[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 274
1. Edkins S, O'Meara S, Parker A, Stevens C, Reis M, Jones S, Greenman C, Davies H, Dalgliesh G, Forbes S, Hunter C, Smith R, Stephens P, Goldstraw P, Nicholson A, Chan TL, Velculescu VE, Yuen ST, Leung SY, Stratton MR, Futreal PA: Recurrent KRAS codon 146 mutations in human colorectal cancer. Cancer Biol Ther; 2006 Aug;5(8):928-32
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent KRAS codon 146 mutations in human colorectal cancer.
  • We report here the identification of recurrent somatic missense mutations at alanine 146, a highly conserved residue in the guanine nucleotide binding domain.
  • We did, however, identify a KRAS A146 mutation in the ML-2 acute myeloid leukemia cell line and an NRAS A146 mutation in the NALM-6 B-cell acute lymphoblastic leukemia line, suggesting that the contribution of codon 146 mutations is not entirely restricted to colorectal cancers or to KRAS.
  • [MeSH-minor] Adenocarcinoma / genetics. Amino Acid Sequence. Carcinoma, Large Cell / genetics. DNA Mutational Analysis. DNA, Neoplasm / genetics. Hong Kong. Humans. Leukemia, Myeloid, Acute / genetics. Molecular Sequence Data. Neoplasm Staging. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Homology, Amino Acid. United States

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • COS Scholar Universe. author profiles.
  • Cellosaurus - a cell line knowledge resource. culture/stock collections - Cell lines described in this publication .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ann Oncol. 2002 Sep;13(9):1438-46 [12196370.001]
  • [Cites] Nature. 2002 Jun 27;417(6892):949-54 [12068308.001]
  • [Cites] Science. 2003 May 9;300(5621):949 [12738854.001]
  • [Cites] Proc Natl Acad Sci U S A. 1978 Mar;75(3):1334-8 [418410.001]
  • [Cites] Nature. 1982 Nov 11;300(5888):143-9 [6290897.001]
  • [Cites] Nature. 1982 Nov 11;300(5888):149-52 [7133135.001]
  • [Cites] Mol Cell Biol. 1988 Jun;8(6):2472-8 [3043178.001]
  • [Cites] Carcinogenesis. 1988 Nov;9(11):2073-9 [2902939.001]
  • [Cites] Mol Cell Biol. 1990 Jan;10(1):405-8 [2403644.001]
  • [Cites] Virus Genes. 1991 Jan;5(1):75-9 [2017878.001]
  • [Cites] Hum Mutat. 1996;8(3):258-61 [8889585.001]
  • [Cites] Mutat Res. 2004 Nov;567(2-3):447-74 [15572290.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Gut. 2005 Sep;54(9):1283-6 [15843421.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7591-5 [16140923.001]
  • [Cites] Nature. 2006 Jan 19;439(7074):358-62 [16273091.001]
  • [Cites] Cancer Res. 2006 Apr 15;66(8):3992-5 [16618717.001]
  • [Cites] J Clin Oncol. 2001 Jan 15;19(2):299-304 [11208819.001]
  • [Cites] Br J Cancer. 2001 Sep 1;85(5):692-6 [11531254.001]
  • [Cites] Science. 2001 Nov 9;294(5545):1299-304 [11701921.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6451-5 [12438234.001]
  • (PMID = 16969076.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA121113; United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / R01 CA121113; United States / NCI NIH HHS / CA / CA062924; United Kingdom / Wellcome Trust / / 077012
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon; 0 / DNA, Neoplasm
  • [Other-IDs] NLM/ PMC2714972; NLM/ UKMS27311
  •  go-up   go-down


2. Tang JM, Meng FY, Chen AW: [Gene expression profile of refractory acute myeloid leukemia (M2a)]. Ai Zheng; 2005 Jun;24(6):676-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Gene expression profile of refractory acute myeloid leukemia (M2a)].
  • BACKGROUND & OBJECTIVE: Recurrence is the major cause of treatment failure of acute myeloid leukemia (AML).
  • This study was to detect differential expression of genes in naive and recurrent/refractory AML, and explore potential mechanisms of recurrent/refractory AML.
  • METHODS: Differential gene expressions of bone marrow mononuclear cells between naive and recurrent/refractory diseases in 5 self-paired patients with AML-M(2a) were detected by DNA microarray.
  • RESULTS: In 925 tested genes, 14 were differentially expressed between naive and recurrent/refractory diseases in the 5 self-paired patients.
  • Of the 14 genes, 12 (involved in signal transduction, DNA replication, regulation of transcription, RNA processing, and regulation of cell cycle) were obviously up-regulated in recurrent diseases, and up-regulation of RRM1 (involved in DNA replication) was the most obvious.
  • CONCLUSIONS: Development of recurrent/refractory AML-M(2a) is concerned with various genes.
  • Up-regulation of these genes suggests that proliferation of recurrent/refractory AML-M(2a) blasts may be higher than that of naive AML-M(2a) blasts.
  • [MeSH-major] Gene Expression Profiling. Immunophenotyping. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / metabolism. Cell Proliferation. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Recurrence. Tumor Suppressor Proteins / metabolism. Up-Regulation

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15946477.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / RRM1 protein, human; 0 / Tumor Suppressor Proteins
  •  go-up   go-down


3. Cunningham I: Extramedullary sites of leukemia relapse after transplant. Leuk Lymphoma; 2006 Sep;47(9):1754-67
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extramedullary sites of leukemia relapse after transplant.
  • Recurrent or residual leukemia found in extramedullary sites after intensive treatments adversely affects prognosis.
  • The most commonly reported sites are soft tissue in acute leukemias and bone in CML.
  • Extramedullary relapse occurred typically within 2 years in ALL, but later in one-third of myeloid leukemias.
  • Intensive therapy has produced lengthy remissions in cases of acute leukemias involving various sites, whereas CML cases, particularly involving bone, were most resistant to treatment.
  • [MeSH-major] Bone Neoplasms / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myeloid, Acute / pathology. Neoplasm Recurrence, Local / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Soft Tissue Neoplasms / pathology. Stem Cell Transplantation


Advertisement
4. Ottone T, Hasan SK, Montefusco E, Curzi P, Mays AN, Chessa L, Ferrari A, Conte E, Noguera NI, Lavorgna S, Ammatuna E, Divona M, Bovetti K, Amadori S, Grimwade D, Lo-Coco F: Identification of a potential "hotspot" DNA region in the RUNX1 gene targeted by mitoxantrone in therapy-related acute myeloid leukemia with t(16;21) translocation. Genes Chromosomes Cancer; 2009 Mar;48(3):213-21
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of a potential "hotspot" DNA region in the RUNX1 gene targeted by mitoxantrone in therapy-related acute myeloid leukemia with t(16;21) translocation.
  • The translocation t(16;21) involving RUNX1 (AML1) and resulting in the RUNX1-CBFA2T3 fusion is a rare but recurrent abnormality mostly found in therapy-related acute myeloid leukemia (t-AML) associated with agents targeting topoisomerase II (topo II).
  • This region contained an ATGCCCCAG nucleotide sequence showing approximately 90% homology to a "hotspot" DNA region ATGCCCTAG present in intron 6 of PML previously identified in therapy-related acute promyelocytic leukemia cases arising following treatment with MTZ.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Mitoxantrone / adverse effects. Translocation, Genetic

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2008 Wiley-Liss, Inc.
  • (PMID = 19023877.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFA2T3 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Phosphoproteins; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 0 / Topoisomerase II Inhibitors; 0 / Tumor Suppressor Proteins; BZ114NVM5P / Mitoxantrone
  •  go-up   go-down


5. Ogura K, Machida T, Nara M, Mayama K, Akagi T, Kubo K: [Long-term complete remission after single therapy with gemtuzumab ozogamicin for refractory AML in an elderly patient]. Gan To Kagaku Ryoho; 2007 Nov;34(11):1881-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • So GO is a more selective agent for acute myeloid leukemia (AML), because the CD33 antigen is expressed on AML, while it is not expressed on normal hematopoietic stem cells and nonhematopoietic tissues.
  • In this study, we report a 76-year-old female with recurrent AML who responded to single therapy with GO, achieving complete remission for more than 1 year after the start of administration, although additional remission induction was impossible.
  • [MeSH-major] Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antineoplastic Agents / administration & dosage. Leukemia, Myeloid, Acute / drug therapy

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18030030.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
  •  go-up   go-down


6. Moon HW, Chang YH, Kim TY, Oh BR, Min HC, Kim BK, Ahn HS, Cho HI, Lee DS: Incidence of submicroscopic deletions vary according to disease entities and chromosomal translocations in hematologic malignancies: investigation by fluorescence in situ hybridization. Cancer Genet Cytogenet; 2007 Jun;175(2):166-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Submicroscopic deletions of genes in recurrent chromosomal rearrangements occur frequently in hematologic malignancies, but their incidences have not been reported clearly.
  • A fluorescence in situ hybridization (FISH) study was conducted in 336 patients with acute lymphoblastic leukemia, 223 patients with acute myeloid leukemia, and 79 patients with chronic myelogenous leukemia.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17556074.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
  •  go-up   go-down


7. Ko M, Huang Y, Jankowska AM, Pape UJ, Tahiliani M, Bandukwala HS, An J, Lamperti ED, Koh KP, Ganetzky R, Liu XS, Aravind L, Agarwal S, Maciejewski JP, Rao A: Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2. Nature; 2010 Dec 9;468(7325):839-43
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2.
  • The gene encoding TET2 resides at chromosome 4q24, in a region showing recurrent microdeletions and copy-neutral loss of heterozygosity (CN-LOH) in patients with diverse myeloid malignancies.
  • Somatic TET2 mutations are frequently observed in myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), MDS/MPN overlap syndromes including chronic myelomonocytic leukaemia (CMML), acute myeloid leukaemias (AML) and secondary AML (sAML).
  • We show here that TET2 mutations associated with myeloid malignancies compromise catalytic activity.
  • Our results demonstrate that Tet2 is important for normal myelopoiesis, and suggest that disruption of TET2 enzymatic activity favours myeloid tumorigenesis.
  • Measurement of 5hmC levels in myeloid malignancies may prove valuable as a diagnostic and prognostic tool, to tailor therapies and assess responses to anticancer drugs.


8. Fung YL, Williams BA: TRALI in 2 cases of leukemia. J Pediatr Hematol Oncol; 2006 Jun;28(6):391-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TRALI in 2 cases of leukemia.
  • We describe transfusion-related acute lung injury (TRALI) in 2 acute leukemia cases to increase awareness of this under reported serious transfusion complication syndrome in multitransfused patients.
  • As each transfused blood product is associated with a potential risk of TRALI, more frequent reports in patients receiving large volume or recurrent transfusion would be expected.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Leukemia, Promyelocytic, Acute / complications. Platelet Transfusion / adverse effects. Respiratory Distress Syndrome, Adult / etiology. Respiratory Distress Syndrome, Adult / therapy

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. FUROSEMIDE .
  • Hazardous Substances Data Bank. OXYGEN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Pediatr Hematol Oncol. 2006 Jun;28(6):328-30 [16794498.001]
  • (PMID = 16794510.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Diuretics; 7LXU5N7ZO5 / Furosemide; 9PHQ9Y1OLM / Prednisolone; S88TT14065 / Oxygen
  •  go-up   go-down


9. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Multiple recurrent chromosomal aberrations have been identified by conventional cytogenetic analysis.
  • [MeSH-major] Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


10. Valent P: Pathogenesis, classification, and therapy of eosinophilia and eosinophil disorders. Blood Rev; 2009 Jul;23(4):157-65
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Eosinophilia is a recurrent feature and diagnostic clue in several hematologic malignancies.
  • Myeloid neoplasms typically presenting with eosinophilia include chronic myeloid leukemia, chronic eosinophilic leukemia (CEL), other myeloproliferative neoplasms, some acute leukemias, advanced mast cell disorders, and rare forms of myelodysplastic syndromes.
  • Endomyocardial fibrosis, the most dangerous cardiovascular complication of the hypereosinophilic state, is frequently detected in PDGFR-mutated neoplasms, specifically in FIP1L1/PDGFRA+ CEL, but is usually not seen in other myeloid neoplasms or reactive eosinophilia, even if eosinophilia is recorded for many years.

  • MedlinePlus Health Information. consumer health - Eosinophilic Disorders.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • SciCrunch. KEGG: Data: Disease Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19246139.001).
  • [ISSN] 1532-1681
  • [Journal-full-title] Blood reviews
  • [ISO-abbreviation] Blood Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
  • [Number-of-references] 74
  •  go-up   go-down


11. Lu G, Yin CC, Medeiros LJ, Abruzzo LV: Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature. Cancer Genet Cytogenet; 2009 Jan 15;188(2):118-23
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature.
  • Deletions within the long arm of chromosome 15, a recurrent abnormality in myeloid malignancies, have been reported previously as a sole abnormality in only eight cases of acute myeloid leukemia (AML).
  • Two cases were acute myelomonocytic leukemia (FAB AML-M4), and one was acute myeloblastic leukemia with maturation (FAB AML-M2).
  • Taken together with the eight previously reported cases, we conclude that deletions in chromosome 15 are associated with AML, both in cases that arise de novo or in the setting of a myeloproliferative disorder or myelodysplastic syndrome.
  • [MeSH-major] Chromosomes, Human, Pair 15. Leukemia, Myeloid, Acute / genetics. Sequence Deletion

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19100517.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 20
  •  go-up   go-down


12. Zhang L, Alsabeh R, Mecucci C, La Starza R, Gorello P, Lee S, Lill M, Schreck R: Rare t(1;11)(q23;p15) in therapy-related myelodysplastic syndrome evolving into acute myelomonocytic leukemia: a case report and review of the literature. Cancer Genet Cytogenet; 2007 Oct 1;178(1):42-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rare t(1;11)(q23;p15) in therapy-related myelodysplastic syndrome evolving into acute myelomonocytic leukemia: a case report and review of the literature.
  • Balanced chromosome rearrangements are the hallmark of therapy-related leukemia that develops in patients treated with topoisomerase II inhibitors.
  • Many of these rearrangements involve recurrent chromosomal sites and associated genes (11q23/MLL, 21q22.3/AML1, and 11p15/NUP98), which can interact with a variety of partner genes.
  • With time, the patient's disorder progressed to acute myelomonocytic leukemia with cytogenetic evidence of clonal evolution.
  • To our knowledge, this is the first report of a patient presenting with a myelodysplastic syndrome with isolated t(1;11) (q23;p15), which evolved into therapy-related acute myeloid leukemia (t-AML).
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 11. Leukemia, Myelomonocytic, Acute / genetics. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Myelodysplastic Syndromes / therapy. Translocation, Genetic


13. McCormack E, Bruserud O, Gjertsen BT: Review: genetic models of acute myeloid leukaemia. Oncogene; 2008 Jun 19;27(27):3765-79
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Review: genetic models of acute myeloid leukaemia.
  • The use of genetically engineered mice (GEM) have been critical in understanding disease states such as cancer, and none more so than acute myelogenous leukaemia (AML), a disease characterized by over 100 distinct chromosomal translocations.
  • A substantial proportion of cases exhibiting recurrent reciprocal translocations at diagnosis, such as t(8;21) or t(15;17) have been exhaustively studied and are currently employed in clinical diagnosis.
  • Furthermore, little emphasis has been paid to the effect of chromosomal translocations other than recurrent genetic abnormalities, with no models reflecting the multiple abnormalities observed in high-risk cases of AML accounting for 8-10% of adult AML.
  • [MeSH-major] Animals, Genetically Modified / genetics. Leukemia, Myeloid, Acute / genetics. Models, Genetic
  • [MeSH-minor] Animals. Chromosome Aberrations. Disease Models, Animal. Exons. Humans. Leukemia, Promyelocytic, Acute / genetics. Mice. Mice, Transgenic. Prognosis


14. Inaba H, Stewart CF, Crews KR, Yang S, Pounds S, Pui CH, Rubnitz JE, Razzouk BI, Ribeiro RC: Combination of cladribine plus topotecan for recurrent or refractory pediatric acute myeloid leukemia. Cancer; 2010 Jan 1;116(1):98-105
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combination of cladribine plus topotecan for recurrent or refractory pediatric acute myeloid leukemia.
  • BACKGROUND: The prognosis after recurrence of pediatric acute myeloid leukemia (AML) is poor, and effective salvage regimens are urgently needed.
  • METHODS: In phase 1 and pilot studies, the authors evaluated the maximum tolerated dose (MTD) and dose-limiting toxicities (DLTs) of a 5-day course of cladribine followed by topotecan in pediatric patients with recurrent/refractory AML.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Topotecan .
  • Hazardous Substances Data Bank. CLADRIBINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 American Cancer Society.
  • [Cites] J Clin Oncol. 2001 Jun 1;19(11):2804-11 [11387351.001]
  • [Cites] Cancer. 2008 Jul 15;113(2):376-82 [18459178.001]
  • [Cites] J Clin Oncol. 2002 Oct 15;20(20):4217-24 [12377965.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):633-40 [12576429.001]
  • [Cites] J Clin Oncol. 2003 Aug 1;21(15):2940-7 [12885813.001]
  • [Cites] Biol Blood Marrow Transplant. 2003 Nov;9(11):706-13 [14652854.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4377-85 [14645428.001]
  • [Cites] Cancer Res. 1973 Nov;33(11):2834-6 [4748440.001]
  • [Cites] Biometrics. 1989 Sep;45(3):925-37 [2790129.001]
  • [Cites] J Clin Invest. 1990 Nov;86(5):1480-8 [1700795.001]
  • [Cites] J Clin Oncol. 1992 Mar;10(3):364-70 [1346800.001]
  • [Cites] J Clin Oncol. 1992 Oct;10(10):1514-8 [1357107.001]
  • [Cites] Cancer Res. 1994 Mar 1;54(5):1235-9 [7906999.001]
  • [Cites] Blood. 1997 Mar 15;89(6):2098-104 [9058732.001]
  • [Cites] J Clin Oncol. 1998 Jun;16(6):2233-7 [9626225.001]
  • [Cites] Clin Cancer Res. 1996 Dec;2(12):1921-30 [9816150.001]
  • [Cites] Blood. 2005 Apr 15;105(8):3051-7 [15632206.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2025-9 [16304569.001]
  • [Cites] J Clin Oncol. 2006 Sep 20;24(27):4499-506 [16983120.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Jan;13(1):1-25 [17222748.001]
  • [Cites] Br J Haematol. 2007 Jan;136(2):229-236 [17278259.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]
  • [Cites] J Clin Oncol. 2002 Mar 15;20(6):1617-24 [11896112.001]
  • (PMID = 19885837.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-31; United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / P30 CA021765-31
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 47M74X9YT5 / Cladribine; 7M7YKX2N15 / Topotecan
  • [Other-IDs] NLM/ NIHMS151111; NLM/ PMC2920745
  •  go-up   go-down


15. Melnick AM: Epigenetics in AML. Best Pract Res Clin Haematol; 2010 Dec;23(4):463-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • All leukemias display aberrant distribution of cytosine methylation, which is most notably distributed in specific and distinct signatures in acute myeloid leukemia (AML).
  • Compared with genetic lesions in AML, epigenetic lesions appear to be more frequent and recurrent.
  • [MeSH-major] DNA Methylation. Epigenesis, Genetic. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010. Published by Elsevier Ltd.
  • (PMID = 21130408.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  •  go-up   go-down


16. Anwar Iqbal M, Al-Omar HM, Owaidah T, Al-Humaidan H, Bhuiyan ZA, Sahovic E: del(6)(p23) in two cases of de novo AML--a new recurrent primary chromosome abnormality. Eur J Haematol; 2006 Sep;77(3):245-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] del(6)(p23) in two cases of de novo AML--a new recurrent primary chromosome abnormality.
  • OBJECTIVE: Previously, deletion 6p23 was generally reported in therapy-related secondary acute myeloid leukemia (AML) as part of complex karyotypes.
  • In this report, we present two young adult patients with de novo AML-M2 and a terminal deletion 6p23 as a sole primary abnormality, confirmed by chromosome 6 specific subtelomeric probes.
  • The common morphological, immunophenotypic, and cytogenetic features in our two patients strongly support a separate new entity of de novo AML with deletion 6p23.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 6 / genetics. Leukemia, Myeloid, Acute / genetics

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16856925.001).
  • [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
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Dek protein, human; 0 / Oncogene Proteins
  •  go-up   go-down


17. Yasar D, Karadogan I, Alanoglu G, Akkaya B, Luleci G, Salim O, Timuragaoglu A, Toruner GA, Berker-Karauzum S: Array comparative genomic hybridization analysis of adult acute leukemia patients. Cancer Genet Cytogenet; 2010 Mar;197(2):122-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Array comparative genomic hybridization analysis of adult acute leukemia patients.
  • We have performed a retrospective array-based comparative hybridization (array-CGH) study on 41 acute leukemia samples [n=17 acute lymphoblastic leukemia (ALL) patients only at diagnosis, n=3 ALL patients both at diagnosis and relapse; n=20 acute myeloid leukemia (AML) patients only at diagnosis and n=1 AML patient both at diagnosis and relapse] using an Agilent 44K array.
  • ALL-specific recurrent abnormalities were RB1 (n=3), PAX5 (n=4), and CDKN2B (n=3) deletions; AML-specific recurrent abnormalities were HOXA9 and HOXA10 (n=2) deletions and NOTCH1 duplication (n=2).
  • Recurrent duplication of the ELK1 oncogene was observed in both ALL (n=2) and AML (n=3) cases.
  • [MeSH-major] Comparative Genomic Hybridization / methods. Oligonucleotide Array Sequence Analysis / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Aberrations. Female. Humans. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged. Mutation. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20193845.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


18. Wang HY, Tirado CA: t(8;21)(q22;q22) Translocation involving AML1 and ETO in B lymphoblastic leukemia [corrected]. Hum Pathol; 2010 Feb;41(2):286-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] t(8;21)(q22;q22) Translocation involving AML1 and ETO in B lymphoblastic leukemia [corrected].
  • t(8;21)(q22;q22) giving rise to RUNX1/RUNX1T1 fusion transcript is a recurrent non-random chromosomal translocation, accounting for approximately 5% of cases of acute myeloid leukemia and 10% of acute myeloid leukemia with maturation.
  • Studies have demonstrated so far that t(8;21)(q22;q22) occurs only in acute myeloid leukemia, and B lymphoblastic leukemia with t(8;21)(q22;q22) has not been reported in the literature.
  • In the present study, we report a 44-year-old woman with a diagnosis of a B lymphoblastic leukemia based on morphology and immunophenotype.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • [ErratumIn] Hum Pathol. 2010 Apr;41(4):620
  • (PMID = 19896694.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
  •  go-up   go-down


19. Sanders MA, Verhaak RG, Geertsma-Kleinekoort WM, Abbas S, Horsman S, van der Spek PJ, Löwenberg B, Valk PJ: SNPExpress: integrated visualization of genome-wide genotypes, copy numbers and gene expression levels. BMC Genomics; 2008;9:41
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CONCLUSION: The combined analyses with the easily accessible software tool SNPExpress will not only facilitate the recognition of recurrent genetic lesions, but also the identification of critical pathogenic genes.
  • [MeSH-minor] Computer Simulation. Genotype. Humans. Leukemia, Myeloid, Acute / genetics. Loss of Heterozygosity / genetics. Markov Chains. Models, Genetic. Oligonucleotide Array Sequence Analysis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Biotechnol. 2000 Sep;18(9):1001-5 [10973224.001]
  • [Cites] BMC Bioinformatics. 2006;7:25 [16420694.001]
  • [Cites] Blood Rev. 2004 Jun;18(2):115-36 [15010150.001]
  • [Cites] Oncogene. 2004 Apr 8;23(15):2716-26 [15048096.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1617-28 [15084694.001]
  • [Cites] Cancer Res. 2004 May 1;64(9):3060-71 [15126342.001]
  • [Cites] Bioinformatics. 2004 May 22;20(8):1233-40 [14871870.001]
  • [Cites] Carcinogenesis. 2004 Aug;25(8):1345-57 [15001537.001]
  • [Cites] Hum Genomics. 2004 May;1(4):287-99 [15588488.001]
  • [Cites] Cancer Res. 2005 Jan 15;65(2):375-8 [15695375.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3053-8 [15833833.001]
  • [Cites] Bioinformatics. 2005 May 1;21(9):1958-63 [15657097.001]
  • [Cites] Cancer Res. 2005 Jul 1;65(13):5561-70 [15994928.001]
  • [Cites] Nature. 2005 Jul 7;436(7047):117-22 [16001072.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6071-9 [16024607.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):334-7 [16015648.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9152-4 [16230371.001]
  • [Cites] Nature. 2005 Oct 27;437(7063):1299-320 [16255080.001]
  • [Cites] PLoS Comput Biol. 2005 Nov;1(6):e65 [16322765.001]
  • [Cites] Bioinformatics. 2006 Jan 1;22(1):7-12 [16267090.001]
  • [Cites] Nat Genet. 2006 May;38(5):500-1 [16642009.001]
  • [Cites] PLoS Comput Biol. 2006 May;2(5):e41 [16699594.001]
  • [Cites] Genome Res. 2006 Aug;16(8):949-61 [16809666.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3887-94 [16864856.001]
  • [Cites] Nucleic Acids Res. 2006;34(14):e100 [16899450.001]
  • [Cites] BMC Bioinformatics. 2006;7:337 [16836741.001]
  • [Cites] Bioinformatics. 2006 Nov 1;22(21):2697-8 [16935928.001]
  • [Cites] OMICS. 2006 Fall;10(3):276-88 [17069508.001]
  • [Cites] BMC Genomics. 2006;7:324 [17192189.001]
  • [Cites] Science. 2007 Feb 9;315(5813):848-53 [17289997.001]
  • [Cites] Nat Genet. 2007 Oct;39(10):1217-24 [17873874.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2382-4 [17554374.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 May 8;98(10):5711-6 [11331760.001]
  • (PMID = 18221515.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2235842
  •  go-up   go-down


20. Cashen AF, Devine H, DiPersio J: Second complete remission in an elderly patient with acute myeloid leukemia retreated with decitabine. Am J Hematol; 2006 Jul;81(7):543-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Second complete remission in an elderly patient with acute myeloid leukemia retreated with decitabine.
  • A 67-year-old man with acute myeloid leukemia (AML) was treated with low-dose decitabine.
  • He developed recurrent AML after discontinuation of decitabine.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Azacitidine / analogs & derivatives. Leukemia, Myeloid, Acute / prevention & control

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16755561.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
  •  go-up   go-down


21. Makishima H, Cazzolli H, Szpurka H, Dunbar A, Tiu R, Huh J, Muramatsu H, O'Keefe C, Hsi E, Paquette RL, Kojima S, List AF, Sekeres MA, McDevitt MA, Maciejewski JP: Mutations of e3 ubiquitin ligase cbl family members constitute a novel common pathogenic lesion in myeloid malignancies. J Clin Oncol; 2009 Dec 20;27(36):6109-16
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutations of e3 ubiquitin ligase cbl family members constitute a novel common pathogenic lesion in myeloid malignancies.
  • PURPOSE: Acquired somatic uniparental disomy (UPD) is commonly observed in myelodysplastic syndromes (MDS), myelodysplastic/myeloproliferative neoplasms (MDS/MPN), or secondary acute myelogenous leukemia (sAML) and may point toward genes harboring mutations.
  • Recurrent UPD11q led to identification of homozygous mutations in c-Cbl, an E3 ubiquitin ligase involved in attenuation of proliferative signals transduced by activated receptor tyrosine kinases.
  • RESULTS: We identified c-Cbl mutations in 5% and 9% of patients with chronic myelomonocytic leukemia (CMML) and sAML, and also in CML blast crisis and juvenile myelomonocytic leukemia (JMML).

  • COS Scholar Universe. author profiles.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 2009 Mar;23(3):610-4 [18818701.001]
  • [Cites] Haematologica. 2008 Oct;93(10):1595-7 [18698078.001]
  • [Cites] Nat Genet. 2004 Sep;36(9):949-51 [15286789.001]
  • [Cites] Oncogene. 1991 Apr;6(4):653-7 [2030914.001]
  • [Cites] Mol Cell Biol. 1998 Aug;18(8):4872-82 [9671496.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Dec;6(12):907-18 [16227975.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1242-3 [16434499.001]
  • [Cites] PLoS Genet. 2005 Dec;1(6):e49 [16444292.001]
  • [Cites] Blood. 2006 Mar 1;107(5):1791-9 [16254134.001]
  • [Cites] J Cell Physiol. 2006 Oct;209(1):21-43 [16741904.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2173-81 [16741247.001]
  • [Cites] PLoS Med. 2006 Jul;3(7):e270 [16834459.001]
  • [Cites] Am J Surg Pathol. 2007 Feb;31(2):233-9 [17255768.001]
  • [Cites] Blood. 2007 Aug 1;110(3):1004-12 [17446348.001]
  • [Cites] Blood. 2007 Aug 1;110(3):1022-4 [17475912.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2058-61 [17525728.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3365-73 [17634407.001]
  • [Cites] PLoS One. 2007;2(11):e1225 [18030353.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1534-42 [17954704.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]
  • [Cites] Blood. 2008 Aug 15;112(4):965-74 [18505780.001]
  • [Cites] Semin Oncol. 2008 Aug;35(4):365-77 [18692687.001]
  • [Cites] Leukemia. 2008 Aug;22(8):1539-41 [18528419.001]
  • [Cites] Cancer Res. 2008 Dec 15;68(24):10349-57 [19074904.001]
  • [Cites] Blood. 2008 Sep 1;112(5):2017-9 [18566322.001]
  • [Cites] Curr Opin Hematol. 2001 Jul;8(4):189-91 [11561153.001]
  • (PMID = 19901108.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K24 HL077522; United States / NHLBI NIH HHS / HL / R01 HL082983; United States / NCRR NIH HHS / RR / U54 RR019391; United States / NHLBI NIH HHS / HL / K24 HL-077522; United States / NHLBI NIH HHS / HL / R01HL-082983; United States / NCRR NIH HHS / RR / S10 RR019391
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Other-IDs] NLM/ PMC3040009
  •  go-up   go-down


22. Sperr WR, Mitterbauer M, Mitterbauer G, Kundi M, Jäger U, Lechner K, Valent P: Quantitation of minimal residual disease in acute myeloid leukemia by tryptase monitoring identifies a group of patients with a high risk of relapse. Clin Cancer Res; 2005 Sep 15;11(18):6536-43
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitation of minimal residual disease in acute myeloid leukemia by tryptase monitoring identifies a group of patients with a high risk of relapse.
  • PURPOSE: Recent data suggest that tryptase is produced by blast cells in a group of patients with acute myeloid leukemia (AML).
  • In 61 patients with de novo AML exhibiting elevated serum tryptase (>15 ng/mL) at diagnosis, tryptase levels were measured serially during and after chemotherapy by a fluoroenzyme immunoassay.
  • In all patients with continuous hematologic CR, tryptase levels remained constantly normal, whereas a recurrent elevation of tryptase in CR was invariably followed by a hematologic relapse.
  • [MeSH-major] Leukemia, Myeloid / pathology. Neoplasm, Residual / pathology. Serine Endopeptidases / blood
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Recurrence, Local. Oncogene Proteins, Fusion / genetics. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors. Survival Analysis. Time Factors. Tryptases

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16166430.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.59 / Tryptases
  •  go-up   go-down


23. Gong H, Liu WL, Zhou JF, Xu HZ: [Expression of mitosis checkpoint gene CHFR in acute leukemia]. Zhonghua Yi Xue Za Zhi; 2005 Apr 27;85(16):1085-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of mitosis checkpoint gene CHFR in acute leukemia].
  • OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with acute leukemia (AL) and its clinical significance.
  • METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with acute myelocytic leukemia (AML) and 22 with acute lymphocytic leukemia (ALL), 45 de novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.
  • (1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent acute lymphoblastic leukemia (ALL) was 0.71, significantly higher than that of the de novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).
  • CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with acute leukemia.
  • Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of acute leukemia to chemotherapy.
  • [MeSH-major] Cell Cycle Proteins / biosynthesis. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16029562.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
  •  go-up   go-down


24. Tanvetyanon T, Stiff PJ: Recurrent steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations. Leuk Lymphoma; 2005 Jan;46(1):151-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations.
  • However, to date, recurrent acute pancreatitis has never been described in association with MDS.
  • The vasculitic syndrome responded rapidly to corticosteroids, but soon after tapering of corticosteroids, acute pancreatitis developed.
  • Finally, his MDS transformed into acute myeloid leukemia (AML); severe acute pancreatitis closely accompanied.
  • All etiologies for recurrent acute pancreatitis were ruled out.
  • The dramatic response of his pancreatitis attacks to immunosuppression suggested its autoimmune origin, while the close relationship in both the timing and severity of acute pancreatitis and MDS/AML suggested that the autoimmune pancreatitis was a paraneoplastic phenomenon related to MDS.


25. Podgornik H, Debeljak M, Zontar D, Cernelc P, Prestor VV, Jazbec J: RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia. Cancer Genet Cytogenet; 2007 Oct 1;178(1):77-81
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia.
  • Amplification of RUNX1 (alias AML1) is a recurrent karyotypic abnormality in childhood acute lymphoblastic leukemia (ALL) that is generally associated with a poor outcome.
  • It does not occur with other primary chromosomal abnormalities in acute ALL.
  • AML1 amplification in acute myelogenous leukemia (AML) is a rare secondary event described mainly in therapy-related cases.
  • AML1 amplification was found in a 13-year-old patient with AML M4/M5 leukemia that occurred 5 years after she had been diagnosed with common B-cell ALL.
  • Conventional cytogenetic, fluorescent in situ hybridization (FISH), and polymerase chain reaction methods revealed no other chromosomal change expected to occur in a disease that we assumed to be a secondary leukemia.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Neoplastic. Leukemia, B-Cell / genetics. Leukemia, B-Cell / pathology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


26. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Mutation

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


27. Erkeland SJ, Verhaak RG, Valk PJ, Delwel R, Löwenberg B, Touw IP: Significance of murine retroviral mutagenesis for identification of disease genes in human acute myeloid leukemia. Cancer Res; 2006 Jan 15;66(2):622-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Significance of murine retroviral mutagenesis for identification of disease genes in human acute myeloid leukemia.
  • Acute myeloid leukemia (AML) is a heterogeneous disease with a variable response to treatment.
  • Recurrent cytogenetic defects and acquired mutations in regulatory genes are associated with AML subtypes and prognosis.
  • Here, we show that mouse leukemia genes identified by retroviral insertion mutagenesis are more frequently differentially expressed in distinct subclasses of adult and pediatric AML than randomly selected genes or genes located more distantly from a virus integration site.
  • Our data support the validity of retroviral insertion mutagenesis in mice for human disease and indicate that combining these murine screens for potential proto-oncogenes with GEP in human AML may help to identify critical disease genes and novel pathogenetic networks in leukemia.
  • [MeSH-major] Gene Expression Profiling. Leukemia, Myeloid / genetics. Mutagenesis, Insertional. Proto-Oncogenes
  • [MeSH-minor] Acute Disease. Adult. Animals. Child. Humans. Mice. Retroviridae / genetics. Signal Transduction. Transcription, Genetic

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16423987.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


28. Barrow PJ, Siriwardena AK: Outcome of hepaticojejunostomy without access loop for repair of iatrogenic bile duct injury at laparoscopic cholecystectomy. J Hepatobiliary Pancreat Surg; 2007;14(4):374-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • There was one death during follow-up, from acute myeloid leukemia.
  • One patient (9%) with a type III injury presented with a symptomatic recurrent biliary stricture 6 months after repair, and was successfully managed by percutaneous biliary dilatation, using a combination of transhepatic and jejunal loop puncture.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17653635.001).
  • [ISSN] 0944-1166
  • [Journal-full-title] Journal of hepato-biliary-pancreatic surgery
  • [ISO-abbreviation] J Hepatobiliary Pancreat Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


29. Druhan LJ, Ai J, Massullo P, Kindwall-Keller T, Ranalli MA, Avalos BR: Novel mechanism of G-CSF refractoriness in patients with severe congenital neutropenia. Blood; 2005 Jan 15;105(2):584-91
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Severe congenital neutropenia (SCN) is a rare disease diagnosed at or soon after birth, characterized by a myeloid maturation arrest in the bone marrow, ineffective neutrophil production, and recurrent infections.
  • In the subset of patients with SCN transforming to acute myeloid leukemia (AML), mutations that truncate the cytoplasmic tail of the G-CSF receptor (G-CSFR) have been detected.
  • Expression of the mutant receptor in either myeloid or lymphoid cells was shown to alter subcellular trafficking of the wild-type (WT) G-CSFR by constitutively heterodimerizing with it.

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15353486.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA75226; United States / NCI NIH HHS / CA / CA82859
  • [Publication-type] Case Reports; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor
  •  go-up   go-down


30. Lengfelder E, Saussele S, Weisser A, Büchner T, Hehlmann R: Treatment concepts of acute promyelocytic leukemia. Crit Rev Oncol Hematol; 2005 Nov;56(2):261-74
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment concepts of acute promyelocytic leukemia.
  • In the past, acute promyelocytic leukemia (APL) was associated with a high risk of early mortality resulting from severe coagulopathy, frequently inducing fatal cerebral hemorrhage.
  • With the introduction of the differentiating agent all-trans retinioc acid (ATRA) APL has changed to the best curable subtype of acute myeloid leukemia (AML).
  • PML/RARalpha, the molecular fusion transcript of the specific translocation t(15;17) represents not only the target for ATRA but also permits a precise diagnosis and provides a marker for the identification of minimal residual or recurrent disease (MRD).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Promyelocytic, Acute / therapy. Stem Cell Transplantation

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • Hazardous Substances Data Bank. ARSENIC TRIOXIDE .
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16236522.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 121
  •  go-up   go-down


31. Yin CC, Abruzzo LV, Qiu X, Apostolidou E, Cortes JE, Medeiros LJ, Lu G: del(15q) is a recurrent minor-route cytogenetic abnormality in the clonal evolution of chronic myelogenous leukemia. Cancer Genet Cytogenet; 2009 Jul;192(1):18-23
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] del(15q) is a recurrent minor-route cytogenetic abnormality in the clonal evolution of chronic myelogenous leukemia.
  • The del(15q) chromosomal abnormality is known to occur in acute leukemias, but has rarely been described in chronic myelogenous leukemia (CML).
  • Bone marrow aspirate smears showed increased blasts in all cases at the time of del(15q) detection, in accelerated phase in two cases and myeloid blast phase in three.
  • These findings indicate that del(15q) is a recurrent cytogenetic abnormality that may be seen at initial presentation of advanced disease or may emerge during disease progression.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 15. Clone Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mod Pathol. 2004 Jan;17(1):96-103 [14657955.001]
  • [Cites] Cancer Genet Cytogenet. 2009 Jan 15;188(2):118-23 [19100517.001]
  • [Cites] Cancer Genet Cytogenet. 2004 Jun;151(2):146-51 [15172752.001]
  • [Cites] Am J Clin Pathol. 2004 Jun;121(6):836-42 [15198355.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):671-84, x [15271399.001]
  • [Cites] Nature. 1973 Jun 1;243(5405):290-3 [4126434.001]
  • [Cites] Cancer. 1999 Dec 15;86(12):2632-41 [10594858.001]
  • [Cites] Cancer Res. 2000 Jan 1;60(1):70-3 [10646855.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3343-56 [11071626.001]
  • [Cites] Arch Pathol Lab Med. 2001 Mar;125(3):437-9 [11231500.001]
  • [Cites] Cancer. 2002 Feb 15;94(4):1102-10 [11920481.001]
  • [Cites] Mod Pathol. 2002 Dec;15(12):1266-72 [12481006.001]
  • [Cites] Int J Cancer. 2003 Aug 10;106(1):74-7 [12794759.001]
  • [Cites] Cancer Genet Cytogenet. 2003 Jul 1;144(1):1-5 [12810248.001]
  • [Cites] Scand J Haematol. 1976 Jul;17(1):17-28 [1066809.001]
  • [Cites] Cancer. 1979 Apr;43(4):1350-7 [445335.001]
  • [Cites] Hum Genet. 1981;58(3):285-93 [6948765.001]
  • [Cites] Cancer. 1985 Feb 1;55(3):535-41 [3965107.001]
  • [Cites] Leuk Res. 1991;15(8):683-91 [1654480.001]
  • [Cites] Cancer Genet Cytogenet. 1991 Aug;55(1):35-8 [1913605.001]
  • [Cites] Leuk Lymphoma. 1993;11 Suppl 1:11-5 [8251885.001]
  • [Cites] Cancer Genet Cytogenet. 1996 Feb;86(2):124-8 [8603337.001]
  • [Cites] Baillieres Clin Haematol. 1997 Jun;10(2):223-31 [9376661.001]
  • [Cites] Leuk Res. 1998 Sep;22(9):845-7 [9716017.001]
  • [Cites] Curr Opin Hematol. 1998 Jul;5(4):302-8 [9747637.001]
  • [Cites] N Engl J Med. 1999 Apr 29;340(17):1330-40 [10219069.001]
  • [Cites] N Engl J Med. 1999 Jul 15;341(3):164-72 [10403855.001]
  • [Cites] Am J Clin Pathol. 2005 Nov;124(5):807-14 [16203287.001]
  • [Cites] Cancer. 2006 Apr 15;106(8):1730-8 [16532439.001]
  • [Cites] J Cell Biochem. 2007 Apr 15;100(6):1376-86 [17131381.001]
  • [Cites] Cancer. 2008 May 15;112(10):2112-8 [18348294.001]
  • [Cites] Cancer. 2008 Oct 1;113(7 Suppl):1933-52 [18798533.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4010-22 [14982876.001]
  • (PMID = 19480932.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS627187; NLM/ PMC4167428
  •  go-up   go-down


32. Nimer SD: Is it important to decipher the heterogeneity of "normal karyotype AML"? Best Pract Res Clin Haematol; 2008 Mar;21(1):43-52
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Almost half of adult acute myelogenous leukemia (AML) is normal cytogenetically, and this subgroup shows a remarkable heterogeneity of genetic mutations at the molecular level and an intermediate response to therapy.
  • The finding of recurrent cytogenetic abnormalities has influenced, in a primary way, the understanding and treatment of leukemias.
  • Although resistance to treatment is associated with specific mutations, the degree to which the leukemia resembles a stem cell in its functional properties may provide greater protection from the effects of treatment.
  • Although usually all of the circulating leukemia cells are cleared following treatment, a small residual population of leukemic cells in the bone marrow persists, making this disease hard to eradicate.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Genet Cytogenet. 1989 Jul 15;40(2):203-16 [2766244.001]
  • [Cites] Blood. 1989 Dec;74(8):2668-73 [2479427.001]
  • [Cites] Clin Lab Med. 1990 Dec;10(4):755-67 [2272173.001]
  • [Cites] Am J Med Genet Suppl. 1990;7:251-61 [2149958.001]
  • [Cites] EMBO J. 1993 Dec;12(12):4481-7 [8223458.001]
  • [Cites] Nat Genet. 1994 Feb;6(2):146-51 [8162068.001]
  • [Cites] Cancer Genet Cytogenet. 1994 Mar;73(1):1-7 [8174068.001]
  • [Cites] J Clin Invest. 1994 Aug;94(2):489-96 [8040301.001]
  • [Cites] Oncogene. 1995 Apr 6;10(7):1423-30 [7731694.001]
  • [Cites] Leuk Res. 2004 Jan;28(1):43-8 [14630079.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1883-90 [14592841.001]
  • [Cites] Nature. 1970 Jun 27;226(5252):1209-11 [4316300.001]
  • [Cites] Nature. 1970 Jun 27;226(5252):1211-3 [4316301.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1975;39 Pt 1:1-7 [50905.001]
  • [Cites] Br J Haematol. 1976 Aug;33(4):451-8 [188440.001]
  • [Cites] Proc Natl Acad Sci U S A. 1977 Feb;74(2):560-4 [265521.001]
  • [Cites] Br J Cancer. 1977 Mar;35(3):265-72 [322689.001]
  • [Cites] Arch Intern Med. 1983 Sep;143(9):1726-31 [6577818.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 May;83(9):2934-8 [3458254.001]
  • [Cites] Prog Clin Biol Res. 1995;393:169-76 [8545449.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jan 21;94(2):569-74 [9012825.001]
  • [Cites] Semin Oncol. 1997 Feb;24(1):17-31 [9045301.001]
  • [Cites] Am J Clin Pathol. 1997 Jun;107(6):653-60 [9169661.001]
  • [Cites] Leuk Lymphoma. 1997 Aug;26(5-6):589-93 [9389365.001]
  • [Cites] Cancer Res. 1998 Sep 15;58(18):4173-9 [9751631.001]
  • [Cites] Mol Cell Biol. 1999 May;19(5):3635-44 [10207087.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Sep 28;96(20):11370-5 [10500183.001]
  • [Cites] J Natl Cancer Inst. 1961 Nov;27:1013-35 [14480645.001]
  • [Cites] Trans Assoc Am Physicians. 1955;68:78-81 [13299314.001]
  • [Cites] Leuk Res. 2006 Aug;30(8):1037-42 [16303180.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6361-9 [16778214.001]
  • [Cites] Mol Cell Biol. 2006 Sep;26(17):6395-402 [16914725.001]
  • [Cites] Br J Haematol. 2006 Sep;134(6):616-9 [16938118.001]
  • [Cites] Br J Haematol. 2006 Nov;135(4):438-49 [16965385.001]
  • [Cites] Haematologica. 2006 Dec;91(12):1653-61 [17145602.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3509-12 [17179228.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5164-7 [17341662.001]
  • [Cites] Oncogene. 2007 Jul 5;26(31):4596-9 [17237811.001]
  • [Cites] J Clin Pathol. 2007 Nov;60(11):1238-43 [17259299.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Sep 24;276(2):673-9 [11027530.001]
  • [Cites] Br J Haematol. 2000 Oct;111(1):190-5 [11091200.001]
  • [Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]
  • [Cites] Leukemia. 2001 Jul;15(7):1001-10 [11455967.001]
  • [Cites] Leukemia. 2001 Aug;15(8):1161-4 [11480556.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]
  • [Cites] J Biol Chem. 2001 Nov 2;276(44):40373-6 [11568179.001]
  • [Cites] Science. 2002 Feb 22;295(5559):1523-5 [11809937.001]
  • [Cites] Cancer Immunol Immunother. 2002 Aug;51(6):299-310 [12111118.001]
  • [Cites] Cell Growth Differ. 2002 Jun;13(6):275-83 [12114217.001]
  • [Cites] J Clin Oncol. 2002 Aug 1;20(15):3254-61 [12149299.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2717-23 [12351377.001]
  • [Cites] Leukemia. 2002 Oct;16(10):1974-83 [12357348.001]
  • [Cites] Hematol J. 2003;4(1):31-40 [12692518.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Jul;37(3):237-51 [12759922.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1986;51 Pt 1:263-73 [3472723.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Sep;84(17):6131-5 [3476934.001]
  • [Cites] Science. 1956 Jul 20;124(3212):127-9 [13337365.001]
  • [Cites] Acta Paediatr Suppl. 1963;:SUPPL146:77-91 [14043522.001]
  • [Cites] Curr Opin Hematol. 2005 Jan;12(1):68-75 [15604894.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] Clin Cancer Res. 2005 Feb 15;11(4):1416-24 [15746041.001]
  • [Cites] Oncogene. 2005 May 26;24(23):3847-52 [15750627.001]
  • [Cites] Blood. 2005 Jul 1;106(1):345-52 [15774615.001]
  • [Cites] Blood. 2005 Jul 1;106(1):318-27 [15784732.001]
  • [Cites] Science. 2005 Oct 28;310(5748):644-8 [16254181.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3958-61 [16081693.001]
  • [Cites] Haematologica. 2005 Dec;90(12):1617-25 [16330434.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9234-42 [16275934.001]
  • [Cites] Leukemia. 2006 Feb;20(2):212-7 [16357841.001]
  • [Cites] J Clin Oncol. 2006 Feb 10;24(5):790-7 [16418499.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):371-81 [16446383.001]
  • [Cites] Cancer Cell. 2006 Mar;9(3):175-87 [16530702.001]
  • [Cites] Pediatr Res. 2006 Apr;59(4 Pt 2):59R-64R [16549550.001]
  • [Cites] Cancer Res. 2006 Apr 1;66(7):3737-46 [16585200.001]
  • (PMID = 18342811.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK052621; United States / NIDDK NIH HHS / DK / R01 DK052621-08; United States / NIDDK NIH HHS / DK / R56 DK052208-09A1; United States / NCI NIH HHS / CA / R01 CA102202-01; United States / NCI NIH HHS / CA / CA102202-01; United States / NIDDK NIH HHS / DK / R56 DK052208; United States / NCI NIH HHS / CA / R01 CA102202; United States / NIDDK NIH HHS / DK / DK052208-09A1; United States / NIDDK NIH HHS / DK / DK052621-08
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 76
  • [Other-IDs] NLM/ NIHMS44325; NLM/ PMC2654590
  •  go-up   go-down


33. Akasaka T, Balasas T, Russell LJ, Sugimoto KJ, Majid A, Walewska R, Karran EL, Brown DG, Cain K, Harder L, Gesk S, Martin-Subero JI, Atherton MG, Brüggemann M, Calasanz MJ, Davies T, Haas OA, Hagemeijer A, Kempski H, Lessard M, Lillington DM, Moore S, Nguyen-Khac F, Radford-Weiss I, Schoch C, Struski S, Talley P, Welham MJ, Worley H, Strefford JC, Harrison CJ, Siebert R, Dyer MJ: Five members of the CEBP transcription factor family are targeted by recurrent IGH translocations in B-cell precursor acute lymphoblastic leukemia (BCP-ALL). Blood; 2007 Apr 15;109(8):3451-61
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Five members of the CEBP transcription factor family are targeted by recurrent IGH translocations in B-cell precursor acute lymphoblastic leukemia (BCP-ALL).
  • CCAAT enhancer-binding protein (CEBP) transcription factors play pivotal roles in proliferation and differentiation, including suppression of myeloid leukemogenesis.
  • Mutations of CEBPA are found in a subset of acute myeloid leukemia (AML) and in some cases of familial AML.
  • Here, using cytogenetics, fluorescence in situ hybridization (FISH), and molecular cloning, we show that 5 CEBP gene family members are targeted by recurrent IGH chromosomal translocations in BCP-ALL.
  • Our findings implicate the CEBP gene family as novel oncogenes in BCP-ALL, and suggest opposing functions of CEBP dysregulation in myeloid and lymphoid leukemogenesis.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17170124.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132670597
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / Immunoglobulin Heavy Chains
  •  go-up   go-down


34. Jones D, Thomas D, Yin CC, O'Brien S, Cortes JE, Jabbour E, Breeden M, Giles FJ, Zhao W, Kantarjian HM: Kinase domain point mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia emerge after therapy with BCR-ABL kinase inhibitors. Cancer; 2008 Sep 1;113(5):985-94
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Kinase domain point mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia emerge after therapy with BCR-ABL kinase inhibitors.
  • BACKGROUND: BCR-ABL kinase domain (KD) mutations are detected in approximately 45% of patients with imatinib-resistant chronic myeloid leukemia.
  • Patterns of KD mutations in Philadelphia chromosome (Ph)-positive acute lympho- blastic leukemia (ALL) are less well studied.
  • METHODS: The authors assessed KD mutations in patients with recurrent Ph-positive ALL after treatments that included 1 or more kinase inhibitors (n = 24 patients) or no prior kinase inhibitor (KI) therapy (n = 12 patients).
  • RESULTS: ABL KD mutations were detected by direct sequencing in 15 of 17 patients (88%) who had recurrent Ph-positive ALL and received prior imatinib (n = 16) or dasatinib (n = 1) treatment and in 6 of 7 patients (86%) who had resistant/recurrent tumors treated with >or=2 KIs compared with 0 of 12 patients with recurrent Ph-positive ALL who never received KIs.
  • Using a more sensitive pyrosequencing method, mutations were not detected at codons 315 and 253 in the diagnostic samples from those 12 patients or in 30 patients with Ph-positive ALL who never developed recurrent disease.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 American Cancer Society.
  • (PMID = 18615627.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / P50 CA100632-010007; United States / NCI NIH HHS / CA / P50 CA100707; United States / NCI NIH HHS / CA / 1P50CA100707-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ NIHMS58345; NLM/ PMC4204653
  •  go-up   go-down


35. Wouters BJ, Louwers I, Valk PJ, Löwenberg B, Delwel R: A recurrent in-frame insertion in a CEBPA transactivation domain is a polymorphism rather than a mutation that does not affect gene expression profiling-based clustering of AML. Blood; 2007 Jan 1;109(1):389-90
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A recurrent in-frame insertion in a CEBPA transactivation domain is a polymorphism rather than a mutation that does not affect gene expression profiling-based clustering of AML.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Polymorphism, Genetic
  • [MeSH-minor] Acute Disease. Cluster Analysis. Cohort Studies. DNA Mutational Analysis. Gene Duplication. Gene Expression Profiling. Humans. Mutagenesis, Insertional. Protein Structure, Tertiary. Transcriptional Activation

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17190859.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human
  •  go-up   go-down


36. Giguère A, Hébert J: CLCA2, a novel RUNX1 partner gene in a therapy-related leukemia with t(1;21)(p22;q22). Cancer Genet Cytogenet; 2010 Oct 15;202(2):94-100
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CLCA2, a novel RUNX1 partner gene in a therapy-related leukemia with t(1;21)(p22;q22).
  • The RUNX1 gene is frequently rearranged in de novo and therapy-related leukemia.
  • In the present study, we identified the CLCA2 gene as a novel fusion partner of RUNX1 in a case of therapy-related acute myeloid leukemia associated with t(1;21)(p22;q22).
  • The RUNX1-CLCA2 fusion is another example of out-of-frame fusion generating truncated RUNX1 isoforms that represent a recurrent molecular mechanism in RUNX1-related leukemias.
  • [MeSH-major] Chloride Channels / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 21 / genetics. Core Binding Factor Alpha 2 Subunit / metabolism. Leukemia / genetics. Leukemia / therapy. Translocation, Genetic / genetics

  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20875871.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CLCA2 protein, human; 0 / Chloride Channels; 0 / Core Binding Factor Alpha 2 Subunit
  •  go-up   go-down


37. Douet-Guilbert N, Arnaud B, Morel F, Le Bris MJ, De Braekeleer M: Cryptic 5' MLL gene insertion in an X-chromosome in acute myeloblastic leukemia. Cancer Genet Cytogenet; 2005 Mar;157(2):178-80
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cryptic 5' MLL gene insertion in an X-chromosome in acute myeloblastic leukemia.
  • We report here on a 43-year-old man presenting with asthenia and pancytopenia who was diagnosed with acute myeloblastic leukemia FAB-M5.
  • The accumulating data on acute myeloblastic leukemia demonstrate that the 5'-MLL insertion in an X-chromosome is a rare but recurrent abnormality associated with leukemia, not only in infants, but also in adults.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, X. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Myeloid-Lymphoid Leukemia Protein

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15721643.001).
  • [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 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


38. Ando T, Mitani N, Matsui K, Yamashita K, Nomiyama J, Tsuru M, Yujiri T, Tanizawa Y: Recurrent extramedullary relapse of acute myelogenous leukemia after allogeneic hematopoietic stem cell transplantation in a patient with the chromosomal abnormality t(8;21) and CD56-positivity. Int J Hematol; 2009 Oct;90(3):374-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent extramedullary relapse of acute myelogenous leukemia after allogeneic hematopoietic stem cell transplantation in a patient with the chromosomal abnormality t(8;21) and CD56-positivity.
  • Isolated extramedullary (EM) relapse of acute myelogenous leukemia (AML) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) is rare.
  • These findings suggest that the graft-versus-leukemia effect may preferentially maintain marrow remission rather than prevent EM relapse.
  • In addition, our findings show that extended survival is possible after EM relapse following allo-HSCT in patients with marrow hematopoiesis of donor origin, and that augmentation of the graft-versus-leukemia effect may be useful.
  • [MeSH-major] Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute. Stomach Neoplasms. Translocation, Genetic


39. Murata M, Ishikawa Y, Ohashi H, Terakura S, Ozeki K, Kiyoi H, Naoe T: Donor cell leukemia after allogeneic peripheral blood stem cell transplantation: a case report and literature review. Int J Hematol; 2008 Jul;88(1):111-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Donor cell leukemia after allogeneic peripheral blood stem cell transplantation: a case report and literature review.
  • A 49-year-old male developed recurrent acute myeloid leukemia 27 months after allogeneic peripheral blood stem cell transplantation (PBSCT) from an HLA-identical brother.
  • Thus, this recipient developed donor cell leukemia (DCL).
  • [MeSH-major] Leukemia, Myeloid, Acute. Living Donors. Peripheral Blood Stem Cell Transplantation

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Organ Donation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Hematol. 2007 Aug;86(2):192-5 [17875537.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):311-21 [15803157.001]
  • [Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 May;12(5):511-7 [16635786.001]
  • [Cites] Bone Marrow Transplant. 2002 Jun;29(12):999-1003 [12098070.001]
  • [Cites] Am J Hematol. 2005 Aug;79(4):294-8 [16044441.001]
  • [Cites] Am J Hematol. 2005 Jun;79(2):142-6 [15929112.001]
  • [Cites] Bone Marrow Transplant. 2008 Jan;41(1):91-2 [17982506.001]
  • [Cites] Lancet. 1971 Feb 6;1(7693):251-5 [4100012.001]
  • [Cites] Br J Haematol. 1989 Nov;73(3):420-2 [2605130.001]
  • [Cites] Am J Hematol. 2000 Jan;63(1):46-53 [10602169.001]
  • [Cites] Haematologica. 2005 Jul;90(7):969-75 [15996934.001]
  • [Cites] Lancet. 1998 Jan 17;351(9097):178-81 [9449873.001]
  • [Cites] Int J Hematol. 2006 May;83(4):301-8 [16757428.001]
  • [Cites] Trends Biochem Sci. 2006 Oct;31(10):589-95 [16911868.001]
  • [Cites] N Engl J Med. 1990 Jun 21;322(25):1794-6 [2189070.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]
  • [Cites] N Engl J Med. 1989 Sep 21;321(12):784-9 [2671734.001]
  • [Cites] Bone Marrow Transplant. 1989 Nov;4(6):643-6 [2573397.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4377-80 [16118319.001]
  • [Cites] Leukemia. 2006 Apr;20(4):744-5 [16437136.001]
  • [Cites] Bone Marrow Transplant. 2001 Oct;28(7):705-7 [11704795.001]
  • [Cites] Nat Genet. 1996 Jul;13(3):350-3 [8673136.001]
  • [Cites] Blood. 2007 Apr 1;109(7):2688-92 [17132724.001]
  • [Cites] J Pediatr Hematol Oncol. 2006 Nov;28(11):763-7 [17114967.001]
  • [Cites] Bone Marrow Transplant. 2002 Mar;29(5):453-6 [11919737.001]
  • [Cites] Leukemia. 2007 Mar;21(3):574-6 [17252020.001]
  • (PMID = 18470599.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha
  • [Number-of-references] 27
  •  go-up   go-down


40. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


41. Dai HP, Xue YQ, Zhou JW, Li AP, Wu YF, Pan JL, Wang Y, Zhang J: LPXN, a member of the paxillin superfamily, is fused to RUNX1 in an acute myeloid leukemia patient with a t(11;21)(q12;q22) translocation. Genes Chromosomes Cancer; 2009 Dec;48(12):1027-36
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] LPXN, a member of the paxillin superfamily, is fused to RUNX1 in an acute myeloid leukemia patient with a t(11;21)(q12;q22) translocation.
  • RUNX1 (previously AML1) is involved in multiple recurrent chromosomal rearrangements in hematological malignances.
  • Recently, we identified a novel fusion between RUNX1 and LPXN from an acute myeloid leukemia (AML) patient with t(11;21)(q12;q22).
  • [MeSH-major] Cell Adhesion Molecules / genetics. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 21 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Phosphoproteins / genetics. Translocation, Genetic / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19760607.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Core Binding Factor Alpha 2 Subunit; 0 / LPXN protein, human; 0 / Oncogene Proteins, Fusion; 0 / Phosphoproteins; 0 / RUNX1 protein, human; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
  •  go-up   go-down


42. Haferlach T: Molecular genetic pathways as therapeutic targets in acute myeloid leukemia. Hematology Am Soc Hematol Educ Program; 2008;:400-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular genetic pathways as therapeutic targets in acute myeloid leukemia.
  • The heterogeneity of acute myeloid leukemia (AML) results from a complex network of cytogenetic aberrations and molecular mutations.
  • Clinical variances within distinct genetically defined subgroups could in part be linked to the interaction of diverse mutation classes, and the subdivision of normal karyotype AML on the basis of recurrent molecular mutations gains increasing relevance for therapeutic decisions.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. ARSENIC TRIOXIDE .
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19074117.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Genetic Markers; 0 / Oxides; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 111
  •  go-up   go-down


43. Verhaak RG, Valk PJ: Genes predictive of outcome and novel molecular classification schemes in adult acute myeloid leukemia. Cancer Treat Res; 2010;145:67-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genes predictive of outcome and novel molecular classification schemes in adult acute myeloid leukemia.
  • The pretreatment karyotype of leukemic blasts is currently the key determinant in therapy decision making in acute myeloid leukemia (AML).
  • The World Health Organization (WHO) has recognized this important information by including, besides clinical, cytological, cytochemical, and immunophenotypical features, recurrent cytogenetic abnormalities in its classification (Table 1).
  • [MeSH-major] Genes, Neoplasm. Leukemia, Myeloid, Acute / genetics


44. Thol F, Weissinger EM, Krauter J, Wagner K, Damm F, Wichmann M, Göhring G, Schumann C, Bug G, Ottmann O, Hofmann WK, Schlegelberger B, Ganser A, Heuser M: IDH1 mutations in patients with myelodysplastic syndromes are associated with an unfavorable prognosis. Haematologica; 2010 Oct;95(10):1668-74
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Myelodysplastic syndromes are a heterogeneous group of hematopoietic stem cell disorders with a high propensity to transform into acute myeloid leukemia.
  • Heterozygous missense mutations in IDH1 at position R132 and in IDH2 at positions R140 and R172 have recently been reported in acute myeloid leukemia.
  • DESIGN AND METHODS: We examined 193 patients with myelodysplastic syndromes and 53 patients with acute myeloid leukemia arising from myelodysplastic syndromes for mutations in IDH1 (R132), IDH2 (R172 and R140), and NPM1 by direct sequencing.
  • RESULTS: We found that mutations in IDH1 occurred with a frequency of 3.6% in myelodysplastic syndromes (7 mutations in 193 patients) and 7.5% in acute myeloid leukemia following myelodysplastic syndromes (4 mutations in 53 patients).
  • Three mutations in codon R140 of IDH2 and one mutation in codon R172 were found in patients with acute myeloid leukemia following myelodysplastic syndromes (7.5%).
  • The presence of IDH1 mutations was associated with a shorter overall survival (HR 3.20; 95% CI 1.47-6.99) and a higher rate of transformation into acute myeloid leukemia (67% versus 28%, P=0.04).
  • CONCLUSIONS: These results suggest that IDH1 mutations are recurrent molecular aberrations in patients with myelodysplastic syndromes, and may become useful as a poor risk marker in these patients.

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Eur J Haematol. 1989 Oct;43(4):271-85 [2684681.001]
  • [Cites] Blood. 2004 Mar 15;103(6):2316-24 [14615365.001]
  • [Cites] Leukemia. 1994 Apr;8(4):638-41 [7512175.001]
  • [Cites] Blood. 1997 Mar 15;89(6):2079-88 [9058730.001]
  • [Cites] Ann Hematol. 1999 Mar;78(3):125-30 [10211754.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2223-31 [16193087.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3898-905 [16912223.001]
  • [Cites] Haematologica. 2007 Jun;92(6):744-52 [17550846.001]
  • [Cites] Br J Haematol. 2007 Nov;139(3):405-14 [17910630.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1807-12 [18772396.001]
  • [Cites] N Engl J Med. 2009 Feb 19;360(8):765-73 [19228619.001]
  • [Cites] J Clin Oncol. 2009 Jun 20;27(18):3000-6 [19380453.001]
  • [Cites] Nat Genet. 2009 Jul;41(7):838-42 [19483684.001]
  • [Cites] Br J Haematol. 2009 Jun;145(6):788-800 [19388938.001]
  • [Cites] N Engl J Med. 2009 Sep 10;361(11):1058-66 [19657110.001]
  • [Cites] N Engl J Med. 2009 Sep 10;361(11):1117; author reply 1117-8 [19741235.001]
  • [Cites] Blood. 2009 Sep 24;114(13):2575-80 [19605847.001]
  • [Cites] N Engl J Med. 2009 Nov 5;361(19):1872-85 [19890130.001]
  • [Cites] Leukemia. 2009 Nov;23(11):2183-6 [19609284.001]
  • [Cites] N Engl J Med. 2010 Jan 28;362(4):369-70 [20107228.001]
  • [Cites] J Clin Oncol. 2010 Feb 1;28(4):578-85 [20038731.001]
  • [Cites] J Exp Med. 2010 Feb 15;207(2):339-44 [20142433.001]
  • [Cites] Cancer Cell. 2010 Mar 16;17(3):225-34 [20171147.001]
  • [Cites] Blood. 2010 Apr 8;115(14):2749-54 [20097881.001]
  • [Cites] J Clin Oncol. 2010 May 10;28(14):2356-64 [20368538.001]
  • [Cites] Blood. 2010 Jul 29;116(4):614-6 [20421455.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Feb;87(4):1377-80 [2406720.001]
  • [Cites] Ann Hematol. 2004 Jun;83(6):336-44 [15034758.001]
  • [Cites] Stat Med. 1986 May-Jun;5(3):255-60 [3738291.001]
  • [Cites] Leukemia. 2004 Mar;18(3):460-5 [14712285.001]
  • [CommentIn] Haematologica. 2010 Oct;95(10):1623-7 [20884716.001]
  • (PMID = 20494930.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human
  • [Other-IDs] NLM/ PMC2948091
  •  go-up   go-down


45. Liedtke M, Cleary ML: Therapeutic targeting of MLL. Blood; 2009 Jun 11;113(24):6061-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The mixed lineage leukemia (MLL) proto-oncogene is a recurrent site of genetic rearrangements in acute leukemias; and since its discovery in 1992, many advances have been made in understanding its role in leukemogenesis.
  • Proteins associated with the MLL core complex or its fusion partners have been isolated and characterized for their critical roles in leukemia pathogenesis.
  • [MeSH-major] Leukemia / therapy. Myeloid-Lymphoid Leukemia Protein / metabolism

  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jun 21;91(13):6236-9 [8016145.001]
  • [Cites] Bioessays. 1995 Oct;17(10):855-63 [7487967.001]
  • [Cites] Nature. 1995 Nov 30;378(6556):505-8 [7477409.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Dec 19;92(26):12160-4 [8618864.001]
  • [Cites] Science. 1997 Apr 18;276(5311):404-7 [9103196.001]
  • [Cites] Blood. 1997 Sep 1;90(5):1799-806 [9292512.001]
  • [Cites] Mol Cell Biol. 1998 Jan;18(1):122-9 [9418860.001]
  • [Cites] EMBO J. 1998 Nov 16;17(22):6723-9 [9822615.001]
  • [Cites] Leukemia. 1999 Oct;13(10):1525-33 [10516753.001]
  • [Cites] Mol Cell Biol. 2004 Dec;24(23):10470-8 [15542854.001]
  • [Cites] Blood. 2005 Jan 15;105(2):812-20 [15374878.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):749-54 [15640349.001]
  • [Cites] Cancer. 2006 Feb 15;106(4):950-6 [16404744.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1307-10 [16617320.001]
  • [Cites] Blood. 2006 Jul 15;108(2):622-9 [16469876.001]
  • [Cites] Leuk Res. 2008 Apr;32(4):633-42 [17875318.001]
  • [Cites] Clin Cancer Res. 2008 Jun 15;14(12):3651-6 [18559577.001]
  • [Cites] Cancer Cell. 2008 Jul 8;14(1):36-46 [18598942.001]
  • [Cites] PLoS Genet. 2008;4(9):e1000190 [18787701.001]
  • [Cites] Nature. 2008 Oct 30;455(7217):1205-9 [18806775.001]
  • [Cites] Trends Cell Biol. 2000 Apr;10(4):147-54 [10740269.001]
  • [Cites] EMBO J. 2000 Sep 1;19(17):4655-64 [10970858.001]
  • [Cites] Cancer Res. 2000 Nov 15;60(22):6227-9 [11103774.001]
  • [Cites] Br J Haematol. 2001 Feb;112(2):315-26 [11167824.001]
  • [Cites] Br J Haematol. 2001 Feb;112(2):358-63 [11167829.001]
  • [Cites] Oncogene. 2001 Feb 15;20(7):874-8 [11314021.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Leukemia. 2006 Aug;20(8):1368-76 [16761017.001]
  • [Cites] Nature. 2006 Aug 17;442(7104):818-22 [16862118.001]
  • [Cites] EMBO J. 2006 Oct 4;25(19):4503-12 [16990798.001]
  • [Cites] Semin Cancer Biol. 2005 Jun;15(3):175-88 [15826832.001]
  • [Cites] J Clin Invest. 2005 Apr;115(4):919-29 [15761502.001]
  • [Cites] Cell. 2005 Apr 22;121(2):167-78 [15851025.001]
  • [Cites] Blood. 2005 Jul 1;106(1):345-52 [15774615.001]
  • [Cites] Blood. 2005 Jul 15;106(2):706-12 [15802527.001]
  • [Cites] Genes Dev. 2005 Aug 15;19(16):1885-93 [16103216.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1605-12 [16034464.001]
  • [Cites] Cell. 2005 Oct 21;123(2):207-18 [16239140.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11367-74 [16357144.001]
  • [Cites] Nat Med. 2006 Jan;12(1):89-98 [16341242.001]
  • [Cites] Leukemia. 2006 Feb;20(2):264-71 [16357833.001]
  • [Cites] Br J Haematol. 2006 Mar;132(5):539-51 [16445826.001]
  • [Cites] J Proteome Res. 2006 Oct;5(10):2743-53 [17022645.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):257-68 [17045204.001]
  • [Cites] Hum Mol Genet. 2007 Jan 1;16(1):92-106 [17135274.001]
  • [Cites] Cancer Res. 2007 Aug 1;67(15):7275-83 [17671196.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Sep 4;104(36):14442-7 [17726105.001]
  • [Cites] Nat Cell Biol. 2007 Oct;9(10):1208-15 [17891136.001]
  • [Cites] Oncogene. 2007 Oct 15;26(47):6766-76 [17934484.001]
  • [Cites] Genes Dev. 2007 Nov 1;21(21):2762-74 [17942707.001]
  • [Cites] Blood. 2007 Dec 15;110(13):4445-54 [17855633.001]
  • [Cites] Leukemia. 2008 Jan;22(1):66-77 [17851551.001]
  • [Cites] Genome Biol. 2002;3(1):REVIEWS3001 [11806834.001]
  • [Cites] Nucleic Acids Res. 2002 Feb 15;30(4):958-65 [11842107.001]
  • [Cites] Blood. 2002 May 15;99(10):3780-5 [11986236.001]
  • [Cites] Lancet. 2002 Jun 1;359(9321):1909-15 [12057554.001]
  • [Cites] Curr Biol. 2002 Jun 25;12(12):1052-8 [12123582.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1270-6 [12406912.001]
  • [Cites] J Cell Sci. 2003 Apr 1;116(Pt 7):1175-86 [12615961.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):173-83 [12620411.001]
  • [Cites] Cell. 2003 Mar 7;112(5):711-23 [12628190.001]
  • [Cites] Blood. 2003 Jul 1;102(1):262-8 [12637319.001]
  • [Cites] Cancer Cell. 2003 Aug;4(2):99-110 [12957285.001]
  • [Cites] Genes Dev. 2003 Sep 15;17(18):2298-307 [12952893.001]
  • [Cites] Cancer Cell. 2003 Sep;4(3):197-207 [14522254.001]
  • [Cites] Leuk Res. 2004 Jan;28(1):19-23 [14630076.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(2):617-28 [14701735.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1823-8 [14615372.001]
  • [Cites] Mol Cell. 2004 Feb 27;13(4):587-97 [14992727.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3192-9 [15070702.001]
  • [Cites] Blood. 2004 May 15;103(10):3876-82 [14751928.001]
  • [Cites] Mol Cell Biol. 2004 Jul;24(13):5639-49 [15199122.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1364-72 [15269783.001]
  • [Cites] Leuk Lymphoma. 2004 May;45(5):1017-24 [15291362.001]
  • [Cites] Cell. 1992 Nov 13;71(4):691-700 [1423624.001]
  • [Cites] Cell. 1992 Nov 13;71(4):701-8 [1423625.001]
  • (PMID = 19289854.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K08 CA120349
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 78
  • [Other-IDs] NLM/ PMC2699228
  •  go-up   go-down


46. Shimoyama M, Yamamoto K, Nishikawa S, Minagawa K, Katayama Y, Matsui T: Duplication of isodicentric chromosome 21, idic(21)(p11.2), leading to pentasomy 21q in acute myeloid leukemia with multilineage dysplasia. Cancer Genet Cytogenet; 2009 Oct;194(1):38-43
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Duplication of isodicentric chromosome 21, idic(21)(p11.2), leading to pentasomy 21q in acute myeloid leukemia with multilineage dysplasia.
  • Isodicentric chromosome 21, idic(21)(p11.2), is a rare but recurrent cytogenetic aberration in acute lymphoblastic leukemia.
  • We describe here a novel case of acute myeloid leukemia (AML) with double idic(21)(p11.2).
  • A 35-year-old man was diagnosed as having de novo AML with multilineage dysplasia because of 30% myeloperoxidase-positive blasts and trilineage dysplasia in the bone marrow.
  • [MeSH-major] Aneuploidy. Chromosomes, Human, Pair 21 / genetics. Gene Duplication. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / blood. Antigens, CD13 / blood. Antigens, CD34 / blood. Antigens, CD7 / blood. Antigens, Differentiation, Myelomonocytic / blood. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. HLA-DR Antigens / blood. Humans. In Situ Hybridization, Fluorescence. Male. Sialic Acid Binding Ig-like Lectin 3. Spectral Karyotyping

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19737652.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, CD7; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / HLA-DR Antigens; 0 / RUNX1 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
  •  go-up   go-down


47. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Monosomy. Neoplasm Proteins / genetics

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


48. Huang KP, Chase AJ, Cross NC, Reiter A, Li TY, Wang TF, Chu SC, Lu XY, Li CC, Kao RH: Evolutional change of karyotype with t(8;9)(p22;p24) and HLA-DR immunophenotype in relapsed acute myeloid leukemia. Int J Hematol; 2008 Sep;88(2):197-201
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evolutional change of karyotype with t(8;9)(p22;p24) and HLA-DR immunophenotype in relapsed acute myeloid leukemia.
  • The rare recurrent translocation of (8;9)(p22;p24) with PCM1-JAK2 fusion was recently characterized in diverse hematological malignancies.
  • Most of them are atypical chronic myeloid leukemia (CML) or other myeloproliferative disorders (MPD), and are predominantly in the male.
  • We report a female patient with acute myeloid leukemia (AML) initially presenting with normal karyotype and negative HLA-DR expression who achieved complete remission after standard chemotherapy.
  • [MeSH-major] Autoantigens / genetics. Cell Cycle Proteins / genetics. HLA-DR Antigens / genetics. Janus Kinase 2 / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 1995 Jun;9(6):972-6 [7596187.001]
  • [Cites] Leukemia. 2002 Oct;16(10):2084-91 [12357361.001]
  • [Cites] Scand J Immunol. 1997 Oct;46(4):379-87 [9350289.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] J Immunol. 1996 Aug 15;157(4):1559-68 [8759739.001]
  • [Cites] Jpn J Ophthalmol. 2001 Jan-Feb;45(1):13-21 [11163041.001]
  • [Cites] J Cell Physiol. 1997 Oct;173(1):110-4 [9326455.001]
  • [Cites] J Immunol. 2001 Feb 15;166(4):2260-9 [11160280.001]
  • [Cites] Cancer Res. 2005 Apr 1;65(7):2662-7 [15805263.001]
  • [Cites] Clin Lab Haematol. 2001 Jun;23(3):173-9 [11553058.001]
  • [Cites] Leukemia. 1998 Sep;12 Suppl 1:S7-12 [9777887.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1692-6 [16034466.001]
  • [Cites] Science. 1997 Nov 14;278(5341):1309-12 [9360930.001]
  • [Cites] Blood. 1999 Jul 15;94(2):694-700 [10397736.001]
  • [Cites] Blood. 1997 Oct 1;90(7):2535-40 [9326218.001]
  • [Cites] Anticancer Res. 1990 Sep-Oct;10(5A):1161-7 [2122794.001]
  • [Cites] Leuk Lymphoma. 1994 Jan;12(3-4):211-22 [7909466.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [Cites] Crit Rev Immunol. 1993;13(3-4):247-68 [8110378.001]
  • [Cites] Hum Pathol. 2005 Oct;36(10):1148-51 [16226118.001]
  • [Cites] Leukemia. 2006 Mar;20(3):536-7 [16424865.001]
  • [Cites] Leukemia. 1995 May;9(5):875-8 [7769851.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] J Clin Invest. 1985 Oct;76(4):1391-7 [2414320.001]
  • [Cites] Oncogene. 2005 Nov 3;24(48):7248-52 [16091753.001]
  • [Cites] Semin Oncol. 1997 Feb;24(1):17-31 [9045301.001]
  • (PMID = 18594780.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Autoantigens; 0 / Cell Cycle Proteins; 0 / HLA-DR Antigens; 0 / Oncogene Proteins, Fusion; 0 / PCM1 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


49. Saunders K, Czepulkowski B, Sivalingam R, Hayes JP, Aldouri M, Sekhar M, Cummins M, Ho A, Mufti GJ: Isochromosome of a deleted 20q: a rare but recurrent chromosome abnormality in myelodysplastic syndromes. Cancer Genet Cytogenet; 2005 Jan 15;156(2):154-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isochromosome of a deleted 20q: a rare but recurrent chromosome abnormality in myelodysplastic syndromes.
  • Interstitial deletion of the long arm of chromosome 20, as the sole abnormality, is commonly observed in myeloid malignancies, including myeloproliferative disorder, myelodysplastic syndrome, and acute myeloid leukemia.

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15642396.001).
  • [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
  •  go-up   go-down


50. Morerio C, Acquila M, Rapella A, Tassano E, Rosanda C, Panarello C: Inversion (11)(p15q22) with NUP98-DDX10 fusion gene in pediatric acute myeloid leukemia. Cancer Genet Cytogenet; 2006 Dec;171(2):122-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inversion (11)(p15q22) with NUP98-DDX10 fusion gene in pediatric acute myeloid leukemia.
  • The inv(11)(p15q22), a rare but recurrent chromosome abnormality that creates a NUP98-DDX10 fusion gene, is associated with de novo or secondary myeloid malignancies.
  • We report a case of acute monocytic leukemia presenting this rearrangement, studied using fluorescence in situ hybridization (FISH) and reverse transcriptase-PCR (RT-PCR).
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 11 / genetics. DEAD-box RNA Helicases / genetics. Gene Fusion. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17116492.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AB040537/ AB040538
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; EC 3.6.1.- / DDX10 protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases
  • [Number-of-references] 12
  •  go-up   go-down


51. Armengol G, Canellas A, Alvarez Y, Bastida P, Toledo JS, Pérez-Iribarne Mdel M, Camós M, Tuset E, Estella J, Coll MD, Caballín MR, Knuutila S: Genetic changes including gene copy number alterations and their relation to prognosis in childhood acute myeloid leukemia. Leuk Lymphoma; 2010 Jan;51(1):114-24
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic changes including gene copy number alterations and their relation to prognosis in childhood acute myeloid leukemia.
  • We studied a series of 68 subjects diagnosed with childhood acute myeloid leukemia (AML) using conventional cytogenetics and fluorescence in situ hybridization (FISH), polymerase chain reaction (PCR) to analyze mutations in FLT3 and NPM1 genes, and/or array comparative genomic hybridization (CGH).
  • They probably correspond to non passenger alterations that cooperate with the recurrent translocations.
  • [MeSH-major] Gene Dosage. Leukemia, Myeloid, Acute / genetics. Mutation


52. Sanada M, Uike N, Ohyashiki K, Ozawa K, Lili W, Hangaishi A, Kanda Y, Chiba S, Kurokawa M, Omine M, Mitani K, Ogawa S: Unbalanced translocation der(1;7)(q10;p10) defines a unique clinicopathological subgroup of myeloid neoplasms. Leukemia; 2007 May;21(5):992-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unbalanced translocation der(1;7)(q10;p10) defines a unique clinicopathological subgroup of myeloid neoplasms.
  • The unbalanced translocation, der(1;7)(q10;p10), is one of the characteristic cytogenetic abnormalities found in myelodysplastic syndromes (MDS) and other myeloid neoplasms.
  • Although described frequently with very poor clinical outcome and possible relationship with monosomy 7 or 7q- (-7/7q-), this recurrent cytogenetic abnormality has not been explored fully.
  • In contrast with other -7/7q- cases, where the abnormality tends to be found in one or more partial karyotypes, der(1;7)(q10;p10) represents the abnormality common to all the abnormal clones and usually appears as a sole chromosomal abnormality during the entire clinical courses, or if not, is accompanied only by a limited number and variety of additional abnormalities, mostly trisomy 8 and/or loss of 20q. der(1;7)(q10;p10)-positive MDS cases showed lower blast counts (P<0.0001) and higher hemoglobin concentrations (P<0.0075) at diagnosis and slower progression to acute myeloid leukemia (P=0.0043) than other -7/7q- cases. der(1;7)(q10;p10) cases showed significantly better clinical outcome than other -7/7q cases (P<0.0001).
  • In conclusion, der(1;7)(q10;p10) defines a discrete entity among myeloid neoplasms, showing unique clinical and cytogenetic characteristics.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics. Translocation, Genetic


53. Ladetto M, Vallet S, Benedetti F, Vitolo U, Martelli M, Callea V, Patti C, Coser P, Perrotti A, Sorio M, Boccomini C, Pulsoni A, Stelitano C, Scimè R, Boccadoro M, Rosato R, De Marco F, Zanni M, Corradini P, Tarella C: Prolonged survival and low incidence of late toxic sequelae in advanced follicular lymphoma treated with a TBI-free autografting program: updated results of the multicenter consecutive GITMO trial. Leukemia; 2006 Oct;20(10):1840-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • (4) actuarial 5-years risk of developing secondary myelodysplasia and acute myeloid leukemia of 3.7%, with most of these events occurring in patients re-treated for recurrent lymphoma.

  • Genetic Alliance. consumer health - Follicular Lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16932351.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin; VB0R961HZT / Prednisone; DHAP protocol; VPD protocol
  •  go-up   go-down


54. Pedersen-Bjergaard J, Christiansen DH, Desta F, Andersen MK: Alternative genetic pathways and cooperating genetic abnormalities in the pathogenesis of therapy-related myelodysplasia and acute myeloid leukemia. Leukemia; 2006 Nov;20(11):1943-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alternative genetic pathways and cooperating genetic abnormalities in the pathogenesis of therapy-related myelodysplasia and acute myeloid leukemia.
  • Alternative genetic pathways were previously outlined in the pathogenesis of therapy-related myelodysplasia (t-MDS) and acute myeloid leukemia (t-AML) based on cytogenetic characteristics.
  • Some of the chromosome aberrations, the recurrent balanced translocations or inversions, directly result in chimeric rearrangement of genes for hematopoietic transcription factors (class II mutations) which disturb cellular differentiation.
  • Therapy-related and de novo myelodysplasia and acute myeloid leukemia seem to share genetic pathways, and surprisingly gene mutations were in general not more frequent in patients with t-MDS or t-AML as compared to similar cases of de novo MDS and AML studied previously.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Chromosome Aberrations. Humans. Mutation


55. MacKinnon RN, Campbell LJ: A comparison of two contrasting recurrent isochromosomes 20 found in myelodysplastic syndromes suggests that retention of proximal 20q is a significant factor in myeloid malignancies. Cancer Genet Cytogenet; 2005 Dec;163(2):176-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A comparison of two contrasting recurrent isochromosomes 20 found in myelodysplastic syndromes suggests that retention of proximal 20q is a significant factor in myeloid malignancies.
  • We speculate that a region of proximal 20q is preferentially retained during deletions of the critical region in MDS and acute myeloid leukemia.


56. Ferguson EC, Talley P, Vora A: Translocation (6;17)(q23;q11.2): a novel cytogenetic abnormality in congenital acute myeloid leukemia? Cancer Genet Cytogenet; 2005 Nov;163(1):71-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translocation (6;17)(q23;q11.2): a novel cytogenetic abnormality in congenital acute myeloid leukemia?
  • Congenital leukemia occurring within 4 weeks of birth is extremely rare and, excluding transient neonatal myeloproliferation associated with Down syndrome, makes up approximately 1% of childhood leukemias.
  • It is usually seen as acute myeloid leukemia (AML), most frequently French-American-British (FAB) types M4 and M5.
  • Recurrent cytogenetic abnormalities have been reported in this group, and in approximately one third of cases the MLL gene at 11q23 is involved.
  • We present a case of congenital leukemia (AML FAB type M1) with an acquired translocation between chromosomes 6 and 17.
  • [MeSH-major] Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 6. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16271959.001).
  • [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
  •  go-up   go-down


57. Rücker FG, Sander S, Döhner K, Döhner H, Pollack JR, Bullinger L: Molecular profiling reveals myeloid leukemia cell lines to be faithful model systems characterized by distinct genomic aberrations. Leukemia; 2006 Jun;20(6):994-1001
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular profiling reveals myeloid leukemia cell lines to be faithful model systems characterized by distinct genomic aberrations.
  • To model and investigate different facets of leukemia pathogenesis, a widely accepted approach is to use immortalized leukemia cell lines.
  • To improve the molecular characterization of these model systems, we analyzed 17 myeloid leukemia cell lines using DNA microarray technology.
  • By array-based comparative genomic hybridization, we identified recurrent genomic DNA gains and losses, as well as high-level amplifications.
  • Comparison with clinical leukemia specimens showed that key signatures were retained, as myeloid cell lines with characteristic cytogenetic aberrations co-clustered with leukemia samples carrying the respective abnormality.
  • Thus, our analyses demonstrate myeloid cell lines to exhibit conserved and stable signatures reflecting the underlying primary cytogenetic aberrations.
  • Our refined molecular characterization of myeloid cell lines supports the utility of cell lines as faithful and powerful model systems and provides additional insights into the molecular mechanisms of leukemogenesis.
  • [MeSH-major] Chromosome Aberrations. Gene Expression Profiling. Leukemia, Myeloid / genetics. Models, Genetic
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Cluster Analysis. Gene Expression Regulation, Leukemic. Humans. Oligonucleotide Array Sequence Analysis

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • SciCrunch. ArrayExpress: Data: Microarray .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16721385.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


58. Lin P, Medeiros LJ, Yin CC, Abruzzo LV: Translocation (3;8)(q26;q24): a recurrent chromosomal abnormality in myelodysplastic syndrome and acute myeloid leukemia. Cancer Genet Cytogenet; 2006 Apr 1;166(1):82-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translocation (3;8)(q26;q24): a recurrent chromosomal abnormality in myelodysplastic syndrome and acute myeloid leukemia.
  • We identified a reciprocal translocation between chromosomes 3 and 8, with breakpoints at bands 3q26 and 8q24, in five patients with myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML).
  • We conclude that the t(3;8)(q26;q24) is a recurrent translocation associated with therapy-related MDS/AML or de novo AML, and is frequently associated with monosomy 7.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 3 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Neoplasm Recurrence, Local / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Female. Humans. Karyotyping. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Mantle-Cell / pathology. Male. Middle Aged. Sarcoma / drug therapy. Sarcoma / pathology


59. Benesch M, Sovinz P, Krammer B, Lackner H, Mann G, Schwinger W, Gadner H, Urban C: Feasibility and toxicity of intrathecal liposomal cytarabine in 5 children and young adults with refractory neoplastic meningitis. J Pediatr Hematol Oncol; 2007 Apr;29(4):222-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We studied feasibility and toxicity of IT administered liposomal cytarabine on a compassionate basis in 5 patients (male, n=4; female, n=1; age at diagnosis 5 to 18 y) with recurrent acute lymphoblastic leukemia (n=3), primary refractory acute myeloid leukemia (n=1), or relapsed medulloblastoma (n=1).

  • Hazardous Substances Data Bank. CYTARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17414563.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Liposomes; 04079A1RDZ / Cytarabine
  •  go-up   go-down


60. Gupta M, Raghavan M, Gale RE, Chelala C, Allen C, Molloy G, Chaplin T, Linch DC, Cazier JB, Young BD: Novel regions of acquired uniparental disomy discovered in acute myeloid leukemia. Genes Chromosomes Cancer; 2008 Sep;47(9):729-39
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel regions of acquired uniparental disomy discovered in acute myeloid leukemia.
  • The acquisition of uniparental disomy (aUPD) in acute myeloid leukemia (AML) results in homozygosity for known gene mutations.
  • Novel recurrent regions of aUPD were uncovered at 2p, 17p, 2q, 17q, 1p, and Xq.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Uniparental Disomy / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2008 Wiley-Liss, Inc.
  • (PMID = 18506749.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6438; United Kingdom / Cancer Research UK / / A6789; United Kingdom / Cancer Research UK / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


61. Shearer BM, Knudson RA, Flynn HC, Ketterling RP: Development of a D-FISH method to detect DEK/CAN fusion resulting from t(6;9)(p23;q34) in patients with acute myelogenous leukemia. Leukemia; 2005 Jan;19(1):126-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of a D-FISH method to detect DEK/CAN fusion resulting from t(6;9)(p23;q34) in patients with acute myelogenous leukemia.
  • The t(6;9)(p23;q34)-DEK/CAN fusion occurs with an incidence of 1-5% in adult patients with acute myelogenous leukemia (AML) and tends to have an unfavorable prognosis at diagnosis.
  • Unfortunately, no commercial or previously published fluorescence in situ hybridization (FISH) strategies exist for this recurrent anomaly.
  • [MeSH-major] Chromosomes, Human, Pair 6. Chromosomes, Human, Pair 9. In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins / genetics. Recombinant Fusion Proteins / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15510206.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DEK-CAN fusion protein, recombinant; 0 / Oncogene Proteins; 0 / Oncogene Proteins, Fusion; 0 / Recombinant Fusion Proteins
  •  go-up   go-down


62. Kornblau SM, McCue D, Singh N, Chen W, Estrov Z, Coombes KR: Recurrent expression signatures of cytokines and chemokines are present and are independently prognostic in acute myelogenous leukemia and myelodysplasia. Blood; 2010 Nov 18;116(20):4251-61
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent expression signatures of cytokines and chemokines are present and are independently prognostic in acute myelogenous leukemia and myelodysplasia.
  • We hypothesized that comprehensive profiling of C&Ckine expression in leukemia would provide greater insight compared with individual analyses.
  • We used multiplex array technology to simultaneously measure the level of 27 C&Ckines in serum from 176 acute myelogenous leukemia (AML) and 114 myelodysplastic syndrome (MDS) patients and 19 normal controls.
  • In conclusion, C&Ckine expression in AML and MDS differs from normal, is similar with one another, and forms recurrent patterns of expression with prognostic relevance.
  • [MeSH-major] Chemokines / blood. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / diagnosis. Myelodysplastic Syndromes / blood. Myelodysplastic Syndromes / diagnosis


63. Montoto S, Canals C, Rohatiner AZ, Taghipour G, Sureda A, Schmitz N, Gisselbrecht C, Fouillard L, Milpied N, Haioun C, Slavin S, Conde E, Fruchart C, Ferrant A, Leblond V, Tilly H, Lister TA, Goldstone AH, EBMT Lymphoma Working Party: Long-term follow-up of high-dose treatment with autologous haematopoietic progenitor cell support in 693 patients with follicular lymphoma: an EBMT registry study. Leukemia; 2007 Nov;21(11):2324-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A total of 375 patients (54%) developed recurrent lymphoma, 10-year progression-free survival (PFS) being 31%.
  • Thirty-nine patients developed secondary myelodysplastic syndrome/acute myeloid leukaemia (MDS/AML), in 34 cases having received TBI as the conditioning regimen.


64. Zwerdling T, Krailo M, Monteleone P, Byrd R, Sato J, Dunaway R, Seibel N, Chen Z, Strain J, Reaman G, Children's Oncology Group: Phase II investigation of docetaxel in pediatric patients with recurrent solid tumors: a report from the Children's Oncology Group. Cancer; 2006 Apr 15;106(8):1821-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II investigation of docetaxel in pediatric patients with recurrent solid tumors: a report from the Children's Oncology Group.
  • The current study was designed to determine response rates to docetaxel in various strata of recurrent solid tumors of childhood and to assess toxicity in a group of patients who were assigned to receive it.
  • One patient each had acute myeloid leukemia, acute lymphoid leukemia, and high-grade glioma reported as secondary malignancies.
  • CONCLUSIONS: Docetaxel demonstrated activity in patients with recurrent Ewing sarcoma but was found to be ineffective for treating the other types of recurrent solid tumors that were studied.

  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. DOCETAXEL .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2006 American Cancer Society
  • (PMID = 16532433.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel
  •  go-up   go-down


65. Osorio S, de la Cámara R, Monteserin MC, Granados R, Oña F, Rodriguez-Tudela JL, Cuenca-Estrella M: Recurrent disseminated skin lesions due to Metarrhizium anisopliae in an adult patient with acute myelogenous leukemia. J Clin Microbiol; 2007 Feb;45(2):651-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent disseminated skin lesions due to Metarrhizium anisopliae in an adult patient with acute myelogenous leukemia.
  • [MeSH-major] Dermatomycoses / microbiology. Hypocreales / classification. Hypocreales / isolation & purification. Leukemia, Myeloid, Acute / complications

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Transpl Infect Dis. 1999 Dec;1(4):247-61 [11428996.001]
  • [Cites] Cornea. 2001 Oct;20(7):765-8 [11588434.001]
  • [Cites] Malar J. 2003 Sep 15;2:29 [14565851.001]
  • [Cites] Pest Manag Sci. 2004 Jul;60(7):639-44 [15260293.001]
  • [Cites] J Med Vet Mycol. 1997 Sep-Oct;35(5):361-3 [9402530.001]
  • [Cites] J Invertebr Pathol. 2006 Jan;91(1):43-9 [16376375.001]
  • [Cites] Med Mycol. 1998 Feb;36(1):51-4 [9776813.001]
  • [Cites] J Clin Microbiol. 1999 Jan;37(1):195-8 [9854089.001]
  • [Cites] J Invertebr Pathol. 2005 Feb;88(2):116-25 [15766928.001]
  • [Cites] Environ Microbiol. 2005 Sep;7(9):1361-8 [16104859.001]
  • [Cites] J Clin Microbiol. 1998 Apr;36(4):1146-50 [9542958.001]
  • (PMID = 17151202.001).
  • [ISSN] 0095-1137
  • [Journal-full-title] Journal of clinical microbiology
  • [ISO-abbreviation] J. Clin. Microbiol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Fungal; 0 / DNA, Ribosomal Spacer
  • [Other-IDs] NLM/ PMC1829053
  •  go-up   go-down


66. Kwan JM, Trafeli JP, DeRienzo D: Atypical cutaneous myeloid infiltrate in myelodysplastic syndrome: a case report. Cutis; 2007 Sep;80(3):223-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical cutaneous myeloid infiltrate in myelodysplastic syndrome: a case report.
  • We report the case of a 31-year-old man with an atypical myeloid dermal infiltrate manifested by a 1.5-year history of recurrent erythematous plaques over his body that previously were shown to be culture positive for Staphylococcus aureus and had responded well to oral antibiotic treatment.
  • Leukemia cutis (LC), a specific dermal infiltrate of malignant hematopoietic cells, particularly is associated with progression to acute leukemia.
  • Nonetheless, the guarded prognosis of this high-risk subtype of MDS mandates continued monitoring for development of LC and progression to leukemia.


67. Seegmiller AC, Kroft SH, Karandikar NJ, McKenna RW: Characterization of immunophenotypic aberrancies in 200 cases of B acute lymphoblastic leukemia. Am J Clin Pathol; 2009 Dec;132(6):940-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of immunophenotypic aberrancies in 200 cases of B acute lymphoblastic leukemia.
  • Morphologic distinction of leukemic lymphoblasts in B acute lymphoblastic leukemia (B-ALL) from their nonneoplastic counterparts in bone marrow (hematogones) can be difficult.
  • Of the 200 cases, 86.5% expressed myeloid-associated antigens, and 19.0% expressed 3 or more.
  • Specific aberrancies correlate with recurrent cytogenetic abnormalities in B-ALL.
  • [MeSH-major] Bone Marrow Cells / pathology. Immunophenotyping / methods. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Precursor Cells, B-Lymphoid / pathology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19926587.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


68. Caramazza D, Hussein K, Siragusa S, Pardanani A, Knudson RA, Ketterling RP, Tefferi A: Chromosome 1 abnormalities in myeloid malignancies: a literature survey and karyotype-phenotype associations. Eur J Haematol; 2010 Mar;84(3):191-200
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromosome 1 abnormalities in myeloid malignancies: a literature survey and karyotype-phenotype associations.
  • It is, therefore, not surprising that recurrent chromosome 1 abnormalities are regularly encountered in both neoplastic and non-neoplastic medical conditions.
  • The current review is focused on myeloid malignancies where we summarize the relevant published literature and discuss specific karyotype-phenotype associations.
  • Although occasionally seen in chronic phase MPN, unbalanced 1;7 translocations, e.g. der(1;7)(q10;p10), are usually seen in acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), and post-MPN AML/MDS.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 1. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics


69. Metzgeroth G, Walz C, Score J, Siebert R, Schnittger S, Haferlach C, Popp H, Haferlach T, Erben P, Mix J, Müller MC, Beneke H, Müller L, Del Valle F, Aulitzky WE, Wittkowsky G, Schmitz N, Schulte C, Müller-Hermelink K, Hodges E, Whittaker SJ, Diecker F, Döhner H, Schuld P, Hehlmann R, Hochhaus A, Cross NC, Reiter A: Recurrent finding of the FIP1L1-PDGFRA fusion gene in eosinophilia-associated acute myeloid leukemia and lymphoblastic T-cell lymphoma. Leukemia; 2007 Jun;21(6):1183-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent finding of the FIP1L1-PDGFRA fusion gene in eosinophilia-associated acute myeloid leukemia and lymphoblastic T-cell lymphoma.
  • Here, we report on seven FIP1L1-PDGFRA-positive patients who presented with acute myeloid leukemia (AML, n=5) or lymphoblastic T-cell non-Hodgkin-lymphoma (n=2) in conjunction with AML or Eos-MPD.
  • [MeSH-major] Eosinophilia / drug therapy. Leukemia, Myeloid / drug therapy. Oncogene Proteins, Fusion / analysis. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / administration & dosage. Receptor, Platelet-Derived Growth Factor alpha. mRNA Cleavage and Polyadenylation Factors
  • [MeSH-minor] Acute Disease. Adult. Aged. Benzamides. Disease-Free Survival. Humans. Imatinib Mesylate. Male. Middle Aged. Myeloproliferative Disorders / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction / methods


70. Quentmeier H, Schneider B, Röhrs S, Romani J, Zaborski M, Macleod RA, Drexler HG: SET-NUP214 fusion in acute myeloid leukemia- and T-cell acute lymphoblastic leukemia-derived cell lines. J Hematol Oncol; 2009;2:3
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] SET-NUP214 fusion in acute myeloid leukemia- and T-cell acute lymphoblastic leukemia-derived cell lines.
  • BACKGROUND: SET-NUP214 fusion resulting from a recurrent cryptic deletion, del(9)(q34.11q34.13) has recently been described in T-cell acute lymphoblastic leukemia (T-ALL) and in one case of acute myeloid leukemia (AML).
  • RESULTS: Of 141 human leukemia/lymphoma cell lines tested, only the T-ALL cell line LOUCY and the AML cell line MEGAL expressed the SET(TAF-Ibeta)-NUP214 fusion gene transcript.
  • [MeSH-major] Histone Chaperones / genetics. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics


71. Xu Q, Wang M, You Q, Wang H, Ye K, Zhan R, Zhou Y: Isolated recurrence of granulocytic sarcoma-two case reports-. Neurol Med Chir (Tokyo); 2009 Dec;49(12):611-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A 29-year-old male presented with an extra- and intracranial mass 10 years after bone marrow transplantation for chronic myeloid leukemia.
  • A 34-year-old female presented with an intracranial mass 3 years after complete remission of acute myeloid leukemia-M2a.
  • The second patient only received whole brain radiotherapy, failed to respond, and died of systemic leukemia later.
  • These two cases demonstrate that neurosurgeons should pay attention to the occurrence of isolated recurrent granulocytic sarcoma, especially in patients with a history of hematologic neoplasm.
  • [MeSH-major] Head and Neck Neoplasms / etiology. Head and Neck Neoplasms / pathology. Leukemia, Myeloid, Acute / complications. Neoplasm Recurrence, Local / pathology. Sarcoma, Myeloid / etiology. Sarcoma, Myeloid / pathology

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Head and Neck Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20035140.001).
  • [ISSN] 1349-8029
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


72. Herry A, Douet-Guilbert N, Morel F, Le Bris MJ, Guéganic N, Berthou C, De Braekeleer M: Isochromosome 5p and related anomalies: a novel recurrent chromosome abnormality in myeloid disorders. Cancer Genet Cytogenet; 2010 Jul 15;200(2):134-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isochromosome 5p and related anomalies: a novel recurrent chromosome abnormality in myeloid disorders.
  • Loss of material from chromosome arm 5q is a common finding in patients with myelodysplastic syndromes (MDS) or acute myeloid leukemia (AML).
  • Isochromosome of the short arm of chromosome 5 and its related abnormalities such as idic(5)(q11) and structurally rearranged i(5)(p10) are rare but recurrent abnormalities; their identification requires a combination of conventional and molecular cytogenetic techniques.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 5. Isochromosomes. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


73. Rubtsov MA, Terekhov SM, Razin SV, Iarovaia OV: Repositioning of ETO gene in cells treated with VP-16, an inhibitor of DNA-topoisomerase II. J Cell Biochem; 2008 May 15;104(2):692-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The translocation t(8;21)(q22;q22) affecting AML1 and ETO genes is known to be one of the frequent chromosome translocations in acute myeloid leukemia.
  • Together, our data corroborate the so called "breakage first" model of the origins of recurrent reciprocal translocation.

  • Hazardous Substances Data Bank. ETOPOSIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2008 Wiley-Liss, Inc.
  • (PMID = 18183572.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Topoisomerase II Inhibitors; 0 / Transcription Factors; 6PLQ3CP4P3 / Etoposide; EC 3.6.4.1 / Myosins
  •  go-up   go-down


74. Fagnoni P, Limat S, Hintzy-Fein E, Martin F, Deconinck E, Cahn JY, Arveux P, Dussaucy A, Woronoff-Lemsi MC: [Cost of hospital-based management of acute myeloid leukemia: from analytical to procedure-based tarification]. Bull Cancer; 2006 Aug;93(8):813-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Cost of hospital-based management of acute myeloid leukemia: from analytical to procedure-based tarification].
  • [Transliterated title] Coûts hospitaliers de prise en charge des leucémies aiguës myéloïdes: de la comptabilité analytique à la T2A.
  • The confrontation of the macro- and micro-economic approaches of hospital costs is a recurrent question, in particular for pathologies where length of stay is highly variable, like acute myeloid leukemias (AML).
  • [MeSH-major] Hospital Costs. Leukemia, Myeloid / economics. Prospective Payment System / economics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Diagnosis-Related Groups / economics. Female. France. Humans. Length of Stay / economics. Male. Middle Aged. Recurrence. Remission Induction. Retrospective Studies

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16935786.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down


75. Sazawal S, Kumar B, Hasan SK, Dutta P, Kumar R, Chaubey R, Mir R, Saxena R: Haematological & molecular profile of acute myelogenous leukaemia in India. Indian J Med Res; 2009 Mar;129(3):256-61
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Haematological & molecular profile of acute myelogenous leukaemia in India.
  • BACKGROUND & OBJECTIVE: Recurrent balanced translocations are generally recognized to be a major parameter for prognostication in acute myeloid leukaemia (AML).
  • FLT3 internal tandem duplication (ITD) mutation was predominant in acute promyelocytic leukaemia patients with bcr3 isoform.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19491417.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 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
  •  go-up   go-down


76. Tamm I: AEG-35156, an antisense oligonucleotide against X-linked inhibitor of apoptosis for the potential treatment of cancer. Curr Opin Investig Drugs; 2008 Jun;9(6):638-46
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Several clinical trials are ongoing and include: two phase I monotherapy clinical trials for the potential treatment of cancer and in patients with solid tumors; a phase I combination clinical trial of AEG-35156 with docetaxel in locally advanced, metastatic, or recurrent solid tumors; four phase I/II combination clinical trials for the potential treatment of pancreatic cancer, advanced breast cancer, advanced NSCLC, and acute myeloid leukemia.

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18516763.001).
  • [ISSN] 1472-4472
  • [Journal-full-title] Current opinion in investigational drugs (London, England : 2000)
  • [ISO-abbreviation] Curr Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AEG 35156; 0 / Oligonucleotides; 0 / Oligonucleotides, Antisense; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human
  • [Number-of-references] 68
  •  go-up   go-down


77. MacKinnon RN, Patsouris C, Chudoba I, Campbell LJ: A FISH comparison of variant derivatives of the recurrent dic(17;20) of myelodysplastic syndromes and acute myeloid leukemia: Obligatory retention of genes on 17p and 20q may explain the formation of dicentric chromosomes. Genes Chromosomes Cancer; 2007 Jan;46(1):27-36
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A FISH comparison of variant derivatives of the recurrent dic(17;20) of myelodysplastic syndromes and acute myeloid leukemia: Obligatory retention of genes on 17p and 20q may explain the formation of dicentric chromosomes.
  • The dic(17;20) is a recurrent unbalanced translocation occurring rarely in myelodysplastic syndromes and acute myeloid leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 20. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Chromosomal Instability. Chromosome Deletion. Humans. In Situ Hybridization, Fluorescence. Karyotyping


78. Tefferi A, Gilliland G: Classification of chronic myeloid disorders: from Dameshek towards a semi-molecular system. Best Pract Res Clin Haematol; 2006;19(3):365-85
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Classification of chronic myeloid disorders: from Dameshek towards a semi-molecular system.
  • Hematological malignancies are phenotypically organized into lymphoid and myeloid disorders, although such a distinction might not be precise from the standpoint of lineage clonality.
  • In turn, myeloid malignancies are broadly categorized into either acute myeloid leukemia (AML) or chronic myeloid disorder (CMD), depending on the presence or absence, respectively, of AML-defining cytomorphologic and cytogenetic features.
  • It has now become evident that most CMD represent clonal stem cell processes where the primary oncogenic event has been characterized in certain instances; Bcr/Abl in chronic myeloid leukemia, FIP1L1-PDGFRA or c-kit(D816V) in systemic mastocytosis, rearrangements of PDGFRB in chronic eosinophilic leukemia, and rearrangements of FGFR1 in stem cell leukemia/lymphoma syndrome.
  • In addition, Bcr/Abl-negative classic myeloproliferative disorders are characterized by recurrent JAK2(V617F) mutations, whereas other mutations affecting the RAS signaling pathway molecules have been associated with juvenile myelomonocytic leukemia.
  • [MeSH-minor] Fusion Proteins, bcr-abl / genetics. Genes, abl. Humans. Janus Kinase 2. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / classification. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Myelodysplastic Syndromes / classification. Myelodysplastic Syndromes / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics. Receptor, Platelet-Derived Growth Factor beta / genetics

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16781478.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 232
  •  go-up   go-down


79. Oda M, Isoyama K, Ito E, Inoue M, Tsuchida M, Kigasawa H, Kato K, Kato S: Survival after cord blood transplantation from unrelated donor as a second hematopoietic stem cell transplantation for recurrent pediatric acute myeloid leukemia. Int J Hematol; 2009 Apr;89(3):374-82
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survival after cord blood transplantation from unrelated donor as a second hematopoietic stem cell transplantation for recurrent pediatric acute myeloid leukemia.
  • The Japan Cord Blood Bank Network (JCBBN) reports the treatment of 22 children with acute myeloid leukemia (AML) who received umbilical cord blood transplantation from unrelated donors (CBT) as their second hematopoietic stem cell transplantation (HSCT).
  • [MeSH-major] Cord Blood Stem Cell Transplantation. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / surgery. Tissue Donors


80. Haltrich I, Csóka M, Kovács G, Fekete G: [Cytogenetic and FISH findings are complementary in childhood ALL]. Magy Onkol; 2008 Sep;52(3):283-91
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Primary genetic abnormalities of leukemia cells have important prognostic significance in childhood acute leukemia.
  • In the last two years 30 newly diagnosed or recurrent childhood ALL bone marrow samples were analyzed for chromosomal abnormalities with conventional G-banding and interphase-fluorescence in situ hybridization (I-FISH) using probes to detect BCR/ABL fusions, cryptic TEL/AML1 and MLL rearrangements and p16(9p21) tumor suppressor gene deletions.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 21. Gene Rearrangement. In Situ Hybridization, Fluorescence. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. Female. Fusion Proteins, bcr-abl / genetics. Gene Deletion. Histone-Lysine N-Methyltransferase. Humans. Interphase. Karyotyping / methods. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Predictive Value of Tests. Prognosis. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Risk Factors. Sensitivity and Specificity

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18845499.001).
  • [ISSN] 0025-0244
  • [Journal-full-title] Magyar onkologia
  • [ISO-abbreviation] Magy Onkol
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down


81. Cucuianu A: Dominant and opportunistic leukemic clones: proposal for a pathogenesis-oriented classification in acute myeloid leukemia. Med Hypotheses; 2005;65(1):107-13
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dominant and opportunistic leukemic clones: proposal for a pathogenesis-oriented classification in acute myeloid leukemia.
  • Despite the common clinical, hematological and prognostic features that define acute myeloid leukemia (AML) there is considerable heterogeneity among individual cases, suggesting different pathogenic pathways.
  • Based on a simple theoretical model, according to the vital characteristics of the leukemic clone (proliferative rate and resistance to apoptosis), I propose a classification of AML into two broad categories: (a) high leukemic clone vitality (HLV) AML or "dominant type" AML, corresponding roughly to the World Health Organization (WHO) classification group of entities "AML with recurrent cytogenetic abnormalities" and (b) low leukemic clone vitality (LLV) or "opportunistic type" AML corresponding to the WHO groups "AML with multilineage dysplasia" and "alkylating agent-related AML".
  • [MeSH-major] Clone Cells. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / etiology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15893127.001).
  • [ISSN] 0306-9877
  • [Journal-full-title] Medical hypotheses
  • [ISO-abbreviation] Med. Hypotheses
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
  •  go-up   go-down


82. Kuriyama K: [Classification of myeloid leukemias]. Nihon Rinsho; 2009 Oct;67(10):1853-62
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Classification of myeloid leukemias].
  • Myeloid leukemia in this series corresponds to the myeloid neoplasms of the 4th WHO classification of pathology and genetics of tumor of haematopoietic and lymphoid tissue.
  • The myeloid neoplasms are composed of six categories, which are 1) myeloproliferative neoplasms (MPN), a new category of 2) myeloid and lymphoid neoplasms with eosinophilia and abnormalities of PDGFRA, PDGFRB or FGFR1, 3) myelodysplastic syndrome (MDS)/MPN, 4) MDS, 5) acute myeloid leukemia (AML) and related precursor neoplasms, and 6) acute leukemias of ambiguous lineage.
  • In MPNs without chronic myelogenous leukemia, the genetic marker of JAK2 V617F is added to the diagnostic criteria for polycythemia vera, essential thrombocythemia and primary myelofibrosis.
  • 22) (p13; q13); RBM15-MKL1 are added to the subtype of AML with recurrent genetic abnormalities, and AML with gene mutations of NPM1 and CEBPA are also added as provisional entities of it.
  • The myeloid neoplasms of the 4th WHO classification are comprehensive and seem to be dynamic by incorporating the results of leukemia researches.
  • [MeSH-major] Leukemia, Myeloid / classification
  • [MeSH-minor] Eosinophilia. Humans. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics. Receptor, Platelet-Derived Growth Factor alpha / genetics. Receptor, Platelet-Derived Growth Factor beta / genetics. World Health Organization

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19860179.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  • [Number-of-references] 14
  •  go-up   go-down


83. Tibes R, Keating MJ, Ferrajoli A, Wierda W, Ravandi F, Garcia-Manero G, O'Brien S, Cortes J, Verstovsek S, Browning ML, Faderl S: Activity of alemtuzumab in patients with CD52-positive acute leukemia. Cancer; 2006 Jun 15;106(12):2645-51
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activity of alemtuzumab in patients with CD52-positive acute leukemia.
  • BACKGROUND: Alemtuzumab is a humanized monoclonal antibody directed against the cell surface antigen CD52 and has demonstrated activity in chronic lymphocytic leukemia and other CD52-positive lymphoproliferative disorders.
  • Because CD52 also is expressed on acute leukemic blasts, the authors investigated the safety and efficacy of alemtuzumab in patients with acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL).
  • METHODS: Fifteen patients with CD52-positive (> or = 20%), recurrent or refractory acute leukemia (9 patients with AML and 6 patients with ALL) received alemtuzumab at a dose of 30 mg intravenously given 3 times a week (dose escalation during Week 1) for a total of 4 to 12 weeks.
  • CONCLUSIONS: Single-agent alemtuzumab was found to have limited activity in recurrent or refractory acute leukemia.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antigens, CD / immunology. Antigens, Neoplasm / immunology. Glycoproteins / immunology. Leukemia, Myeloid / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antibodies, Monoclonal, Humanized. Bacteremia / diagnosis. Bacteremia / etiology. Bone Marrow / drug effects. Bone Marrow / pathology. Disease Progression. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Female. Fungemia / diagnosis. Fungemia / etiology. Humans. Male. Middle Aged. Pneumonia / diagnosis. Pneumonia / etiology. Treatment Outcome

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 American Cancer Society.
  • (PMID = 16688777.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
  •  go-up   go-down


84. Alvarez S, Cigudosa JC: Gains, losses and complex karyotypes in myeloid disorders: a light at the end of the tunnel. Hematol Oncol; 2005 Mar;23(1):18-25
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gains, losses and complex karyotypes in myeloid disorders: a light at the end of the tunnel.
  • Complex karyotypes are seen in approximately 15% of de novo MDS/AML and in up to 50% of therapy-related MDS/AML.
  • On the basis of the available data from several studies of AML with complex karyotypes, similar findings on recurrent breakpoints and frequently lost and gained chromosomal regions have been observed.
  • [MeSH-major] Chromosomes, Human / genetics. Gene Expression Regulation, Leukemic / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Translocation, Genetic
  • [MeSH-minor] Chromosome Segregation / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor Alpha 2 Subunit / metabolism. DNA Repair / genetics. Gene Amplification / genetics. Gene Expression Profiling / methods. Genome, Human / genetics. Histone-Lysine N-Methyltransferase. Humans. Karyotyping. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Neoplasm, Residual / genetics. Neoplasm, Residual / metabolism. Neoplasm, Residual / therapy. Risk Factors

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2005 John Wiley & Sons, Ltd.
  • (PMID = 16142824.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / RUNX1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 53
  •  go-up   go-down


85. Strehl S, Nebral K, König M, Harbott J, Strobl H, Ratei R, Struski S, Bielorai B, Lessard M, Zimmermann M, Haas OA, Izraeli S: ETV6-NCOA2: a novel fusion gene in acute leukemia associated with coexpression of T-lymphoid and myeloid markers and frequent NOTCH1 mutations. Clin Cancer Res; 2008 Feb 15;14(4):977-83
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ETV6-NCOA2: a novel fusion gene in acute leukemia associated with coexpression of T-lymphoid and myeloid markers and frequent NOTCH1 mutations.
  • Cytogenetic analysis of six cases of childhood acute lymphoblastic leukemia revealed a novel recurrent t(8;12)(q13;p13), suggesting involvement of ETV6.
  • RESULTS: We have identified a novel recurrent t(8;12)(q13;p13), which results in a fusion between the transcriptional repressor ETV6 (TEL) and the transcriptional coactivator NCOA2 (TIF2) in six cases of childhood leukemia expressing both T-lymphoid and myeloid antigens.
  • In addition, ETV6-NCOA2 leukemia shows a high frequency of heterozygous activating NOTCH1 mutations, which disrupt the heterodimerization or the PEST domains.
  • CONCLUSIONS: The ETV6-NCOA2 fusion may define a novel subgroup of acute leukemia with T-lymphoid and myeloid features, which is associated with a high prevalence of NOTCH1 mutations.
  • [MeSH-major] Nuclear Receptor Coactivator 2 / genetics. Oncogene Fusion / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18281529.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ETS translocation variant 6 protein; 0 / NCOA2 protein, human; 0 / NOTCH1 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Receptor, Notch1; 0 / Repressor Proteins
  •  go-up   go-down


86. Huh JY, Chung S, Oh D, Kang MS, Eom HS, Cho EH, Han MH, Kong SY: Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature. Korean J Lab Med; 2010 Apr;30(2):117-21
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature.
  • The translocation t(10;11)(p13;q14q21) has been found to be recurrent in acute lymphoblastic and myeloid leukemias, and results in the fusion of the clathrin assembly lymphoid myeloid leukemia (CALM) gene with the AF10 gene; these genes are present on chromosomes 11 and 10, respectively.
  • Because the CALM-AF10 rearrangement is a rare chromosomal abnormality, it is not included in routine molecular tests for acute leukemia.
  • Both patient samples showed expression of the homeobox A gene cluster and the histone methyltransferase hDOT1L, which suggests that they mediate leukemic transformation in CALM-AF10-positive and mixed-lineage leukemia-AF10-positive leukemias.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Monomeric Clathrin Assembly Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20445327.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MLLT10 protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Transcription Factors; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 14
  •  go-up   go-down


87. Yanada M, Suzuki M, Kawashima K, Kiyoi H, Kinoshita T, Emi N, Saito H, Naoe T: Long-term outcomes for unselected patients with acute myeloid leukemia categorized according to the World Health Organization classification: a single-center experience. Eur J Haematol; 2005 May;74(5):418-23
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcomes for unselected patients with acute myeloid leukemia categorized according to the World Health Organization classification: a single-center experience.
  • The actual utility of a new classification system of acute myeloid leukemia (AML) recently introduced by the World Health Organization (WHO) has not been thoroughly investigated yet.
  • AML with recurrent genetic abnormalities accounted for 26%, AML with multilineage dysplasia for 29%, therapy-related AML for 13%, and AML not otherwise categorized for 32% of classifiable cases.
  • [MeSH-major] Leukemia, Myeloid / classification. Leukemia, Myeloid / therapy

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15813916.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  •  go-up   go-down


88. Park TS, Cheong JW, Song J, Choi JR: Therapy-related myelodysplastic syndrome with der(17)t(12;17)(q13;p13) as a new recurrent cytogenetic abnormality after treatment for chronic lymphocytic leukemia. Leuk Res; 2009 Jul;33(7):1001-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related myelodysplastic syndrome with der(17)t(12;17)(q13;p13) as a new recurrent cytogenetic abnormality after treatment for chronic lymphocytic leukemia.
  • He was initially diagnosed with chronic lymphocytic leukemia (CLL) and treated with six cycles of fludarabine, cyclophosphamide, and rituximab chemotherapy.
  • The chromosomal abnormality der(17)t(12;17)(q13;p13) is very rare in hematologic malignancies, and has been reported in only two patients with therapy-related acute myeloid leukemia (t-AML).
  • In addition, we suggest that der(17)t(12;17)(q13;p13) should be considered a new recurrent, nonrandom chromosomal abnormality in patients with t-MDS/AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics. Translocation, Genetic / genetics


89. von Neuhoff C, Reinhardt D, Sander A, Zimmermann M, Bradtke J, Betts DR, Zemanova Z, Stary J, Bourquin JP, Haas OA, Dworzak MN, Creutzig U: Prognostic impact of specific chromosomal aberrations in a large group of pediatric patients with acute myeloid leukemia treated uniformly according to trial AML-BFM 98. J Clin Oncol; 2010 Jun 1;28(16):2682-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic impact of specific chromosomal aberrations in a large group of pediatric patients with acute myeloid leukemia treated uniformly according to trial AML-BFM 98.
  • PURPOSE: Because cytogenetic data are essential for risk stratification of childhood acute myeloid leukemia (AML), the impact of chromosomal aberrations is crucial.
  • CONCLUSION: Because the prognostic value of rare recurrent chromosomal aberrations still has to be elucidated, these data will contribute to future risk stratification for the treatment of pediatric AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Chromosome Aberrations. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20439630.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZRP63D75JW / Idarubicin; ICE protocol 4
  •  go-up   go-down


90. Dombret H, Preudhomme C, Boissel N: Core binding factor acute myeloid leukemia (CBF-AML): is high-dose Ara-C (HDAC) consolidation as effective as you think? Curr Opin Hematol; 2009 Mar;16(2):92-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Core binding factor acute myeloid leukemia (CBF-AML): is high-dose Ara-C (HDAC) consolidation as effective as you think?
  • PURPOSE OF REVIEW: Core binding factor acute myeloid leukemia (CBF-AML) corresponds to two distinct subtypes of AML characterized by recurrent favorable chromosome translocations, namely t(8;21) and inv(16)/t(16;16).
  • [MeSH-major] Core Binding Factors / genetics. Cytarabine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics


91. Bacher U, Kern W, Schnittger S, Hiddemann W, Haferlach T, Schoch C: Population-based age-specific incidences of cytogenetic subgroups of acute myeloid leukemia. Haematologica; 2005 Nov;90(11):1502-10
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Population-based age-specific incidences of cytogenetic subgroups of acute myeloid leukemia.
  • BACKGROUND AND OBJECTIVES: It is well known that the different cytogenetic subgroups of acute myeloid leukemia (AML) show different age-specific frequencies.
  • There were also different age-specific incidences of some recurrent molecular mutations.
  • [MeSH-major] Cytogenetics. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16266897.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Genetic Markers
  •  go-up   go-down


92. Abbas S, Lugthart S, Kavelaars FG, Schelen A, Koenders JE, Zeilemaker A, van Putten WJ, Rijneveld AW, Löwenberg B, Valk PJ: Acquired mutations in the genes encoding IDH1 and IDH2 both are recurrent aberrations in acute myeloid leukemia: prevalence and prognostic value. Blood; 2010 Sep 23;116(12):2122-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acquired mutations in the genes encoding IDH1 and IDH2 both are recurrent aberrations in acute myeloid leukemia: prevalence and prognostic value.
  • Somatic mutations in isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) were recently demonstrated in acute myeloid leukemia (AML), but their prevalence and prognostic impact remain to be explored in large extensively characterized AML series, and also in various other hematologic malignancies.
  • Moreover, we identified IDH mutations in 2 JAK2 V617F myeloproliferative neoplasias (n = 96), a single case of acute lymphoblastic leukemia (n = 96), and none in chronic myeloid leukemias (n = 81).
  • [MeSH-major] Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Mutation

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20538800.001).
  • [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] EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


93. Kim IS, Kim HJ, Yoo KH, Sung KW, Kim SH: A boy with acute lymphoblastic leukemia acquired clonal and nonclonal cytogenetic abnormalities including del(7q) and del(20q) without clinical evidence of disease after sex-mismatched cord blood transplantation. J Pediatr Hematol Oncol; 2006 Aug;28(8):540-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A boy with acute lymphoblastic leukemia acquired clonal and nonclonal cytogenetic abnormalities including del(7q) and del(20q) without clinical evidence of disease after sex-mismatched cord blood transplantation.
  • An 8-year-old boy was diagnosed with precursor B-cell acute lymphoblastic leukemia.
  • Del(7q) and del(20q), 2 recurrent chromosomal aberrations in myeloid neoplasia, might represent underlying genomic instability in this patient, not the direct culprits of dysplasia or leukemogenesis.

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16912597.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


94. Pan J, Xue Y, Qiu H, Chen S, Zhang J, Wu Y, Shen J, Wang Y: A pericentric inv(9)(p22q34) of the der(9)t(9;22)(q34;q11.2) is a recurrent secondary anomaly in Ph-positive leukemia. Cancer Genet Cytogenet; 2010 Dec;203(2):333-40
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A pericentric inv(9)(p22q34) of the der(9)t(9;22)(q34;q11.2) is a recurrent secondary anomaly in Ph-positive leukemia.
  • A pericentric inv(9)(p22q34) of the derivative chromosome 9 that resulted from a standard t(9;22)(q34;q11.2) was identified by R-banding karyotypic analysis and fluorescence in situ hybridization (FISH) assays in 4 (0.18%) of 2,200 Philadelphia chromosome (Ph)-positive leukemia patients, including 3 with chronic myeloid leukemia (CML) in chronic phase and 1 with acute myeloid leukemia (AML) in our hospital since 2004.
  • Reverse transcriptase-polymerase chain reaction revealed a b3a2 type of BCR/ABL1 fusion transcript in all of them, proving their disease to be Ph-positive leukemia.
  • On reviewing the literature, only two solitary Ph-positive leukemia patients have been noticed to have the inv(9)(p22q34) anomaly.
  • These two patients, together with our four documented patients, indicate that inv(9)(p22q34) is a novel, rare, but recurrent secondary chromosomal abnormality for Ph-positive leukemia.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21156255.001).
  • [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
  •  go-up   go-down


95. Malinge S, Ragu C, Della-Valle V, Pisani D, Constantinescu SN, Perez C, Villeval JL, Reinhardt D, Landman-Parker J, Michaux L, Dastugue N, Baruchel A, Vainchenker W, Bourquin JP, Penard-Lacronique V, Bernard OA: Activating mutations in human acute megakaryoblastic leukemia. Blood; 2008 Nov 15;112(10):4220-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activating mutations in human acute megakaryoblastic leukemia.
  • Oncogenic activation of tyrosine kinase signaling pathway is recurrent in human leukemia.
  • To gain insight into the oncogenic process leading to acute megakaryoblastic leukemia (AMKL), we performed sequence analyses of a subset of oncogenes known to be activated in human myeloid and myeloproliferative disorders.
  • [MeSH-major] Down Syndrome / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Mutation. Neoplasm Proteins / genetics


96. Paggetti J, Largeot A, Aucagne R, Jacquel A, Lagrange B, Yang XJ, Solary E, Bastie JN, Delva L: Crosstalk between leukemia-associated proteins MOZ and MLL regulates HOX gene expression in human cord blood CD34+ cells. Oncogene; 2010 Sep 9;29(36):5019-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Crosstalk between leukemia-associated proteins MOZ and MLL regulates HOX gene expression in human cord blood CD34+ cells.
  • MOZ and MLL, encoding a histone acetyltransferase (HAT) and a histone methyltransferase, respectively, are targets for recurrent chromosomal translocations found in acute myeloblastic or lymphoblastic leukemia.
  • In MOZ (MOnocytic leukemia Zinc-finger protein)/CBP- or mixed lineage leukemia (MLL)-rearranged leukemias, abnormal levels of HOX transcription factors have been found to be critical for leukemogenesis.
  • In CD34+ cells, depletion of MLL causes release of MOZ from HOX promoters, which is correlated to defective histone activation marks, leading to repression of HOX gene expression and alteration of commitment of CD34+ cells into myeloid progenitors.
  • [MeSH-major] Antigens, CD34 / metabolism. Fetal Blood / metabolism. Histone Acetyltransferases / physiology. Homeodomain Proteins / genetics. Myeloid-Lymphoid Leukemia Protein / physiology

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20581860.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Histones; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / WDR5 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human
  •  go-up   go-down


97. Levine RL, Loriaux M, Huntly BJ, Loh ML, Beran M, Stoffregen E, Berger R, Clark JJ, Willis SG, Nguyen KT, Flores NJ, Estey E, Gattermann N, Armstrong S, Look AT, Griffin JD, Bernard OA, Heinrich MC, Gilliland DG, Druker B, Deininger MW: The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia. Blood; 2005 Nov 15;106(10):3377-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia.
  • Recently, we and others identified a single recurrent somatic activating mutation (JAK2V617F) in the Janus kinase 2 (JAK2) tyrosine kinase in the myeloproliferative disorders (MPDs) polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.
  • We used direct sequence analysis to determine if the JAK2V617F mutation was present in acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML)/atypical chronic myelogenous leukemia (aCML), myelodysplastic syndrome (MDS), B-lineage acute lymphoblastic leukemia (ALL), T-cell ALL, and chronic lymphocytic leukemia (CLL).
  • These data indicate that the JAK2V617F allele is present in acute and chronic myeloid malignancies but not in lymphoid malignancies.


98. Hejlik DP, Nagarajan L: Deletion of 5q in myeloid leukemia cells HL-60: an L1 element-mediated instability. Cancer Genet Cytogenet; 2005 Jan 15;156(2):97-103
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Deletion of 5q in myeloid leukemia cells HL-60: an L1 element-mediated instability.
  • Complete and partial deletions of chromosome 5 are recurrent anomalies associated with refractory myelogenous leukemia.
  • We have analyzed a complex rearrangement of chromosome band 5q both in the primary leukemic cells of the patient from whom the acute myelogenous leukemia (AML) cell line HL-60 was derived and in the HL-60 cells in culture.
  • The resulting genomic fragment is found inserted into a telomeric locus (D5S89), with loss of 4.1 Mbp of in-between sequences, encoding one or more candidate myeloid leukemia suppressor genes.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15642388.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA66982
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  •  go-up   go-down


99. Pagel JM, Gooley TA, Rajendran J, Fisher DR, Wilson WA, Sandmaier BM, Matthews DC, Deeg HJ, Gopal AK, Martin PJ, Storb RF, Press OW, Appelbaum FR: Allogeneic hematopoietic cell transplantation after conditioning with 131I-anti-CD45 antibody plus fludarabine and low-dose total body irradiation for elderly patients with advanced acute myeloid leukemia or high-risk myelodysplastic syndrome. Blood; 2009 Dec 24;114(27):5444-53
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic hematopoietic cell transplantation after conditioning with 131I-anti-CD45 antibody plus fludarabine and low-dose total body irradiation for elderly patients with advanced acute myeloid leukemia or high-risk myelodysplastic syndrome.
  • Fifty-eight patients older than 50 years with advanced acute myeloid leukemia (AML) or high-risk myelodysplastic syndrome (MDS) were treated with (131)I-BC8 Ab and fludarabine plus 2 Gy total body irradiation.
  • The estimated probability of recurrent malignancy at 1 year is 40%, and the 1-year survival estimate is 41%.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Acute Disease. Aged. Antibodies / administration & dosage. Antibodies / immunology. Antigens, CD45 / immunology. Combined Modality Therapy. Female. Humans. Iodine Radioisotopes / pharmacokinetics. Male. Middle Aged. Risk Factors. Survival Analysis. Survival Rate. Tissue Distribution. Transplantation, Homologous. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Whole-Body Irradiation


100. Jäger R, Gisslinger H, Passamonti F, Rumi E, Berg T, Gisslinger B, Pietra D, Harutyunyan A, Klampfl T, Olcaydu D, Cazzola M, Kralovics R: Deletions of the transcription factor Ikaros in myeloproliferative neoplasms. Leukemia; 2010 Jul;24(7):1290-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Transformation to acute leukemia is a major complication of myeloproliferative neoplasms (MPNs), however, the genetic changes leading to transformation remain largely unknown.
  • We screened nine patients with post-MPN leukemia for chromosomal aberrations using microarray karyotyping.
  • Deletions on the short arm of chromosome 7 (del7p) emerged as a recurrent defect.
  • We further examined the frequency of IKZF1 deletions in a total of 29 post-MPN leukemia and 526 MPN patients without transformation and observed a strong association of IKZF1 deletions with post-MPN leukemia in two independent cohorts.
  • IKZF1 deletions were observed in both undifferentiated and differentiated myeloid cell types, indicating that IKZF1 loss does not cause differentiation arrest but rather renders progenitors susceptible to transformation, most likely through chromosomal instability.






Advertisement