered to be the most valuable prognostic factor in acute non-lymphocytic leukemia (ANLL), a very heterogeneous disease.
  • Some 14 were classified as M1, 20 as M2, 19 as M3 , 3 as M4, 1 as M5 and 1 as M6.
  • Trisomy of chromosome 8 (+8) was the most frequent numerical alteration in 3 patients with M1, M2 and M6.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Iran / epidemiology. Karyotyping. Leukemia, Promyelocytic, Acute / epidemiology. Leukemia, Promyelocytic, Acute / genetics. Male. Middle Aged

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  • (PMID = 17059342.001).
  • [ISSN] 1513-7368
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Thailand
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54. Nakamura S, Okinaka K, Hirano I, Ono T, Sugimoto Y, Shigeno K, Fujisawa S, Shinjo K, Ohnishi K: KIS induces proliferation and the cell cycle progression through the phosphorylation of p27Kip1 in leukemia cells. Leuk Res; 2008 Sep;32(9):1358-65
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  • [Title] KIS induces proliferation and the cell cycle progression through the phosphorylation of p27Kip1 in leukemia cells.
  • We showed that KIS protein directly interacted with p27(Kip1) protein, and reduction of KIS inhibited the S10 phosphorylation of p27(Kip1) in leukemia cells.
  • We showed that KIS mRNA expression was increased in primary leukemia specimens (acute myelogenous leukemia (AML); 37, myelodysplastic syndrome (MDS); 72, acute lymphoblastic leukemia (ALL); 23), and the mean ratios of KIS to G3PDH in AML, MDS and ALL specimens were 3.62+/-0.68, 3.27+/-0.73 and 3.17+/-0.58, respectively.
  • Moreover, we found that KIS protein was overexpressed in all 132 adults cases of various leukemias, including 37 AML (8 M1, 12 M2, 2 M3, 7 M4, 8 M5), 72 MDS (42 RAEB-I, 30 REAB-II) and 23 ALL (23 L2).
  • This study demonstrates that the elevated levels of KIS protein in leukemia cells promote the cell cycle progression in leukemia cells.
  • [MeSH-major] Cell Cycle / physiology. Cell Proliferation. Intracellular Signaling Peptides and Proteins / metabolism. Intracellular Signaling Peptides and Proteins / physiology. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Protein-Serine-Threonine Kinases / physiology

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  • (PMID = 18384876.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / UHMK1 protein, human
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55. Vehreschild JJ, Krüger K, Kurzai O, Wickenhauser C, Behringer K, Töx U, Cornely OA: Salvage therapy of refractory chronic disseminated candidiasis in a patient with acute myeloid leukaemia and secondary prophylaxis during allogeneic stem cell transplantation. Mycoses; 2006;49 Suppl 1:42-7
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  • [Title] Salvage therapy of refractory chronic disseminated candidiasis in a patient with acute myeloid leukaemia and secondary prophylaxis during allogeneic stem cell transplantation.
  • We report on the treatment course of a 27-year-old male patient with acute myeloid leukaemia M1 and chronic disseminated candidiasis.
  • [MeSH-major] Antifungal Agents / therapeutic use. Candidiasis / drug therapy. Leukemia, Myeloid, Acute / complications. Salvage Therapy. Triazoles / therapeutic use

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  • (PMID = 16961582.001).
  • [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 / Triazoles; 6TK1G07BHZ / posaconazole
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56. Aydin-Sayitoglu M, Hatirnaz O, Erensoy N, Ozbek U: Role of CYP2D6, CYP1A1, CYP2E1, GSTT1, and GSTM1 genes in the susceptibility to acute leukemias. Am J Hematol; 2006 Mar;81(3):162-70
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  • [Title] Role of CYP2D6, CYP1A1, CYP2E1, GSTT1, and GSTM1 genes in the susceptibility to acute leukemias.
  • Acute leukemias (ALs) are heterogeneous diseases.
  • Functional polymorphisms in the genes encoding detoxification enzymes cause inter-individual differences, which contribute to leukemia susceptibility.
  • The CYP2D6, CYP1A1, CYP2E1, GSTT1, and GSTM1 polymorphisms in ALL (n = 156) and AML (n = 94) patients and 140 healthy controls were genotyped by PCR and/or PCR-RFLP using blood or bone marrow samples.
  • Patients with ALL and AML had a higher prevalence of the GSTM1 deletions compared to controls but only the difference among adult AML patients (OR = 2.1, 95% CI = 1.0-4.2) was statistically significant.
  • The CYP2D6*3 variant allele frequency was lower in the overall acute leukemia patients (0.6%) compared to controls (P = 0.03).
  • CYP2D6*1/*3 genotype frequency also showed a protective association in AML patients (OR = 0.09, 95% CI = 0.01-1.7; P = 0.04).
  • We also found a risk association for CYP2E1*5 in ALL and AML (OR = 3.6, 95% CI = 1.4-9.4 and OR = 3.9, 95% CI = 1.4-10.5, respectively).
  • No association was found for the studied CYP2D6*4, CYP1A1*2A, and GSTT1"null" variants and the risk of acute leuke-mia (ALL or AML).
  • This case-control study suggests a contribution of CYP2E1, CYP2D6, and GSTM1 "null" variants to the development of acute leukemias.
  • [MeSH-major] Cytochrome P-450 CYP1A1 / genetics. Cytochrome P-450 CYP2D6 / genetics. Cytochrome P-450 CYP2E1 / genetics. Genetic Predisposition to Disease. Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16493615.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.14.13.- / Cytochrome P-450 CYP2E1; EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 1.14.14.1 / Cytochrome P-450 CYP2D6; 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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57. Tempescul A, Guillerm G, Douet-Guilbert N, Morel F, Le Bris MJ, De Braekeleer M: Translocation (10;17)(p15;q21) is a recurrent anomaly in acute myeloblastic leukemia. Cancer Genet Cytogenet; 2007 Jan 1;172(1):74-6
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  • [Title] Translocation (10;17)(p15;q21) is a recurrent anomaly in acute myeloblastic leukemia.
  • We report here two cases of patients with acute myeloblastic leukemia, type M1 (FAB classification), associated with a t(10;17)(p15;q21).
  • Four other patients with this translocation have been reported, three of them having acute undifferentiated or poorly differentiated leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 17175384.001).
  • [ISSN] 0165-4608
  • [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 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / retinoic acid receptor alpha; 143220-95-5 / PML protein, human
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58. Ahmad F, Dalvi R, Mandava S, Das BR: Acute Myelogeneous Leukemia (M0/M1) with novel chromosomal abnormality of t(14;17) (q32; q11.2). Am J Hematol; 2007 Jul;82(7):676-8
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  • [Title] Acute Myelogeneous Leukemia (M0/M1) with novel chromosomal abnormality of t(14;17) (q32; q11.2).
  • Acute Myelogeneous Leukemia (AML) is a heterogeneous disease with respect to morphology, immunophenotype, and genetic rearrangements.
  • In this study, we report a case whose clinical features were suggestive of AML-M1 subtype with t(14;17) (q32; q11.2) karyotype involving rearrangement of chromosomal segments 17q11.2 and 14q32.
  • This is the first report of novel chromosomal translocation in this subset of AML and has not yet been reported elsewhere.
  • [MeSH-major] Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 17177193.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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59. Trivedi PJ, Patel PS, Brahmbhatt MM, Patel BP, Gajjar SB, Dalal EN, Shukla SN, Shah PM, Bakshi SR: A new recurring chromosome 13 abnormality in two older patients with de novo acute myeloid leukemia: An Indian experience. Indian J Hum Genet; 2009 Sep;15(3):137-9
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  • [Title] A new recurring chromosome 13 abnormality in two older patients with de novo acute myeloid leukemia: An Indian experience.
  • We report here two cases of trisomy 13 in acute myeloid leukemia M1 subtype. short-term unstimulated bone marrow and peripheral blood lymphocyte culture showed 47, XY, +13 in all metaphase plates and trisomy 13 was confirmed with whole chromosome paint probes.
  • Trisomy 13 in AML-M1 is a rare numerical abnormality.
  • This is the first Indian report of sole trisomy 13 in AML-M1.

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  • (PMID = 21088719.001).
  • [ISSN] 0971-6866
  • [Journal-full-title] Indian journal of human genetics
  • [ISO-abbreviation] Indian J Hum Genet
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2922630
  • [Keywords] NOTNLM ; Acute myeloid leukemia-M1 / recurrent / sole abnormality / trisomy 13
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60. Ardianto B, Sugimoto T, Kawano S, Kasagi S, Jauharoh SN, Kurimoto C, Tatsumi E, Morikawa K, Kumagai S, Hayashi Y: The HPB-AML-I cell line possesses the properties of mesenchymal stem cells. J Exp Clin Cancer Res; 2010;29:163
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  • [Title] The HPB-AML-I cell line possesses the properties of mesenchymal stem cells.
  • BACKGROUND: In spite of its establishment from the peripheral blood of a case with acute myeloid leukemia (AML)-M1, HPB-AML-I shows plastic adherence with spindle-like morphology.
  • In addition, lipid droplets can be induced in HPB-AML-I cells by methylisobutylxanthine, hydrocortisone, and indomethacin.
  • These findings suggest that HPB-AML-I is similar to mesenchymal stem cells (MSCs) or mesenchymal stromal cells rather than to hematopoietic cells.
  • METHODS: To examine this possibility, we characterized HPB-AML-I by performing cytochemical, cytogenetic, and phenotypic analyses, induction of differentiation toward mesenchymal lineage cells, and mixed lymphocyte culture analysis.
  • RESULTS: HPB-AML-I proved to be negative for myeloperoxidase, while surface antigen analysis disclosed that it was positive for MSC-related antigens, such as CD29, CD44, CD55, CD59, and CD73, but not for CD14, CD19, CD34, CD45, CD90, CD105, CD117, and HLA-DR.
  • Karyotypic analysis showed the presence of complicated abnormalities, but no reciprocal translocations typically detected in AML cases.
  • Following the induction of differentiation toward adipocytes, chondrocytes, and osteocytes, HPB-AML-I cells showed, in conjunction with extracellular matrix formation, lipid accumulation, proteoglycan synthesis, and alkaline phosphatase expression.
  • Mixed lymphocyte culture demonstrated that CD3+ T-cell proliferation was suppressed in the presence of HPB-AML-I cells.
  • CONCLUSIONS: We conclude that HPB-AML-I cells appear to be unique neoplastic cells, which may be derived from MSCs, but are not hematopoietic progenitor cells.

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  • (PMID = 21144016.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3016278
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61. Mu QT, Chen ZM, Lou JY, Cheng YZ, Wang YG, Ni WM, Wang HP, Xu H, Yu YB, Jin J: [Cytogenetic analysis of 154 case of acute myeloid leukemia with t(8;21)]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2010 May;39(3):236-40
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  • [Title] [Cytogenetic analysis of 154 case of acute myeloid leukemia with t(8;21)].
  • OBJECTIVE: To investigate the cytogenetic features of acute myeloid leukemia (AML) with t(8;21).
  • METHODS: The clinical characteristics of 154 cases of acute myeloid leukemia with t(8;21) in our hospital were analyzed retrospectively.
  • According to the chromosome karyotype, all cases were divided into three groups: the group without additional chromosome abnormality, the group with single sex chromosome loss and the group with additional chromosome abnormalities other than sex chromosome loss.
  • RESULT: In this study, according to FAB classification, there were 127 cases of M2 (82.5%), 15 of M5 (9.7%), 6 of M4 (3.9%), 4 of M1(2.6%) and 2 of M0(1.3%).
  • Cytogenetically, 85 (55.2%) AML patients with t(8;21) had additional chromosome abnormalities.
  • In the group of t(8;21) with additional chromosome abnormalities, 11 cases (35.5%) were non-M2 AML, higher than that in single t(8;21) group (17.4%)(P<0.05); however, there was no significant difference between the group of single t(8;21) and the group of t(8;21) with single sex chromosome loss(P>0.05).
  • CONCLUSION: t(8;21) translocation is usually accompanied by additional chromosome abnormalities, particularly in M2; while t(8;21) with additional chromosome abnormalities other than sex chromosome loss is more frequently observed in non-M2 AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics

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  • (PMID = 20544983.001).
  • [ISSN] 1008-9292
  • [Journal-full-title] Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
  • [ISO-abbreviation] Zhejiang Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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62. Liu YR, Wang YZ, Chen SS, Chang Y, Fu JY, Li LD, Wang H, Yu H, Jiang B, Huang XJ: [Analysis of immunophenotype and leukemia associated immunophenotype in 610 patients with acute myeloid leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2007 Nov;28(11):731-6
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  • [Title] [Analysis of immunophenotype and leukemia associated immunophenotype in 610 patients with acute myeloid leukemia].
  • OBJECTIVE: To analyze the immunophenotype and leukemia associated immunophenotype (LAIP) of leukemia cells from patients with acute myeloid leukemia (AML) in minimal residual disease (MRD) detection.
  • METHODS: Four-color multiparametric flow cytometry (FCM) with CD45/SSC gating was used to determine the expression of the following antibodies of CD7, CD117, CD33, CD34, CD10, CD19, CD56, CD38, CD13, CD14, CD64, CD9, CD16, CD2, CD5, CD11b, CD123, HLA-DR in 610 AML patients and 20 normal bone marrow (NBM) samples.
  • In AML patients, most cases were CD117+ (95.08%), CD38+ (94.74%), CD9+ (84.93%), CD33+ (84.60%), HLA-DR+ (77.23%) and CD13 (75.25%).
  • 86.39% of AML patients were found to have at least one LAIP, the highest incidence being in AML-M1 and M3 subtypes and the lowest in AML-M4Eo subtype.
  • For asynchronous antigen expression, CD34+ CD64+, CD117+ CD11b+ , CD34+ CD38(-/dim) and CD34+ HLA-DR(-/dim) were seldom expressed on normal BMMNCs (about 0.01%), and the logarithm difference between AML and NBM was larger than 3.0, being the more sensitive LAIP.
  • CONCLUSION: MRD detection by multiparameter flow cytometry can be applied to more than 80% of AML patients.
  • [MeSH-major] Immunophenotyping. Leukemia, Myeloid, Acute / immunology. Neoplasm, Residual / diagnosis

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  • (PMID = 18457262.001).
  • [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
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63. Wang L, Xu WL, Meng HT, Qian WB, Mai WY, Tong HY, Mao LP, Tong Y, Qian JJ, Lou YJ, Chen ZM, Wang YG, Jin J: FLT3 and NPM1 mutations in Chinese patients with acute myeloid leukemia and normal cytogenetics. J Zhejiang Univ Sci B; 2010 Oct;11(10):762-70
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  • [Title] FLT3 and NPM1 mutations in Chinese patients with acute myeloid leukemia and normal cytogenetics.
  • Mutations of fms-like tyrosine kinase 3 (FLT3) and nucleophosmin (NPM1) exon 12 genes are the most common abnormalities in adult acute myeloid leukemia (AML) with normal cytogenetics.
  • To assess the prognostic impact of the two gene mutations in Chinese AML patients, we used multiplex polymerase chain reaction (PCR) and capillary electrophoresis to screen 76 AML patients with normal cytogenetics for mutations in FLT3 internal tandem duplication (FLT3/ITD) and exon 12 of the NPM1 gene.
  • Significantly more FLT3/ITD aberration was detected in subjects with French-American-British (FAB) M1 (42.8%).
  • Our results indicate that the FLT3/ITD mutation might be a prognostic factor for an unfavorable outcome in Chinese AML subjects with normal cytogenetics, while NPM1 mutation may be a favorable prognostic factor for OS and RFS in the presence of FLT3/ITD.
  • [MeSH-major] Asian Continental Ancestry Group / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 20872983.001).
  • [ISSN] 1862-1783
  • [Journal-full-title] Journal of Zhejiang University. Science. B
  • [ISO-abbreviation] J Zhejiang Univ Sci B
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antigens, CD7; 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
  • [Other-IDs] NLM/ PMC2950237
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64. Barragan E, Collado M, Cervera J, Martin G, Bolufer P, Roman J, Sanz MA: The GST deletions and NQO1*2 polymorphism confers interindividual variability of response to treatment in patients with acute myeloid leukemia. Leuk Res; 2007 Jul;31(7):947-53
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  • [Title] The GST deletions and NQO1*2 polymorphism confers interindividual variability of response to treatment in patients with acute myeloid leukemia.
  • Functional polymorphisms in the genes encoding detoxification enzymes could modify the response to treatment in acute myeloid leukemia and therefore affect the final clinical outcome.
  • In the present study, we genotyped 153 patients diagnosed with de novo acute myeloid leukemia (AML) to clarify the influence of the genetic polymorphisms CYP1A1*2A, CYP3A4*1B, CYP2E1*5B, del{GSTT1}, del{GSTM1}, and NQO1*2 on disease outcome.
  • The del{GSTM1} showed a higher frequency in females (62%) than in males (41%) (P=0.01).
  • [MeSH-major] Gene Deletion. Glutathione Transferase / genetics. Leukemia, Myeloid / genetics. NAD(P)H Dehydrogenase (Quinone) / genetics. Polymorphism, Genetic / genetics
  • [MeSH-minor] Acute Disease. Cytochrome P-450 CYP1A1 / genetics. Cytochrome P-450 CYP2E1 / genetics. Cytochrome P-450 CYP3A. Cytochrome P-450 Enzyme System / genetics. Disease-Free Survival. Female. Genotype. Humans. Male. Middle Aged. Survival Rate. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 17118447.001).
  • [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] 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.13.- / Cytochrome P-450 CYP2E1; EC 1.14.13.67 / CYP3A4 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 1.14.14.1 / Cytochrome P-450 CYP3A; 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; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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65. Das P, Shaik AP, Bammidi VK: Meta-analysis study of glutathione-S-transferases (GSTM1, GSTP1, and GSTT1) gene polymorphisms and risk of acute myeloid leukemia. Leuk Lymphoma; 2009 Aug;50(8):1345-51
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  • [Title] Meta-analysis study of glutathione-S-transferases (GSTM1, GSTP1, and GSTT1) gene polymorphisms and risk of acute myeloid leukemia.
  • To investigate the association of glutathione-S-transferase (GST) polymorphisms with the risk of acute myeloid leukemia (AML), a meta-analysis of case-control studies published between 1998 and 2009 was performed.
  • Statistically, significant increased risk of AML was observed with GSTM1 while borderline significance was seen with GSTT1 null genotypes.
  • However, fixed-effects model showed significant risk of AML in the presence of null genotypes of GSTM1 and GSTT1(p < 0.05).
  • Significant heterogeneity was found between studies relating to GSTP1 (p = 0.162), however, no heterogeneity was seen in studies that evaluated GSTM1 (Q-value = 44; I(2) = 70.9; p-value < 0.01]; and GSTT1 (Q-value = 26.03; I(2) = 57.74; p-value < 0.01] polymorphisms.
  • From the limited studies on the association of GSTP1 with risk of AML, the role of this gene cannot be ascertained fully.
  • Significant association of these three genes with risk of AML must be evaluated further with respect to population, smoking, eating habits, ethnicity, and race.
  • [MeSH-major] Glutathione S-Transferase pi / genetics. Glutathione Transferase / genetics. Leukemia, Myeloid / genetics. Neoplasm Proteins / genetics. Polymorphism, Genetic
  • [MeSH-minor] Acute Disease. Alleles. Carcinogens / pharmacokinetics. Case-Control Studies. Confounding Factors (Epidemiology). Gene Frequency. Genetic Predisposition to Disease. Genotype. Humans. Models, Genetic. Odds Ratio. Risk. Selection Bias


66. Syampurnawati M, Tatsumi E, Furuta K, Takenokuchi M, Nakamachi Y, Kawano S, Kumagai S, Saigo K, Matsui T, Takahashi T, Nagai K, Yabe H, Kondo S, Hayashi Y: HLA-DR-negative AML (M1 and M2): FLT3 mutations (ITD and D835) and cell-surface antigen expression. Leuk Res; 2007 Jul;31(7):921-9
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  • [Title] HLA-DR-negative AML (M1 and M2): FLT3 mutations (ITD and D835) and cell-surface antigen expression.
  • FLT3 mutations and cell-surface antigen were investigated in 29 DR-negative (DR(-)) M1/M2 AML samples in comparison with 30 DR-positive (DR(+)) M1/M2 AML samples.
  • Our results indicated that FLT3 mutation is the most common gene alteration found in the DR(-) M1/M2 AML.
  • These results are important for further characterizing this phenotypic AML entity.
  • [MeSH-major] Antigens, Surface / metabolism. HLA-DR Antigens / metabolism. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 17056111.001).
  • [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 / Antigens, CD34; 0 / Antigens, CD7; 0 / Antigens, Surface; 0 / HLA-DR Antigens; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.1.3.48 / Antigens, CD45
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67. Shafarenko M, Liebermann DA, Hoffman B: Egr-1 abrogates the block imparted by c-Myc on terminal M1 myeloid differentiation. Blood; 2005 Aug 1;106(3):871-8
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  • [Title] Egr-1 abrogates the block imparted by c-Myc on terminal M1 myeloid differentiation.
  • Thus, understanding functional interactions between genes that regulate normal blood cell development, including cell growth and differentiation, and how their altered expression contributes to leukemia, is important for rational drug design.
  • Ectopic expression of Egr-1 in M1 myeloblastic leukemia cells was observed to activate the macrophage differentiation program in the absence of the differentiation inducer interleukin 6 (IL-6) and to promote terminal differentiation in its presence.
  • In addition, we have shown that deregulated expression of the proto-oncogene c-myc blocks the myeloid terminal differentiation program.
  • Here we show that restoring expression of Egr-1 in M1 cells that express deregulated c-Myc abrogates the c-Myc block in terminal differentiation, resulting in cells that undergo functional macrophage maturation.

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  • (PMID = 15840692.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 1 RO1 CA59774; United States / NCI NIH HHS / CA / 1 RO1 CA81168; United States / NCI NIH HHS / CA / CA88261-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Early Growth Response Protein 1; 0 / Egr1 protein, mouse; 0 / Immediate-Early Proteins; 0 / Myc protein, mouse; 0 / Proto-Oncogene Proteins c-myc; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1895156
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68. Bungaro S, Raghavan M, Dell'Oro MG, Paolucci P, Young BD, Biondi A, Cazzaniga G: Assessment of submicroscopic genetic lesions by single nucleotide polymorphism arrays in a child with acute myeloid leukemia and FLT3-internal tandem duplication. Haematologica; 2006 Jul;91(7):998-1000
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  • [Title] Assessment of submicroscopic genetic lesions by single nucleotide polymorphism arrays in a child with acute myeloid leukemia and FLT3-internal tandem duplication.
  • The same FLT3-internal tandem duplication (ITD) positive clone was detected at diagnosis and relapse, but not at birth, in a child with M1 acute myeloid leukemia.
  • [MeSH-major] Gene Deletion. Leukemia, Myeloid, Acute / genetics. Oligonucleotide Array Sequence Analysis / methods. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16757411.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6438; United Kingdom / Cancer Research UK / / A6789
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [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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69. Callera F, Mulin CC, Rosa ES, Melo DB, Melo CM: High prevalence of morphological subtype FAB M1 in adults with de novo acute myeloid leukemia in São José dos Campos, São Paulo. Sao Paulo Med J; 2006 Jan 5;124(1):45-7
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  • [Title] High prevalence of morphological subtype FAB M1 in adults with de novo acute myeloid leukemia in São José dos Campos, São Paulo.
  • CONTEXT AND OBJECTIVE: Geographical variations have been described in acute myelogenous leukemia (AML).
  • The aim of this study was to demonstrate the high prevalence of French-American-British (FAB) M1 subtype in adults with de novo AML in São José dos Campos, State of São Paulo, Brazil.
  • METHODS: Records from 39 consecutive adult patients with de novo AML referred to Hospital Pio XII between January 2002 and September 2004 were reviewed.
  • Peripheral blood and blood marrow smears were reviewed blindly by five hematologists and classified according to FAB criteria.
  • The rates of remission, relapse, mortality according treatment phase, survival and leukemia-free survival were calculated.
  • RESULTS: The prevalence of each category as determined via a consensus among five observers was M0: 0%; M1: 43.6%; M2: 30.7%; M3: 12.8%; M4: 5.1%; M5: 2.6%: M6: 2.6%; and M7: 2.6%.
  • The survival rate was 30% and leukemia-free survival was 33%.
  • CONCLUSIONS: The study demonstrated a high prevalence of FAB M1 subtype in adults with de novo AML in São José dos Campos.
  • Our data suggest the occurrence of different regional prevalences of FAB AML categories in Brazil.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology

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  • (PMID = 16612463.001).
  • [ISSN] 1516-3180
  • [Journal-full-title] São Paulo medical journal = Revista paulista de medicina
  • [ISO-abbreviation] Sao Paulo Med J
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
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70. McManus PM: Classification of myeloid neoplasms: a comparative review. Vet Clin Pathol; 2005 Sep;34(3):189-212
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  • [Title] Classification of myeloid neoplasms: a comparative review.
  • Classification of myeloid neoplasms in veterinary medicine was modeled in the early 1990s after French-American-British and National Cancer Institute systems used in human medicine.
  • WHO revisions lower the blast threshold from 30% to 20% for diagnosing acute myeloid leukemia (AML) and expand and redefine AML categories.
  • AML is now subdivided into 4 broad groups:.
  • 1) AML with recurrent genetic abnormalities, 2) AML with multilineage dysplasia, 3) AML with previous chemotherapy and/or radiation, and 4) AML, not otherwise categorized.
  • AML alphanumeric designations (M1, M2, etc) have been discontinued as numbers of subtypes have increased.
  • At least 10% of cells from each of 2 lineages must display atypia for a diagnosis of RCMD.
  • That threshold is 50% for diagnosing AML with multilineage dysplasia.
  • Chronic myelomonocytic leukemia has been removed from the MDS category and included in a new category of diseases that have features of both MDS and chronic leukemia.


71. Wang J, Wang T, Li S, Lin L, Gang Y: [Flt-3/ITD mutation in pediatric leukemia and its clinical significance]. Ai Zheng; 2007 Jan;26(1):58-63
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  • [Title] [Flt-3/ITD mutation in pediatric leukemia and its clinical significance].
  • BACKGROUND & OBJECTIVE: Flt-3 internal tandem duplication (Flt-3/ITD) in transmembrane region is the most frequently identified mutation in Flt-3 gene, which is the most frequently happened in acute myeloid leukemia (AML) and correlated to prognosis.
  • This study was to explore the correlation of Flt-3/ITD mutation to the occurrence of pediatric leukemia, and analyze its clinical significance.
  • METHODS: Flt-3/ITD mutation status in bone marrow samples from 302 children with leukemia, including 122 cases of AML, 124 cases of acute lymphoblastic leukemia (ALL), 17 cases of juvenile chronic myelogenous leukemia (JCML), and 39 cases of myelodysplastic syndromes (MDS), were examined by polymerase chain reaction (PCR) and sequencing.
  • RESULTS: Of the 122 AML patients, 98 (80.32%) had Flt-3 gene products in bone marrow.
  • Flt-3/ITD mutation was detected in 21 (17.21%) of the 122 patients; the mutation rates were 42.86% (3/7) in M0, 22.22% (2/9) in M1, 12.90% (4/31) in M2, 44.44% (8/18) in M4, and 15.38% (4/26) in M5.
  • Of the 19 AML patients with Flt3/ITD mutation, the median survival time was 13.5 months (0-47 months), which was significantly shorter than that of the patients without Flt-3/ITD mutation (P<0.05).
  • Chromosome karyotype analysis showed chromosome abnormity, including t(11; 12)(p15; q13), inv16(q21; q23), and t(6; 9)(p23; q23), in 3 AML patients with Flt-3/ITD.
  • CONCLUSIONS: Flt-3/ITD mutations are usually detected in AML, seldom in ALL, not in MDS and JCML.
  • Flt-3/ITD mutation is correlated to AML onset and progress.
  • Flt-3/ITD is a significant marker to analyze AML prognosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Base Sequence. Child. Child, Preschool. Chromosome Aberrations. DNA, Neoplasm / genetics. Female. Follow-Up Studies. Gene Expression Regulation, Neoplastic. Humans. Infant. Leukemia, Myelomonocytic, Juvenile / genetics. Leukemia, Myelomonocytic, Juvenile / metabolism. Male. Molecular Sequence Data. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / metabolism. Prognosis

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  • (PMID = 17222369.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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72. 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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73. Reisch N, Roehnisch T, Sadeghi M, Greiner L, Regenbogen C, Rieger J, Emmerich B, Oduncu F: AML M1 presenting with recurrent acute large arterial vessel thromboembolism. Leuk Res; 2007 Jun;31(6):869-71
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  • [Title] AML M1 presenting with recurrent acute large arterial vessel thromboembolism.
  • Acute leukemia may be associated with coagulopathy, predominantly severe bleeding diathesis caused by disseminated intravascular coagulation (DIC) and/or hyperfibrinolysis.
  • Disordered hemostasis is characteristic for acute promyelocytic leukemia (APL, FAB M3).
  • We report a case of severe recurrent acute arterial thromboembolism at presentation in AML FAB M1.
  • Most likely, the ischemic events in our patient resulted from leukemia as the thrombus material included many leukemic blasts.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Thromboembolism / etiology
  • [MeSH-minor] Adult. Amputation. Disseminated Intravascular Coagulation / etiology. Female. Hemorrhagic Disorders / etiology. Humans. Iliac Artery / pathology. Iliac Artery / radiography. Ischemia / etiology. Ischemia / pathology. Ischemia / radiography. Ischemia / surgery. Leg / blood supply. Leg / pathology. Leg / radiography. Leg / surgery. Leukemia, Promyelocytic, Acute / complications

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  • (PMID = 17011031.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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74. Ozkan A, Ali R, Ozkalemkas F, Ozcelik T, Ozkocaman V: Acute myeloblastic leukaemia (AML-M1) presenting with prominent gingival hypertrophy. Eur J Haematol; 2007 Jun;78(6):547
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  • [Title] Acute myeloblastic leukaemia (AML-M1) presenting with prominent gingival hypertrophy.
  • [MeSH-major] Gingival Diseases / physiopathology. Leukemia, Myeloid, Acute / physiopathology

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  • (PMID = 17331137.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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75. Harani MS, Adil SN, Shaikh MU, Kakepoto GN, Khurshid M: Frequency of fab subtypes in acute myeloid leukemia patients at Aga Khan University Hospital Karachi. J Ayub Med Coll Abbottabad; 2005 Jan-Mar;17(1):26-9
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  • [Title] Frequency of fab subtypes in acute myeloid leukemia patients at Aga Khan University Hospital Karachi.
  • BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous disease.
  • The commonly used method for diagnosis and classification is based on FAB criteria using morphology and cytochemical stains.
  • The aim of present study is to determine the frequency of various sub types in acute myeloid leukemia using FAB criteria in our population.
  • This will aid in the correct diagnosis of acute leukemia and hence proper management of the patients.
  • The patients were diagnosed on the basis of bone marrow morphology using FAB classification.
  • AML-M4 was the predominant French-American-British (FAB) subtype (36.2%) followed by M2 (30.25%), M3 (10.4%), M1 (8.7%), M0 (7.7%), M5a (3.5%), M5b (2.5%) and M6 (0.8%).
  • CONCLUSIONS: The most common FAB subtype observed in our study was Acute myelomonocytic leukemia (M4) which is in accordance with studies reported from Saudia Arabia and a previous study reported from our institution.
  • However,other national and international studies have reported Myeloblastic Leukemia with maturation (M2) as the predominant subtype of AML.
  • [MeSH-major] Leukemia, Myeloid / classification
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Case-Control Studies. Child. Child, Preschool. Female. Hospitals, University. Humans. Infant. Male. Middle Aged. Pakistan

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  • (PMID = 15929522.001).
  • [ISSN] 1025-9589
  • [Journal-full-title] Journal of Ayub Medical College, Abbottabad : JAMC
  • [ISO-abbreviation] J Ayub Med Coll Abbottabad
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
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76. Kang LC, Dunphy CH: Immunoreactivity of MIC2 (CD99) and terminal deoxynucleotidyl transferase in bone marrow clot and core specimens of acute myeloid leukemias and myelodysplastic syndromes. Arch Pathol Lab Med; 2006 Feb;130(2):153-7
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  • [Title] Immunoreactivity of MIC2 (CD99) and terminal deoxynucleotidyl transferase in bone marrow clot and core specimens of acute myeloid leukemias and myelodysplastic syndromes.
  • CONTEXT: MIC2 ("thymus leukemia") antigen has been shown to be expressed by T cells and monocytes, as well as B cells and granulocyte-lineage cells.
  • It is most intensely expressed by the most immature thymus T-lineage cells and is more intensely expressed by CD34-positive/CD33-positive myeloid cells (compared to more mature myeloid cells) and the earliest CD34-positive/CD10-positive B-cell precursor cells (compared to cells of later B-cell precursor stages).
  • It has also been shown to be expressed in a few terminal deoxynucleotidyl transferase (TdT)-positive myeloid processes, but has been uniformly negative in TdT-negative myeloid processes.
  • A more recent study showed that 43% of acute myeloid leukemias (AMLs) and 55% of chloromas express CD99, concluding that CD99 is commonly expressed in AML and rarely seen in myeloproliferative disorders, myelodysplastic syndromes, or normal bone marrow.
  • Although this study speculated that MIC2 expression was probably not limited to TdT-positive AML, there was no comparison with TdT reactivity in this study.
  • OBJECTIVE: Since AML and high-grade myelodysplastic syndrome may occasionally be difficult to distinguish morphologically from acute lymphoblastic leukemia and ES/ PNET, we undertook a study to analyze MIC2 expression in conjunction with TdT reactivity in distinguishing AML or high-grade myelodysplastic syndrome from acute lymphoblastic leukemia and ES/PNET.
  • DESIGN: We studied bone marrow core and clot paraffin specimens from AML (classified according to criteria of the World Health Organization; n = 49), myelodysplastic syndromes (n = 4), precursor B-cell acute lymphoblastic leukemia (n = 4), ES/PNET (n = 1), and normal bone marrow (n = 3) with MIC2 (CD99) and TdT immunohistochemistry.
  • RESULTS: Overall, CD99 was expressed in 24 (49%) of 49 AML cases, including all (11/11) TdT-positive cases.
  • CD99 was expressed in all subtypes of AML except M5.
  • Expression of TdT was limited to a subset of AML-M0, -M1, -M2, and -M4, and AML with multilineage dysplasia.
  • An M5 AML may likely be excluded based on a uniform TdT-negative/CD99-negative immunophenotype.
  • [MeSH-major] Antigens, CD / metabolism. Bone Marrow / metabolism. Cell Adhesion Molecules / metabolism. DNA Nucleotidylexotransferase / metabolism. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism
  • [MeSH-minor] Diagnosis, Differential. Flow Cytometry. Humans. Immunohistochemistry. Neuroectodermal Tumors, Primitive / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Retrospective Studies. Sarcoma, Ewing / diagnosis

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  • (PMID = 16454553.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; EC 2.7.7.31 / DNA Nucleotidylexotransferase
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77. Wei J, Zhou XF, Zhao F, Zhou JF, Chen Y: Immunologic characteristics and prognosis of myelodysplastic syndrome new subtype: refractory anemia with excess blasts-II. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Feb;17(1):111-6
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  • 35 cases of adult patients with de novo MDS were investigated.
  • 47 cases of acute myeloid leukemia (AML) M1, 51 cases of AML-M(2) and 38 cases of acute lymphocytic leukemia (ALL) were selected as control.
  • CD13 in RAEB-II was significantly higher than that in refractory cytopenia with or without multilineage dysplasia (RA/RCMD) (p < 0.01) and REAB-I (p < 0.05); CD33, CD117 (p < 0.05) and stem cell antigen CD34 (p < 0.01) in RAEB-II were significantly higher than that in RCMD (p < 0.01), but no statistically significant difference was found as compared with RAEB-I (p > 0.05).
  • Compared with AML-M(1) and AML-M(2), no significant difference of CD13 and CD117 in RAEB-II was found (p > 0.05).
  • CD33 (p < 0.01) and CD34 (p < 0.05) were significantly lower than that in AML-M(1), but no significant difference was found as compared with AML-M(2) (p > 0.05); CD15 (p < 0.01) and CD11b (p < 0.05) was significantly lower than that in M(2), but no significant difference was found as compared with AML-M(1) (p > 0.05); MPO was significantly lower than that in AML-M(1) and M(2) (p < 0.05); HLA-DR was significantly higher than that on AML-M(2) (p < 0.05), but no significant difference was found as compared with AML-M(1) (p > 0.05).
  • RAEB-II did not express CD2, CD3, CD5 and CD8 (positive rate 0%, p < 0.01) when compared with T-ALL; CD4 (p < 0.05) and CD7 (p < 0.01) were significantly lower than that in T-ALL.
  • RAEB-II did not express CD19 and CD20 (positive rate 0%, p < 0.01) as compared with B-ALL; CD10, CD22 and cCD79a were significantly lower than that in B-ALL (p < 0.05).
  • It is concluded that RAEB-II expresses mainly myeloid antigen without or with little expression of lymphoid antigen.


78. Novotny JR, Müller-Beissenhirtz H, Herget-Rosenthal S, Kribben A, Dührsen U: Grading of symptoms in hyperleukocytic leukaemia: a clinical model for the role of different blast types and promyelocytes in the development of leukostasis syndrome. Eur J Haematol; 2005 Jun;74(6):501-10
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  • [Title] Grading of symptoms in hyperleukocytic leukaemia: a clinical model for the role of different blast types and promyelocytes in the development of leukostasis syndrome.
  • OBJECTIVE: Patients with hyperleukocytic leukaemia were graded according to the severity of symptoms possibly caused by leukostasis to evaluate the effectiveness of therapy and to test the relative contribution of blast type and count of blasts and promyelocytes in the development of leukostasis syndrome.
  • METHODS: Ninety-five patients (59 male, 36 female, median age 52 yr) with hyperleukocytic leukaemia [leukocytes above 50 x 10(9)/L, 48 acute myeloid leukaemia (AML), 31 chronic myeloid leukaemia (CML), 13 acute lymphoblastic leukaemia (ALL), three chronic myelomonocytic leukaemia (CMML)] were grouped according to the presence or absence and severity of neurologic, pulmonary and other symptoms into four categories (no, possible, probable and highly probable leukostasis syndrome).
  • RESULTS: Patients with myeloid leukaemia (AML M1/M2, CML) which scored as highly probable leukostasis showed significantly higher WBC (P = 0.011), lower haemoglobin (P = 0.004), higher peripheral blast counts (P = 0.004) and higher total of peripheral blasts plus promyelocytes (P < 0.001) compared with the lower probability groups.
  • In leukaemia involving the monocytic lineage (AML M4/M5, CMML) no significant differences were found in any of these factors between patients with highly probable leukostasis and the other patients.
  • We further demonstrate that the mechanisms of leukostasis are different in myeloid leukaemia as compared with leukaemia with involvement of the monocytic lineage.
  • [MeSH-major] Blast Crisis / pathology. Leukemia, Myeloid / pathology. Myelodysplastic Syndromes / pathology

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  • (PMID = 15876254.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Hemoglobins
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79. Kebriaei P, Kline J, Stock W, Kasza K, Le Beau MM, Larson RA, van Besien K: Impact of disease burden at time of allogeneic stem cell transplantation in adults with acute myeloid leukemia and myelodysplastic syndromes. Bone Marrow Transplant; 2005 May;35(10):965-70
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  • [Title] Impact of disease burden at time of allogeneic stem cell transplantation in adults with acute myeloid leukemia and myelodysplastic syndromes.
  • The impact of disease burden on the outcome of patients with acute myeloid leukemia (AML) undergoing allogeneic stem cell transplantation (SCT) has not been well defined.
  • Data from several retrospective series suggest that overt leukemia at the time of transplant increases the risk of relapse.
  • We reviewed the outcomes of 68 consecutive adults with AML (n=60) or myelodysplastic syndromes (MDS) (n=8) who received an allogeneic SCT at the University of Chicago between May 1986 and October 2002 to confirm the importance of currently recognized risk factors for overall survival (OS) and progression-free survival (PFS).
  • AML subtypes based on the FAB classification were as follows: M0=9, M1=9, M2=16, M3=2, M4=16, M5=3, M6=5.
  • Using standard morphologic criteria, 34 patients were in complete remission (CR) and 34 had visible leukemia present.
  • (1) increased percentage of blasts in the bone marrow at the time of SCT, (2) presence of acute graft-versus-host disease, (3) mismatched donor, (4) Zubrod performance score of >/=2, and (5) age >/=45 years.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy


80. Zhang Y, Yang L, Li R, Zhang L, Zhang MR, Xiao ZJ: [The effects of glutathione S-transferase (GSTT1 and GSTM1) genes polymorphisms on treatment efficacy and prognosis of acute myeloid leukemia]. Zhonghua Nei Ke Za Zhi; 2006 Mar;45(3):213-6
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  • [Title] [The effects of glutathione S-transferase (GSTT1 and GSTM1) genes polymorphisms on treatment efficacy and prognosis of acute myeloid leukemia].
  • OBJECTIVE: To investigate the impact of GSTT1 and GSTM1 genotypes on response, drug side effects and prognosis of acute myeloid leukemia (AML).
  • METHODS: GSTT1 and GSTM1 genotypes were analysed in 180 AML patients with PCR.
  • The risk of ALT abnormality in patients with GSTM1 null is 2.593 times higher than that in patients with GSTM1 present (P = 0.016, 95% CI 1.176 - 5.717). (3) Overall survival and relapse-free survival of GSTT1 and GSTM1 double-present patients were significantly better than those in patients of GSTT1 null/GSTM1 null (mean overall survival was 68.4 months vs 38.5 months, P = 0.028, and mean relapse-free survival was 73.5 months vs 34.9 months, P = 0.014, respectively).
  • CONCLUSION: GSTT1 and GSTM1 genotypes were apparently related with response, drug side effects and prognosis of patients with AML.
  • GSTT1 and GSTM1 genotype might be useful in selecting appropriate chemotherapy regimens for patients with AML.
  • [MeSH-major] Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / drug therapy. Polymorphism, Genetic

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  • (PMID = 16624155.001).
  • [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] 0 / Antineoplastic Agents; 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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81. Coates PJ, Rundle JK, Lorimore SA, Wright EG: Indirect macrophage responses to ionizing radiation: implications for genotype-dependent bystander signaling. Cancer Res; 2008 Jan 15;68(2):450-6
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  • Delayed effects are genotype dependent with CBA/Ca mice, but not C57BL/6 mice, susceptible to the induction of damage and also radiation-induced acute myeloid leukemia.
  • The profiles classify macrophages derived from CBA/Ca mice as M1-like (pro-inflammatory) and those from C57BL/6 mice as M2-like (anti-inflammatory); measurements of NOS2 and arginase activity in normal bone marrow macrophages confirm these findings.
  • After irradiation in vivo, but not in vitro, C57BL/6 macrophages show a reduction in NOS2 and an increase in arginase activities, indicating a further M2 response, whereas CBA/Ca macrophages retain an M1 phenotype.

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  • (PMID = 18199539.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Opsonin Proteins; 0 / Receptors, Scavenger
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82. Tapinassi C, Gerbino E, Malazzi O, Micucci C, Gasparini P, Najera MJ, Calasanz MJ, Odero MD, Pelicci PG, Belloni E: A new dic(7;12)(p12.21;p12.2) chromosome aberration in a case of acute myeloid leukemia. Cancer Genet Cytogenet; 2008 Sep;185(2):102-5
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  • [Title] A new dic(7;12)(p12.21;p12.2) chromosome aberration in a case of acute myeloid leukemia.
  • A new dic(7;12)(p12.21;p12.2) chromosome aberration was identified in an acute myeloid leukemia with FAB-M1 morphology and was cloned.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 7. Leukemia, Myeloid, Acute / genetics


83. Kadam PS, Jain HV, Parikh PM, Saikia TK, Agarwal S, Ambulkar I: Emergence of an unrelated highly aberrant clone in an AML patient at relapse four months after peripheral blood stem cell transplantation. Indian J Hum Genet; 2007 Sep;13(3):114-8
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  • [Title] Emergence of an unrelated highly aberrant clone in an AML patient at relapse four months after peripheral blood stem cell transplantation.
  • We report a case of AML-M1 with 5q aberration at diagnosis.

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  • (PMID = 21957359.001).
  • [ISSN] 0971-6866
  • [Journal-full-title] Indian journal of human genetics
  • [ISO-abbreviation] Indian J Hum Genet
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3168137
  • [Keywords] NOTNLM ; Acute myeloid leukemia / emergence / intense chemotherapy / mutagenic effects / peripheral blood stem cell transplantation / unusual aberrant clone
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84. Schnittger S, Haferlach C, Ulke M, Alpermann T, Kern W, Haferlach T: IDH1 mutations are detected in 6.6% of 1414 AML patients and are associated with intermediate risk karyotype and unfavorable prognosis in adults younger than 60 years and unmutated NPM1 status. Blood; 2010 Dec 16;116(25):5486-96
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  • [Title] IDH1 mutations are detected in 6.6% of 1414 AML patients and are associated with intermediate risk karyotype and unfavorable prognosis in adults younger than 60 years and unmutated NPM1 status.
  • Mutations in the IDH1 gene at position R132 coding for the enzyme cytosolic isocitrate dehydrogenase are known in glioma and have recently been detected also in acute myeloid leukemia (AML).
  • To further clarify the role of this mutation in AML, we have analyzed IDH1R132 in 1414 AML patients.
  • IDH1-mutated cases more often had AML without maturation/French-American-British M1 (P < .001), an immature immunophenotype, and female sex (8.7% vs 4.7% in male, P = .003) compared with IDH1wt cases.
  • In conclusion, these data show that IDH1R132 may significantly add information regarding characterization and prognostication in AML.
  • [MeSH-major] Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Nuclear Proteins / genetics

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  • (PMID = 20805365.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human
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85. Graf M, Reif S, Kröll T, Hecht K, Nuessler V, Schmetzer H: Expression of MAC-1 (CD11b) in acute myeloid leukemia (AML) is associated with an unfavorable prognosis. Am J Hematol; 2006 Apr;81(4):227-35
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  • [Title] Expression of MAC-1 (CD11b) in acute myeloid leukemia (AML) is associated with an unfavorable prognosis.
  • There is evidence to suggest, that cellular adhesion molecules and receptors could play a role in leukemia, e.g., through altered adhesive qualities of leukemic blasts.
  • We have studied the expression of the beta2-integrin Mac-1 (CD11b) on mononuclear cells in 48 patients with AML at first diagnosis by flow cytometry using a direct fluorescein-conjugated antibody.
  • Within the FAB types, we observed a high expression rate in cases with M5 (100% MAC-1+ cases, 73% MAC-1+ cells), M4 (75% MAC-1+ cases, 48% MAC-1+ cells) and in cases with FAB-M1 with 71% MAC-1+ cases and 29% MAC-1+ cells.
  • For clinical evaluations only patients treated according to the protocols of the German AML Cooperative Group (AML-CG) were included (n = 29, cases with AML-M3 were excluded).
  • We can conclude that AML cases with high MAC-1 expression are characterized by a worse prognosis.
  • Evaluation of MAC-1 expression in AML might therefore contribute clinically important data with respect to develop new therapies that influence the interactions between integrins like MAC-1 on leukemic cells and endothelial or immunoreactive cells.
  • [MeSH-major] Antigens, CD11b / blood. Biomarkers, Tumor / blood. Blast Crisis / blood. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / blood

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16550517.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Biomarkers, Tumor; 0 / Macrophage-1 Antigen
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86. Nikolaievs'kyĭ VV: [Distribution of Mycobacterium tuberculosis strains in the south of Ukraine based on genotyping data]. Mikrobiol Z; 2006 Sep-Oct;68(5):52-61
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  • Other epidemiological groups were represented by the family strains T1, LAM1, LAM4, LAM5, S and Haarlem.

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  • (PMID = 17388120.001).
  • [ISSN] 1028-0987
  • [Journal-full-title] Mikrobiolohichnyĭ zhurnal (Kiev, Ukraine : 1993)
  • [ISO-abbreviation] Mikrobiol. Z.
  • [Language] ukr
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antitubercular Agents; 0 / DNA, Bacterial
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87. Øyan AM, Bø TH, Jonassen I, Gjertsen BT, Bruserud Ø, Kalland KH: cDNA microarray analysis of non-selected cases of acute myeloid leukemia demonstrates distinct clustering independent of cytogenetic aberrations and consistent with morphological signs of differentiation. Int J Oncol; 2006 May;28(5):1065-80
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  • [Title] cDNA microarray analysis of non-selected cases of acute myeloid leukemia demonstrates distinct clustering independent of cytogenetic aberrations and consistent with morphological signs of differentiation.
  • Acute myeloid leukemia (AML) is a heterogeneous disease with respect to biology and clinical course.
  • In an attempt to address this question, we performed cDNA microarray analysis on peripheral blood samples of 25 patients with newly diagnosed AML with high blast counts.
  • Leave-one-out crossvalidation (LOOCV) showed with high accuracy that gene expression classifiers could predict if leukaemia samples belonged to the FAB AML-M1 or to the FAB AML-M2 groups.
  • Except for an accumulation of samples classified as FAB M1 and M2 in cluster 3, there was no evident relationship between the clusters and the FAB classification.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Oligonucleotide Array Sequence Analysis


88. Schepers H, Geugien M, van der Toorn M, Bryantsev AL, Kampinga HH, Eggen BJ, Vellenga E: HSP27 protects AML cells against VP-16-induced apoptosis through modulation of p38 and c-Jun. Exp Hematol; 2005 Jun;33(6):660-70
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  • [Title] HSP27 protects AML cells against VP-16-induced apoptosis through modulation of p38 and c-Jun.
  • OBJECTIVE: To investigate 1) the signal transduction pathways affected by heat shock protein 27 (HSP27) expression; and 2) the expression and regulation of HSP27 in acute myeloid leukemia (AML).
  • HSP27 expression and activation was investigated in AML blasts through Western blot analysis.
  • Although HSP27 was highly expressed and phosphorylated in primitive monocytic AML blasts (M4-M5, 91%, n=11) and undetectable in myeloid blasts (M1-M2, n=5), VP-16-mediated apoptosis correlated moderately with HSP27 expression.
  • This is likely due to the co-expression of p21Waf1/Cip1, which is in the majority of the monocytic AML M4-M5 blasts constitutively localized in the cytoplasm.
  • 2) HSP27 is expressed and activated in monocytic AML blasts;.
  • [MeSH-major] Apoptosis / drug effects. Etoposide / pharmacology. Heat-Shock Proteins / physiology. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Adaptor Proteins, Signal Transducing. Carrier Proteins / metabolism. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p21. Enzyme-Linked Immunosorbent Assay. Humans. Immunoprecipitation. Intracellular Signaling Peptides and Proteins / metabolism. MAP Kinase Kinase Kinase 5 / metabolism. Nuclear Proteins / metabolism. Proto-Oncogene Proteins c-jun / metabolism. RNA Interference. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 15911090.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / CDKN1A protein, human; 0 / Carrier Proteins; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DAXX protein, human; 0 / Heat-Shock Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins c-jun; 6PLQ3CP4P3 / Etoposide; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinase 5; EC 2.7.11.25 / MAP3K5 protein, human
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89. Polák J, Marková J, Schwarz J, Maaloufová J, Volková Z, Cermák J, Haskovec C: [The use of quantitative assessment of Wilms tumour gene 1 for monitoring of residual disease in acute myeloid leukemia patients]. Cas Lek Cesk; 2006;145(1):36-42
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  • [Title] [The use of quantitative assessment of Wilms tumour gene 1 for monitoring of residual disease in acute myeloid leukemia patients].
  • BACKGROUND: Despite a considerable effort, the majority of acute myeloid leukaemia (AML) patients do not have a suitable specific molecular marker for monitoring minimal residual disease (MRD).
  • METHODS AND RESULTS: We measured the expression of WT1 at diagnosis and during treatment of the acute myeloid leukaemia (AML) patients.
  • The expression of WT1 was measured by the quantitative real-time RT-PCR in peripheral leukocytes from 56 AML at diagnosis and 7 patients with AML transformed from myelodysplastic syndromes (MDS).
  • The WT1 expression was significantly elevated (up to 3 orders of magnitude) in peripheral blood samples (PB) of AML patients at diagnosis compared to PB samples of healthy donors (P < 0.0001).
  • The level of WT1 expression depends particularly on FAB AML subtype, with the highest being found in AML patients with subtypes M4, M1, M3 and AML transformed from MDS.
  • Conversely, AML patients with M2 and with the presence of AML1/ET0 at presentation showed a significantly lower expression of the WT1 gene compared to the remaining AML patients at presentation (P = 0,005).
  • Further, sequence samples of 12 AML patients under long-term surveillance were tested for the WT1 expression in parallel with the expression of specific MRD markers--fusion genes: AMLI/ETO, PML/RARalpha and CBFB/MYH11.
  • CONCLUSIONS: Our results, in accordance with some of the previously published ones, show that WT1 expression seems to be a suitable marker of minimal residual disease in AML patients.
  • [MeSH-major] Genes, Wilms Tumor. Leukemia, Myeloid / diagnosis
  • [MeSH-minor] Acute Disease. Biomarkers, Tumor / analysis. Core Binding Factor Alpha 2 Subunit / analysis. Genetic Markers. Humans. Neoplasm Proteins / analysis. Neoplasm, Residual. Oncogene Proteins, Fusion / analysis. Plant Proteins

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  • (PMID = 16468240.001).
  • [ISSN] 0008-7335
  • [Journal-full-title] Casopís lékar̆ů c̆eských
  • [ISO-abbreviation] Cas. Lek. Cesk.
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Biomarkers, Tumor; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Genetic Markers; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Plant Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 139874-82-1 / RT-TIP protein, Nicotiana tabacum
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90. Suzuki R, Ohtake S, Takeuchi J, Nagai M, Kodera Y, Hamaguchi M, Miyawaki S, Karasuno T, Shimodaira S, Ohno R, Nakamura S, Naoe T: The clinical characteristics of CD7+ CD56+ acute myeloid leukemias other than M0. Int J Hematol; 2010 Mar;91(2):303-9
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  • [Title] The clinical characteristics of CD7+ CD56+ acute myeloid leukemias other than M0.
  • Immunological phenotyping of acute leukemia have provided enormous and important information for the classification and lineage determination of leukemia.
  • Forty-nine patients with CD7(+) CD56(+) acute myeloid leukemia (AML) were analyzed.
  • There were 17 patients of M0, which corresponded to myeloid/NK cell precursor acute leukemia, and 32 patients of AML other than M0 (9 each for M1 and M2, one for M3, 3 for M4, 4 for M5 and 6 for M7).
  • Age distribution was similar between these two groups, but CD7(+) CD56(+) M0 showed significant male predominance than CD7(+) CD56(+) M1-M7 (M:F = 15:2 vs. 15:17, P = 0.006).
  • These findings suggest that extramedullary involvement of myeloid/NK cell precursor acute leukemia is not directly derived from the presence of CD7 and CD56 antigens on leukemic cells.
  • The poor prognosis of CD7(+) CD56(+) M1-M7 suggests that this phenotype may act as a prognostic factor for AML, but this should be confirmed in further studies.
  • [MeSH-major] Antigens, CD56 / metabolism. Antigens, CD7 / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / metabolism. Leukemia, Myeloid, Acute

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  • (PMID = 20111912.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Antigens, CD7; 0 / Biomarkers, Tumor; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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91. Graf M, Reif S, Hecht K, Kroell T, Nuessler V, Schmetzer H: Expression of poliovirus receptor-related proteins PRR1 and PRR2 in acute myeloid leukemia: first report of surface marker analysis, contribution to diagnosis, prognosis and implications for future therapeutical strategies. Eur J Haematol; 2005 Dec;75(6):477-84
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  • [Title] Expression of poliovirus receptor-related proteins PRR1 and PRR2 in acute myeloid leukemia: first report of surface marker analysis, contribution to diagnosis, prognosis and implications for future therapeutical strategies.
  • There is evidence to suggest, that those receptors could have a role in leukemia.
  • We have studied the expression of PRR molecules PRR1 and PRR2 on mononuclear bone marrow (BM) cells of 55 patients with acute myeloid leukemia (AML) at first diagnosis by FACS-analysis using directly Phycoerythrin-labeled markers (PRR1 clone R1.302.12; PRR2 clone R2.477.1) in combination with other Fluorescein conjugated antibodies to evaluate the blast phenotype in AML.
  • We could demonstrate, that on average 35% PRR1(+) or 45% PRR2(+) cells in AML were found.
  • Within FAB-types we observed a high PRR1 expression in cases with M3 and M4 and lowest expressions in M0 and M5; a high PRR2 expression was found in cases with M3, M4, M5 and M1 and lowest expressions in M0 and M2.
  • Qui-square analyses showed, that 3 of 4 cases with FAB-type M3 (P = 0.03) or a favorable karyotype (P = 0.04) were found in the group with >7% PRR1(+) cells, due to only few cases available a similar correlation, however, could not be found in cases with >78% PRR2(+) cells.
  • We can conclude, that blasts in AML regularly express PRR1 and PRR2.
  • [MeSH-major] Biomarkers, Tumor. Cell Adhesion Molecules. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / diagnosis. Membrane Glycoproteins

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  • (PMID = 16313259.001).
  • [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] 0 / Antigens, CD34; 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules; 0 / Membrane Glycoproteins; 0 / nectins
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92. Gibbs JD, Liebermann DA, Hoffman B: Egr-1 abrogates the E2F-1 block in terminal myeloid differentiation and suppresses leukemia. Oncogene; 2008 Jan 3;27(1):98-106
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  • [Title] Egr-1 abrogates the E2F-1 block in terminal myeloid differentiation and suppresses leukemia.
  • Previously, we have shown that ectopic expression of the zinc finger transcription factor Egr-1 in M1 myeloblastic leukemia cells promotes terminal differentiation with interleukin-6 (IL-6).
  • In addition, we have shown that deregulated expression of the oncogene E2F-1 blocks the myeloid terminal differentiation program, resulting in proliferation of immature cells in the presence of IL-6.
  • Here it is shown that the positive regulator of differentiation Egr-1 abrogates the E2F-1-driven block in myeloid terminal differentiation.
  • The M1E2F-1/Egr-1 cells underwent G(0)/G(1) arrest and functional macrophage maturation following treatment with IL-6.
  • Previously, we reported that Egr-1 abrogated the block in terminal myeloid differentiation imparted by deregulated c-myc, which blocks differentiation at a later stage than E2F-1, resulting in cells that have the characteristics of functionally mature macrophages that did not undergo G(0)/G(1) arrest.
  • Taken together, this work extends and highlights the tumor suppressor role of Egr-1, with Egr-1 behaving as a tumor suppressor against two oncogenes, each blocking myeloid differentiation by a different mechanism.
  • [MeSH-major] Cell Differentiation / physiology. Early Growth Response Protein 1 / physiology. Growth Inhibitors / physiology. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / prevention & control. Myeloid Cells / metabolism. Myeloid Cells / pathology. Tumor Suppressor Proteins / physiology

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  • (PMID = 17599039.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA081168
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / E2F1 Transcription Factor; 0 / E2F1 protein, human; 0 / E2f1 protein, mouse; 0 / Early Growth Response Protein 1; 0 / Egr1 protein, mouse; 0 / Growth Inhibitors; 0 / Interleukin-6; 0 / Tumor Suppressor Proteins
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93. Nakade Y, Fujimura M, Ohkura N, Waseda Y, Yamazakis H, Inuzuka K, Ikeda H, Oe H, Nanbu Y, Takamuralo T, Sakai Y, Wada T: [A case of bronchiolitis obliterans caused by allogeneic hematopoietic stem cell transplantation diagnosed with a body plethysmograph]. Rinsho Byori; 2010 Sep;58(9):906-11
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  • A 19-year-old woman with acute myeloid leukemia (M1) was treated with allogeneic hematopoietic stem cell transplantation.
  • The pathological diagnosis made using biopsied lung, obtained by a right lower partial lobectomy, was constrictive bronchiolitis.
  • [MeSH-major] Bronchiolitis Obliterans / diagnosis. Bronchiolitis Obliterans / etiology. Hematopoietic Stem Cell Transplantation / adverse effects. Plethysmography, Whole Body
  • [MeSH-minor] Adult. Female. Humans. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 20963951.001).
  • [ISSN] 0047-1860
  • [Journal-full-title] Rinsho byori. The Japanese journal of clinical pathology
  • [ISO-abbreviation] Rinsho Byori
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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94. Yan M, Kanbe E, Peterson LF, Boyapati A, Miao Y, Wang Y, Chen IM, Chen Z, Rowley JD, Willman CL, Zhang DE: A previously unidentified alternatively spliced isoform of t(8;21) transcript promotes leukemogenesis. Nat Med; 2006 Aug;12(8):945-9
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  • The t(8;21)(q22;q22) translocation is one of the most common genetic abnormalities in acute myeloid leukemia (AML), identified in 15% of all cases of AML, including 40-50% of FAB M2 subtype and rare cases of M0, M1 and M4 subtypes.
  • Although alterations of gene expression and hematopoietic cell proliferation have been reported in the presence of AML1-ETO, its expression does not lead to the development of leukemia.
  • Expression of AML1-ETO9a leads to rapid development of leukemia in a mouse retroviral transduction-transplantation model.
  • More importantly, coexpression of AML1-ETO and AML1-ETO9a results in the substantially earlier onset of AML and blocks myeloid cell differentiation at a more immature stage.
  • [MeSH-major] Alternative Splicing. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 16892037.001).
  • [ISSN] 1078-8956
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA096735; United States / NCI NIH HHS / CA / CA104509; United States / NHLBI NIH HHS / HL / F32HL079900
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Protein Isoforms
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95. Hsiao HH, Yang MY, Liu YC, Hsiao HP, Tseng SB, Chao MC, Liu TC, Lin SF: RBM15-MKL1 (OTT-MAL) fusion transcript in an adult acute myeloid leukemia patient. Am J Hematol; 2005 May;79(1):43-5
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  • [Title] RBM15-MKL1 (OTT-MAL) fusion transcript in an adult acute myeloid leukemia patient.
  • The t(1;22)(p13;q13) is a nonrandom chromosomal abnormality in acute leukemia with the fusion oncogene, RBM15-MKL1 (OTT-MAL), identified recently.
  • However, this abnormality has been described only in infants and young children with acute megakaryoblastic leukemia (AMKL).
  • We report a 59-year-old male patient with the diagnosis of acute myeloid leukemia, subtype M1, who harbors an abnormal chromosome +der(1)t(1;22)(p13;q13).
  • This unusual abnormality is rare in adult cases of leukemia, and in children it is restricted to AMKL.
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 5. DNA-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Base Sequence. DNA Primers. Humans. Male. Reverse Transcriptase Polymerase Chain Reaction. Trans-Activators

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  • [Copyright] 2005 Wiley-Liss, Inc.
  • (PMID = 15849773.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / MKL1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / RBM15 protein, human; 0 / RNA-Binding Proteins; 0 / Trans-Activators
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96. Xia Q, Wang HX, Wang J, Zhang JY, Liu BY, Li AL, Lv M, Hu MR, Yu M, Feng JN, Yang SC, Zhang XM, Shen BF: Proteomic analysis of interleukin 6-induced differentiation in mouse myeloid leukemia cells. Int J Biochem Cell Biol; 2005 Jun;37(6):1197-207
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  • [Title] Proteomic analysis of interleukin 6-induced differentiation in mouse myeloid leukemia cells.
  • Cytokine-induced differentiation of myeloid leukemia cells has important therapeutic implications, but the mechanism remains to be clarified.
  • M1 cell, a mouse acute myeloid leukemia cell line, which underwent growth inhibition, terminal differentiation and apoptosis in response to IL-6, was selected as an experimental model to study on the molecular mechanisms of myeloid cell differentiation on a proteome-wide scale.
  • Our data provide novel information for a better understanding of the mechanisms by which terminal differentiation of acute myeloid leukemia cells induced by IL-6.
  • [MeSH-major] Cell Differentiation / drug effects. Interleukin-6 / pharmacology. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. Proteomics

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  • (PMID = 15778084.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Cstb protein, mouse; 0 / Cystatins; 0 / Interleukin-6; 0 / Membrane Proteins; 0 / Recombinant Proteins; 88844-95-5 / Cystatin B; EC 1.11.1.- / Peroxidases; EC 1.11.1.15 / Peroxiredoxins; EC 4.1.2.13 / Fructose-Bisphosphate Aldolase
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97. Liu QX, Chen HC, Liu XF, Cao YF, Zhang J, Liu J: [Study on the relationship between polymorphisms of Cyp1A1, GSTM1, GSTT1 genes and the susceptibility to acute leukemia in the general population of Hunan province]. Zhonghua Liu Xing Bing Xue Za Zhi; 2005 Dec;26(12):975-9
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  • [Title] [Study on the relationship between polymorphisms of Cyp1A1, GSTM1, GSTT1 genes and the susceptibility to acute leukemia in the general population of Hunan province].
  • OBJECTIVE: Based on the distribution of genetic polymorphisms regarding phase I metabolic enzyme cytochrome P450 1A1 (CYP1A1) and phase II metabolic enzymes glutathione S-transferase GSTM1 and GSTT1 genotypes in acute leukemia patients and health controls among general population of Hunan in China, this study was to explore the relationship between these gene polymorphisms and the susceptibility to acute leukemia.
  • METHODS: Using case-control methodology, we studied 204 healthy controls and 232 patients with acute leukemia, of which 112 patients were suffering acute lymphoblastic leukemia (ALL) and 120 with acute non-lymphoblastic leukemia (ANLL).
  • The incidences of GSTM1 -/- and GSTT1 -/- combined genotype in ALL, ANLL and control group were 33.0%, 40.0% and 27.5%, of which the difference between ANLL group and control group was statistically significant (P < 0.05) and CYP1A1 gene heterozygous mutation type or homozygous mutation type combined with GSTM1 -/- and GSTT1 -/- increased the risk of ANLL (OR value 1.890, 95% CI: 1.084-3.295).
  • CONCLUSION: These results indicated that both the variation of CYP1A1 gene or GSTT1 -/- genotype alone might not be associated with the susceptibility of acute leukemia while GSTM1 -/- genotype alone or combined with GSTT1 -/- or the 3801 T-C variation of CYP1A1 gene were correlated with ANLL.
  • [MeSH-major] Cytochrome P-450 CYP1A1 / genetics. Genetic Predisposition to Disease. Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16676594.001).
  • [ISSN] 0254-6450
  • [Journal-full-title] Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi
  • [ISO-abbreviation] Zhonghua Liu Xing Bing Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] EC 1.14.14.1 / Cytochrome P-450 CYP1A1; 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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98. Oh SH, Park TS, Cho SY, Kim MJ, Huh J, Kim B, Song SA, Lee JY, Jun KR, Shin JH, Kim HR, Lee JN: Acute myeloid leukemia associated with t(10;17)(p13-15;q12-21) and phagocytic activity by leukemic blasts: a clinical study and review of the literature. Cancer Genet Cytogenet; 2010 Oct 1;202(1):43-6
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  • [Title] Acute myeloid leukemia associated with t(10;17)(p13-15;q12-21) and phagocytic activity by leukemic blasts: a clinical study and review of the literature.
  • Translocation (10;17)(p13-15;q12-21) in acute leukemia is rarely reported in the literature.
  • Here, we present both a novel t(10;17) case study and a review of relevant literature on t(10;17) in acute leukemia (10 cases).
  • In summary, we came to the following preliminary conclusions: t(10;17) is associated with poorly differentiated acute leukemia subtype [90%; eight cases of acute myeloid leukemia (AML M0, M1) and one case of acute undifferentiated leukemia], phagocytic activity by blasts occurs (30%), and the survival time was short in three of the seven t(10;17) cases for whom follow-up data were available (median, 8 months).
  • [MeSH-major] Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 17. Leukemia / drug therapy. Leukemia / genetics. Translocation, Genetic

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20804920.001).
  • [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 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 1.11.1.7 / Peroxidase; ZS7284E0ZP / Daunorubicin
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99. 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).
  • Although new FLT3 mutations are being increasing by investigated, the role of FLT3 expression levels in wild type as well as in mutated FLT3 has only been infrequently addressed.
  • 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).
  • The expression levels were correlated with clinical parameters, FAB types, cytogenetics, flow cytometry, microarray analysis, FLT3 mutations, further molecular aberrations and prognosis.
  • 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.
  • These results correlate with the FLT3 receptor surface expression (CD135) detected by flow cytometry (p<0.001), showing the highest CD135 expression in FAB M5.
  • 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.
  • Furthermore, our data indicate that FLT3 expression and signaling are closely associated with FAB M5.
  • [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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100. Haferlach T, Kohlmann A, Klein HU, Ruckert C, Dugas M, Williams PM, Kern W, Schnittger S, Bacher U, Löffler H, Haferlach C: AML with translocation t(8;16)(p11;p13) demonstrates unique cytomorphological, cytogenetic, molecular and prognostic features. Leukemia; 2009 May;23(5):934-43
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  • [Title] AML with translocation t(8;16)(p11;p13) demonstrates unique cytomorphological, cytogenetic, molecular and prognostic features.
  • Balanced chromosomal rearrangements define distinct entities in acute myeloid leukemia (AML).
  • Here, we present 13 AML cases with t(8;16)(p11;p13) with observed low incidence (13/6124 patients), but more frequent presentation in therapy-related AML than in de novo AML (7/438 versus 6/5686, P=0.00001).
  • Cytomorphology was characterized by parallel positive myeloperoxidase and non-specific esterase staining, therefore, French-American-British (FAB)-classification was impossible and origin of the AML with t(8;16) from an early stem cell with myeloid and monoblastic potential is hypothesized.
  • Using gene expression profiling on 407 cases, patients with t(8;16) were compared to AML FAB subtypes with normal karyotype.
  • Principal component analyses demonstrated that AML with t(8;16) were distinct from FAB subtypes M1, M4, M5a/b.
  • When further compared to AML showing balanced rearrangements, that is, current WHO categories t(15;17), t(8;21), inv(16) and t(11q23)/MLL, AML with t(8;16) cases were clustered close to t(11q23)/MLL sharing commonly expressed genes.
  • Subsequently, a pairwise comparison discriminated AML with t(8;16) from AML with t(11q23)/MLL, thus defining a highly unique signature for AML with t(8;16).
  • In conclusion, AML with t(8;16) demonstrates unique cytomorphological, cytogenetic, molecular and prognostic features and is a specific subtype of AML.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Mapping. Cytogenetic Analysis. Female. Gene Expression Profiling. Gene Regulatory Networks. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein. Oligonucleotide Array Sequence Analysis. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
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  • (PMID = 19194466.001).
  • [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 / MLL protein, human; 0 / RNA, Messenger; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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