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[Title] Effect of clathrin assembly lymphoid myeloid leukemia protein depletion on clathrin coat formation.

The endocytic accessory clathrin assembly lymphoid myeloid leukemia protein (CALM) is the ubiquitously expressed homolog of the neuron-specific protein AP180 that has been implicated in the retrieval of synaptic vesicle.

[MeSH-minor] Cell Membrane / metabolism. Coated Pits, Cell-Membrane / ultrastructure. Endosomes / metabolism. HeLa Cells. Humans. RNA Interference. Transcription Factor AP-2 / metabolism. trans-Golgi Network / metabolism

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Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

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(PMID = 16262731.001).

[ISSN] 1398-9219

[Journal-full-title] Traffic (Copenhagen, Denmark)

[ISO-abbreviation] Traffic

[Language] eng

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

[Publication-country] Denmark

[Chemical-registry-number] 0 / Clathrin; 0 / Monomeric Clathrin Assembly Proteins; 0 / PICALM protein, human; 0 / Transcription Factor AP-2

   

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

[Title] [Major molecular response to imatinib in a patient with acute mixed lineage leukemia expressing a novel BCR/ABL transcript].

OBJECTIVE: To identify the novel BCR/ABL transcript in a patient with acute mixed lineage leukemia (AMLL), and to evaluate the imatinib treatment response by quantitatively monitoring the aberrant BCR/ABL.

Morphological analysis of the bone marrow showed the myeloid blast cells accounted for 66%, and immunophenotyping analysis showed 2 groups of aberrant blast cells: myeloid and B lineage.

Chemical therapy and bone marrow transplantation failed to control the disease, and a novel BCR/ABL transcript (GenBank: EF423615) was found by using several detection protocols.

[MeSH-major] Fusion Proteins, bcr-abl / genetics. Leukemia, Biphenotypic, Acute / drug therapy. Leukemia, Biphenotypic, Acute / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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(PMID = 19552835.001).

[ISSN] 0376-2491

[Journal-full-title] Zhonghua yi xue za zhi

[ISO-abbreviation] Zhonghua Yi Xue Za Zhi

[Language] chi

[Publication-type] Case Reports; 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; EC 2.7.10.2 / Fusion Proteins, bcr-abl

   

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

[Title] Detection of FLT3 gene and FLT3/ITD mutation by polymerase chain reaction-single-strand conformation polymorphism in patients with acute lymphoblastic leukemia.

OBJECTIVE: To analyze Fms-like tyrosine kinase 3 (FLT3) gene and FLT3 internal tandem duplication (ITD) mutation in acute lymphoblastic leukemia (ALL) patients of different immunological subtypes.

The positivity rate of FLT3 gene in pre-pre B-lineage ALL, pre-B-ALL, B-lineage ALL and T-lineage ALL cases were 93.3% (14/15), 77.8% (14/18), 41.7% (5/12) and 28.6% (4/14), respectively.

Two cases (3.2%) were found to have FLT3/ITD mutation, which were also positive for myeloid antigen expression and diagnosed as acute mixed-lineage leukemia, showing leukocytosis and high percentage of bone marrow blast cells with poor prognosis.

CONCLUSIONS: FLT3 gene can be detected in both B-and T-lineage ALL patients, but more frequently in the former.

In B-lineage ALL patients, FLT3 gene is more frequent in cases with undifferentiated than those with differentiated blast cells.

FLT3/ITD is rarely detected in ALL patients and FLT3/ITD mutation detection might be helpful to identify the genotypes and evaluate the prognosis of acute leukemia.

[MeSH-major] Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor Protein-Tyrosine Kinases / genetics. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics

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(PMID = 16234090.001).

[ISSN] 1000-2588

[Journal-full-title] Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA

[ISO-abbreviation] Di Yi Jun Yi Da Xue Xue Bao

[Language] eng

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

[Publication-country] China

[Chemical-registry-number] EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

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

[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

   

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

[Title] [Report of a case of hybrid acute leukemia with t (12; 22) and literature review].

OBJECTIVE: To report a hybrid acute leukemia (HAL) patient with t (12;.

Leukemia surface markers were detected by anti-biotin-biotin complex and monoclonal antibodies.

RESULTS: The clinical and hematological findings were compatible with the diagnosis of HAL.

Lymphoid and myeloid markers were positive on the leukemia cells.

22) translocation is a rare chromosome abnormality in leukemia.

This translocation as a cytogenetic marker for poor-prognosis in leukemia needs to be further studied.

[MeSH-major] Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 22 / genetics. Leukemia, Biphenotypic, Acute / genetics. Translocation, Genetic

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(PMID = 16875585.001).

[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] Case Reports; English Abstract; Journal Article; Review

[Publication-country] China

[Number-of-references] 20

   

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

[Title] Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL).

METHODS: Pts ≥ 21 years (yrs) with primary refractory or relapsed ALL, NYHA class < 3, and a cardiac ejection fraction ≥ 45% were eligible.

Twenty-one pts had pre-B ALL, 5 pts pre-T/T ALL, 1 pt mature B ALL, and 3 pts biphenotypic acute leukemias.

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(PMID = 27961382.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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

[Title] [Clinical characteristics and immunophenotypes of mixed-lineage acute leukemia].

The aim of study was to analyze the clinical, biological features, treatment outcome and prognosis of mixed-lineage acute leukemia (MAL).

48 MAL patients diagnosed according to European Group of International Leukemia (EGIL) scoring system were retrospectively analyzed and the analysis results were compared with that from 68 cases of AML and 61 cases of ALL.

The results showed that the incidence of MAL in acute leukemia was 9.6%.

The median of white blood cell count in MAL was significantly higher than that of non-mixed-lineage cases (AML and ALL) observed during the same period (P < 0.05).

Coexpression of myeloid and B lymphoid antigens in MAL patients was predominant, its rate was 70.9%.

The coexpression rate of T lymphoid and myeloid antigens was 20.8%, coexpression of B, T lymphoid and myeloid antigens was 8.3%.

In MAL Ph chromosome abnormality incidence was 25% and was significantly higher than that in AML group (0%) (P < 0.01), but was not statistical defference with that in ALL group (16.7%) (P > 0.05).

It is concluded that MAL is supposed to be originated from stem cells, coexpression of lymphoid/myeloid antigens is the major feature of MAL which accompanies many poor prognosis factors and lower CR rate.

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(PMID = 17605883.001).

[ISSN] 1009-2137

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

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

[Language] CHI

[Publication-type] English Abstract; Journal Article

[Publication-country] China

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

   

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

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

[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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(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

   

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

[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

   

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

[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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(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] China

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

   

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

[Title] B-Lymphoid and myeloid lineages biphenotypic acute leukemia with t(8;21)(q22;q22).

By analyzing the characteristics of morphology, immune phenotype, chromosome karyotype and clinical manifestations of six cases of B-lymphoid and myeloid lineages biphenotypic acute leukemia (BAL) with t(8;21)(q22;q22), a new subgroup of BAL was reported.

Immunophenotype revealed B-lymphoid and myeloid lineages positive, together with frequent and high expression of CD34 and CD33, and weak expression of HLA-DR.

Chemotherapy for myeloid and lymphoid leukemia simultaneously produced good response in the patients.

q22) might be a new subgroup of BAL, and it was suggested that the leukemia clone with t(8;21)(q22;q22) might have originated from an early phase of hematopoiesis, and AML1/ETO fusion gene might be related to differentiation of B lymphocyte.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Translocation, Genetic

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(PMID = 18288568.001).

[ISSN] 0925-5710

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD79; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / CD79A protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3

   

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

[Title] V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia.

Translocations of proto-oncogenes to the B-cell or T-cell antigen receptor loci in acute T- or B-cell leukemia and lymphoma have been, in most cases, accredited to V(D)J or switch recombination depending on the location of the breakpoint at the receptor locus.

[MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Recombination, Genetic. Translocation, Genetic. VDJ Recombinases / metabolism

[MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Cells, Cultured. DNA Breaks. DNA-Binding Proteins / genetics. Fibroblasts. Genes, T-Cell Receptor. Homeodomain Proteins / genetics. LIM Domain Proteins. Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / genetics. Metalloproteins / genetics. Mice. Receptors, Antigen, B-Cell / genetics. TCF Transcription Factors / genetics. Transcription Factor 7-Like 1 Protein

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(PMID = 19455608.001).

[ISSN] 1098-2264

[Journal-full-title] Genes, chromosomes & cancer

[ISO-abbreviation] Genes Chromosomes Cancer

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Receptors, Antigen, B-Cell; 0 / TCF Transcription Factors; 0 / Tcf7l1 protein, mouse; 0 / Tlx1 protein, mouse; 0 / Transcription Factor 7-Like 1 Protein; EC 2.7.10.2 / Lymphocyte Specific Protein Tyrosine Kinase p56(lck); EC 2.7.7.- / VDJ Recombinases

   

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

[Title] [Skin lesions and myelodysplastic syndrome as initial manifestations of biphenotypic acute leukemia].

The aim of this study was to investigate the clinical, pathological and biological features of biphenotypic acute leukemia.

The results showed that extramedullary skin lesions and myelodysplasia occurred before the onset of overt disease.

At the time of diagnosis, this case had more than 30% blasts in bone marrow with meningeal involvement.

Flow cytometry revealed the co-expression of myeloid antigens (cMPO, CD33 and CD117) and T-lymphoid antigens (cCD3, CD5, CD7, dual expression of CD4 and CD8).

All above-mentioned results led to the diagnosis of biphenotypic acute leukemia.

It is concluded that the biphenotypic acute leukemia is an uncommon type of leukemia which may be preceded by myelodysplastic syndrome and has aggressive clinical and biological behavior.

Immunophenotype, cytogenetics and molecular analysis can contribute to early diagnosis of BAL and evaluation of prognosis.

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(PMID = 17956670.001).

[ISSN] 1009-2137

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

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

[Language] CHI

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD43; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase

   

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

CONCLUSION: Pancreatic myeloid and lymphoid leukemia show single or multiple mass lesions of homogeneous low attenuation and poor contrast enhancement on CT that is radiographically indistinguishable from that of pancreatic lymphoma.

[MeSH-major] Biliary Tract Neoplasms / radiography. Leukemia / radiography. Pancreatic Neoplasms / radiography. Radiographic Image Enhancement / methods

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(PMID = 17515381.001).

[ISSN] 1546-3141

[Journal-full-title] AJR. American journal of roentgenology

[ISO-abbreviation] AJR Am J Roentgenol

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Contrast Media

   

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

To study the FLT3 gene expression and its internal tandem duplication in hematologic malignancies and its clinical significance, polymerase chain reaction (PCR) and DNA sequencing were used to detect the FLT3/ITD mutation in blast cells of bone marrow from 86 patients with hematologic malignancies, including 32 cases of acute myeoloid leukemia (AML), 18 cases of acute lymphoblastic leukemia (ALL), 2 cases of acute hybrid leukemia (AHL), 12 cases of myelodysplastic syndromes (MDS), 10 cases of chronic myelogenous leukemia (CML), 3 cases of non-Hodgkin's lymphoma (NHL) and 9 cases of multiple myeloma (MM).

FLT3/ITD was associated with a higher peripheral blood white cell count (p < 0.01), higher percentage of bone marrow blast cells (p < 0.01) and lower complete mission rate.

FLT3/ITD mutation is associated with higher peripheral blood white cell count, higher percentage of bone marrow blast cells and lower complete remission rate, FIT3/IID gene mutation may be used to predict prognosis of patients with AML.

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(PMID = 17708788.001).

[ISSN] 1009-2137

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

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

[Language] CHI

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

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

[Title] Aberrant cytokine signaling in leukemia.

Abnormalities of cytokine and growth factor signaling pathways are characteristic of all forms of leukemia: lymphoid and myeloid, acute and chronic.

In this review, our current knowledge of leukemic cell cytokine signaling will be summarized, and some speculations on the significance and implications of these insights will be advanced.

A better understanding of aberrant cytokine signaling in leukemia should provide additional targets for the rational therapy of these diseases.

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(PMID = 17934482.001).

[ISSN] 0950-9232

[Journal-full-title] Oncogene

[ISO-abbreviation] Oncogene

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA090576; United States / NCI NIH HHS / CA / R01 CA105043; United States / NCI NIH HHS / CA / CA090576; United States / NCI NIH HHS / CA / CA105043

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

[Publication-country] England

[Chemical-registry-number] 0 / Cytokines

[Number-of-references] 139

[Other-IDs] NLM/ NIHMS579951; NLM/ PMC4344827

   

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

MLL, involved in many chromosomal translocations associated with acute myeloid and lymphoid leukemia, has >50 known partner genes with which it is able to form in-frame fusions.

Characterizing important downstream target genes of MLL and of MLL fusion proteins may provide rational therapeutic strategies for the treatment of MLL-associated leukemia.

To this end, we developed inducible MLL-AF4 fusion cell lines in different backgrounds.

Overexpression of MLL-AF4 does not lead to increased proliferation in either cell line, but rather, cell growth was slowed compared with similar cell lines inducibly expressing truncated MLL.

We found that in the MLL-AF4-induced cell lines, the expression of the cyclin-dependent kinase inhibitor gene CDKN1B was dramatically changed at both the RNA and protein (p27kip1) levels.

Further, we confirmed CDKN1B promoter binding by ChIP in MLL-AF4 as well as in MLL-AF9 leukemia cell lines.

Our results suggest that CDKN1B is a downstream target of MLL and of MLL-AF4, and that, depending on the background cell type, MLL-AF4 inhibits or activates CDKN1B expression.

This finding may have implications in terms of leukemia stem cell resistance to chemotherapy in MLL-AF4 leukemias.

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(PMID = 16169901.001).

[ISSN] 0027-8424

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / CA104300; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / CA78438; United States / NCI NIH HHS / CA / R01 CA104300; United States / NCI NIH HHS / CA / CA81269

[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.

[Publication-country] United States

[Chemical-registry-number] 0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein

[Other-IDs] NLM/ PMC1236570

   

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

[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]

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(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

   

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

[Title] Clinicopathologic analysis of acute myeloid leukemia in a single institution: biphenotypic acute myeloid leukemia may not be an aggressive subtype.

BACKGROUND: Most acute leukemias are classified as lymphoid or myeloid lineages by standard microscopic morphology, cytochemistry and a panel of immunologic markers.

The World Health Organization classification of acute leukemia incorporates morphologic, cytogenetic, immunologic and clinical features to define the entities that are biologically homogeneous and that have clinical relevance.

The purpose of this study was to determine the clinicopathologic characteristics of acute myeloid leukemia (AML) in Taiwan.

The median age at onset of disease was 49 years (range, 2-78 years), which was younger in biphenotypic AML (23.5 years) and older in multilineage dysplasia-related AML (61 years).

There were 9 cases (13%) with recurrent cytogenetic abnormality, 7 (10%) multilineage dysplasia-related, 7 (10%) therapy-related, 39 (56%) not other categorized and 8 (11%) of ambiguous lineage.

The median survivals of therapyrelated, multilineage dysplasia-related and biphenotypic AML were 2 months, 9 months and 30.5 months, respectively.

Biphenotypic AML may not be an aggressive subtype.

[MeSH-major] Leukemia, Myeloid, Acute / pathology

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(PMID = 17631462.001).

[ISSN] 1726-4901

[Journal-full-title] Journal of the Chinese Medical Association : JCMA

[ISO-abbreviation] J Chin Med Assoc

[Language] eng

[Publication-type] Journal Article

[Publication-country] China (Republic : 1949- )

   

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

[Title] [Biologic features of 688 cases of childhood acute leukemia-a single centre retrospective study].

OBJECTIVE: To investigate the biologic features of childhood acute leukemia in the northern region of China through a small cohort study in a single center.

METHODS: The medical records of 688 children with acute leukemia (age< or =15 years) who were initially diagnosed at Blood Disease Hospital of Chinese Academy of Medical Sciences from October 2003 to June 2006 were retrospectively studied.

RESULTS: Four hundred children were diagnosed as acute lymphoblastic leukemia (ALL), with a peak incidence at ages of 1-4 years.

Two hundred and eighteen children were classified into B-cell ALL, and 34 into T-cell ALL.

E2A-PBX1 fusion gene was expressed in 3.9% of children with B-cell ALL.

Two hundred and twenty-two children were diagnosed as acute myeloid leukemia (AML), with a peak incidence at ages of 10-15 years.

Acute hybrid leukemia (AHL) was confirmed in 24 children (4.2%), with a median age of 9 years.

Seventy-four percent of the children with (AHL) had mainly CD13 and CD33 expression in myeloid antigen integral.

CONCLUSIONS: There are differences in the biologic features of childhood acute leukemia between the northern region of China and other regions and races, which suggests that there might be differences in the pathogenesis of childhood acute leukemia in different environmental exposures.

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

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(PMID = 19849934.001).

[ISSN] 1008-8830

[Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics

[ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi

[Language] chi

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

[Publication-country] China

   

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

[Title] Low turnover bone disease in Egyptian children with acute leukemia.

The aim of this work was to study bone turnover markers, calcium homeostasis and bone mineral density (BMD) in children with acute leukemia at diagnosis, after induction chemotherapy, and during maintenance therapy to delineate abnormalities present.

After evaluation of L2-L4 BMD using dual-energy X-ray absorptiometry in patients with acute myeloid and lymphoid leukemia at presentation and after treatment, the results were compared to 352 healthy age- and sex-matched Egyptian controls.

Osteopenia was observed at diagnosis and during treatment in patients with acute leukemia.

At diagnosis osteopenia was observed in 27 patients (62.8%): 10 (23.3%) had non severe osteopenia and 17 (39.5%) had severe osteopenia.

Parathyroid hormone (PTH) (pg/ml) levels demonstrated non significant differences between children with acute leukemia at different stages of therapy and controls, while, 25 (OH) D3 (ng/ml) was significantly lower in acute leukemia patients at different stages of therapy compared to controls (p<0.001).

Osteocalcin (ng/ml) is significantly lower in patients at different stages of the disease compared to controls (p<0.001) but there was no significant difference between patients at different stages of therapy.

Deoxy-pyridoline cross links showed non-significant difference between the different types of acute leukemia and with controls.

Osteopenia is a significant problem in children with acute leukemia at presentation and after chemotherapy.

Osteopenia in acute leukemia appears to be of the low turnover type (decreased osteoblastic activity and decreased bone mineralization).

[MeSH-major] Bone Density. Bone Diseases, Metabolic / blood. Bone Remodeling. Leukemia / blood

[MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Cholecalciferol / blood. Egypt. Humans. Infant. Male. Osteoblasts / metabolism. Osteocalcin / blood. Parathyroid Hormone / blood

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(PMID = 16085546.001).

[ISSN] 1024-5332

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

[ISO-abbreviation] Hematology

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Parathyroid Hormone; 104982-03-8 / Osteocalcin; 1C6V77QF41 / Cholecalciferol

   

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

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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(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

   

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

Hepatitis C virus (HCV) which is one of the endemic viral infections in Egypt is not only hepatotropic, but also a lymphotropic virus and has many extrahepatic manifestations as mixed cryoglobulinemia and non-Hodgkin's lymphoma.

We studied gene expression profile of 20 B-cell non-Hodgkin's lymphoma with HCV infection and 20 B-cell non-Hodgkin's lymphoma without HCV infection as a control group by c-DNA microarray.

Also, HCV was associated with overexpression of the genes related to myeloid/lymphoid leukemia and B lymphoma as MLLT3, BAL, influences the overexpression of transcription regulator genes as TATA box binding protein (TBP) and may influence the overexpression of some immunoglobulin genes as immunoglobulin superfamily containing leucine gene in B cells resulting in overproduction of immunoglobulins in B-lymphocyte disorders.

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(PMID = 23082489.001).

[ISSN] 1110-4902

[Journal-full-title] The Egyptian journal of immunology

[ISO-abbreviation] Egypt J Immunol

[Language] ENG

[Publication-type] Journal Article

[Publication-country] Egypt

[Chemical-registry-number] 0 / Immunoglobulins; 0 / MLLT3 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / PARP9 protein, human; 0 / TATA-Box Binding Protein; 0 / TBP protein, human; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / CASP4 protein, human; EC 3.4.22.- / Caspases, Initiator; EC 3.4.22.36 / Caspase 1

   

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

The chromosomal translocation t(4;11)(q21;q23) is the most frequent genetic aberration of the human MLL gene, resulting in high-risk acute lymphoblastic leukemia (ALL).

Recipients of AF4.MLL- or double-transduced LSPCs developed pro-B ALL, B/T biphenotypic acute leukemia, or mixed lineage leukemia.

Transplantation of MLL.AF4- or mock-transduced LSPCs did not result in disease development during an observation period of 13 months.

These findings indicate that the expression of the AF4.MLL fusion protein is capable of inducing acute lymphoblastic leukemia even in the absence of the MLL.AF4 fusion protein.

In view of recent findings, these results may imply that t(4;11) leukemia is based on 2 oncoproteins, providing an explanation for the very early onset of disease in humans.

[MeSH-major] Cell Transformation, Neoplastic / metabolism. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Leukemic. Myeloid-Lymphoid Leukemia Protein / metabolism. Nuclear Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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(PMID = 20194896.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Aff1 protein, mouse; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse

   

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

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

   

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

[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

   

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

[Title] Cryptic insertion into 11q23 of MLLT10 not involved in t(1;15;11;10)(p36;q11;q23;q24) in infant acute biphenotypic leukemia.

This report describes a case of infant acute biphenotypic leukemia with t(1;15;11;10)(p36;q11;q23;q24).

In real-time quantitative PCR with primers that recognized the DNA sequence of the two sites of fusion point, the minimal residual disease (MRD) levels changed in parallel with other clinical markers.

[MeSH-major] Leukemia, Biphenotypic, Acute / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics

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(PMID = 19380030.001).

[ISSN] 1873-4456

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / MLLT10 protein, human; 0 / Transcription Factors

   

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

[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

   

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

[Title] Identification and molecular characterization of recurrent genomic deletions on 7p12 in the IKZF1 gene in a large cohort of BCR-ABL1-positive acute lymphoblastic leukemia patients: on behalf of Gruppo Italiano Malattie Ematologiche dell'Adulto Acute Leukemia Working Party (GIMEMA AL WP).

The BCR-ABL1 fusion gene defines the subgroup of acute lymphoblastic leukemia (ALL) with the worst clinical prognosis.

The IKZF1 deletion also was identified in the progression of chronic myeloid leukemia to lymphoid blast crisis (66%) but never in myeloid blast crisis or chronic-phase chronic myeloid leukemia or in patients with acute myeloid leukemia.

[MeSH-major] Base Sequence / genetics. Chromosomes, Human, Pair 7 / genetics. Fusion Proteins, bcr-abl / genetics. Ikaros Transcription Factor / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Deletion

[MeSH-minor] Adolescent. Adult. Aged. Blast Crisis / genetics. Blast Crisis / metabolism. Cell Line, Tumor. Codon, Initiator / genetics. Codon, Initiator / metabolism. Cohort Studies. Exons / genetics. Female. Gene Expression Regulation, Leukemic / genetics. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Male. Microarray Analysis. Middle Aged. Polymorphism, Single Nucleotide

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[ErratumIn] Blood. 2010 Sep 23;116(12):2196

(PMID = 19589926.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Codon, Initiator; 0 / IKZF1 protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 2.7.10.2 / Fusion Proteins, bcr-abl

   

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

NF1 inactivation occurs in specific human cancers, including juvenile myelomonocytic leukemia, an aggressive myeloproliferative disorder of childhood.

However, evidence suggests that Nf1 loss alone does not cause leukemia.

We therefore hypothesized that inactivation of the Nf1 tumor suppressor gene requires cooperating mutations to cause acute leukemia.

One of these genes, Bcl11a, confers a growth advantage in cultured Nf1 mutant hematopoietic cells and causes early onset of leukemia of either myeloid or lymphoid lineage in mice when expressed in Nf1-deficient bone marrow.

Importantly, Bcl11a is expressed in human chronic myelomonocytic leukemia and juvenile myelomonocytic leukemia samples.

These findings suggest that deregulated Bcl11a cooperates with Nf1 in leukemogenesis, and a therapeutic strategy targeting the BCL11A pathway may prove beneficial in the treatment of leukemia.

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(PMID = 18948576.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / CA84221

[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 / BCL11A protein, human; 0 / Bcl11a protein, mouse; 0 / CDKN1A protein, human; 0 / Carrier Proteins; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Neurofibromin 1; 0 / Nuclear Proteins

[Other-IDs] NLM/ PMC2635073

   

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

[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

   

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

Proteolysis of alpha- and beta2-adaptins, as well as the accessory clathrin adaptors epsin 1, adaptor protein 180, and the clathrin assembly lymphoid myeloid leukemia protein, was detected in brain tissues after experimentally induced ischemia and in cases of human Alzheimer disease.

[MeSH-major] Adaptor Protein Complex alpha Subunits / metabolism. Adaptor Protein Complex beta Subunits / metabolism. Alzheimer Disease / metabolism. Brain / metabolism. Calpain / metabolism. Clathrin / metabolism. Endocytosis. Neurons / metabolism

[MeSH-minor] Adaptor Proteins, Vesicular Transport. Animals. Brain Ischemia / genetics. Brain Ischemia / metabolism. Brain Ischemia / pathology. Calcium / metabolism. Cell Line. Cell Membrane / genetics. Cell Membrane / metabolism. Cell Membrane / pathology. Female. Glutamic Acid / metabolism. Humans. Hydrolysis. Male. Membrane Lipids / genetics. Membrane Lipids / metabolism. Monomeric Clathrin Assembly Proteins / genetics. Monomeric Clathrin Assembly Proteins / metabolism. Rats. Rats, Sprague-Dawley. Rats, Wistar

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(PMID = 19240038.001).

[ISSN] 0021-9258

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Protein Complex alpha Subunits; 0 / Adaptor Protein Complex beta Subunits; 0 / Adaptor Proteins, Vesicular Transport; 0 / Clathrin; 0 / Membrane Lipids; 0 / Monomeric Clathrin Assembly Proteins; 0 / PICALM protein, human; 0 / Picalm protein, rat; 0 / epsin; 3KX376GY7L / Glutamic Acid; EC 3.4.22.- / Calpain; SY7Q814VUP / Calcium

[Other-IDs] NLM/ PMC2673311

   

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

[Title] Risk of leukemia and multiple myeloma associated with exposure to benzene and other organic solvents: evidence from the Italian Multicenter Case-control study.

BACKGROUND: While there is a general consensus about the ability of benzene to induce acute myeloid leukemia (AML), its effects on chronic lymphoid leukemia and multiple myeloma (MM) are still under debate.

We conducted a population-based case-control study to evaluate the association between exposure to organic solvents and risk of myeloid and lymphoid leukemia and MM.

METHODS: Five hundred eighty-six cases of leukemia (and 1,278 population controls), 263 cases of MM (and 1,100 population controls) were collected.

There were elevated point estimates for the associations between medium/high benzene exposure and chronic lymphatic leukemia (OR = 1.8, 95% CI = 0.9-3.9) and MM (OR = 1.9, 95% CI = 0.9-3.9).

Risks of chronic lymphatic leukemia were somewhat elevated, albeit with wide confidence intervals, from medium/high exposure to xylene and toluene as well.

Our results support the association between benzene, xylene, and toluene and chronic lymphatic leukemia and between benzene and MM with longer latencies than have been observed for AML in other studies.

[MeSH-major] Benzene / adverse effects. Leukemia, Lymphoid / chemically induced. Multiple Myeloma / chemically induced. Occupational Exposure / adverse effects. Solvents / adverse effects

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[Copyright] Copyright 2008 Wiley-Liss, Inc.

(PMID = 18651579.001).

[ISSN] 1097-0274

[Journal-full-title] American journal of industrial medicine

[ISO-abbreviation] Am. J. Ind. Med.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA51086

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

[Publication-country] United States

[Chemical-registry-number] 0 / Solvents; 0 / Xylenes; 3FPU23BG52 / Toluene; J64922108F / Benzene

   

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

Melarsoprol, a water-insoluble drug, is mainly used in the treatment of trypanosomiasis and has demonstrated an in vitro activity on myeloid and lymphoid leukemia derived cell lines.

However, the cytotoxic properties of melarsoprol on K562 and U937 human leukemia cell lines was not modified by complexation.

[MeSH-minor] Cell Line, Tumor. Cell Survival / drug effects. Drug Compounding. Drug Stability. Humans. Kinetics. Magnetic Resonance Spectroscopy. Molecular Structure. Solubility

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(PMID = 16253447.001).

[ISSN] 0378-5173

[Journal-full-title] International journal of pharmaceutics

[ISO-abbreviation] Int J Pharm

[Language] eng

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

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclodextrins; ZF3786Q2E8 / Melarsoprol

   

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

[Title] [Biphenotypic and bilineal acute leukemias].

Human acute leukemias (AL) are classified as myeloid or lymphoid according to cytomorphology and the expression of leukocyte differentiation antigens/CD-markers.

However, in the minority of cases leukemic cells express markers of more than one lineage, which has led to the introduction of a new subgroup of acute leukemias termed mixed or biphenotypic acute leukemias (BAL).

In an effort to distinguish between BAL and those AL with aberrant expression of markers of other lineage, the European Group for the Immunological Characterization of Acute Leukemias (EGIL) has proposed a scoring system in which CD-markers are assigned a score of 0.5, 1.0 or 2.0, depending on the specificity of a particular antigen for myeloid, B- and/or T-lymphoid lineage, respectively.

The new WHO classification of hematologic tumors has adopted the EGIL criteria for BAL and introduced a new group of AL termed 'AL of ambiguous lineage'.

In addition to BAL in which a single cell population expresses both myeloid and lymphoid differentiation markers, this new group of leukemias also comprises cases that present with two separate blast populations (acute bilineal leukemia, aBLL).

In general, BAL accounts for less than 5% of all AL cases, whereas aBLL is a rare disease constituting 1%-2% of AL cases that contains B- or T-lymphoid along with myeloid blasts.

Chromosome abnormalities are frequent in both entities with a relatively high incidence of Philadelphia chromosome and rearrangements involving 11q23, especially in cases with B- and myeloid involvement.

Unfortunately, optimal therapy is not known, although regimens designed for acute lymphoblastic leukemia may result in a better response rate.

[MeSH-major] Leukemia, Biphenotypic, Acute

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(PMID = 19209464.001).

[ISSN] 1330-0164

[Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti

[ISO-abbreviation] Acta Med Croatica

[Language] hrv

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Croatia

[Number-of-references] 30

   

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

A 46-year-old male with refractory biphenotypic acute leukemia was treated with doxorubicin (days 1-3, 15-17), vincristine (days 1, 8, 15, 22), prednisolone (days 1-28), and L-asparaginase (L-ASP: days 15-28) as reinduction therapy.

[MeSH-major] Asparaginase / adverse effects. Brain / pathology. Brain Diseases / chemically induced. Brain Diseases / diagnosis

[MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Doxorubicin / administration & dosage. Humans. Hypertension / chemically induced. Leukemia / drug therapy. Male. Middle Aged. Prednisolone / administration & dosage. Seizures / chemically induced. Vincristine / administration & dosage

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(PMID = 16862982.001).

[ISSN] 0485-1439

[Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology

[ISO-abbreviation] Rinsho Ketsueki

[Language] jpn

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 9PHQ9Y1OLM / Prednisolone; EC 3.5.1.1 / Asparaginase

   

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

[Title] Clinico-hematological profile in biphenotypic acute leukemia.

BACKGROUND: We present a clinico-hematological profile and treatment outcome of Biphenotypic Acute Leukemia (BAL).

MATERIAL AND METHODS: Diagnosis was based on WHO classification, including clinical details, morphology, cytochemistry, immunophenotyping, and molecular genetics.

We included those cases, which fulfilled the European Group for the Immunological Characterization of Acute Leukemia's (EGIL's) scoring system criteria for the diagnosis of BAL, as per recommendation of the WHO classification.

B-Myeloid (14 cases) followed by T-Myeloid BAL (13 cases) were the commonest subtypes.

Polymorphous population of blasts (16 cases) was commonly associated with T-Myeloid BAL (10 cases).

BCR ABL fusion positivity was a common cytogenetic abnormality (seven cases).

CONCLUSIONS: Pediatric BAL and T-B lymphoid BAL have a better prognosis.

BCR-ABL expression is an important prognostic factor, as these cases will be labeled as Chronic myeloid leukemia (CML) in blast crisis with biphenotypic expression and treated accordingly.

[MeSH-major] Immunophenotyping. Leukemia, Biphenotypic, Acute / blood. Leukemia, Biphenotypic, Acute / diagnosis

[MeSH-minor] Adolescent. Adult. Case-Control Studies. Child. Child, Preschool. Disease Progression. Female. Hematologic Tests. Humans. Incidence. Male. Middle Aged. Phenotype. Retrospective Studies. Young Adult

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(PMID = 19346652.001).

[ISSN] 0019-509X

[Journal-full-title] Indian journal of cancer

[ISO-abbreviation] Indian J Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] India

   

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

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

   

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

[Title] Safety of imatinib in chronic myeloid leukemia in blastic crisis presenting as cholestatic jaundice.

Acute leukemia presenting as cholestatic jaundice is rare.

It can occur due to granulocytic sarcoma compressing the bile ducts in case of acute myeloid leukemia.

We report a case of chronic myeloid leukemia in lymphoid blast cell crisis presenting with severe cholestatic jaundice due to diffuse infiltration of the liver sinusoids with lymphoblasts.

[MeSH-major] Antineoplastic Agents / administration & dosage. Blast Crisis / drug therapy. Jaundice, Obstructive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Liver Neoplasms / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage

[MeSH-minor] Adult. Benzamides. Diagnosis, Differential. Drug-Related Side Effects and Adverse Reactions. Humans. Imatinib Mesylate. Male

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[Copyright] 2007 S. Karger AG, Basel

(PMID = 17804901.001).

[ISSN] 1421-9662

[Journal-full-title] Acta haematologica

[ISO-abbreviation] Acta Haematol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Switzerland

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

   

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

We have analyzed gene expression data from three different kinds of samples: normal human tissues, human cancer cell lines, and leukemic cells from lymphoid and myeloid leukemia pediatric patients.

Analysis of the expression levels of these two groups of genes in the human cancer cell lines and leukemias identified genes that were highly expressed in cancer cells but not in their normal counterparts and, thus, were overexpressed in the cancers.

The different cancer cell lines and leukemias varied in the number and identity of these overexpressed genes.

[MeSH-minor] Adenocarcinoma / genetics. Cell Line. Cell Line, Tumor. Health. Humans. Leukemia / classification. Leukemia / genetics. Multigene Family / genetics

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(PMID = 16339305.001).

[ISSN] 0027-8424

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] eng

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

[Publication-country] United States

[Other-IDs] NLM/ PMC1317977

   

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

[Title] Clofarabine for the treatment of acute lymphoblastic leukemia.

A marked improvement in the outcome of patients with acute lymphoblastic leukemia has been achieved with chemotherapeutic agents developed between the 1950s and 1970s.

As the limits of optimizing the use of old drugs are reached, most adults with acute lymphoblastic leukemia still succumb to their disease and leukemia remains the leading cause of nonaccidental death in children.

Clofarabine, a next-generation deoxyadenosine analog, has demonstrated significant activity in children and adults with refractory lymphoid and myeloid leukemia in early clinical trials and was granted approval for use in children with acute lymphoblastic leukemia in second or higher relapse.

[MeSH-major] Adenine Nucleotides / therapeutic use. Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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(PMID = 17288522.001).

[ISSN] 1744-8328

[Journal-full-title] Expert review of anticancer therapy

[ISO-abbreviation] Expert Rev Anticancer Ther

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 762RDY0Y2H / clofarabine

[Number-of-references] 36

   

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

[Title] Acute biphenotypic leukemia arising in a patient with essential thrombocythemia.

Acute leukemia is an uncommon complication of patients with essential thrombocythemia (ET).

We describe a patient with ET, who transformed to acute biphenotypic leukemia 4 and 1/2 years after initial ET diagnosis.

Acute biphenotypic leukemia was confirmed on bone marrow studies and immunophenotyping.

Complete remission (CR) was achieved with induction chemotherapy for acute leukemia.

To our knowledge, this is a rare event of acute biphenotypic leukemic transformation of a patient with ET.

[MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 20 / genetics. Leukemia / complications. Leukemia / genetics. Thrombocythemia, Essential / complications

[MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Cytogenetic Analysis. Female. Follow-Up Studies. Humans. Hydroxyurea / adverse effects. Hydroxyurea / therapeutic use. Middle Aged. Quinazolines / adverse effects. Quinazolines / therapeutic use. Remission Induction. Treatment Outcome

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(PMID = 16823822.001).

[ISSN] 0361-8609

[Journal-full-title] American journal of hematology

[ISO-abbreviation] Am. J. Hematol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Quinazolines; 0 / anagrelide; X6Q56QN5QC / Hydroxyurea

   

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

Cyclic-AMP response element binding protein (CREB) is a transcription factor that functions in glucose homeostasis, growth-factor- dependent cell survival, proliferation and memory.

Data from our laboratory shows that a 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.

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 one year.

Thus, CREB acts as a proto-oncogene 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-minor] Animals. Bone Marrow Cells / metabolism. Cell Line, Tumor. Cell Proliferation. Cell Survival. Cell Transformation, Neoplastic. Gene Expression Regulation, Neoplastic. Glucose / metabolism. Granulocyte-Macrophage Colony-Stimulating Factor / metabolism. Humans. Leukemia, Myeloid, Acute / metabolism. Mice. Mice, Transgenic. Neoplasms / metabolism. Phenotype. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proto-Oncogene Proteins / chemistry. Signal Transduction. Up-Regulation

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(PMID = 16096372.001).

[ISSN] 1551-4005

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

[ISO-abbreviation] Cell Cycle

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Cyclic AMP Response Element-Binding Protein; 0 / Proto-Oncogene Proteins; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; IY9XDZ35W2 / Glucose

[Number-of-references] 18

   

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

[Title] Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature.

The translocation t(10;11)(p13;q14q21) has been found to be recurrent in acute lymphoblastic and myeloid leukemias, and results in the fusion of the clathrin assembly lymphoid myeloid leukemia (CALM) gene with the AF10 gene; these genes are present on chromosomes 11 and 10, respectively.

Because the CALM-AF10 rearrangement is a rare chromosomal abnormality, it is not included in routine molecular tests for acute leukemia.

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

   

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

[Title] Withaferin A induces apoptosis by activating p38 mitogen-activated protein kinase signaling cascade in leukemic cells of lymphoid and myeloid origin through mitochondrial death cascade.

Here we demonstrate how WA exhibits a strong growth-inhibitory effect on several human leukemic cell lines and on primary cells from patients with lymphoblastic and myeloid leukemia in a dose-dependent manner, showing no toxicity on normal human lymphocytes and primitive hematopoietic progenitor cells.

WA-mediated decrease in cell viability was observed through apoptosis as demonstrated by externalization of phosphatidylserine, a time-dependent increase in Bax/Bcl-2 ratio; loss of mitochondrial transmembrane potential, cytochrome c release, caspases 9 and 3 activation; and accumulation of cells in sub-G0 region based on DNA fragmentation.

WA caused increased levels of Bax in response to MAPK signaling, which resulted in the initiation of mitochondrial death cascade, and therefore it holds promise as a new, alternative, inexpensive chemotherapeutic agent for the treatment of patients with leukemia of both lymphoid and myeloid origin.

[MeSH-major] Apoptosis / drug effects. Ergosterol / analogs & derivatives. Leukemia. MAP Kinase Signaling System / physiology. Mitochondria. Tumor Cells, Cultured / drug effects. p38 Mitogen-Activated Protein Kinases / metabolism

[MeSH-minor] Animals. Caspase Inhibitors. Caspases / metabolism. Cell Survival / drug effects. Dose-Response Relationship, Drug. Enzyme Activation. Humans. Medicine, Traditional. Membrane Potential, Mitochondrial / drug effects. Mice. Molecular Structure. Plants, Medicinal / chemistry. Poly(ADP-ribose) Polymerases / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Withanolides. bcl-2-Associated X Protein / metabolism

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(PMID = 18987975.001).

[ISSN] 1573-675X

[Journal-full-title] Apoptosis : an international journal on programmed cell death

[ISO-abbreviation] Apoptosis

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Caspase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Small Interfering; 0 / Withanolides; 0 / bcl-2-Associated X Protein; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspases; L6DO3QW4K5 / withaferin A; Z30RAY509F / Ergosterol

   

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

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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[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

   

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

[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

Genetic Alliance. consumer health - Acute Biphenotypic Leukemia.

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.

Genetic Alliance. consumer health - Leukemia, Myeloid.

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[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

   

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

BACKGROUND: The RUNX1 transcription factor gene is frequently mutated in sporadic myeloid and lymphoid leukemia through translocation, point mutation or amplification.

It is also responsible for a familial platelet disorder with predisposition to acute myeloid leukemia (FPD-AML).

The disruption of the largely unknown biological pathways controlled by RUNX1 is likely to be responsible for the development of leukemia.

We have used multiple microarray platforms and bioinformatic techniques to help identify these biological pathways to aid in the understanding of why RUNX1 mutations lead to leukemia.

1) cell lines with RUNX1 mutations from FPD-AML patients, 2) over-expression of RUNX1 and CBFbeta, and 3) Runx1 knockout mouse embryos using either cDNA or Affymetrix microarrays.

A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous RUNX1 point mutations in patients with FPD-AML impair cell proliferation, microtubule dynamics and possibly genetic stability.

CONCLUSION: This work is the first large-scale study attempting to identify the genetic networks regulated by RUNX1, a master regulator in the development of the hematopoietic system and leukemia.

The biological pathways and target genes controlled by RUNX1 will have considerable importance in disease progression in both familial and sporadic leukemia as well as therapeutic implications.

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(PMID = 18671852.001).

[ISSN] 1471-2164

[Journal-full-title] BMC genomics

[ISO-abbreviation] BMC Genomics

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / R01 DK058161; United States / NHLBI NIH HHS / HL / R01 HL079507; United States / NIDDK NIH HHS / DK / DK58161; United States / NHLBI NIH HHS / HL / HL079507

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

[Publication-country] England

[Chemical-registry-number] 0 / CBFB protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / RUNX1 protein, human; 0 / Runx1 protein, mouse

[Other-IDs] NLM/ PMC2529319

   

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

[Title] Inactivation of HOXA genes by hypermethylation in myeloid and lymphoid malignancy is frequent and associated with poor prognosis.

We aimed to study the role of DNA methylation as an inducer of HOX gene silencing in leukemia.

EXPERIMENTAL DESIGN: Three hundred and seventy-eight samples of myeloid and lymphoid leukemia were quantitatively analyzed (by COBRA analysis and pyrosequencing of bisulfite-modified DNA) for methylation of eight HOXA and HOXB cluster genes.

The biological significance of the methylation identified was studied by expression analysis and through re-expression of HOXA5 in a chronic myeloid leukemia (CML) blast crisis cell line model.

RESULTS: Here, we identify frequent hypermethylation and gene inactivation of HOXA and HOXB cluster genes in leukemia.

In particular, hypermethylation of HOXA4 and HOXA5 was frequently observed (26-79%) in all types of leukemias studied.

HOXA6 hypermethylation was predominantly restricted to lymphoid malignancies, whereas hypermethylation of other HOXA and HOXB genes was only observed in childhood leukemia.

Furthermore, re-expression of HOXA5 in CML blast crisis cells resulted in the induction of markers of granulocytic differentiation.

CONCLUSION: We propose that in addition to the oncogenic role of some HOX family members, other HOX genes are frequent targets for gene inactivation and normally play suppressor roles in leukemia development.

[MeSH-major] DNA Methylation. Homeodomain Proteins / genetics. Leukemia / genetics

[MeSH-minor] Blast Crisis. CpG Islands. Humans. Leukemia, Lymphoid / genetics. Leukemia, Lymphoid / mortality. Leukemia, Lymphoid / pathology. Leukemia, Myeloid / genetics. Leukemia, Myeloid / mortality. Leukemia, Myeloid / pathology. Prognosis

MedlinePlus Health Information. consumer health - Leukemia.

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(PMID = 17785556.001).

[ISSN] 1078-0432

[Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research

[ISO-abbreviation] Clin. Cancer Res.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / HOXA5 protein, human; 0 / Homeodomain Proteins; 127609-92-1 / HOXA4 protein, human

   

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

[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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(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

   

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

We have found that domains containing the adapter complex 2 (AP2)-coated vesicle adapter and the endocytic accessory proteins CALM (clathrin assembly lymphoid myeloid leukemia protein), epsin, and eps15/eps15R (EGF receptor pathway substrate 15-related) nevertheless persist at the plasma membrane.

[MeSH-major] Cell Membrane / metabolism. Cell Surface Extensions / metabolism. Clathrin / metabolism

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(PMID = 16735469.001).

[ISSN] 0027-8424

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Protein Complex 2; 0 / Adaptor Proteins, Vesicular Transport; 0 / Clathrin; 0 / epsin

[Other-IDs] NLM/ PMC1482644