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As far as could be ascertained, this infection has never been reported in a patient with leukaemia.

We describe what we believe to be the first such case of C. violaceum sepsis, in a 16-year-old female patient with acute biphenotypic leukaemia, which developed during the neutropenic phase after intensive chemotherapy.

[MeSH-minor] Adolescent. Antifungal Agents / pharmacology. Candidiasis / complications. Candidiasis / drug therapy. Female. Humans. Leukemia / complications. Neutropenia / complications. South Africa / epidemiology. Treatment Outcome

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(PMID = 18809561.001).

[ISSN] 0022-2615

[Journal-full-title] Journal of medical microbiology

[ISO-abbreviation] J. Med. Microbiol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antifungal Agents

   

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Biphenotypic acute leukemia (BAL) is a relatively rare subtype of acute leukemia characterized by the presence of both myeloid and lymphoid cell surface antigens.

A variety of luciferase-based reporter assays revealed that P2RY8 increased both the trans-activation activities of CREB and Elk-1 as well as the transcriptional activities of the serum response element and enhancer-promoter fragments of the c-Fos and c-Myc genes.

Quantitation of P2RY8 mRNA in CD34(+) cells of bone marrow showed that P2RY8 expression is frequently increased in leukemia patients, especially in those with refractory disease.

Our data thus reveal an abundant expression of P2RY8 in leukemic cells and its unexpected role in the pathogenesis of acute leukemia.

[MeSH-major] Gene Expression Regulation, Leukemic. Leukemia / genetics. Leukemia / metabolism. Receptors, Purinergic / physiology. Receptors, Purinergic P2 / metabolism. Receptors, Purinergic P2Y / metabolism. Receptors, Purinergic P2Y / physiology. Retroviridae / metabolism

[MeSH-minor] 3T3 Cells. Animals. Antigens, CD34 / biosynthesis. Bone Marrow Cells / metabolism. Cell Line, Tumor. DNA, Complementary / genetics. Gene Library. Humans. Mice. Mice, Nude. Transcription, Genetic

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Guide to Pharmacology. gene/protein/disease-specific - P2RY8 - data and references .

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(PMID = 17487742.001).

[ISSN] 1042-8194

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD34; 0 / DNA, Complementary; 0 / P2RY8 protein, human; 0 / P2RY9 receptor, human; 0 / P2RY9 receptor, mouse; 0 / Receptors, Purinergic; 0 / Receptors, Purinergic P2; 0 / Receptors, Purinergic P2Y

   

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[Title] Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia.

We report a case of acute mixed-lineage leukemia, as seen in a 65 year-old female with MLL gene amplification and biallelic loss of wild type p53 gene.

The diagnosis was based on the findings that her bone marrow (BM) blasts expressed cytoplasmic CD3 (cyCD3), B-lineage antigens and myeloid antigens accompanied by clonal rearrangements of IgH gene.

Add (11q23) abnormality was found in sideline karyotypes as well as the stemline abnormality of dic(17;20) (p11;q11).

[MeSH-major] Gene Amplification. Leukemia, Biphenotypic, Acute / genetics. Translocation, Genetic

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(PMID = 20505276.001).

[ISSN] 1880-9952

[Journal-full-title] Journal of clinical and experimental hematopathology : JCEH

[ISO-abbreviation] J Clin Exp Hematop

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

   

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[Title] Expression of IAP-family proteins in adult acute mixed lineage leukemia (AMLL).

To determine the apoptosis-resistant mechanism in adult acute mixed lineage leukemia (AMLL) with biphenotypic blasts responsible for resistance against chemotherapy, the expression levels of IAP-family proteins in AMLL bone marrow cells were analyzed by quantitative RT-PCR.

These findings suggest that higher expression of various IAPs is associated with the chemotherapy-resistant nature of this specific type of leukemia.

[MeSH-major] Apoptosis. Biomarkers, Tumor / metabolism. Bone Marrow Cells / metabolism. Leukemia, Biphenotypic, Acute / metabolism. Proteins / metabolism

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Flow Cytometry. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Inhibitor of Apoptosis Proteins. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / metabolism. Leukemia, Monocytic, Acute / pathology. Male. Microtubule-Associated Proteins / analysis. Microtubule-Associated Proteins / metabolism. Middle Aged. Neoplasm Proteins. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 15726601.001).

[ISSN] 0361-8609

[Journal-full-title] American journal of hematology

[ISO-abbreviation] Am. J. Hematol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proteins; 0 / RNA, Messenger

   

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[Title] Potential use of the Macrobrachium rosenbergii lectin for diagnosis of T-cell acute lymphoblastic leukemia.

T-cell acute lymphoblastic leukemia is the most common form of cancer in children.

Lectins are proteins or glycoproteins from plants or animals that recognize oligossacharides on the cell surface and have been used to characterize the structural changes of oligosaccharides in leukemias.

In this study, we used the lectin from the freshwater prawn Macrobrachium (M. rosenbergii), specific for acetyl groups in sialylated glycans, because increased sialylation of glycoproteins and glycolipids has been identified in lymphoblastic leukemias.

We compared the specificity of the M. rosenbergii lectin for lymphoblastic leukemias with the specificities of the lectins from Triticum vulgaris, Solanum tuberosum, Arachis hipogaea, and Phytolacca americana.

By morphologic and phenotype characterization with a panel of monoclonal antibodies, we identified four types of leukemias from 106 leukemia patients: 11 cases of T-cell acute lymphoblastic leukemia, 61 cases of B-cell acute lymphoblastic leukemia, 24 cases of acute myeloblastic leukemia, and 10 cases of acute biphenotypic leukemia.

As determined by cytofluorometric assays, nine of the eleven cases with T-cell acute lymphoblastic leukemia (8 +/- 3 years old) were specifically identified with the lectin from M. rosenbergii.

In contrast, only six cases of B-cell leukemia, one case of myeloblastic leukemia, and 2 cases of biphenotypic leukemia were identified with this M. rosenbergii lectin.

The other lectins tested showed no capacity to differentiate, in a significant manner, any of the four types of leukemias tested.

Thus, the lectin from M. rosenbergii could be considered a useful tool for the diagnosis and study of T-cell acute lymphoblastic leukemia.

[MeSH-major] Lectins. Leukemia, Biphenotypic, Acute / diagnosis. Palaemonidae / chemistry

[MeSH-minor] Animals. Antibodies, Monoclonal. Antigens, CD45 / analysis. Antigens, Neoplasm / immunology. Child. Diagnosis, Differential. Flow Cytometry. Humans. Lymphocytes / drug effects. Lymphocytes / metabolism. Phenotype

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(PMID = 18212483.001).

[ISSN] 0040-8727

[Journal-full-title] The Tohoku journal of experimental medicine

[ISO-abbreviation] Tohoku J. Exp. Med.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Japan

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Lectins; EC 3.1.3.48 / Antigens, CD45

   

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[Title] Identification of new markers discriminating between myeloid and lymphoid acute leukemia.

BACKGROUND: The heterogeneity of acute myeloid leukemia (AML) with respect to biology and clinical course resides in the fact that patients belonging to the same group show marked differences in their response to chemotherapy, necessitating a refinement of AML classification.

RESULTS: We have shown that two downregulated genes in AML, those encoding guanine nucleotide-binding protein gamma11 (GNG11) and amphiregulin (AREG), are also downregulated in B-lineage acute lymphoblastic leukemia (B-ALL) and T-lineage acute lymphoblastic leukemia (T-ALL) patients.

A second gene, that encoding ceruloplasmin (CP), is upregulated in AML but not in B-ALL and T-ALL.

Our study is the first to analyze these genes in AML, B-ALL, T-ALL and chronic leukemia (myeloid and lymphoid) patients by RT-PCR.

This rapid and sensitive method could be used to screen these genes in different types of leukemia.

[MeSH-major] Biomarkers, Tumor / metabolism. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Adolescent. Adult. Aged. Amphiregulin. Cell Line, Tumor. Ceruloplasmin / genetics. Ceruloplasmin / metabolism. Diagnosis, Differential. EGF Family of Proteins. Female. GTP-Binding Protein alpha Subunits, Gq-G11 / genetics. GTP-Binding Protein alpha Subunits, Gq-G11 / metabolism. Gene Expression Profiling. Glycoproteins / genetics. Glycoproteins / metabolism. Humans. Intercellular Signaling Peptides and Proteins / genetics. Intercellular Signaling Peptides and Proteins / metabolism. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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(PMID = 20670477.001).

[ISSN] 1607-8454

[Journal-full-title] Hematology (Amsterdam, Netherlands)

[ISO-abbreviation] Hematology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / AREG protein, human; 0 / Amphiregulin; 0 / Biomarkers, Tumor; 0 / EGF Family of Proteins; 0 / Glycoproteins; 0 / Intercellular Signaling Peptides and Proteins; EC 1.16.3.1 / Ceruloplasmin; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gq-G11

   

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Donor leukocyte infusions (DLI) in the allogeneic hematopoietic transplant setting can provide a clinically relevant boost of immunity to reduce opportunistic infections and to increase graft-versus-leukemia activity.

However, significant apoptosis occurs in proliferating T cells, diminishing the yield and skewing the CD4/CD8 ratio in the T-cell population, jeopardizing the potential efficacy of DLI.

Recognizing that infused T lymphocytes will need to meet microbial antigens in secondary lymphoid organs to generate effectors, we also show that expansion with IL-7 promotes the preservation of a polyclonal broad T-cell receptor repertoire and a surface phenotype that favors lymph node homing.

Expanded lymphocytes lack alloreactivity against recipient and other allogeneic cells, indicating a favorable safety profile from graft-versus-host disease.

Nevertheless, expanded T cells can be primed subsequently against lymphoid and myeloid leukemia cells to generate tumor-specific cytotoxic T cells.

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[Copyright] Copyright 2010 AACR.

[Cites] Bone Marrow Transplant. 1999 Dec;24(11):1229-33 [10642813.001]

[Cites] Blood. 2009 Mar 26;113(13):2999-3007 [19008454.001]

[Cites] Blood. 2001 Mar 1;97(5):1491-7 [11222398.001]

[Cites] Nat Immunol. 2000 Nov;1(5):426-32 [11062503.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8732-7 [11447288.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Jul 31;98(16):9277-82 [11470908.001]

[Cites] Biol Blood Marrow Transplant. 2001;7(8):454-66 [11569891.001]

[Cites] Blood. 2001 Oct 1;98(7):2256-65 [11568014.001]

[Cites] Scand J Immunol. 2001 Nov;54(5):501-5 [11696202.001]

[Cites] Nat Med. 2002 Jan;8(1):47-53 [11786906.001]

[Cites] Blood. 2002 Oct 1;100(7):2642-9 [12239180.001]

[Cites] Stem Cells. 2003;21(3):296-303 [12743324.001]

[Cites] J Immunol. 2003 Jul 1;171(1):61-8 [12816983.001]

[Cites] Exp Hematol. 2003 Aug;31(8):708-14 [12901976.001]

[Cites] Blood. 2003 Sep 15;102(6):2004-13 [12763934.001]

[Cites] J Clin Invest. 2003 Oct;112(7):1095-107 [14523046.001]

[Cites] J Virol. 2004 Sep;78(18):9740-9 [15331707.001]

[Cites] Biol Blood Marrow Transplant. 2004 Nov;10(11):772-83 [15505608.001]

[Cites] Immunol Today. 1990 Jun;11(6):211-6 [2162180.001]

[Cites] Bone Marrow Transplant. 1994 Oct;14(4):545-53 [7858529.001]

[Cites] Eur J Immunol. 1997 Mar;27(3):633-40 [9079802.001]

[Cites] Immunol Lett. 1997 Oct;59(1):21-8 [9334853.001]

[Cites] Blood. 1998 Jul 1;92(1):11-8 [9639493.001]

[Cites] J Immunol. 1998 Dec 1;161(11):5909-17 [9834071.001]

[Cites] Am J Reprod Immunol. 1998 Nov;40(5):319-25 [9870074.001]

[Cites] Bone Marrow Transplant. 1999 Apr;23(8):783-8 [10231140.001]

[Cites] Immunology. 1999 Jan;96(1):35-47 [10233676.001]

[Cites] Nat Rev Immunol. 2004 Nov;4(11):856-67 [15516965.001]

[Cites] Clin Immunol. 2005 Jan;114(1):30-41 [15596407.001]

[Cites] Immunology. 2005 Mar;114(3):322-35 [15720434.001]

[Cites] Clin Exp Immunol. 2005 Jul;141(1):10-8 [15958064.001]

[Cites] Bioinformatics. 2005 Aug 15;21(16):3394-400 [15955781.001]

[Cites] Blood. 2006 Feb 15;107(4):1325-31 [16269610.001]

[Cites] Cytotherapy. 2006;8(2):149-57 [16698688.001]

[Cites] J Immunother. 2006 May-Jun;29(3):313-9 [16699374.001]

[Cites] Immunol Rev. 2006 Jun;211:154-63 [16824125.001]

[Cites] Biol Blood Marrow Transplant. 2006 Sep;12(9):919-27 [16920557.001]

[Cites] Leuk Lymphoma. 2006 Jul;47(7):1222-8 [16923550.001]

[Cites] Blood. 2006 Sep 1;108(5):1770-3 [16675712.001]

[Cites] Cytotherapy. 2007;9(2):111-22 [17453963.001]

[Cites] Biol Blood Marrow Transplant. 2007 Oct;13(10):1135-44 [17889349.001]

[Cites] Blood. 2007 Oct 15;110(8):2803-10 [17595335.001]

[Cites] Blood. 2007 Dec 15;110(13):4543-51 [17671230.001]

[Cites] Biol Blood Marrow Transplant. 2008 Jan;14(1):16-27 [18158957.001]

[Cites] Bone Marrow Transplant. 2008 Jan;41(2):193-8 [17982497.001]

[Cites] J Exp Med. 2008 Jul 7;205(7):1701-14 [18573906.001]

[Cites] Biol Blood Marrow Transplant. 2008 Oct;14(10):1190-6 [18804050.001]

[Cites] Biol Blood Marrow Transplant. 2009 Jan;15(1 Suppl):162-8 [19147099.001]

[Cites] Blood. 2000 Aug 1;96(3):885-93 [10910901.001]

(PMID = 20530666.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] ENG

[Grant] United States / NHLBI NIH HHS / HL / R01 HL091749; United States / NHLBI NIH HHS / HL / 7R01HL091749; United States / NCI NIH HHS / CA / R01 CA132110; United States / NIAID NIH HHS / AI / UC6 AI058607; United States / NIAID NIH HHS / AI / P30 AI051445; United States / NHLBI NIH HHS / HL / R01 HL091749-04; United States / NCI NIH HHS / CA / R01-CA132110; United States / NCI NIH HHS / CA / R01 CA132110-03; United States / NCI NIH HHS / CA / CA132110-03; United States / NIAID NIH HHS / AI / UC6 AI58607; United States / NIAID NIH HHS / AI / P30 AI51445

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD137; 0 / Antigens, CD28; 0 / Antigens, CD3; 0 / Interleukin-7; 0 / Receptors, Antigen, T-Cell, alpha-beta; 126465-35-8 / Perforin; 147205-72-9 / CD40 Ligand

[Other-IDs] NLM/ NIHMS203765; NLM/ PMC2896454

   

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A systematic approach that starts from the registration of new diagnosis and complete follow-up can be of help for the study of treatment and evolution of these complications.

Its aim is to improve the speed, quality and integration of information related to subjects with febrile event, ultimately resulting in improving patients' care.Patients included adults and children with acute and chronic myeloid or lymphoid leukemia, Hodgkin's and non-Hodgkin's lymphoma, myelodysplastic syndrome, or multiple myeloma.

The registry also included data regarding event onset in hematopoietic stem cell transplants (HSCTs).

[MeSH-minor] Hematopoietic Stem Cell Transplantation. Humans. Incidence. Italy. Prospective Studies

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(PMID = 20227988.001).

[ISSN] 1973-9478

[Journal-full-title] Journal of chemotherapy (Florence, Italy)

[ISO-abbreviation] J Chemother

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Italy

[Investigator] Levis A; Leoni P; Liso V; Baccarani M; Cortellazzo S; Rossi G; Russo D; La Nasa G; Storti S; Giustolisi R; Morabito F; Cuneo A; Bosi A; Capalbo SF; Cascavilla N; Ghio R; Carella A; Brugiatelli M; Ciceri F; Martinelli G; Morra E; Pogliani E; Mettivier V; Carli M; Abbadessa V; Musso M; Aricò M; Lazzarino M; Visani G; Fioritoni G; Di Bartolomeo P; Vallisa D; Petrini M; Favre C; Olivieri A; Gugliotta L; Leone G; Amadori S; De Rossi G; De Fabritiis P; Majolino I; D'Arco A; Lauria F; Mazza P; Fagioli F; Gherlinzoni F; Chesesi T; Rodeghiero F

   

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[Title] Fulminant septicemia of Bacillus cereus resistant to carbapenem in a patient with biphenotypic acute leukemia.

A 33-year-old man was suffering from febrile neutropenia (FN) on day 15 after the start of remission-induction therapy for biphenotypic acute leukemia under gut decontamination with polymyxin B and nystatin.

If B. cereus resistant to carbapem increases, our method of gut decontamination with polymyxin B and nystatin may have to be changed to one containing a new quinolone for the prevention of septicemia.

[MeSH-major] Bacillus cereus / drug effects. Bacteremia / microbiology. Carbapenems / therapeutic use. Leukemia, Biphenotypic, Acute / complications

[MeSH-minor] Adult. Anti-Bacterial Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Stem / microbiology. Brain Stem / pathology. Fever / drug therapy. Gram-Positive Bacterial Infections / complications. Gram-Positive Bacterial Infections / diagnosis. Gram-Positive Bacterial Infections / drug therapy. Gram-Positive Bacterial Infections / pathology. Humans. Liver / microbiology. Liver / ultrastructure. Lung / microbiology. Lung / ultrastructure. Male. Microbial Sensitivity Tests. Neutropenia / drug therapy. Remission Induction. beta-Lactam Resistance

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(PMID = 18936889.001).

[ISSN] 1341-321X

[Journal-full-title] Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy

[ISO-abbreviation] J. Infect. Chemother.

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Japan

[Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Carbapenems

   

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Increased erythrocyte mean corpuscular volume (MCV) is frequently found among DS infants and remains elevated throughout life in two-thirds of patients, making interpretation of red cell indices for diagnosis of nutritional anemias or bone marrow failure disorders more challenging.

Transient myeloproliferative disorder (TMD) associated with pancytopenia, hepatosplenomegaly, and circulating immature WBCs, is found almost exclusively in DS infants with an incidence of approximately 10%.

Despite the high rate of spontaneous regression, TMD can be a preleukemic disorder in 20-30% of children with DS.

There is an increased risk of leukemia with an equal incidence of lymphoid and myeloid leukemia.

Acute megakaryocytic leukemia (AMKL) subtype is the most common form of acute myeloid leukemia (AML) in this setting, and is uncommon in children without DS.

Children with DS and leukemia are more sensitive to some chemotherapeutic agents such as methotrexate than other children which requires careful monitoring for toxicity.

Although the risk for leukemia is higher in individuals with DS, these patients have a lower risk of developing solid tumors, with the exception of germ cell tumors, and perhaps retinoblastoma and lymphoma.

[MeSH-major] Down Syndrome / complications. Hematologic Diseases / diagnosis. Hematologic Diseases / etiology. Neoplasms / diagnosis. Neoplasms / etiology

[MeSH-minor] Child. Female. Humans. Infant. Leukemia / diagnosis. Leukemia / etiology. Male. Myeloproliferative Disorders / diagnosis. Myeloproliferative Disorders / etiology

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(PMID = 17048354.001).

[ISSN] 1552-4868

[Journal-full-title] American journal of medical genetics. Part C, Seminars in medical genetics

[ISO-abbreviation] Am J Med Genet C Semin Med Genet

[Language] eng

[Grant] United States / NCI NIH HHS / CA / 2T32 CA 09307

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Number-of-references] 72

   

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[Title] Comparison between CD19 and CD20 expression patterns on acute leukemic cells.

In order to provide the evidences for CD19 as a better antibody targeting molecule for B lineage acute leukemias than CD20 through the multi-parameter flow-cytometry analysis of leukemia cells, the samples from 321 patients with acute leukemia (AL) were immunophenotyped by multi-color flow cytometry and CD45/SSC gating strategy followed by the analysis of CD19 and CD20 expression.

The results showed that the positive rate of CD19 (115/116, 99.1%) in 116 cases with B lineage acute lymphoblastic leukemia (B lineage ALL) was significantly higher than that of CD20 (33/116, 28.4%) (P < 0.01); in 17 patients with B lineage/Myeloid (B/My) acute mixed lineage leukemia (AMLL), the former positive rate (17/17, 100%) was also higher than the latter (5/17, 29.4%) (P < 0.01).

Both of the two antigens were negative in 29 patients with acute T lymphoblastic leukemia and 7 patients with T/My AMLL.

The positive rates of CD19 and CD20 in 152 patients with acute myeloid leukemia (AML) were 7.2% and 2.0%, respectively.

The difference of the fluorescence intensity between the two antigens on the cells from each patient with B lineage ALL or B/My AMLL was statistically significant (t = 20.68, P < 0.001).

The specificity of CD19 and CD20 in B lymphocytic lineage was 92.3% (132/143) and 92.7% (38/41), respectively, while the sensitivity was 99.2% (132/133) and 28.6% (38/133), respectively, the former sensitivity was significantly higher than the latter (chi(2) = 144.018, P = 0.001).

It is concluded that CD19 continuously and steadily express on almost all subtypes of B lineage leukemic cells with homogeneous pattern while only a small number of leukemias express CD20.

These indicate that CD19 may be a better antibody targeting molecule than CD20 for patients with B-lineage acute leukemia.

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(PMID = 16403255.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] ENG

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD20

   

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[Title] Analysis of FLT3 internal tandem duplication and D835 mutations in Chinese acute leukemia patients.

Genomic aberrations of Fms-like tyrosine kinase 3 (FLT3), including internal tandem duplication (ITD) and point mutations, have been demonstrated in 25-30% of adults acute myeloid leukemia (AML) and are markers of poor prognosis.

FLT3/ITD and D835 mutations were analyzed in 194 Chinese patients with acute leukemia and myelodysplastic syndromes (MDS) by polymerase chain reaction (PCR).

However, neither aberrations was found in 25 patients with acute lymphoblastic leukemia (ALL), 2 acute hybrid leukemia, 17 MDS and 7 chronic myeloid leukemia in blast crisis (CML-BC).

[MeSH-major] Leukemia / genetics. Mutation, Missense. Tandem Repeat Sequences. fms-Like Tyrosine Kinase 3 / genetics

[MeSH-minor] Acute Disease. Adolescent. Adult. Amino Acid Sequence. Asian Continental Ancestry Group / genetics. DNA Mutational Analysis. Female. Humans. Leukocytosis. Male. Middle Aged. Molecular Sequence Data. Myelodysplastic Syndromes / genetics. Prognosis. Remission Induction

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(PMID = 15996732.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

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[Title] Cytogenetic manifestation of chromosome 11 duplication/amplification in acute myeloid leukemia.

Gene amplification is a frequent genetic abnormality in solid tumors, and many oncogenes are activated in this way.

In acute myeloid leukemia (AML), a frequent target of gene amplification is chromosome 11, particularly chromosome region 11q23, including the MLL (myeloid/lymphoid leukemia) gene.

[MeSH-major] Chromosomes, Human, Pair 11 / genetics. Gene Amplification. Gene Duplication. Leukemia, Myeloid, Acute / genetics. Trisomy

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[Copyright] Copyright 2010 Elsevier Inc. All rights reserved.

(PMID = 20471515.001).

[ISSN] 1873-4456

[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

   

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[Title] Induction of apoptosis in lymphoid and myeloid leukemia.

Defects in the core machinery of the apoptosis pathway contribute to chemoresistance and poor outcomes in patients with acute leukemia.

This review highlights compounds that target the mitochondrial, death receptor, and convergence pathways of caspase activation that are being developed for the treatment of acute leukemia.

[MeSH-major] Apoptosis / physiology. Leukemia, Lymphoid / therapy. Leukemia, Myeloid / therapy

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[Cites] J Biol Chem. 1998 Mar 20;273(12):6916-20 [9506996.001]

[Cites] J Med Chem. 2003 Sep 25;46(20):4259-64 [13678404.001]

[Cites] Cancer Res. 2003 Nov 15;63(22):7724-32 [14633697.001]

[Cites] J Med Chem. 2004 Aug 12;47(17):4147-50 [15293984.001]

[Cites] Cancer Cell. 2005 May;7(5):457-68 [15894266.001]

[Cites] Nature. 1999 Oct 21;401(6755):818-22 [10548111.001]

[Cites] Curr Treat Options Oncol. 2003 Jun;4(3):211-8 [12718798.001]

[Cites] Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1252-6 [9990010.001]

[Cites] Cancer Res. 2004 Oct 15;64(20):7183-90 [15492230.001]

[Cites] EMBO J. 2005 Feb 9;24(3):645-55 [15650747.001]

[Cites] Haematologica. 2004 Mar;89(3):363-4 [15020280.001]

[Cites] Cancer Res. 1999 Jan 15;59(2):336-41 [9927043.001]

[Cites] Cell Death Differ. 2002 Sep;9(9):881-92 [12181739.001]

[Cites] Science. 1998 Aug 28;281(5381):1312-6 [9721091.001]

[Cites] J Mol Biol. 2000 Sep 8;302(1):171-88 [10964568.001]

[Cites] Chem Biol. 2003 Aug;10(8):759-67 [12954335.001]

[Cites] Blood. 2005 May 15;105(10):4043-50 [15687241.001]

[Cites] Leukemia. 2003 Nov;17(11):2122-9 [12931220.001]

[Cites] Mol Cell. 2003 Feb;11(2):519-27 [12620238.001]

[Cites] Cell. 2001 Mar 9;104(5):781-90 [11257231.001]

[Cites] Cell. 2001 Mar 9;104(5):769-80 [11257230.001]

[Cites] EMBO J. 1999 Oct 1;18(19):5242-51 [10508158.001]

[Cites] J Biol Chem. 1999 Jun 18;274(25):17941-5 [10364241.001]

[Cites] Science. 2004 Sep 3;305(5689):1471-4 [15353805.001]

[Cites] Cell. 2001 Mar 9;104(5):791-800 [11257232.001]

[Cites] Leukemia. 1995 Jan;9(1):131-8 [7845007.001]

[Cites] J Am Chem Soc. 2004 Dec 29;126(51):16686-7 [15612682.001]

[Cites] Science. 1997 Feb 21;275(5303):1132-6 [9027315.001]

[Cites] Cancer Cell. 2004 Jan;5(1):25-35 [14749124.001]

[Cites] Nature. 1998 Dec 10;396(6711):580-4 [9859993.001]

[Cites] Br J Haematol. 2003 Jun;121(5):730-8 [12780787.001]

[Cites] Blood. 2001 Dec 15;98(13):3541-53 [11739155.001]

[Cites] J Biol Chem. 2000 Oct 27;275(43):33777-81 [10934209.001]

[Cites] Cell Death Differ. 2004 Apr;11(4):372-80 [14765132.001]

[Cites] Cancer Gene Ther. 2005 May;12(5):509-14 [15706355.001]

[Cites] Cancer Res. 2004 Nov 1;64(21):7927-35 [15520199.001]

[Cites] J Biol Chem. 1999 Apr 23;274(17):11549-56 [10206961.001]

[Cites] Cell. 1997 Nov 14;91(4):443-6 [9390553.001]

[Cites] J Med Chem. 2004 Aug 26;47(18):4417-26 [15317454.001]

[Cites] Br J Haematol. 2001 Mar;112(3):706-13 [11260076.001]

[Cites] Leukemia. 1999 Oct;13(10):1574-80 [10516759.001]

[Cites] Mol Cell Biol. 2000 Jun;20(11):3781-94 [10805722.001]

[Cites] J Biol Chem. 2002 Jun 21;277(25):22320-9 [11940602.001]

[Cites] J Med Chem. 2004 May 6;47(10):2430-40 [15115387.001]

[Cites] Trends Neurosci. 2000 May;23(5):222-9 [10782128.001]

[Cites] Clin Cancer Res. 2003 Jul;9(7):2826-36 [12855663.001]

[Cites] Science. 2004 Sep 3;305(5689):1466-70 [15353804.001]

[Cites] Cell Growth Differ. 2000 May;11(5):261-7 [10845427.001]

[Cites] Nat Med. 1999 Feb;5(2):157-63 [9930862.001]

[Cites] Mol Cell Biol. 2004 Aug;24(16):7003-14 [15282301.001]

[Cites] Leuk Res. 1998 Jan;22(1):81-7 [9585084.001]

[Cites] Leukemia. 2002 Jan;16(1):67-73 [11840265.001]

[Cites] Cancer Res. 2004 Oct 15;64(20):7570-8 [15492284.001]

[Cites] J Biol Chem. 1998 Oct 16;273(42):27084-90 [9765224.001]

[Cites] Ann N Y Acad Sci. 2005 Nov;1058:215-34 [16394139.001]

[Cites] Nature. 2005 Jun 2;435(7042):677-81 [15902208.001]

[Cites] Leukemia. 1997 Dec;11(12):2075-8 [9447823.001]

[Cites] Cancer Res. 2002 May 1;62(9):2462-7 [11980633.001]

[Cites] EMBO J. 1999 Jul 1;18(13):3586-95 [10393175.001]

[Cites] Nat Med. 2000 May;6(5):564-7 [10802713.001]

[Cites] J Biol Chem. 1999 Jan 29;274(5):3189-98 [9915859.001]

[Cites] Cancer Res. 2005 Mar 15;65(6):2378-86 [15781653.001]

[Cites] Genes Dev. 1998 Jun 1;12(11):1551-70 [9620844.001]

[Cites] Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7124-9 [10860979.001]

[Cites] Cell Death Differ. 2006 Feb;13(2):179-88 [16322751.001]

[Cites] Mol Biol Cell. 2003 Jan;14(1):78-92 [12529428.001]

[Cites] Br J Haematol. 2000 Jul;110(1):154-60 [10930993.001]

(PMID = 17040621.001).

[ISSN] 1523-3790

[Journal-full-title] Current oncology reports

[ISO-abbreviation] Curr Oncol Rep

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Receptors, Death Domain; EC 3.4.22.- / Caspases

[Number-of-references] 68

   

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[Title] Successful voriconazole treatment of invasive pulmonary aspergillosis in a patient with acute biphenotypic leukemia.

A 23-year old woman with acute biphenotypic leukemia (ABL) complained of chest pain with cough, high fever and hemoptysis during induction chemotherapy, although she had been treated with anti-biotics and micafungin.

We made a clinical diagnosis of invasive pulmonary aspergillosis (IPA) based on a consolidation in the right upper lung field on a chest radiograph as well as a high level of serum beta-D-glucan (with no evidence of tuberculosis and candidiasis).

Later, we discovered an air-crescent sign by CT scan that supported the diagnosis of IPA.

Serological tests and CT findings can aid in early diagnosis of IPA, which, along with treatment for IPA, will improve clinical outcomes.

[MeSH-major] Antifungal Agents / therapeutic use. Invasive Pulmonary Aspergillosis / drug therapy. Leukemia, Biphenotypic, Acute / complications. Pyrimidines / therapeutic use. Triazoles / therapeutic use

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(PMID = 19727206.001).

[ISSN] 0386-300X

[Journal-full-title] Acta medica Okayama

[ISO-abbreviation] Acta Med. Okayama

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Antifungal Agents; 0 / Pyrimidines; 0 / Triazoles; JFU09I87TR / Voriconazole

   

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[Title] Outcomes of CAG regimen for refractory biphenotypic acute leukemia patients.

OBJECTIVE: To evaluated the efficiency of low-dose cytosine arabinoside plus aclarubicin with concurrent administration of granulocyte colony-stimulating factor (CAG) regimen for refractory biphenotypic acute leukemia (BAL).

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(PMID = 19848320.001).

[ISSN] 1001-9294

[Journal-full-title] Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih

[ISO-abbreviation] Chin. Med. Sci. J.

[Language] ENG

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 74KXF8I502 / Aclarubicin

   

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[Title] Concomitant t(4;11) and t(1;19) in a patient with biphenotypic acute leukemia.

[MeSH-major] Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Chromosomes, Human, Pair 4 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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(PMID = 17693199.001).

[ISSN] 0165-4608

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] United States

   

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AP180 and clathrin assembly lymphoid myeloid leukemia protein (CALM) are clathrin accessory proteins that promote the formation of clathrin-coated vesicles.

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(PMID = 15558718.001).

[ISSN] 0021-9967

[Journal-full-title] The Journal of comparative neurology

[ISO-abbreviation] J. Comp. Neurol.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Monomeric Clathrin Assembly Proteins; 0 / Picalm protein, rat; 0 / clathrin assembly protein AP180

   

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[Title] Biological features and outcome of biphenotypic acute leukemia: a case series.

BACKGROUND: Biphenotypic acute leukemia (BAL) is a distinct entity that is immunophenotypically defined by the European Group for the Immunological Classification of Leukemia (EGIL) scoring system and accounts for less than 5% of all acute leukemia cases.

Since it is a rare and heterogeneous form of acute leukemia with an allegedly poor outcome, there is no consensus on the best treatment approach in these patients.

PATIENTS AND METHODS: Using the EGIL system, we identified 21 cases (3.9%) of BAL from 535 newly diagnosed acute leukemia patients in an 11-year period.

RESULTS: There were ten cases of myeloid+B-lymphoid leukemia, eight cases of myeloid+T-lymphoid, one case of B+T-lymphoid and two cases of trilineage (myeloid+B+T-lymphoid leukemia).

Patients that received acute lymphoblastic leukemia-oriented chemotherapy had a higher CR rate compared with those who received acute myeloid leukemia-oriented chemotherapy (100% vs. 60%, P = .007).

The white blood cell count at diagnosis was found to have statistically significant impact on survival.

CONCLUSION: Despite the progress in the treatment of acute leukemia, the prognosis of BAL remains poor and treatment protocols devised explicitly for this entity should be investigated in prospective collaborative studies.

[MeSH-major] Leukemia, Biphenotypic, Acute / pathology. Leukemia, Biphenotypic, Acute / therapy

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Disease-Free Survival. Female. Humans. Immunophenotyping. Male. Middle Aged. Prognosis. Stem Cell Transplantation. Treatment Outcome. Young Adult

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(PMID = 20058478.001).

[ISSN] 1658-3876

[Journal-full-title] Hematology/oncology and stem cell therapy

[ISO-abbreviation] Hematol Oncol Stem Cell Ther

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

   

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[Title] Prophylaxis of central nervous system leukemia: a case of chronic myeloid leukemia with lymphoid blast crisis treated with imatinib mesylate.

BACKGROUND: Chronic myeloid leukemia (CML) in blast crisis has a dismal prognosis.

METHODS: A child with CML in lymphoid blast crisis was diagnosed by complete hematological and bone marrow examination.

There was no central nervous system (CNS) leukemia at presentation.

Results of cerebrospinal fluid taken for cytopathology showed CNS leukemia.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blast Crisis / drug therapy. Central Nervous System Neoplasms / prevention & control. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / administration & dosage

[MeSH-minor] Anti-Inflammatory Agents / administration & dosage. Benzamides. Blood Cell Count. Chemoprevention / methods. Child. Clinical Protocols. Cytarabine / administration & dosage. Drug Therapy, Combination. Female. Humans. Hydrocortisone / administration & dosage. Imatinib Mesylate. Injections, Spinal. Methotrexate / therapeutic use. Remission Induction

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[Cites] Clin Cancer Res. 2003 Oct 15;9(13):4674-81 [14581336.001]

[Cites] Blood. 1983 Jan;61(1):85-91 [6571717.001]

[Cites] Ann Hematol. 2004 Jun;83(6):401-2 [14673623.001]

[Cites] Am J Med. 1993 Jan;94(1):69-74 [8420302.001]

[Cites] N Engl J Med. 2001 Apr 5;344(14):1038-42 [11287973.001]

[Cites] Leuk Lymphoma. 2004 Apr;45(4):695-8 [15160941.001]

[Cites] Blood. 2004 Nov 1;104(9):2655-60 [15231574.001]

[Cites] FDA Consum. 2001 Jul-Aug;35(4):6 [11692893.001]

[Cites] N Engl J Med. 2002 Feb 28;346(9):645-52 [11870241.001]

[Cites] N Engl J Med. 1983 Oct 6;309(14):826-31 [6412140.001]

(PMID = 18661773.001).

[ISSN] 1708-8569

[Journal-full-title] World journal of pediatrics : WJP

[ISO-abbreviation] World J Pediatr

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 04079A1RDZ / Cytarabine; 8A1O1M485B / Imatinib Mesylate; WI4X0X7BPJ / Hydrocortisone; YL5FZ2Y5U1 / Methotrexate

   

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[Title] Unusual childhood biphenotypic acute leukemia with a yet unreported t(3;13)(p25.1;q13).

[MeSH-major] Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 3 / genetics. Killer Cells, Natural / pathology. Leukemia, Myeloid, Acute / pathology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Translocation, Genetic / genetics

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(PMID = 20338638.001).

[ISSN] 1873-5835

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] England

   

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[Title] Diagnosis of biphenotypic acute leukemia: a paradigmatic approach.

Biphenotypic acute leukemia (BAL), or acute leukemia with a single population of blasts coexpressing markers of two different lineages, is a rare clinical entity.

To define BAL, a scoring system was proposed by the European Group of Immunological Markers for Leukemias (EGIL) in 1995.

However, increasing evidence suggests that this system has limitations, as acknowledged by the 2008 World Health Organization (WHO) Classification of Tumors of Hematopoietic and Lymphoid Tissues.

We propose a new paradigmatic approach to defining BAL based on recent clinical studies of BAL and advances in immunologic marker definition and cytogenetics, and applied our new approach to 8 cases of "BAL" among a cohort of 742 new acute leukemias in our Cancer Center.

By our new criteria, 6 cases were reclassified as acute lymphoblastic leukemia (ALL), while only 2 were still classified as BAL.

[MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis

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[Cites] Arch Pathol Lab Med. 2001 Jul;125(7):948-50 [11419984.001]

[Cites] Am J Clin Pathol. 1998 Feb;109(2):211-20 [9583894.001]

[Cites] Am J Hematol. 2001 Oct;68(2):69-74 [11559944.001]

[Cites] Exp Hematol. 2002 Mar;30(3):205-11 [11882357.001]

[Cites] Br J Haematol. 2003 Dec;123(5):842-9 [14632775.001]

[Cites] Cancer Res. 2004 Oct 15;64(20):7399-404 [15492262.001]

[Cites] Nature. 1975 Dec 4;258(5534):454-6 [1059878.001]

[Cites] Br J Haematol. 1976 Aug;33(4):451-8 [188440.001]

[Cites] Blood. 1981 Sep;58(3):648-52 [6973348.001]

[Cites] Blood. 1983 Apr;61(4):718-25 [6572534.001]

[Cites] Blood. 1983 Jun;61(6):1138-45 [6404327.001]

[Cites] Hum Pathol. 1998 May;29(5):498-504 [9596274.001]

[Cites] Am J Hematol. 1998 Jul;58(3):241-3 [9662278.001]

[Cites] Cytometry. 1998 Aug 15;34(4):198-202 [9725460.001]

[Cites] Haematologica. 1999 Aug;84(8):699-706 [10457405.001]

[Cites] Cancer. 2004 Dec 15;101(12):2788-801 [15481055.001]

[Cites] Exp Mol Pathol. 2005 Aug;79(1):39-41 [16005710.001]

[Cites] Cancer Genet Cytogenet. 2005 Nov;163(1):62-7 [16271957.001]

[Cites] Blood. 2007 May 1;109(9):3697-705 [17218387.001]

[Cites] Exp Mol Pathol. 2007 Aug;83(1):138-41 [17434163.001]

[Cites] Br J Haematol. 2007 Jul;138(2):213-6 [17593028.001]

[Cites] Exp Mol Pathol. 2007 Dec;83(3):471-3 [17963747.001]

[Cites] Trends Biochem Sci. 2008 Feb;33(2):51-7 [18201888.001]

[Cites] Int J Hematol. 2008 Mar;87(2):132-6 [18288568.001]

[Cites] Leuk Lymphoma. 2008 Apr;49(4):700-9 [18398737.001]

[Cites] Cancer Genet Cytogenet. 2008 Aug;185(1):28-31 [18656690.001]

[Cites] Blood. 2009 May 21;113(21):5083-9 [19131545.001]

[Cites] J Biol Chem. 2000 Mar 24;275(12):8633-40 [10722703.001]

[Cites] Am J Clin Pathol. 2000 Jun;113(6):823-30 [10874883.001]

[Cites] J Chin Med Assoc. 2007 Jul;70(7):269-73 [17631462.001]

[Cites] Leukemia. 2007 Nov;21(11):2264-70 [17611554.001]

[Cites] Pathology. 1986 Jan;18(1):99-110 [3014425.001]

[Cites] EMBO J. 1988 Nov;7(11):3457-64 [2463161.001]

[Cites] Leukemia. 1989 Mar;3(3):170-81 [2465463.001]

[Cites] Br J Haematol. 1990 Jun;75(2):202-7 [2372506.001]

[Cites] Blood. 1990 Aug 15;76(4):808-13 [2166608.001]

[Cites] Blood. 1992 Jul 15;80(2):470-7 [1378322.001]

[Cites] J Immunol. 1992 Oct 1;149(7):2281-5 [1382094.001]

[Cites] Leukemia. 1993 Apr;7(4):489-98 [7681917.001]

[Cites] Blood. 1993 Aug 1;82(3):853-7 [8338949.001]

[Cites] J Exp Med. 1993 Sep 1;178(3):1049-55 [7688784.001]

[Cites] Blood. 1993 Sep 1;82(5):1599-607 [8395912.001]

[Cites] J Pathol. 1993 Oct;171(2):99-104 [7506772.001]

[Cites] Am J Clin Pathol. 1994 Mar;101(3):296-9 [7510927.001]

[Cites] Br J Haematol. 1994 Jun;87(2):273-81 [7947267.001]

[Cites] Leukemia. 1995 Oct;9(10):1783-6 [7564526.001]

[Cites] Am J Clin Pathol. 1996 Jun;105(6):761-8 [8659452.001]

[Cites] Am J Clin Pathol. 1996 Aug;106(2):185-91 [8712171.001]

[Cites] Br J Haematol. 1997 Oct;99(1):101-6 [9359509.001]

[Cites] Br J Haematol. 1998 Jan;100(1):147-55 [9450804.001]

[Cites] Am J Clin Pathol. 2001 Jul;116(1):25-33 [11447748.001]

(PMID = 19918331.001).

[ISSN] 1936-2625

[Journal-full-title] International journal of clinical and experimental pathology

[ISO-abbreviation] Int J Clin Exp Pathol

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor

[Other-IDs] NLM/ PMC2776262

[Keywords] NOTNLM ; ALL / AML / Biphenotypic acute leukemia / EGIL / classification

   

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[Title] The ultrastructure of hybrid acute leukemia: a study of 15 cases.

The objective of this study was to investigate the ultrastructural characteristics of hybrid acute leukemia (HAL).

By TEM, 5 out 15 cases of HAL were consistent with immunophenotyping (3 cases of biphenotypic type, and 2 cases of biclonal type with granulocytes and lymphocytes); 2 cases were suspected as HAL.

Most of the blast cells of biphenotypic HAL showed lymphoid features, except some cases containing MPO positive granules in blasts, while a few cases exhibited monocytic or nonspecific features.

TEM offers advantages in the diagnosis of biclonal type HAL and biphenotypic HAL positive for MPO.

However, it is difficult to differentiate MPO-negative cases of biphenotypic HAL from ALL and a few cases may be misinterpreted as M5 by TEM.

[MeSH-major] Granulocyte Precursor Cells / ultrastructure. Leukemia, Myeloid, Acute / diagnosis. Lymphocytes / ultrastructure. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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(PMID = 16257860.001).

[ISSN] 0191-3123

[Journal-full-title] Ultrastructural pathology

[ISO-abbreviation] Ultrastruct Pathol

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] EC 1.11.1.7 / Peroxidase

   

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[Title] Isolated extraocular muscle involvement as the ophthalmic manifestation of leukaemia.

BACKGROUND: Clinical and imaging features of patients with orbital leukaemia primarily involving extraocular muscles were evaluated.

METHODS: This retrospective case series includes patients with leukaemia whose only ophthalmic manifestation was extraocular muscle enlargement.

Demographic data, clinical information on the systemic disease, prominent ocular signs and symptoms, computed tomography and magnetic resonance imaging characteristics, treatments applied and the outcomes were collected.

Acute myeloid leukaemia was the diagnosis in two patients, and chronic lymphocytic leukaemia, chronic myeloid leukaemia and biphenotypic acute leukaemia were found in one patient each, respectively.

Restricted ocular motility was the most common finding.

In one patient who had no prior history of leukaemia, an incisional biopsy established the diagnosis.

CONCLUSIONS: Leukaemic infiltration of extraocular muscles is a rare and late manifestation of the advanced disease associated with relapse and there seems to be a predilection for the lateral rectus muscle.

[MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Leukemic Infiltration. Oculomotor Muscles / pathology. Orbital Neoplasms / diagnosis

[MeSH-minor] Child. Child, Preschool. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Ocular Motility Disorders / diagnosis. Prognosis. Retrospective Studies. Tomography, X-Ray Computed

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[CommentIn] Clin Exp Ophthalmol. 2010 Aug;38(6):651 [20553299.001]

(PMID = 19702712.001).

[ISSN] 1442-9071

[Journal-full-title] Clinical & experimental ophthalmology

[ISO-abbreviation] Clin. Experiment. Ophthalmol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Australia

   

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[Title] Role of cyclic AMP response element binding protein in human leukemias.

Acute myeloid leukemia (AML) in adults has a 20% 5-year disease-free survival despite treatment with aggressive cytotoxic chemotherapy.

Previous work from our laboratory demonstrated that the majority of patients with acute lymphoid and myeloid leukemia overexpress CREB in the bone marrow.

CREB overexpression is associated with poor initial outcome of clinical disease in AML patients.

CREB is a transcription factor that functions in glucose homeostasis, growth-factor-dependent cell survival, and memory.

To study its role in hematopoiesis, we overexpressed CREB in leukemia cell lines and in mice.

CREB overexpression resulted in increased survival and proliferation of myeloid cells and blast-transformation of bone marrow progenitor cells from transgenic mice expressing CREB in the myeloid lineage.

CREB transgenic mice also develop myeloproliferative disease after 1 year.

Thus, CREB acts as a protooncogene to regulate hematopoiesis and contributes to the leukemia phenotype.

Our results suggest that CREB-dependent pathways may serve as targets for directed therapies in leukemia in the future.

[MeSH-major] Cyclic AMP Response Element-Binding Protein / genetics. Leukemia / metabolism

[MeSH-minor] Acute Disease. Animals. Cell Line, Tumor. Cell Survival. Disease-Free Survival. Hematopoiesis / genetics. Humans. Mice. Mice, Transgenic. Mutation. Transcription Factors / genetics. Up-Regulation

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[Copyright] (c) 2005 American Cancer Society.

(PMID = 16196046.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA16042; United States / NCI NIH HHS / CA / CA68221

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Cyclic AMP Response Element-Binding Protein; 0 / Transcription Factors

[Number-of-references] 30

   

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[Title] Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias.

The t(9;22) BCR/ABL fusion is associated with over 90% of chronic myelogenous and 25% of acute lymphocytic leukemia.

Chromosome 11q23 translocations in acute myeloid and lymphoid leukemia cells demonstrate myeloid lymphoid leukemia (MLL) fusions with over 40 gene partners, like AF9 and AF4 on chromosomes 9 and 4, respectively.

Therapy-related leukemia is associated with the above gene rearrangements following the treatment with topoisomerase II (topo II) inhibitors.

In this report, using cell lines and primary cells, chromatin structural elements were analyzed in BCR, ABL and AF4 and, for comparison, in MLL2, which is a homolog to MLL, but not associated with chromosome translocations.

Although MLL2 was expressed in all cell lines tested, except for the presence of one DNAse I site in the promoter, no other structural elements were found in MLL2.

A NHR model presented demonstrates the importance of chromatin structure in chromosome translocations involved with leukemia.

[MeSH-major] Chromatin / chemistry. Chromosome Breakage. Chromosomes, Human / genetics. Leukemia / genetics. Leukemia / metabolism. Translocation, Genetic

[MeSH-minor] Acute Disease. Cell Line, Tumor. Cells, Cultured. Chronic Disease. Humans. K562 Cells. Proto-Oncogene Proteins c-bcr / chemistry. Proto-Oncogene Proteins c-bcr / genetics. Recombination, Genetic

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[Cites] Biochemistry. 1997 May 20;36(20):5934-9 [9166762.001]

[Cites] Cell. 1985 May;41(1):127-32 [2986841.001]

[Cites] Gene. 2002 May 29;291(1-2):251-7 [12095698.001]

[Cites] EMBO J. 1990 Apr;9(4):1319-27 [2323342.001]

[Cites] Science. 1994 Jan 28;263(5146):515-8 [8290959.001]

[Cites] Curr Biol. 2000 Jul 27-Aug 10;10(15):923-6 [10959840.001]

[Cites] Leukemia. 1996 Feb;10(2):372-7 [8637251.001]

[Cites] J Cell Biochem. 2001;82(2):299-309 [11527155.001]

[Cites] Genomics. 1995 May 1;27(1):67-82 [7665185.001]

[Cites] Annu Rev Biochem. 1989;58:351-75 [2549853.001]

[Cites] Proc Natl Acad Sci U S A. 1994 Jun 21;91(13):6236-9 [8016145.001]

[Cites] Oncogene. 1989 May;4(5):559-67 [2657572.001]

[Cites] Oncogene. 1990 Nov;5(11):1669-73 [2267134.001]

[Cites] Oncogene. 2001 May 24;20(23):2900-7 [11420702.001]

[Cites] J Cell Biol. 2001 Dec 10;155(6):899-910 [11739403.001]

[Cites] Genes Chromosomes Cancer. 2002 Apr;33(4):331-45 [11921269.001]

[Cites] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4790-5 [10758153.001]

[Cites] EMBO J. 2002 Oct 1;21(19):5269-80 [12356743.001]

[Cites] Genes Chromosomes Cancer. 2001 Oct;32(2):144-54 [11550282.001]

[Cites] Genes Chromosomes Cancer. 2003 Apr;36(4):393-401 [12619163.001]

[Cites] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2076-80 [2832845.001]

[Cites] Nucleic Acids Res. 1997 Feb 1;25(3):511-7 [9016589.001]

[Cites] Cancer Res. 1999 Jul 15;59(14 ):3357-62 [10416593.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Aug 14;98 (17 ):9802-7 [11493704.001]

[Cites] Oncogene. 1998 Dec 3;17(22):2921-31 [9879998.001]

[Cites] J Cell Sci. 2004 Sep 1;117(Pt 19):4583-90 [15331666.001]

[Cites] Nucleic Acids Res. 1988 Jun 24;16(12):5533-56 [2838820.001]

[Cites] Proc Natl Acad Sci U S A. 1989 Jul;86(14):5497-501 [2546156.001]

[Cites] Cell. 1995 Dec 29;83(7):1137-48 [8548801.001]

[Cites] J Cell Biochem Suppl. 2000;Suppl 35:3-22 [11389527.001]

[Cites] Hum Mol Genet. 1998 May;7(5):767-76 [9536079.001]

[Cites] Hum Mol Genet. 2000 Jul 1;9(11):1671-9 [10861294.001]

[Cites] Mol Cell Biol. 1991 Oct;11(10):4973-84 [1656219.001]

[Cites] Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14535-40 [10588740.001]

[Cites] Cell Mol Life Sci. 2002 Feb;59(2):373-85 [11915950.001]

[Cites] Mol Cell Biol. 1997 Jul;17(7):4070-9 [9199342.001]

[Cites] Biochem J. 1994 Nov 1;303 ( Pt 3):681-95 [7980433.001]

[Cites] Blood. 1996 Apr 1;87(7):2649-58 [8639880.001]

[Cites] Proc Natl Acad Sci U S A. 1993 May 15;90(10 ):4631-5 [8506309.001]

[Cites] Hum Mol Genet. 2002 Jun 1;11(12):1391-7 [12023981.001]

[Cites] J Biol Chem. 2002 Jun 14;277(24):21458-67 [11940566.001]

[Cites] Hum Mutat. 2003 Sep;22(3):229-44 [12938088.001]

[Cites] Cell. 1992 Nov 13;71(4):701-8 [1423625.001]

[Cites] Oncogene. 1998 Dec 10;17 (23 ):3035-44 [9881706.001]

[Cites] Genomics. 1999 Jul 15;59(2):187-92 [10409430.001]

[Cites] Leuk Res. 2002 Aug;26(8):713-20 [12191565.001]

[Cites] Br J Haematol. 1999 Apr;105(1):256-64 [10233389.001]

[Cites] Blood. 2000 Feb 1;95(3):738-43 [10648381.001]

[Cites] Oncogene. 1999 Dec 23;18(56):7975-84 [10637508.001]

[Cites] Cancer Res. 1995 Jan 1;55(1):34-8 [7805037.001]

[Cites] Cancer Res. 1996 Apr 15;56(8):1855-62 [8620504.001]

[Cites] Blood. 1996 Mar 1;87(5):1912-22 [8634439.001]

[Cites] Nature. 2001 Sep 27;413(6854):435-8 [11574892.001]

[Cites] Cancer Lett. 2003 Apr 10;193(1):1-9 [12691817.001]

[Cites] Leukemia. 1997 Sep;11(9):1571-4 [9305614.001]

[Cites] Chromosoma. 1996 Aug;105(2):122-33 [8753702.001]

[Cites] Leukemia. 1999 Dec;13(12):2107-13 [10602437.001]

[Cites] Cancer Res. 1993 Oct 1;53(19):4489-92 [8402620.001]

[Cites] Mol Cell Biol. 1999 Apr;19(4):2986-97 [10082566.001]

[Cites] Hum Genet. 2003 Jul;113(1):80-91 [12665971.001]

[Cites] Blood. 1998 Nov 15;92(10):3793-803 [9808573.001]

[Cites] Genomics. 1998 Jan 15;47(2):217-29 [9479494.001]

[Cites] Blood. 2001 Dec 15;98(13):3778-83 [11739186.001]

[Cites] Genes Dev. 2001 Dec 15;15(24):3237-42 [11751629.001]

[Cites] Genes Chromosomes Cancer. 2002 Sep;35(1):92-6 [12203795.001]

[Cites] Cancer Res. 2001 Jun 1;61(11):4550-5 [11389089.001]

[Cites] Blood. 1990 Aug 1;76(3):597-601 [2198962.001]

[Cites] Genetics. 2002 Apr;160(4):1363-73 [11973293.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):9882-7 [12114534.001]

[Cites] Genes Chromosomes Cancer. 2004 Nov;41(3):257-65 [15334549.001]

[Cites] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4411-3 [10781030.001]

[Cites] FASEB J. 2004 Jan;18(1):173-5 [14630694.001]

[Cites] Genes Chromosomes Cancer. 2002 Apr;33(4):362-78 [11921271.001]

[Cites] Mol Pharmacol. 1998 Jul;54(1):78-85 [9658192.001]

[Cites] Cancer Res. 2004 Apr 15;64(8):2656-62 [15087374.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Mar 5;99(5):3070-5 [11867721.001]

[Cites] Semin Hematol. 1999 Oct;36(4 Suppl 7):59-72 [10595755.001]

[Cites] Chromosoma. 1991 Feb;100(2):97-102 [1849068.001]

[Cites] Leukemia. 1998 Mar;12(3):346-52 [9529129.001]

[Cites] Leukemia. 1995 Aug;9(8):1305-12 [7643617.001]

(PMID = 16572268.001).

[ISSN] 0340-6717

[Journal-full-title] Human genetics

[ISO-abbreviation] Hum. Genet.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies

[Publication-country] Germany

[Chemical-registry-number] 0 / Chromatin; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr

   

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[Title] Biphenotypic acute leukemia with t(15;17).

Biphenotypic acute leukemias (BAL) represent 5% of all acute leukemias.

Immunophenotype revealed the compromise of myeloid and B-lymphoid lineages.

This report describes a BAL case with an unfrequent cytogenetic abnormality, and highlights the importance of correlating the results of multiple diagnostic methods in order to establish a correct diagnosis and treatment in BAL patients.

[MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia / genetics

[MeSH-minor] Acute Disease. Child. Chromosome Aberrations. Chromosomes, Human, Pair 8 / genetics. Female. Flow Cytometry / methods. Gene Rearrangement. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence / methods. Neoplasm, Residual / diagnosis. Neoplasm, Residual / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Trisomy

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(PMID = 16019491.001).

[ISSN] 1042-8194

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

   

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[Title] [Detection of point mutation at second tyrosine kinase domain of FLT3 gene in acute myeloid leukemia].

OBJECTIVE: To evaluate the prevalence of a novel FLT3 activating mutation in tyrosine kinase domain (TDK) in acute leukemia patients and its clinical implication.

METHODS: Genomic DNA from bone marrow mononuclear cells of 143 cases of acute myeloid leukemia (AML), 25 acute lymphocytic leukemia (ALL), 2 acute hybrid leukemia (AHL), 17 myelodysplastic syndromes (MDS) and 7 chronic myelogenous leukemia in blast crisis (CML-BC) was screened by polymerase chain reaction (PCR) and gel electrophoresis for FLT3-TKD point mutations.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. fms-Like Tyrosine Kinase 3 / genetics

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(PMID = 16185475.001).

[ISSN] 0253-2727

[Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi

[ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

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Bone marrow biopsy and peripheral blood film confirmed the diagnosis of an acute biphenotypic leukaemia.

This case report highlights the fact that bone pain associated with a normal peripheral blood count may be the presentation of an acute haematological disorder in both adults and children.

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(PMID = 16137555.001).

[ISSN] 0953-6205

[Journal-full-title] European journal of internal medicine

[ISO-abbreviation] Eur. J. Intern. Med.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Netherlands

   

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[Title] Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital.

To characterize the biology and optimal therapy of acute mixed-lineage leukemia in children, we reviewed the pathologic and clinical features, including response to therapy, of 35 patients with mixed-lineage leukemia.

The majority of cases (91%) had blasts cells that simultaneously expressed either T-lineage plus myeloid markers (T/myeloid, n = 20) or B-lineage plus myeloid markers (B/myeloid, n = 12).

Overall survival rates for the B/myeloid and T/myeloid subgroups were not significantly different from each other or from the rate for acute myeloid leukemia (AML) but were inferior to the outcome in children with acute lymphoblastic leukemia (ALL).

Analysis of gene-expression patterns identified a subset of biphenotypic leukemias that did not cluster with T-cell ALL, B-progenitor ALL, or AML.

We propose that treatment for biphenotypic leukemia begin with one course of AML-type induction therapy, with a provision for a switch to lymphoid-type induction therapy with a glucocorticoid, vincristine, and L-asparaginase if the patient responds poorly.

We also suggest that hematopoietic stem cell transplantation is often not required for cure of these patients.

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[Cites] J Immunol Methods. 2000 Sep 21;243(1-2):59-75 [10986407.001]

[Cites] Leukemia. 2000 Dec;14(12):2286-94 [11187920.001]

[Cites] Nucleic Acids Res. 2002 Jan 1;30(1):207-10 [11752295.001]

[Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]

[Cites] J Clin Oncol. 2002 Oct 15;20(20):4217-24 [12377965.001]

[Cites] J Clin Oncol. 2003 Aug 15;21(16):3084-91 [12915598.001]

[Cites] Br J Haematol. 2003 Dec;123(5):842-9 [14632775.001]

[Cites] Cancer. 2003 Dec 15;98(12):2715-22 [14669294.001]

[Cites] Br J Haematol. 2004 Jun;125(6):814-5 [15180872.001]

[Cites] Br J Cancer. 1977 Jan;35(1):1-39 [831755.001]

[Cites] Blood. 1985 Nov;66(5):1115-23 [3931724.001]

[Cites] Blood. 1990 Jan 1;75(1):198-202 [2294988.001]

[Cites] Leukemia. 1990 Feb;4(2):121-6 [2137547.001]

[Cites] N Engl J Med. 1991 Mar 21;324(12):800-8 [1997852.001]

[Cites] Blood. 1991 Sep 1;78(5):1327-37 [1878594.001]

[Cites] J Clin Oncol. 1992 Sep;10(9):1419-29 [1517785.001]

[Cites] Leukemia. 1995 Oct;9(10):1783-6 [7564526.001]

[Cites] Blood. 1995 Oct 15;86(8):3097-108 [7579404.001]

[Cites] Leukemia. 1996 Aug;10(8):1283-7 [8709632.001]

[Cites] Haematologica. 1997 Jan-Feb;82(1):64-6 [9107085.001]

[Cites] Blood. 1997 Jul 1;90(1):28-35 [9207434.001]

[Cites] Br J Haematol. 1998 Jan;100(1):147-55 [9450804.001]

[Cites] Leukemia. 1998 Dec;12(12):2038 [9844938.001]

[Cites] J Clin Oncol. 1998 Dec;16(12):3768-73 [9850020.001]

[Cites] Haematologica. 1999 Aug;84(8):699-706 [10457405.001]

[Cites] Blood. 2004 Dec 1;104(12):3679-87 [15226186.001]

[Cites] Leukemia. 2005 Dec;19(12):2125-9 [16281077.001]

[Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]

[Cites] Bioinformatics. 2006 Aug 15;22(16):1979-87 [16777905.001]

[Cites] Br J Haematol. 2007 Jul;138(2):213-6 [17593028.001]

[Cites] Blood. 2007 Aug 15;110(4):1271-7 [17456722.001]

[Cites] Leukemia. 2007 Nov;21(11):2264-70 [17611554.001]

[CommentIn] Blood. 2009 May 21;113(21):5036 [19470432.001]

(PMID = 19131545.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA-21765

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Other-IDs] NLM/ PMC2686179

   

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We previously showed that S-adenosylmethionine (SAMe) and its metabolite methylthioadenosine (MTA) blocked lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNFalpha) expression in RAW (murine macrophage cell line) and Kupffer cells at the transcriptional level without affecting nuclear factor kappa B nuclear binding.

LPS increased the binding of histone methyltransferases Set1 and myeloid/lymphoid leukemia to these promoters, which was unaffected by SAMe or MTA.

Exogenous SAMe is unstable and converts spontaneously to MTA, which is stable and cell-permeant.

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[Cites] Annu Rev Med. 1994;45:491-503 [8198398.001]

[Cites] J Immunol. 1991 Sep 1;147(5):1694-700 [1715367.001]

[Cites] Immunology. 1996 Dec;89(4):558-62 [9014821.001]

[Cites] Biochem Biophys Res Commun. 1997 Jul 30;236(3):655-60 [9245708.001]

[Cites] Am J Physiol. 1999 May;276(5 Pt 1):G1069-73 [10329995.001]

[Cites] J Hepatol. 1999 Jun;30(6):1081-9 [10406187.001]

[Cites] Biochem J. 1999 Aug 15;342 ( Pt 1):21-5 [10432295.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8603-8 [15941828.001]

[Cites] J Biol Chem. 2005 Jul 1;280(26):24824-38 [15870070.001]

[Cites] J Biol Chem. 2006 Jun 23;281(25):17180-8 [16613853.001]

[Cites] Biochem J. 2007 Jan 1;401(1):87-96 [16953798.001]

[Cites] Cell. 2007 Mar 9;128(5):889-900 [17320163.001]

[Cites] Cell. 2007 Mar 23;128(6):1077-88 [17320160.001]

[Cites] Hepatology. 2007 May;45(5):1306-12 [17464973.001]

[Cites] Proc Natl Acad Sci U S A. 2007 Jun 26;104(26):10835-40 [17578910.001]

[Cites] Cell. 2007 Jul 13;130(1):77-88 [17632057.001]

[Cites] Gastroenterology. 2007 Jul;133(1):207-18 [17631143.001]

[Cites] Nature. 2001 Mar 1;410(6824):116-20 [11242053.001]

[Cites] Science. 2001 Aug 10;293(5532):1074-80 [11498575.001]

[Cites] Mol Cell Biol. 2001 Oct;21(20):7065-77 [11564889.001]

[Cites] J Hepatol. 2001 Dec;35(6):692-9 [11738094.001]

[Cites] Mol Cell. 2001 Dec;8(6):1207-17 [11779497.001]

[Cites] Am J Physiol Gastrointest Liver Physiol. 2002 Aug;283(2):G256-65 [12121871.001]

[Cites] J Clin Invest. 2002 Sep;110(5):643-50 [12208865.001]

[Cites] Nature. 2002 Sep 26;419(6905):407-11 [12353038.001]

[Cites] Mol Cell Biol. 2003 Jan;23(2):526-33 [12509451.001]

[Cites] Nat Neurosci. 2004 Mar;7(3):229-35 [14770186.001]

[Cites] Hepatology. 2004 Apr;39(4):1088-98 [15057913.001]

[Cites] Cell. 2004 Jun 11;117(6):721-33 [15186774.001]

[Cites] Am J Physiol Gastrointest Liver Physiol. 2004 Aug;287(2):G352-62 [15064230.001]

[Cites] J Virol. 2004 Nov;78(22):12308-19 [15507618.001]

[Cites] Biochem Biophys Res Commun. 1981 May 29;100(2):523-31 [6791639.001]

[Cites] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386.001]

[Cites] J Exp Med. 1990 Jan 1;171(1):35-47 [2104921.001]

[Cites] Mol Cell Biol. 1990 Apr;10(4):1498-506 [2181276.001]

[Cites] Cell. 1995 May 19;81(4):641-50 [7538909.001]

(PMID = 18393372.001).

[ISSN] 1527-3350

[Journal-full-title] Hepatology (Baltimore, Md.)

[ISO-abbreviation] Hepatology

[Language] ENG

[Grant] United States / NIAAA NIH HHS / AA / T32 AA007578; None / None / / R01 AT001576-05; United States / NCCIH NIH HHS / AT / R01 AT001576-05; United States / NIAAA NIH HHS / AA / AA007578-07; United States / NIAAA NIH HHS / AA / AA12677; United States / NIDDK NIH HHS / DK / R01 DK051719-11; United States / NCCIH NIH HHS / AT / R01 AT001576; United States / NIDDK NIH HHS / DK / DK048522-139003; United States / NIDDK NIH HHS / DK / R01 DK051719; United States / NIAAA NIH HHS / AA / T32 AA07578; United States / NCCIH NIH HHS / AT / AT1576; United States / NIAAA NIH HHS / AA / T32 AA007578-07; United States / NIDDK NIH HHS / DK / DK48522; United States / NIAAA NIH HHS / AA / R01 AA013847; United States / NIAAA NIH HHS / AA / R01 AA012677; United States / NIDDK NIH HHS / DK / DK051719-11; United States / NIAAA NIH HHS / AA / R01 AA012677-05; United States / NIDDK NIH HHS / DK / DK51719; United States / NIAAA NIH HHS / AA / R01 AA013847-05; United States / NIDDK NIH HHS / DK / P30 DK048522; United States / NIAAA NIH HHS / AA / AA13847; United States / NIDDK NIH HHS / DK / P30 DK048522-139003; United States / NIAAA NIH HHS / AA / AA012677-05; United States / NIAAA NIH HHS / AA / AA013847-05

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Chromatin; 0 / DNA Primers; 0 / Histones; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 63231-63-0 / RNA; 7LP2MPO46S / S-Adenosylmethionine

[Other-IDs] NLM/ NIHMS49821; NLM/ PMC2408693

   

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[Title] [Biphenotypic acute leukaemia with Burkitt-like cytology].

[Transliterated title] Leucémie aiguë biphénotypique avec aspect cytologique de type Burkitt.

Biphenotypic acute leukaemia (BAL) represents about 5% of adult acute leukaemia.

Based on a previously described scoring system, the European Group for Immunologic Classification of Leukaemia (EGIL) proposed a set of diagnostic criteria for BAL.

This scoring system is based on the number and degree of the specificity of several markers for myeloid or T/B lymphoid blasts.

Here, we report the case of a BAL with Burkitt-like cytology, corresponding to "the acute lymphoblastic leukaemia, Burkitt type" L3 for the FAB classification.

By flow cytometry, the blasts showed a positivity for B lymphoid cytoplasmic (CD79a and mu) and membrane (CD19, CD22, CD24, IgM) markers AND a positivity for the myeloid (CD13, CD33, CD65, CD15) markers.

[MeSH-major] Leukemia, Biphenotypic, Acute / genetics

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(PMID = 19654084.001).

[ISSN] 0003-3898

[Journal-full-title] Annales de biologie clinique

[ISO-abbreviation] Ann. Biol. Clin. (Paris)

[Language] fre

[Publication-type] English Abstract; Journal Article

[Publication-country] France

   

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[Title] [Therapeutic results in patients with biphenotypic acute leukemia at Sapporo Medical University Hospital].

We reviewed the results of 6 patients with biphenotypic acute leukemia (BAL) which the diagnostic standard of the European Group for the Immunological Characterization of Leukemia (EGIL) at Sapporo Medical University Hospital between 2006 and 2008.

Among them, 4 were B lymphoid and myeloid, 2 were T lymphoid and myeloid, and one was T/B lymphoid.

Two of 4 patients did not attain complete remission, and two relapsed after first treatment with acute myeloblastic leukemia (AML) protocol.

On the other hand, two showed complete remission after the acute lymphoblastic leukemia (ALL) protocol.

One of 4 patients survived who had been treated with hematopoietic stem cell transplantation as a post-remission therapy.

[MeSH-major] Leukemia, Biphenotypic, Acute / drug therapy

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(PMID = 20948276.001).

[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

   

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[Title] Mixed phenotype acute leukemia with t(11;19)(q23;p13.3)/ MLL-MLLT1(ENL), B/T-lymphoid type: A first case report.

The majority of cases of acute leukemia belong to a specific lineage origin, either lymphoid or myeloid, and therefore are classified as acute lymphoblastic leukemia (ALL) or acute myelogenous leukemia (AML), based on morphologic features and cytochemical and immunophenotypic profile of the blast cells.

A minority of acute leukemias however, show no clear evidence of differentiation along a single lineage.

These are now classified under acute leukemias of ambiguous lineage by the most recent WHO classification and account for <4% of all cases of acute leukemia [1].

They include leukemias with no lineage specific antigens (acute undifferentiated leukemias) and those with blasts that express antigens of more than one lineage to such degree that it is not possible to assign the leukemia to any one particular lineage with certainty (mixed phenotype acute leukemias).

The latter can either be leukemias with two distinct populations of blasts, each expressing antigens of a different lineage (historically referred to as "bilineal" leukemias) or a single blast population expressing antigens of multiple lineages (historically referred to as "biphenotypic" acute leukemias) [2].

Acute leukemias of ambiguous lineage may harbor a variety of genetic lesions.

Those with t(9;22)(q34;q11) or translocations associated with mixed lineage leukemias (MLL) gene, i.e., t(11;V)(q23;V), occur frequently enough and are associated with distinct features, that are considered as separate entities according to the recent WHO classification.

Co-expression of myeloid and B-lymphoid antigens is most common in mixed phenotype acute leukemia (MPAL), followed by co-expression of myeloid and T-lymphoid antigens, accounting for 66-70% and 23-24% of MLLs, respectively.

Coexpression of B- and T-lineage associated antigens or antigens of all three lineages is exceedingly rare, accounting for <5% of MLLs [3,4].

The requirements for assigning more than one lineage to a single blast population has been established by current WHO classification [1].

[MeSH-major] Antigens, Neoplasm / blood. Chromosomes, Human, Pair 11 / ultrastructure. Chromosomes, Human, Pair 19 / ultrastructure. Immunophenotyping. Leukemia / classification. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

[MeSH-minor] Acute Disease. Adult. Antigens, CD / analysis. Bone Marrow / pathology. Cell Lineage. Gene Rearrangement. Humans. In Situ Hybridization, Fluorescence. Male. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Transcription Factors / genetics

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(PMID = 20513125.001).

[ISSN] 1096-8652

[Journal-full-title] American journal of hematology

[ISO-abbreviation] Am. J. Hematol.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / MLL-ENL oncoprotein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein

   

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[Title] Non-specific interstitial pneumonia as the initial presentation of biphenotypic acute leukemia: a case report.

We present a 46-year-old woman with recent-onset rheumatologic illness who developed pulmonary symptoms as the presenting feature of biphenotypic acute leukaemia.

Corticosteroid therapy resulted in resolution of both her pulmonary and rheumatologic symptoms, and her pulmonary symptoms did not recur following treatment of her leukemia.

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[Cites] Leuk Lymphoma. 2002 Nov;43(11):2083-92 [12533032.001]

[Cites] J Am Acad Dermatol. 2001 Mar;44(3):530-1 [11209130.001]

[Cites] Am J Respir Crit Care Med. 2008 Jun 15;177(12):1338-47 [18388353.001]

[Cites] Crit Rev Oncol Hematol. 2007 Aug;63(2):100-10 [17391977.001]

[Cites] Intern Med. 2004 Aug;43(8):721-6 [15468974.001]

[Cites] Semin Respir Crit Care Med. 2006 Dec;27(6):652-8 [17195141.001]

[Cites] Respiration. 2005 Jan-Feb;72(1):39-45 [15753633.001]

[Cites] Haematologica. 1997 Jan-Feb;82(1):64-6 [9107085.001]

[Cites] Br J Haematol. 2007 Jul;138(2):213-6 [17593028.001]

(PMID = 19918465.001).

[ISSN] 1757-1626

[Journal-full-title] Cases journal

[ISO-abbreviation] Cases J

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2769415

   

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[Title] [Biphenotypic Acute Leukemia with BCR-ABL mRNA Transcript b3a2 Type: A Case Report with Review of the Literature.].

Biphenotypic acute leukemia (BAL) is a subtype of leukemia of ambiguous lineage in the World Health Organization classification system.

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(PMID = 18156734.001).

[ISSN] 1598-6535

[Journal-full-title] The Korean journal of laboratory medicine

[ISO-abbreviation] Korean J Lab Med

[Language] kor

[Publication-type] English Abstract; Journal Article

[Publication-country] Korea (South)

   

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[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.

The first patient (case 1) was diagnosed with T-cell ALL, and the second patient (case 2) was diagnosed with AML.

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.

The first patient (case 1) relapsed after double-unit cord blood transplantation; there was no evidence of relapse in the second patient (case 2) after allogenic peripheral blood stem cell transplantation.

Since CALM-AF10- positive leukemias have been shown to have poor prognosis with conventional therapy, molecular tests for CALM-AF10 rearrangement would be necessary to detect minimal residual disease during follow-up.

[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

[MeSH-minor] Adolescent. Adult. Bone Marrow / pathology. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 11. Cord Blood Stem Cell Transplantation. Female. Histone-Lysine N-Methyltransferase / genetics. Histone-Lysine N-Methyltransferase / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Male. Recurrence. Translocation, Genetic

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(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

   

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[Title] Immunophenotypic profile of acute leukemia: critical analysis and insights gained at a tertiary care center in India.

BACKGROUND: To analyze the spectrum of various types and subtypes of acute leukemia.

METHODS: Two thousand five hundred and eleven consecutive new referral cases of acute leukemia (AL) were evaluated based on WHO classification.

RESULTS: It included 1,471 cases (58%) of acute lymphoblastic leukemia (ALL), 964 cases (38%) of acute myeloid leukemia (AML), 45 cases (1.8%) of chronic myelogenous leukemia in blast crisis (CMLBC), 37 cases (1.5%) of biphenotypic acute leukemia (BAL), 1 case of Triphenotypic AL, and 2 cases of acute undifferentiated leukemia (AUL).

Common subtypes of ALL were B-cell ALL (76%), which comprised of intermediate stage/CALLA positive (73%), early precursor/proBALL (3%).

T-cell ALL constituted 24% (351 cases) of ALL.

CMLBC was commonly of myeloid blast crisis subtype (40 cases).

CONCLUSION: B-cell ALL was the commonest subtype in children and AML in adults.

CD13 was most sensitive and CD117 most specific for determining myeloid lineage.

A minimal primary panel of nine antibodies consisting of three myeloid markers (CD13, CD33, and CD117), B-cell lymphoid marker (CD19), T-cell marker (CD7), with CD45, CD10, CD34, and HLADR could assign lineage to 92% of AL.

Cytogenetics findings lead to a change in the diagnostic subtype of myeloid malignancy in 38 (1.5%) cases.

[MeSH-major] Immunophenotyping. Leukemia / immunology. Leukemia / pathology

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Cytogenetic Analysis. Female. Histocytochemistry. Humans. In Situ Hybridization. India. Infant. Infant, Newborn. Male. Middle Aged. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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[Copyright] (c) 2008 Clinical Cytometry Society.

(PMID = 18803279.001).

[ISSN] 1552-4957

[Journal-full-title] Cytometry. Part B, Clinical cytometry

[ISO-abbreviation] Cytometry B Clin Cytom

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Transforming human blood stem and progenitor cells: a new way forward in leukemia modeling.

MLL-AF9 (MA9) is a leukemia fusion gene formed upon translocation of the AF9 gene on chromosome 9 and the MLL gene on chromosome 11.

MA9 is commonly found in acute myeloid leukemia (AML) and occasionally in acute lymphoid leukemia and is associated with intermediate to poor outcome.

We have recently described a model system whereby we expressed the MA9 fusion gene in human CD34(+) Umbilical Cord Blood (UCB) cells and showed that these cells transformed to acute myeloid or lymphoid leukemia when injected into immunodeficient mice.

The Mixed Lineage Leukemia (MLL) oncogenes are unique in this model system in that they promote full transformation of primary human blood cells, while all other leukemia-associated oncogenes tested thus far have induced only partial phenotypes.

Here we provide an update on the use of this system for modeling human leukemia and its potential application for therapeutic testing of novel compounds to treat the disease.

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[Cites] Leukemia. 2002 Sep;16(9):1818-26 [12200698.001]

[Cites] Leukemia. 2008 Nov;22(11):2029-40 [18685615.001]

[Cites] Genes Dev. 2003 Dec 15;17(24):3029-35 [14701873.001]

[Cites] Proc Natl Acad Sci U S A. 2004 May 18;101(20):7618-23 [15128949.001]

[Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]

[Cites] EMBO J. 1994 Feb 15;13(4):928-33 [8112307.001]

[Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]

[Cites] Nature. 1999 Jul 29;400(6743):464-8 [10440377.001]

[Cites] Blood. 2006 Feb 1;107(3):1166-73 [16234360.001]

[Cites] Nature. 2006 Aug 17;442(7104):818-22 [16862118.001]

[Cites] Cancer Cell. 2006 Oct;10(4):257-68 [17045204.001]

[Cites] Science. 2007 Apr 27;316(5824):600-4 [17463288.001]

[Cites] Exp Hematol. 2007 May;35(5):782-92 [17577927.001]

[Cites] Exp Hematol. 2007 Oct;35(10):1538-49 [17889721.001]

[Cites] Cancer Cell. 2007 Nov;12(5):467-78 [17996650.001]

[Cites] Methods Enzymol. 2008;439:365-93 [18374178.001]

[Cites] Cancer Cell. 2008 May;13(5):432-40 [18455126.001]

[Cites] Leukemia. 2008 May;22(5):898-904 [18354486.001]

[Cites] Cancer Cell. 2008 Jun;13(6):483-95 [18538732.001]

[Cites] Leukemia. 2008 Sep;22(9):1803-6 [18668135.001]

[Cites] Leukemia. 2003 Apr;17(4):760-3 [12682634.001]

(PMID = 18948748.001).

[ISSN] 1551-4005

[Journal-full-title] Cell cycle (Georgetown, Tex.)

[ISO-abbreviation] Cell Cycle

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA118319; United States / NCI NIH HHS / CA / K01 CA090370; United States / NCRR NIH HHS / RR / M01 RR 08084; United States / NCRR NIH HHS / RR / M01 RR008084; United States / NCI NIH HHS / CA / CA118319-04; United States / NCI NIH HHS / CA / R01 CA118319-04; United States / NCI NIH HHS / CA / CA118319; United States / NCI NIH HHS / CA / CA90370

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / MLL-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.6.5.2 / rac GTP-Binding Proteins

[Other-IDs] NLM/ NIHMS169825; NLM/ PMC2812025

   

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[Title] Erythroid/B-cell biphenotypic acute leukemia first case report.

[MeSH-major] B-Lymphocytes / pathology. Erythroid Cells / pathology. Leukemia, Biphenotypic, Acute / pathology

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(PMID = 19458630.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD

   

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The MLL gene, located within band 11q23, has been shown to be involved in translocations with a large variety of reciprocal sites in both lymphoid and myeloid leukemia and has also been shown to undergo submicroscopic self-fusion/partial duplication.

The frequency and clinical correlations of MLL gene amplification in leukemia will need careful follow-up, since the frequently cryptic amplification described in these cases may not generally provoke confirmatory FISH studies.

A common cytogenetic profile of 5 q-, -17/17 p-, -18/18 q-, and a missing or abnormal chromosome 11, may help direct appropriate follow-up studies.

Both genes also show a high degree of diversity of pathogenic mechanisms of leukemia evolution, including numerous reciprocal fusion genes in transformation to either AML or ALL and gain of function amplification.

[MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins / genetics

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(PMID = 16026782.001).

[ISSN] 0014-4800

[Journal-full-title] Experimental and molecular pathology

[ISO-abbreviation] Exp. Mol. Pathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase

   

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[Title] [Study on the clinical characteristics of adult biphenotypic acute leukaemia].

OBJECTIVE: To analyze the clinical and biological characteristics and prognosis of adult biphenotypic acute leukaemia (BAL).

The chemotherapy regimens were accordingly for acute lymphoblastic leukaemia (ALL), acute myeloid leukaemia (AML) or for both ALL and AML.

(1) The incidence of BAL in acute leukaemias was 6.7%, with a male predominance and 52.3% of BAL patients had WBC > or = 30 x 10(9)/L and 16.9% WBC > or = 100 x 10(9)/L. (2) Percentages of coexpression of myeloid and B lymphoid antigens were 81.5%, of myeloid and T lymphoid antigens 10.8%, of myeloid, B- and T lymphoid antigens 4.6%, and of B and T lymphoid antigens 3.1%. (3) Normal and abnormal karyotypes accounted for 41.5% and 58.5%, respectively in 53 BAL patients with karyotype analysis.

(1) High white blood cell count and coexpression of myeloid/B lymphoid antigens are common in BAL. (2) Abnormal karyotypes and Ph (+) or bcr-abl( +) often happen. (3) The treatment outcome of BAL is poor.

[MeSH-major] Leukemia, Biphenotypic, Acute

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(PMID = 19563029.001).

[ISSN] 0253-2727

[Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi

[ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

   

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[Title] Leukemic infiltration of the lung following allogeneic hematopoietic stem cell transplantation.

Pulmonary leukemic infiltration (PLI) is more common than generally recognized, but accurate antemortem diagnosis with pathological proof is rarely achieved.

We describe herein the clinical courses of two patients with PLI following hematopoietic stem cell transplantation (HSCT).

One case is a male patient with acute biphenotypic leukemia, and the other is a female patient with myelodysplastic syndrome.

Moreover, the former case presented PLI as the initial manifestation of relapsed leukemia and the latter was accompanied with the fungal pneumonia.

High-resolution computed tomography (HRCT) of the chest at onset of PLI showed diffuse small nodular lesions along peribronchovascular bundle, and diagnosis of leukemic infiltration was made based on pathological findings obtained from transbronchial lung biopsy.

Thus, radiological and pathological corroborating assessment was important to reach the correct diagnosis.

[MeSH-major] Hematopoietic Stem Cell Transplantation / adverse effects. Leukemic Infiltration / diagnosis. Lung Neoplasms / etiology

[MeSH-minor] Adult. Female. Humans. Leukemia / pathology. Lung / pathology. Male. Middle Aged. Myelodysplastic Syndromes / diagnosis. Myelodysplastic Syndromes / etiology. Opportunistic Infections. Transplantation, Homologous

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[Cites] Br J Haematol. 1998 Mar;100(4):680-7 [9531334.001]

[Cites] Chest. 1990 Mar;97(3):674-8 [2407452.001]

[Cites] Br J Haematol. 2003 Mar;120(6):1058-61 [12648078.001]

[Cites] Bone Marrow Transplant. 1994;14 Suppl 4:S19-28 [7728120.001]

[Cites] AJR Am J Roentgenol. 2000 Feb;174(2):517-21 [10658733.001]

[Cites] Radiat Med. 2003 Jan-Feb;21(1):7-15 [12801138.001]

[Cites] Clin Chest Med. 1990 Jun;11(2):323-32 [2189666.001]

[Cites] Bone Marrow Transplant. 2001 Sep;28(5):425-34 [11593314.001]

[Cites] Eur Radiol. 2002 Jan;12 (1):166-74 [11868094.001]

[Cites] Semin Respir Crit Care Med. 2005 Oct;26(5):514-9 [16267702.001]

[Cites] Bone Marrow Transplant. 2000 Jun;25(12):1263-8 [10871731.001]

[Cites] Annu Rev Med. 1992;43:425-35 [1580600.001]

[Cites] Bone Marrow Transplant. 2007 Sep;40(5):465-72 [17618318.001]

[Cites] Chest. 1990 Nov;98(5):1233-9 [2225971.001]

[Cites] Chest. 1996 Apr;109(4):1066-77 [8635332.001]

(PMID = 19093164.001).

[ISSN] 1865-3774

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

   

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[Title] Clinical and biological characteristics of adult biphenotypic acute leukemia in comparison with that of acute myeloid leukemia and acute lymphoblastic leukemia: a case series of a Chinese population.

BACKGROUND: Biphenotypic acute leukemia is a rare disorder that is difficult to diagnose.

It displays features of both myeloid and lymphoid lineage.

There is still a lack of studies in biphenotypic acute leukemia in a Chinese population.

We present here a comprehensive investigation of the clinical and biological characteristics, and outcome of biphenotypic acute leukemia in our hospital in over a seven year period.

DESIGN AND METHODS: We retrospectively analyzed 452 adult acute leukemia patients diagnosed according to French-American-British (FAB) classification and biphenotypic acute leukemia diagnosed according to European Group for the Immunological Characterization of Leukemias (EGIL) classification, respectively.

Biological characteristics, response to treatment, and outcome were examined in biphenotypic acute leukemia patients and compared with that in acute myeloid leukemia and acute lymphoblastic leukemia patients with complete follow-up profiles diagnosed in the same period.

RESULTS: Of 452 acute leukemia patients, 21 cases (4.6%) were diagnosed as biphenotypic acute leukemia.

Among them, 14 (66.7%) were B lymphoid and myeloid, 5 (23.8%) were T lymphoid and myeloid, one (4.8%) was T/B lymphoid and one (4.8%) was trilineage differentiation.

When compared with acute myeloid leukemia and acute lymphoblastic leukemia, patients with biphenotypic acute leukemia showed significantly higher incidence of CD34 antigen expression, unfavorable karyotypes, and extramedullary infiltration (p<0.05).

In this cohort of patients with biphenotypic acute leukemia, t(9;22) was the most common abnormality in chromosome structure.

The median disease-free survival and overall survival in biphenotypic acute leukemia patients was five months and ten months, respectively, significantly shorter than those in acute myeloid leukemia and acute lymphoblastic leukemia patients (p<0.05).

CONCLUSIONS: The prognosis of biphenotypic acute leukemia patients is poor when compared with de novo acute myeloid leukemia or acute lymphoblastic leukemia.

Biphenotypic acute leukemia patients showed a much higher incidence of CD34 antigen expression, complex abnormal karyotype, extramedullary infiltration, relapse, and resistance to therapy after relapse.

[MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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[Cites] Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7521-6 [10861016.001]

[Cites] Zhonghua Xue Ye Xue Za Zhi. 2000 Jul;21(7):352-4 [11877003.001]

[Cites] Nature. 2008 Apr 10;452(7188):768-72 [18401412.001]

[Cites] Nat Rev Immunol. 2002 Feb;2(2):127-32 [11910894.001]

[Cites] Blood. 2002 Sep 15;100(6):1965-71 [12200353.001]

[Cites] Zhonghua Zhong Liu Za Zhi. 2002 Jul;24(4):375-7 [12408768.001]

[Cites] Ann Intern Med. 1985 Oct;103(4):620-5 [3862359.001]

[Cites] Blood. 1990 Aug 15;76(4):808-13 [2166608.001]

[Cites] Ann Hematol. 1991 Feb;62(1):16-21 [2031964.001]

[Cites] N Engl J Med. 1993 Sep 23;329(13):909-14 [8361504.001]

[Cites] Leukemia. 1995 Oct;9(10):1783-6 [7564526.001]

[Cites] Leukemia. 1996 Aug;10(8):1283-7 [8709632.001]

[Cites] Haematologica. 1997 Jan-Feb;82(1):64-6 [9107085.001]

[Cites] Blood. 1997 Oct 15;90(8):2863-92 [9376567.001]

[Cites] Br J Haematol. 1998 Jan;100(1):147-55 [9450804.001]

[Cites] Haematologica. 1999 Aug;84(8):699-706 [10457405.001]

[Cites] Am J Hematol. 2005 Mar;78(3):173-80 [15726601.001]

[Cites] Leukemia. 2006 Apr;20(4):620-6 [16437134.001]

[Cites] Br J Haematol. 2007 Jul;138(2):213-6 [17593028.001]

[Cites] Leukemia. 2007 Nov;21(11):2264-70 [17611554.001]

[Cites] Int J Hematol. 2008 Mar;87(2):132-6 [18288568.001]

[Cites] Leuk Lymphoma. 2008 Apr;49(4):700-9 [18398737.001]

[Cites] Nature. 2008 Apr 10;452(7188):764-7 [18401411.001]

[CommentIn] Haematologica. 2009 Dec;94(12):1778-80; author reply 1780 [19996120.001]

[CommentIn] Haematologica. 2009 Jul;94(7):891-3 [19570749.001]

(PMID = 19454497.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Italy

[Chemical-registry-number] 0 / Antigens, CD34

[Other-IDs] NLM/ PMC2704302

   

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[Title] [Clinical characteristics and outcomes of 59 patients with acute lymphoblastic leukemia positive for BCR/ABL].

OBJECTIVE: To study the clinical characteristics and outcomes of BCR/ABL-positive acute lymphoblastic leukemia (BCR/ABL360888725-ALL) and screen the prognostic factors for BCR/ABL360888725-ALL.

METHODS: From January 2001 to May 2008, 59 patients (median age of 32 years ranging from 3 to 69 years) with the diagnosis of BCR/ABL360888725-ALL by fluorescence in situ hybridization received induction chemotherapy with VDLP-/+Ara-C regimen.

The patients who failed to respond to the chemotherapy received subsequent consolidation chemotherapy with imatinib (400-800 mg/day) (17 cases) or allogeneic hematopoietic stem cell transplantation (allo-HSCT) (16 cases).

In patients with peripheral white blood cell (WBC) count <30=10(9)/L, 30-99.9(9)/L and > or =100(9)/L, the CR rates were 75.0% (18/24), 56.3% (9/15) and 26.3% (5/19) (P=0.006), and the overall survival probability of 2 years ( OSs of 2-yrs) was 24.7%, 22.5% and 21.1%, respectively (P=0.180).

According to the FAB classification, 56 cases were divided into L1, L2 and biphenotypic acute leukemia (BAL) subgroups, and their CR rates were 66.7% (6/9), 63.2% (24/38) and 22.2% (2/9) (P=0.029), with OSs of 2-yrs of 22.2%, 27.0% and 22.0%, respectively (P=0.623).

In terms of immunophenotype grouping by EGIL, the patients with ALL, myeloid antigen-positive ALL and BAL had CR rates of 61.1% (11/18), 60.6% (20/33) and 12.5% (1/8) (P=0.039), and the OSs of 2-yrs of 22.7%, 21.0% and 18.8%, respectively (P=0.643).

In 55 patients with known karyotype, the CR rates were 71.4%(5/7), 70.8% (17/24) and 37.5% (9/24) in normal, sole t(9;22) abnormality, t(9;22) with additional abnormalities groups (P=0.046), with the OSs of 2-yrs of 42.9%, 34.0% and 7.3%, respectively (P=0.000).

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Genes, abl / genetics. Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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(PMID = 19304540.001).

[ISSN] 1673-4254

[Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University

[ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

   

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Topoisomerase II (Topo II) inhibitors are cell cycle-specific DNA-damaging agents and often correlate with secondary leukemia with chromosomal translocations involving the mixed-lineage leukemia/myeloid lymphoid leukemia (MLL) gene on chromosome 11 band q23 (11q23).

[MeSH-major] Cell Cycle / physiology. Chromosome Aberrations / chemically induced. Etoposide / pharmacology. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic

[MeSH-minor] Bone Neoplasms. Cell Division. Cell Line. Cell Line, Tumor. Chromosome Banding. Chromosomes, Human, Pair 11. Cloning, Molecular. G2 Phase. Gene Expression Regulation. Gene Expression Regulation, Neoplastic. Histone-Lysine N-Methyltransferase. Humans. Osteosarcoma

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[Cites] Mutat Res. 2000 Mar 3;466(1):9-15 [10751720.001]

[Cites] J Biol Chem. 1996 Nov 15;271(46):29238-44 [8910583.001]

[Cites] Br J Haematol. 2000 Apr;109(1):13-23 [10848777.001]

[Cites] Leukemia. 2000 Jun;14(6):1014-7 [10865966.001]

[Cites] Blood. 2000 Jul 1;96(1):24-33 [10891426.001]

[Cites] Cancer Res. 2001 Mar 15;61(6):2542-6 [11289128.001]

[Cites] Med Pediatr Oncol. 2001 May;36(5):525-35 [11340607.001]

[Cites] Annu Rev Genet. 2001;35:673-745 [11700297.001]

[Cites] Carcinogenesis. 2002 Jan;23(1):19-24 [11756219.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Jan 22;99(2):925-30 [11805335.001]

[Cites] Mol Cell Biol. 2002 Feb;22(4):1049-59 [11809797.001]

[Cites] Blood. 2002 Mar 15;99(6):1909-12 [11877259.001]

[Cites] Genes Chromosomes Cancer. 2002 Apr;33(4):331-45 [11921269.001]

[Cites] Genes Chromosomes Cancer. 2002 Apr;33(4):395-400 [11921273.001]

[Cites] Lancet Oncol. 2002 Apr;3(4):235-43 [12067686.001]

[Cites] Nat Genet. 2002 Sep;32(1):185-90 [12195425.001]

[Cites] Nat Rev Cancer. 2003 Mar;3(3):155-68 [12612651.001]

[Cites] Blood. 2003 May 1;101(9):3622-7 [12511424.001]

[Cites] Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5057-62 [12679524.001]

[Cites] Curr Med Chem Anticancer Agents. 2003 Jul;3(4):271-90 [12769773.001]

[Cites] J Clin Oncol. 2003 Jun 1;21(11):2123-37 [12775738.001]

[Cites] Cancer Cell. 2003 May;3(5):449-58 [12781363.001]

[Cites] Cancer Causes Control. 1996 Nov;7(6):581-90 [8932918.001]

[Cites] Curr Opin Struct Biol. 1998 Feb;8(1):26-32 [9519293.001]

[Cites] Leukemia. 1998 Mar;12(3):346-52 [9529129.001]

[Cites] J Clin Oncol. 1999 Feb;17(2):569-77 [10080601.001]

[Cites] EMBO J. 1999 Jul 1;18(13):3564-74 [10393173.001]

[Cites] Oncologist. 1999;4(3):225-40 [10394590.001]

[Cites] Nature. 2004 Nov 18;432(7015):316-23 [15549093.001]

[Cites] Nature. 2004 Nov 18;432(7015):338-41 [15549096.001]

[Cites] Mol Cell. 2004 Dec 22;16(6):991-1002 [15610741.001]

[Cites] Mol Cell. 2004 Dec 22;16(6):1003-15 [15610742.001]

[Cites] N Engl J Med. 2005 Apr 14;352(15):1529-38 [15829534.001]

[Cites] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4790-5 [10758153.001]

[Cites] Cancer Cell. 2003 Aug;4(2):99-110 [12957285.001]

[Cites] Blood. 2004 Jan 1;103(1):283-90 [12969974.001]

[Cites] Science. 2004 Jan 2;303(5654):92-5 [14704429.001]

[Cites] Nat Genet. 2004 Apr;36(4):331-4 [15054488.001]

[Cites] Cancer Res. 1974 Aug;34(8):1788-93 [4210356.001]

[Cites] J Cell Biol. 1975 Sep;66(3):521-30 [1057547.001]

[Cites] J Biol Chem. 1984 Nov 10;259(21):13560-6 [6092381.001]

[Cites] Mol Cell Biol. 1987 Sep;7(9):3119-23 [2823120.001]

[Cites] Proc Natl Acad Sci U S A. 1988 Feb;85(4):1086-90 [2829215.001]

[Cites] N Engl J Med. 1989 Jul 20;321(3):136-42 [2787477.001]

[Cites] Cancer Res. 1993 Jul 1;53(13):2954-6 [8319201.001]

[Cites] Lancet. 1993 Oct 2;342(8875):819-20 [8104269.001]

[Cites] Blood. 1996 Mar 1;87(5):1912-22 [8634439.001]

[Cites] Blood. 1996 Apr 1;87(7):2649-58 [8639880.001]

[Cites] Cell. 1996 Jun 14;85(6):853-61 [8681380.001]

[ErratumIn] J Clin Invest. 2006 Aug;116(8):2306-7

(PMID = 16357944.001).

[ISSN] 0021-9738

[Journal-full-title] The Journal of clinical investigation

[ISO-abbreviation] J. Clin. Invest.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6PLQ3CP4P3 / Etoposide; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase

[Other-IDs] NLM/ PMC1312016