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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

   

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

BACKGROUND: Fusion of the MOZ and TIF2 genes by an inv (8) (p11q13) translocation has been identified in patients with acute mixed-lineage leukemia.

Stable expression of MOZ-TIF2 inhibited retinoic acid (RA) inducible endogenous CD11b and C/EBPbeta gene response.

[MeSH-minor] Acute Disease. Blotting, Western. Carrier Proteins / genetics. Carrier Proteins / metabolism. Corticosterone. Genes, Reporter. Humans. Leukemia, Myeloid / genetics. Receptors, Androgen / genetics. Receptors, Estrogen / genetics

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(PMID = 17697320.001).

[ISSN] 1476-4598

[Journal-full-title] Molecular cancer

[ISO-abbreviation] Mol. Cancer

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Carrier Proteins; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Androgen; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Estrogen; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human; W980KJ009P / Corticosterone

[Other-IDs] NLM/ PMC2048977

   

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

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

[Title] Prognosis of children with mixed phenotype acute leukemia treated on the basis of consistent immunophenotypic criteria.

BACKGROUND: Mixed phenotype acute leukemia (MPAL) represents a diagnostic and therapeutic dilemma.

The European Group for the Immunological Classification of Leukemias (EGIL) scoring system unambiguously defines MPAL expressing aberrant lineage markers.

DESIGN AND METHODS: Simple immunophenotypic criteria were used to classify all cases of childhood acute leukemia in order to provide therapy directed against acute lymphoblastic leukemia or acute myeloid leukemia.

Prognosis, genotype and immunoglobulin/T-cell receptor gene rearrangement status were analyzed.

RESULTS: The incidences of MPAL were 28/582 and 4/107 for children treated with acute lymphoblastic leukemia and acute myeloid leukemia regimens, respectively.

In immunophenotypic principal component analysis, MPAL treated as T-cell acute lymphoblastic leukemia clustered between cases of non-mixed T-cell acute lymphoblastic leukemia and acute myeloid leukemia, while other MPAL cases were included in the respective non-mixed B-cell progenitor acute lymphoblastic leukemia or acute myeloid leukemia clusters.

Analogously, immunoglobulin/T-cell receptor gene rearrangements followed the expected pattern in patients treated as having acute myeloid leukemia (non-rearranged, 4/4) or as having B-cell progenitor acute lymphoblastic leukemia (rearranged, 20/20), but were missing in 3/5 analyzed cases of MPAL treated as having T-cell acute lymphobastic leukemia.

In patients who received acute lymphoblastic leukemia treatment, the 5-year event-free survival of the MPAL cases was worse than that of the non-mixed cases (53+/-10% and 76+/-2% at 5 years, respectively, P=0.0075), with a more pronounced difference among B lineage cases.

The small numbers of MPAL cases treated as T-cell acute lymphoblastic leukemia or as acute myeloid leukemia hampered separate statistics.

CONCLUSIONS: Simple immunophenotypic criteria are useful for therapy decisions in MPAL.

In B lineage leukemia, MPAL confers poorer prognosis.

However, our data do not justify a preferential use of current acute myeloid leukemia-based therapy in MPAL.

[MeSH-major] Immunophenotyping. Leukemia / diagnosis. Leukemia / therapy. Phenotype

[MeSH-minor] Adolescent. Child. Child, Preschool. Diagnosis, Differential. Follow-Up Studies. Humans. Infant. Infant, Newborn. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Prognosis. Receptors, Antigen, T-Cell / immunology

MedlinePlus Health Information. consumer health - Childhood Leukemia.

MedlinePlus Health Information. consumer health - Leukemia.

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(PMID = 20145275.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

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

[Publication-country] Italy

[Chemical-registry-number] 0 / Receptors, Antigen, T-Cell

[Other-IDs] NLM/ PMC2878790

   

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

[Title] Acute mixed lineage leukemia and a t(6;14)(q25;q32) in two adults.

Acute mixed lineage leukemia (AMLL) is a rare form of leukemia in which both myeloid and lymphoid markers are present.

Few chromosome abnormalities have been identified associated with this form of leukemia.

A translocation involving the long arms of chromosomes 6 and 14 was previously described in four young individuals with acute leukemia and in three of these cases the diagnosis was mixed lineage.

[MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 6. Leukemia, Biphenotypic, Acute / genetics. Translocation, Genetic

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(PMID = 18656690.001).

[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

   

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

[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

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

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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

   

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

[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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(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

   

[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] [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] 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] Therapy-related, mixed phenotype acute leukemia with t(1;21)(p36;q22) and RUNX1 rearrangement.

We describe here a new case of therapy-related acute leukemia with t(1;21)(p36;q22).

Immunophenotypic analyses revealed that blasts were positive for CD19, CD79a, and cytCD22, as well as MPO, CD13, and CD33, fulfilling the diagnostic criteria of mixed phenotype acute leukemia, B/myeloid.

The patient died of disease progression after 10 months.

Thus, acute leukemia with t(1;21) and RUNX1 rearrangement could be associated with B/myeloid mixed phenotype as well as previous topoisomerase II inhibitor therapy and poor prognoses.

[MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics

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[Copyright] 2010 Elsevier Inc. All rights reserved.

(PMID = 20682397.001).

[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 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human

   

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

[Title] [Successful treatment with clarithromycin for Mixed phenotype acute leukemia, T/myeloid, NOS].

The diagnosis was Mixed phenotype acute leukemia, T/myeloid, NOS.

This clinical course suggests CAM is effective for this leukemia.

[MeSH-major] Anti-Bacterial Agents / administration & dosage. Clarithromycin / administration & dosage. Leukemia / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

[MeSH-minor] Acute Disease. Aged. Drug Synergism. Drug Therapy, Combination. Female. Humans. Pneumonia, Bacterial / complications. Pneumonia, Bacterial / drug therapy. Prednisolone / administration & dosage

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(PMID = 20467229.001).

[ISSN] 0485-1439

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

[ISO-abbreviation] Rinsho Ketsueki

[Language] jpn

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

[Publication-country] Japan

[Chemical-registry-number] 0 / Anti-Bacterial Agents; 9PHQ9Y1OLM / Prednisolone; H1250JIK0A / Clarithromycin

   

[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] [Successful selection of chemotherapy based on cell surface antigens in a patient with mixed phenotype acute leukemia].

The patient was diagnosed as having mixed phenotype acute leukemia, T/myeloid, NOS, according to the WHO classification.

After initial treatment, residual leukemic cells with CD13, CD33 and MPO were detected by FCM; therefore, he received re-induction chemotherapy for AML, and achieved CR.

Acute leukemia of ambiguous lineage is a relatively rare subtype in acute leukemia and standard chemotherapy has not been established.

[MeSH-major] Antigens, Surface. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia / drug therapy. Leukemia / immunology

[MeSH-minor] Acute Disease. Cyclophosphamide. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Humans. Male. Middle Aged. Prednisolone / administration & dosage. Treatment Outcome. Vincristine / administration & dosage

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(PMID = 20534955.001).

[ISSN] 0485-1439

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

[ISO-abbreviation] Rinsho Ketsueki

[Language] jpn

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

[Publication-country] Japan

[Chemical-registry-number] 0 / Antigens, Surface; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; ZS7284E0ZP / Daunorubicin

   

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

[Title] [A study of mixed phenotype acute leukemia based on the 2008 World Health Organization classification].

BACKGROUND: We evaluated the clinical significance of revised 2008 WHO classification needed to diagnose mixed phenotype acute leukemia (MPAL).

METHODS: A total of 22 MPAL patients, previously diagnosed by applying the scoring system of the European Group for Immunological Classification of Acute Leukemias (EGIL) were reclassified based on the 2008 WHO classification.

RESULTS: In 2008 WHO classification, the number of monoclonal antibodies (mAbs) required for assigning more than one lineage was markedly decreased, from 26 to 11, compared with that of EGIL.

Seventeen of the 22 MPAL patients were reclassified as MPAL with following details: 6 MPAL with t(9;22)(q34;q11.2); BCR-ABL1, 1 MPAL with t(v;11q23); MLL rearranged, 7 MPAL, B/Myeloid, not otherwise specified (NOS) and 3 MPAL, T/Myeloid, NOS.

Five patients were excluded from MPAL in the revised classification: 4 cytoplasmic myeloperoxidase (cMPO)-negative and 1 CD19-negative.

One patient with cCD79a, CD20, CD38, cMPO and CD15, whose diagnosis was reclassified from MPAL to AML has survived during the study period.

CONCLUSIONS: Because of decreased number of mAbs needed, it is possible that acute leukemia panel is designed to include all mAbs required to diagnose MPAL according to 2008 WHO classification.

When diagnosing MPAL, it is critical to figure out positivity in either cMPO or CD19, and AML expressing more than 2 lymphoid antigens are considered as MPAL.

[MeSH-major] Leukemia / diagnosis

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antibodies, Monoclonal / immunology. Child. Chromosomes, Human. Female. Fusion Proteins, bcr-abl / metabolism. Humans. Infant. Male. Middle Aged. Phenotype. Philadelphia Chromosome. Survival Analysis. World Health Organization

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(PMID = 21157134.001).

[ISSN] 1598-6535

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

[ISO-abbreviation] Korean J Lab Med

[Language] kor

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

[Publication-country] Korea (South)

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 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] Mixed-phenotype acute leukemia relapse in the iris.

Mixed-phenotype acute leukemia is a rare condition with no previously reported intraocular involvement.

We present clinical, radiologic, and cytologic findings of leukemic intraocular relapse in a 23-month-old girl, with lineage switch presenting as conjunctivitis after allogeneic bone marrow transplantation.

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[Copyright] Copyright © 2010 American Association for Pediatric Ophthalmology and Strabismus. Published by Mosby, Inc. All rights reserved.

(PMID = 20863726.001).

[ISSN] 1528-3933

[Journal-full-title] Journal of AAPOS : the official publication of the American Association for Pediatric Ophthalmology and Strabismus

[ISO-abbreviation] J AAPOS

[Language] ENG

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / MLL-AF10 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein

   

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

[Title] Mixed-phenotype acute leukemia: historical overview and a new definition.

Acute leukemia with a mixed phenotype is a rare disease and comprises 2-5% of all acute leukemias.

These disorders have been known historically by a variety of names, such as mixed lineage leukemia, bilineal leukemia and biphenotypic leukemia, and the criteria for diagnosis have often been arbitrary.

The scoring criteria proposed by the European Group for the Immunological Characterization of Leukemias represented a major attempt to define this disorder.

However, the relative weight given to some markers and the lack of lineage specificity of most markers have raised questions regarding the significance of this approach.

In 2008, the World Health Organization classification of hematopoietic and lymphoid tumors proposed a simpler diagnostic algorithm, which relies on fewer and more lineage-specific markers to define mixed-phenotype acute leukemia (MPAL).

MPAL with t(9;22) and MLL rearrangement have been separated.

Several studies have suggested that patients with acute leukemia of mixed phenotype have a worse clinical outcome when compared with matched controls with acute myeloid leukemia or acute lymphoblastic leukemia.

Further studies are needed to confirm the significance of MPAL as currently defined, to determine a standardized treatment approach and to better understand the biological and clinical aspects of this disease.

[MeSH-major] Leukemia / genetics

[MeSH-minor] Acute Disease. Antigens, CD / analysis. Biomarkers, Tumor / analysis. Blast Crisis / pathology. Gene Rearrangement. Humans. Leukemia, B-Cell / classification. Leukemia, B-Cell / genetics. Leukemia, T-Cell / classification. Leukemia, T-Cell / genetics. Phenotype

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(PMID = 20844566.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

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

   

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

[Title] Infantile mixed phenotype acute leukemia (bilineal and biphenotypic) with t(10;11)(p12;q23);MLL-MLLT10.

We report a case of a 6-month-old boy with a mixed phenotype acute leukemia (MPAL), bilineal and biphenotypic immunophenotype (B-lymphoid lineage and combined B-lymphoid and monocytic lineage) with t(10;11)(p12;q23);MLL-MLLT10.

He was treated with acute myeloid leukemia protocol and in complete remission at 7-month follow-up.

To the best of our knowledge, this is the first reported MLL-MLLT10 rearranged case presenting as MPAL in an infant.

From a clinical practice standpoint, this case illustrates the importance of detection of MLL rearrangement due to its prognostic implication and the effectiveness of flow cytometry immunophenotyping in diagnosing MPAL and monitoring minimal residual disease.

[MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 11 / genetics. Leukemia, Biphenotypic, Acute / genetics. Leukemia, Monocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics

[MeSH-minor] Flow Cytometry. Gene Rearrangement. Humans. Immunophenotyping. Infant. Karyotyping. Male. Neoplasm, Residual / genetics. Neoplasm, Residual / pathology. Neoplasm, Residual / therapy. Phenotype. Prognosis. Remission Induction

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[Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.

(PMID = 20299091.001).

[ISSN] 1873-5835

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / MLL-AF10 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein

   

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

[Title] Clinical characteristics and outcome of children with biphenotypic acute leukemia.

BACKGROUND: Knowledge concerning the clinical and biological presentation, as well as the outcome of treatment, of biphenotypic acute leukemia in children is limited.

DESIGN AND METHODS: This retrospective review analyzes the clinical features and outcome of children with biphenotypic acute leukemia diagnosed and treated over an 8-year period.

According to the EGIL scoring system 24 (3.7%) of 633 patients with acute leukemia were classified as having biphenotypic acute leukemia.

The diagnostic work-up and results were reviewed specifically for this study in the light of the newly published WHO criteria for the diagnosis of leukemia of ambiguous lineage.

Based on these criteria, 11 (1.7%) patients were categorized according to the new nomenclature as having mixed phenotype acute leukemia.

The majority of the patients (58.3%) had a B-lymphoid/myeloid phenotype, followed by the T-lymphoid/myeloid phenotype.

The most frequent chromosomal abnormality involved the 14q32 locus.

Patients received therapy based on a treatment regimen for acute lymphocytic leukemia regimen, which included myeloid-effective agents.

The survival of those patients who underwent hematopoietic stem cell transplantation in first complete remission was not different from that of the patients who were treated with chemotherapy alone (overall survival: 70.1% versus 81.1%, respectively, p=0.39; event-free survival: 70.1% versus 76.2%, respectively, p=0.75).

The outcome of the 11 patients who were retrospectively classified as having mixed phenotype acute leukemia according to the new WHO criteria was excellent, with no relapses or deaths occurring among these patients.

CONCLUSIONS: An acute lymphocytic leukemia type of induction therapy, using agents that are active against lymphoid and myeloid leukemias, appears to be more effective in achieving and maintaining complete remissions regardless of whether the patients are classified according to EGIL criteria or the new WHO criteria.

Hematopoietic stem cell transplantation may not be necessary for all patients in first complete remission.

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

[MeSH-minor] Antigens, CD / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Flow Cytometry. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Outcome Assessment (Health Care) / methods. Remission Induction. Retrospective Studies

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(PMID = 19713227.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

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

[Other-IDs] NLM/ PMC2791935

   

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

[Title] PAX-5: a valuable immunohistochemical marker in the differential diagnosis of lymphoid neoplasms.

OBJECTIVE: Undifferentiated tumors and hematolymphoid neoplasms can be diagnostically challenging due to potential overlap of morphologic features and variant antigen expression.

PAX-5, a transcription factor expressed throughout B-cell maturation, is detected in most B-cell neoplasms including those that lack expression of mature B-cell markers, such as classical Hodgkin lymphoma (cHL), B-lymphoblastic leukemia and B-cell lymphomas following rituximab therapy.

The lack of PAX-5 expression in most CD30-positive non-hematopoietic malignancies (embryonal carcinoma and seminoma) and T-cell lymphomas, such as anaplastic large cell lymphoma (ALCL), suggests that the absence of PAX-5 may be used to confirm non-B-cell lineage.

DESIGN: Diagnostic lymph node, decalcified core bone marrow biopsies and tissue sections from 111 archived paraffin-embedded tissue blocks and a tissue lymphoma microarray were immunostained using a monoclonal antibody to PAX-5.

RESULTS: Nuclear PAX-5 immunoreactivity was detected in 88% (36/41) of Hodgkin lymphoma, all cases of diffuse large B-cell lymphoma (n=72), small B-cell lymphomas (n=5), B-lymphoblastic leukemia/lymphoma and mixed phenotype acute leukemia with B-cell lineage (n=5).

PAX-5 was not detected in ALCL (n=22), T-cell lymphoblastic leukemia/lymphoma, mixed phenotype acute leukemia with T-cell lineage (n=5), acute myeloid leukemia (n=4), carcinoid tumors with typical morphology (n=5), melanoma (n=3), and undifferentiated/metastatic tumors (n=8).

Non-neoplastic bone marrow sections showed scattered nuclear staining in small B-cell lymphocytes/hematogones.

CONCLUSION: Overall, our results demonstrate that including PAX-5 in a panel with other immunomarkers helps establish B-cell lineage and increases diagnostic yield.

[MeSH-major] B-Cell-Specific Activator Protein / analysis. Biomarkers, Tumor / analysis. Lymphoma / diagnosis

[MeSH-minor] Diagnosis, Differential. Hodgkin Disease / diagnosis. Humans. Immunohistochemistry. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis

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[Cites] Am J Surg Pathol. 2009 May;33(5):775-80 [19145202.001]

[Cites] J Clin Pathol. 2007 Jun;60(6):709-14 [16837628.001]

[Cites] Am J Surg Pathol. 2002 Oct;26(10):1343-50 [12360049.001]

(PMID = 20660931.001).

[ISSN] 1554-6179

[Journal-full-title] Clinical medicine & research

[ISO-abbreviation] Clin Med Res

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / PAX5 protein, human

[Other-IDs] NLM/ PMC2910102

   

[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

[MeSH-minor] Adolescent. Adult. Child. Female. Humans. Immunophenotyping. Male. Microscopy, Electron, Transmission. Middle Aged. Peroxidase / metabolism. Phenotype

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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.

A 52-year-old man was diagnosed with acute leukemia of mixed phenotype.

[MeSH-minor] Adult. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Humans. Interphase. Karyotyping. Leukemia / diagnosis. Leukemia / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Male. Metaphase. Middle Aged. Phenotype. Translocation, Genetic

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(PMID = 21157160.001).

[ISSN] 1598-6535

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

[ISO-abbreviation] Korean J Lab Med

[Language] kor

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

[Publication-country] Korea (South)

   

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

[Title] Discrepant immunophenotypic characteristics between the lymph node and bone marrow in two mixed-phenotype acute leukemia patients.

The immunophenotypic profile of hematological malignancies is usually consistent among different sites of involvement; this consistency allows reliable diagnosis from peripheral blood, bone marrow, or lymph node, especially in cases of acute leukemia.

Here, we report two Korean patients with acute leukemia where the results of immunophenotypic analysis of the bone marrow specimen were different from those of immunohistochemical studies of a biopsy sample of a cervical lymph node, particularly with respect to myeloperoxidase and CD3.

The clinical significance of the immunophenotypic disparity found in the patients still remains unknown; however, discrepancies between the different anatomic sites that are simultaneously involved can occur in a subset of leukemia patients.

Therefore, integration of all the relevant results, including those of the bone marrow studies, may be helpful for accurate diagnosis and selecting appropriate treatment modalities.

[MeSH-major] Bone Marrow / pathology. Immunophenotyping / methods. Leukemia / diagnosis. Lymph Nodes / pathology

[MeSH-minor] Acute Disease. Adolescent. Adult. Antigens, CD3 / metabolism. Female. Flow Cytometry. Humans. Male. Peroxidase / metabolism. Phenotype

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(PMID = 19893347.001).

[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

[Publication-country] Korea (South)

[Chemical-registry-number] 0 / Antigens, CD3; EC 1.11.1.7 / Peroxidase

   

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

The aim of this study was to assess the results of surgical treatment of multiple primary adenocarcinomas of the lung (MPAL) analyzing the radiological and histological features.

METHODS: From 1988 to 2005, 26 patients underwent surgical treatment for MPAL at our department, for a total of 52 tumors.

RESULTS: Thirty-seven tumors were classified as solid, two as ground-glass opacities (GGO) and 13 as mixed solid/GGO tumors on the basis of CT scan evaluation.

CONCLUSIONS: Surgical treatment of MPAL is associated with favorable results.

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(PMID = 19169994.001).

[ISSN] 0171-6425

[Journal-full-title] The Thoracic and cardiovascular surgeon

[ISO-abbreviation] Thorac Cardiovasc Surg

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

   

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

METHODS: One hundred thirty-four patients with congenital heart disease were randomly allocated to one of 3 groups according to the cardioplegia formula used: the high-potassium (HP) group (K(+), 20 mmol/L), 46 patients; the high-potassium adenosine-lidocaine (HPAL) group (K(+), 20 mmol/L; adenosine, 0.7 mmol/L; and lidocaine, 0.7 mmol/L), 44 patients; and the moderate-potassium adenosine-lidocaine (MPAL) group (K(+), 10 mmol/L; adenosine, 0.7 mmol/L; and lidocaine, 0.7 mmol/L), 44 patients.

RESULTS: At the end of cardiopulmonary bypass and modified ultrafiltration, the systolic and pulse pressures of the MPAL group were significantly increased compared with the respective values of the HP group.

At the time points of 1 to 12 hours after reperfusion, the levels of serum cardiac troponin I were significantly decreased in the MPAL group compared with those in the HP and HPAL groups.

CONCLUSIONS: The MPAL cardioplegia formula was associated with better myocardial protective effects.

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(PMID = 19114188.001).

[ISSN] 1097-685X

[Journal-full-title] The Journal of thoracic and cardiovascular surgery

[ISO-abbreviation] J. Thorac. Cardiovasc. Surg.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Cardioplegic Solutions; 0 / Cardiotonic Agents; 98PI200987 / Lidocaine; K72T3FS567 / Adenosine; RWP5GA015D / Potassium

   

[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] 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

[MeSH-minor] Adolescent. Adult. Aged, 80 and over. Antigens, Neoplasm / analysis. Biomarkers, Tumor / genetics. Biomarkers, Tumor / immunology. Child. Female. Humans. Immunophenotyping. Male. Middle Aged. Phenotype. Retrospective Studies. World Health Organization. Young Adult

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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

   

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

[Title] Molecular basis of the mixed lineage leukemia-menin interaction: implications for targeting mixed lineage leukemias.

Chromosomal translocations targeting the mixed lineage leukemia (MLL) gene result in MLL fusion proteins that are found in aggressive human acute leukemias.

Disruption of MLL by such translocations leads to overexpression of Hox genes, resulting in a blockage of hematopoietic differentiation that ultimately leads to leukemia.

Altogether, our work establishes the molecular basis of the menin interaction with MLL and MLL fusion proteins and provides the necessary foundation for development of small molecule inhibitors targeting this interaction in leukemias with MLL translocations.

[MeSH-major] Myeloid-Lymphoid Leukemia Protein / chemistry. Proto-Oncogene Proteins / chemistry

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(PMID = 20961854.001).

[ISSN] 1083-351X

[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 / MEN1 protein, human; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase

[Other-IDs] NLM/ PMC3003368

   

[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] 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] 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.

[Transliterated title] Porphyrie cutanée tardive chez un enfant greffé de moelle.

His past medical history revealed acute biphenotypic leukaemia with complete remission after allogeneic hematopoietic stem cell transplantation (unrelated donor).

Complications of bone marrow transplant comprised anaemia (treated by blood transfusions), primary cytomegalovirus (CMV) infection, pulmonary aspergillosis and acute digestive graft-versus-host disease.

The diagnosis of type I sporadic PCT was based on high levels of porphyria and normal erythrocytic uroporphyrinogen decarboxylase activity.

The causative role of bone marrow transplantation in the development of PCT could be related to several triggering factors: primary CMV infection, hepatotoxic drugs, blood transfusion and possible chronic hepatic graft-versus-host disease.

[MeSH-major] Bone Marrow Transplantation / adverse effects. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Biphenotypic, Acute / therapy. Porphyria Cutanea Tarda / diagnosis. Porphyria Cutanea Tarda / therapy

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[Copyright] Copyright © 2010 Elsevier Masson SAS. All rights reserved.

(PMID = 20932445.001).

[ISSN] 0151-9638

[Journal-full-title] Annales de dermatologie et de vénéréologie

[ISO-abbreviation] Ann Dermatol Venereol

[Language] fre

[Publication-type] Case Reports; 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] Constitutional pericentric inversion 9 in Korean patients with chronic myelogenous leukemia.

BACKGROUND: Although the pericentric inversion of chromosome 9, inv(9)(p11q13), is generally considered a normal variation, it is also associated with solid tumors and several hematologic malignancies such as biphenotypic acute leukemia, ALL, AML, and myeloproliferative neoplasms.

The purpose of this retrospective study was to investigate the frequency and clinical features of CML patients with concomitant inv(9) and t(9;22)(q34;q11.2) variation at our institution.

METHODS: We reviewed the bone marrow chromosome database entries between October 2006 and December 2008 to identify patients with concomitant inv(9) and t(9;22) variations.

RESULTS: Among the 51 CML patients, 4 (7.8%) had concomitant inv(9) and t(9;22) variations.

[MeSH-major] Asian Continental Ancestry Group / genetics. Chromosome Inversion. Chromosomes, Human, Pair 9. Leukemia, Myeloid, Acute / genetics

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(PMID = 20603579.001).

[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

[Publication-country] Korea (South)

   

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

[Title] Mixed lineage leukemia: a structure-function perspective of the MLL1 protein.

Several acute lymphoblastic and myelogenous leukemias are correlated with alterations in the human mixed lineage leukemia protein-1 (MLL1) gene.

Despite the important biological role of SET1 family enzymes and their involvement in human leukemias, relatively little is understood about how these enzymes work.

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(PMID = 20236310.001).

[ISSN] 1742-4658

[Journal-full-title] The FEBS journal

[ISO-abbreviation] FEBS J.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA140522-02; United States / NCI NIH HHS / CA / R01 CA140522; United States / NCI NIH HHS / CA / R01 CA140522-02; United States / NCI NIH HHS / CA / R01CA140522

[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 / Histones; 0 / Ligands; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; K3Z4F929H6 / Lysine

[Number-of-references] 61

[Other-IDs] NLM/ NIHMS209384; NLM/ PMC2892832

   

[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.

[Title] c-Myb binds MLL through menin in human leukemia cells and is an important driver of MLL-associated leukemogenesis.

Mixed-lineage leukemia (MLL) is a proto-oncogene frequently involved in chromosomal translocations associated with acute leukemia.

Recent data suggest that the MYB proto-oncogene, which is an important regulator of hematopoietic cell development, has a role in leukemogenesis driven by the MLL-ENL fusion protein, but exactly how is unclear.

Silencing MYB in human leukemic cell lines and primary patient material evoked a global decrease in H3K4 methylation, an unexpected decrease in HOXA9 and MEIS1 gene expression, and decreased MLL and menin occupancy in the HOXA9 gene locus.

The finding that c-Myb has the ability to direct epigenetic marks, along with its participation in an autoregulatory feedback loop with genes known to transform hematopoietic cells, lends mechanistic and translationally relevant insight into its role in MLL-associated leukemogenesis.

[MeSH-major] Leukemia / metabolism. Myeloid-Lymphoid Leukemia Protein / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-myb / metabolism

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(PMID = 20093773.001).

[ISSN] 1558-8238

[Journal-full-title] The Journal of clinical investigation

[ISO-abbreviation] J. Clin. Invest.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P01 CA072765; United States / NCI NIH HHS / CA / 2P01CA072765-11

[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 / DNA-Binding Proteins; 0 / Histones; 0 / Homeodomain Proteins; 0 / MEN1 protein, human; 0 / MLL protein, human; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myb; 0 / Recombinant Fusion Proteins; 0 / homeobox protein HOXA9; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase

[Other-IDs] NLM/ PMC2810070

   

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

[Title] Acute myelogenous leukemia cells with the MLL-ELL translocation convert morphologically and functionally into adherent myofibroblasts.

We show in this paper that non-adherent leukemia blasts can change into myofibroblasts.

When myeloblasts from two cases of acute myelogenous leukemia with a fusion product comprising mixed lineage leukemia and RNA polymerase II elongation factor, were cultured long term, their morphology changed to that of myofibroblasts with similar molecular characteristics to the parental myeloblasts.

The original leukemia blasts, when cultured on the leukemia blast-derived myofibroblasts, grew extensively.

Leukemia blasts can create their own microenvironment for proliferation.

[MeSH-major] Chromosomes, Human, Pair 11 / genetics. Fibroblasts / pathology. Leukemia, Myeloid, Acute / pathology. Myeloid-Lymphoid Leukemia Protein / genetics. Myoblasts / pathology. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

[MeSH-minor] Cell Adhesion. Cell Line, Tumor. Humans. Karyotyping

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

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[Copyright] Copyright 2009 Elsevier Inc. All rights reserved.

(PMID = 19932689.001).

[ISSN] 1090-2104

[Journal-full-title] Biochemical and biophysical research communications

[ISO-abbreviation] Biochem. Biophys. Res. Commun.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / MLL-ELL fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein

   

[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.

[Title] On the mechanism of multiple lysine methylation by the human mixed lineage leukemia protein-1 (MLL1) core complex.

The mixed lineage leukemia protein-1 (MLL1) is a member of the SET1 family of H3K4 methyltransferases and is frequently rearranged in acute leukemias.

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(PMID = 19556245.001).

[ISSN] 0021-9258

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

[ISO-abbreviation] J. Biol. Chem.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA140522

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

[Publication-country] United States

[Chemical-registry-number] 0 / ASH2L protein, human; 0 / DNA-Binding Proteins; 0 / DPY30 protein, human; 0 / Histones; 0 / MLL protein, human; 0 / Multiprotein Complexes; 0 / Nuclear Proteins; 0 / RBP5 protein, human; 0 / Retinol-Binding Proteins, Cellular; 0 / Transcription Factors; 0 / WDR5 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; K3Z4F929H6 / Lysine

[Other-IDs] NLM/ PMC2782018

   

[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] [Clinical study on prognosis of acute leukemia subtypes Ly + AML and My + ALL].

The purpose of this study was to investigate the prognosis of acute myelogenous leukemia (AML), acute lymphoblastic leukemia (ALL), lymphoid antigen-positive acute myeloid leukemia (Ly + AML), myeloid antigen-positive acute leukemia (My + ALL) and biphenotypic acute leukemia (BAL).

Immunophenotyping was performed on medullary specimens of 197 acute leukemia (AL) patients by using three-color flow cytometry analysis and CD45/SSC gating.

The results showed that in Ly + AML, CD7 was the most common (53.8%) as compared to other lymphoid markers, however, in My + ALL CD13 was the most common (47.2%) as compared to other myeloid markers.

It is concluded that since Ly + AML has lymphoid markers, and the prognosis of Ly + AML is worse than AML, the clinical therapy for Ly + AML should contain both AML and ALL.

Though My + ALL had myeloid markers, no significant difference was found between My + ALL and ALL, it might be supposed that their therapy could be the same.

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(PMID = 17493361.001).

[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; 0 / Antigens, CD7; EC 3.4.11.2 / Antigens, CD13

   

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

[Title] The role of HOX genes in malignant myeloid disease.

Recent studies indicate that a common characteristic of poor prognosis acute myeloid leukemia is dysregulated expression of a key group of these Hox proteins.

The purpose of this review is to outline recent progress in understanding the role that dysregulation of HOX-gene expression plays in the pathogenesis of myeloid leukemogenesis.

RECENT FINDINGS: A number of recent studies correlate increased expression of HOXA-genes with poor prognosis cytogenetics in acute myeloid leukemia and mixed lineage leukemia.

Many such studies also document co-overexpression of homeodomain proteins of the Meis and Pbx families in poor prognosis leukemia.

SUMMARY: These findings suggest that a key characteristic of poor prognosis acute myeloid leukemia is increased, differentiation-stage inappropriate expression of the Abd HoxA proteins and their DNA-binding partners.

Such results suggest that dysregulation of the 'Hox code' is important in the pathogenesis of myeloid malignancy.

[MeSH-major] Genes, Homeobox / physiology. Leukemia, Myeloid / genetics

[MeSH-minor] Chromosome Aberrations. Gene Expression Regulation, Leukemic. Histone-Lysine N-Methyltransferase. Humans. Myeloid-Lymphoid Leukemia Protein / physiology

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(PMID = 17255784.001).

[ISSN] 1065-6251

[Journal-full-title] Current opinion in hematology

[ISO-abbreviation] Curr. Opin. Hematol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase

[Number-of-references] 44

   

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

Chromosomal translocation is a common cause of leukaemia and the most common chromosome translocations found in leukaemia patients involve the mixed lineage leukaemia (MLL) gene.

AF10 is one of more than 30 MLL fusion partners in leukaemia.

In addition to MLL, AF10 has also been reported to fuse to CALM (clathrin-assembly protein-like lymphoid-myeloid) in patients with T-cell acute lymphoblastic leukaemia (T-ALL) and acute myeloid leukaemia (AML).

Thus, our study establishes CALM-AF10 fusion as a cause of leukaemia and reveals that mistargeting of hDOT1L and upregulation of Hoxa5 through H3K79 methylation is the underlying mechanism behind leukaemia caused by CALM-AF10 fusion.

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[ErratumIn] Nat Cell Biol. 2006 Oct;8(10):1178

(PMID = 16921363.001).

[ISSN] 1465-7392

[Journal-full-title] Nature cell biology

[ISO-abbreviation] Nat. Cell Biol.

[Language] ENG

[Grant] United States / NIAID NIH HHS / AI / AI48407; United States / NIAID NIH HHS / AI / R56 AI048407; United States / NHLBI NIH HHS / HL / R21 HL072240; United States / NIAID NIH HHS / AI / R01 AI080432; United States / NIGMS NIH HHS / GM / R01 GM068804; United States / NIAID NIH HHS / AI / R01 AI077454; United States / NIGMS NIH HHS / GM / GM68804; United States / NHLBI NIH HHS / HL / HL72240; United States / NIAID NIH HHS / AI / R01 AI048407

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

[Publication-country] England

[Chemical-registry-number] 0 / HOXA5 protein, human; 0 / Homeodomain Proteins; 0 / Hoxa5 protein, mouse; 0 / MLLT10 protein, human; 0 / Mllt10 protein, mouse; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Phosphoproteins; 0 / Transcription Factors; EC 2.1.1.- / DOT1L protein, human; EC 2.1.1.- / Methyltransferases

[Other-IDs] NLM/ NIHMS684864; NLM/ PMC4425349

   

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

[Title] Infant acute lymphoblastic leukemia with t(11;16)(q23;p13.3) and lineage switch into acute monoblastic leukemia.

Rearrangements of the mixed-lineage leukemia (MLL) gene have been associated with a poor prognosis in infant acute lymphoblastic leukemia (ALL).

Previously, MLL translocations involving the CREP-binding protein (CREBBP) gene at chromosome band 16p13.3 have primarily been reported in treatment-related acute myeloid leukemia, after chemotherapy for other primary malignancies using topoisomerase II inhibitors.

We report a case of de novo infant ALL with t(11;16)(q23;p13.3).

After chemotherapy, this patient developed an acute monoblastic leukemia (M5b) with retention of the t(11;16)(q23;p13.3), indicating that this is a lineage switch of the original leukemic clone.

[MeSH-major] Cell Lineage. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 16 / genetics. Leukemia, Monocytic, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics

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(PMID = 16843104.001).

[ISSN] 0165-4608

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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

[Title] IMC-EB10, an anti-FLT3 monoclonal antibody, prolongs survival and reduces nonobese diabetic/severe combined immunodeficient engraftment of some acute lymphoblastic leukemia cell lines and primary leukemic samples.

The class III receptor tyrosine kinase FLT3 is expressed on the blasts of >90% of patients with B-lineage acute lymphoblastic leukemias (ALL).

In addition, it is expressed at extremely high levels in ALL patients with mixed lineage leukemia rearrangements or hyperdiploidy and is sometimes mutated in these same patients.

In this report, we investigate the effects of treating ALL cell lines and primary samples with human anti-FLT3 monoclonal antibodies (mAb) capable of preventing binding of FLT3 ligand.

In vitro studies, examining the ability of two anti-FLT3 mAbs (IMC-EB10 and IMC-NC7) to affect FLT3 activation and downstream signaling in ALL cell lines and primary blasts, yielded variable results.

FLT3 phosphorylation was consistently inhibited by IMC-NC7 treatment, but in some cell lines, IMC-EB10 actually stimulated FLT3 activation, possibly as a result of antibody-mediated receptor dimerization.

Through antibody-dependent, cell-mediated cytotoxicity, such an antibody could still prove efficacious against leukemia cells in vivo.

In fact, IMC-EB10 treatment significantly prolonged survival and/or reduced engraftment of several ALL cell lines and primary ALL samples in nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice.

Moreover, fluorescence-activated cell sorting and PCR analysis of IMC-EB10-treated NOD/SCID mice surviving 150 days post-leukemic cell injection revealed that FLT3 immunotherapy reduced leukemic engraftment below the level of detection in these assays (<0.001%).

[MeSH-major] Antibodies, Monoclonal / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. fms-Like Tyrosine Kinase 3 / immunology

[MeSH-minor] Animals. Cell Line, Tumor. Child. Cytotoxicity, Immunologic. Female. Humans. Immunization, Passive / methods. Killer Cells, Natural / immunology. Male. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Transplantation. Signal Transduction / drug effects

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(PMID = 16651440.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / CA62924; United States / NCI NIH HHS / CA / CA70970; United States / NCI NIH HHS / CA / CA90668; United States / NCRR NIH HHS / RR / RR00171

[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 / Antibodies, Monoclonal; 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.

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