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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

   

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

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

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(PMID = 16137555.001).

[ISSN] 0953-6205

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

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

[Language] eng

[Publication-type] Journal Article

[Publication-country] Netherlands

   

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

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

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

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

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

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

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

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

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(PMID = 19654084.001).

[ISSN] 0003-3898

[Journal-full-title] Annales de biologie clinique

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

[Language] fre

[Publication-type] English Abstract; Journal Article

[Publication-country] France

   

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

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

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

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

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

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

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

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(PMID = 20948276.001).

[ISSN] 0385-0684

[Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy

[ISO-abbreviation] Gan To Kagaku Ryoho

[Language] jpn

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

[Publication-country] Japan

   

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[Title] 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] Switzerland

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

   

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[Title] [Expression of PTEN mRNA in acute leukemia and its clinical significance].

OBJECTIVE: To explore PTEN gene expression and its clinical significance in acute leukemia.

METHODS: The expression levels of PTEN mRNA in 5 leukemia cell lines, 87 patients with acute leukemias (AL), including 59 acute myeloid leukemia (AML), 26 acute lymphoblastic leukemia (ALL), and 2 acute hybrid leukemia, 21 AL in complete remission (AL-CR), 31 chronic myelogenous leukemia (CML) and 14 normal controls were assayed by RT-PCR.

RESULTS: PTEN mRNA was detected in K562 cell line, but not in Kasumi-1, HL-60, U937, Nalm-6 cell lines.

The decreased level of PTEN mRNA had a positive correlation with poor-prognostic factors (high white blood cell count of > or = 20 x 10(9)/L and chromosome abnormality).

[MeSH-major] Leukemia / metabolism. PTEN Phosphohydrolase / metabolism

[MeSH-minor] Cell Line, Tumor. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 16383243.001).

[ISSN] 0253-2727

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

[ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi

[Language] chi

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

[Publication-country] China

[Chemical-registry-number] 0 / RNA, Messenger; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase

   

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

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

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

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(PMID = 18393372.001).

[ISSN] 1527-3350

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

[ISO-abbreviation] Hepatology

[Language] ENG

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

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

[Publication-country] United States

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

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

   

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[Title] 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

   

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

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

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(PMID = 18156734.001).

[ISSN] 1598-6535

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

[ISO-abbreviation] Korean J Lab Med

[Language] kor

[Publication-type] English Abstract; Journal Article

[Publication-country] Korea (South)

   

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

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

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

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

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

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

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

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

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

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

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

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

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

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[Copyright] (c) 2008 Clinical Cytometry Society.

(PMID = 18803279.001).

[ISSN] 1552-4957

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

[ISO-abbreviation] Cytometry B Clin Cytom

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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

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

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

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

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

[MeSH-major] Leukemia, Biphenotypic, Acute

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(PMID = 19563029.001).

[ISSN] 0253-2727

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

[ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

   

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

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

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

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

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

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

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

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

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

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(PMID = 19093164.001).

[ISSN] 1865-3774

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

   

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

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

It displays features of both myeloid and lymphoid lineage.

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

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

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

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

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

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

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

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

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

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

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

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

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(PMID = 19454497.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

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

[Publication-country] Italy

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

[Other-IDs] NLM/ PMC2704302

   

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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

   

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[Title] The versatile mixed lineage leukaemia gene MLL and its many associations in leukaemogenesis.

The marked association of abnormalities of chromosome 11 long arm, band q23, with human leukaemia led to the identification of the 11q23 gene called MLL (or HTRX, HRX, TRX1, ALL-1).

MLL can become fused with one of a remarkable panoply of genes from other chromosome locations in individual leukaemias, leading to either acute myeloid or lymphoid tumours (hence the name MLL for mixed lineage leukaemia).

The unusual finding that a single protein could be involved in both myeloid and lymphoid malignancies and that the truncated protein could do so as a fusion with very disparate partners has prompted studies to define the molecular role of MLL-fusions in leukaemogenesis and to the development of MLL-controlled mouse models of leukaemogenesis.

[MeSH-major] Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Leukemia / metabolism. Leukemia / pathology. Myeloid-Lymphoid Leukemia Protein / metabolism

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(PMID = 15826832.001).

[ISSN] 1044-579X

[Journal-full-title] Seminars in cancer biology

[ISO-abbreviation] Semin. Cancer Biol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein

[Number-of-references] 123

   

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

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

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

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

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

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

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

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

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

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(PMID = 19304540.001).

[ISSN] 1673-4254

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

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

[Language] chi

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

[Publication-country] China

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

   

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

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

[MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Banding. Fatal Outcome. Humans. Karyotyping. Male. Middle Aged. Phenotype

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(PMID = 17693199.001).

[ISSN] 0165-4608

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] United States

   

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[Title] Leukaemia lineage specification caused by cell-specific Mll-Enl translocations.

Chromosomal translocations involving the Mixed-Lineage Leukaemia (MLL) gene underlie many human leukaemias and MLL rearrangements are found in both acute myelogenous and acute lymphoblastic leukaemias.

To assess the functionally relevant haematopoietic cell contexts for MLL fusions to be tumorigenic, we have generated different lines of mice in which de novo Mll-associated translocations occur.

Translocations between Mll and Enl cause myeloid neoplasias, initiating in stem cells or progenitors while no tumours arose when the translocation was restricted to the B-cell compartment.

Despite the absence of tumorigenesis, Mll-Enl translocations did occur and Mll-Enl fusion mRNA was expressed in B-cell-restricted translocators.

[MeSH-major] B-Lymphocytes / pathology. Cell Lineage. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. T-Lymphocytes / pathology. Translocation, Genetic

[MeSH-minor] Animals. Antigens, CD19 / genetics. Antigens, CD19 / physiology. Cells, Cultured. Histone-Lysine N-Methyltransferase. Integrases / metabolism. Mice. Myeloid Progenitor Cells / cytology. Myeloid Progenitor Cells / metabolism. Nuclear Proteins / genetics. Nuclear Proteins / physiology. Phenotype. Recombination, Genetic. Stem Cells / cytology. Stem Cells / metabolism

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(PMID = 17906700.001).

[ISSN] 1476-5594

[Journal-full-title] Oncogene

[ISO-abbreviation] Oncogene

[Language] eng

[Grant] United Kingdom / Medical Research Council / / G0600914; United Kingdom / Medical Research Council / / MC/ U105178807; United Kingdom / Medical Research Council / /

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

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD19; 0 / Mllt3 protein, mouse; 0 / Neoplasm 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; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases

   

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In this study, we focus on two closely related clathrin assembly proteins, AP180 and CALM (clathrin assembly lymphoid myeloid leukemia protein), in the developing embryonic rat brain.

[MeSH-minor] Animals. Cell Line. Clathrin / metabolism. Clathrin-Coated Vesicles / metabolism. Female. Neurons / cytology. Neurons / metabolism. Pregnancy. Rats. Stem Cells / cytology. Stem Cells / metabolism

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(PMID = 20653035.001).

[ISSN] 1096-9861

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

[ISO-abbreviation] J. Comp. Neurol.

[Language] eng

[Grant] United States / Intramural NIH HHS / / Z99 AG999999

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

[Publication-country] United States

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

[Other-IDs] NLM/ NIHMS215726; NLM/ PMC2909614

   

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[Title] Acute leukemia of ambiguous lineage, biphenotype, without CD34, TdT or TCR-rearrangement.

Biphenotypic acute leukemia (BAL) is a rare entity that comprises 0.5-3% of all acute leukemias and probably arises from multipotent progenitor cells.

We report the case of a 41-year-old man with BAL having myeloid and T-lymphoid lineage phenotypes.

This pattern is rarely encountered and suggests that the blast cells were possibly considered immature with aspects of differentiation indicating myeloid lineage, rather than T-lymphoid lineage.

[MeSH-major] Antigens, CD34 / genetics. Cell Lineage / genetics. DNA Nucleotidylexotransferase / genetics. Gene Rearrangement / genetics. Leukemia, Biphenotypic, Acute / genetics. Receptors, Antigen, T-Cell. Receptors, Antigen, T-Cell, alpha-beta / genetics. Receptors, Antigen, T-Cell, gamma-delta / genetics

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(PMID = 19687594.001).

[ISSN] 1349-7235

[Journal-full-title] Internal medicine (Tokyo, Japan)

[ISO-abbreviation] Intern. Med.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Antigens, CD34; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta; EC 2.7.7.31 / DNA Nucleotidylexotransferase

   

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[Title] Solution structure of the nonmethyl-CpG-binding CXXC domain of the leukaemia-associated MLL histone methyltransferase.

The mixed-lineage leukaemia (MLL) CXXC domain selectively binds nonmethyl-CpG DNA, and is required for transformation by MLL fusion proteins that commonly arise from recurrent chromosomal translocations in infant and secondary treatment-related acute leukaemias.

These data provide a template for the design of specifically targeted therapeutics for poor prognosis MLL-associated leukaemias.

[MeSH-major] CpG Islands / genetics. Histone-Lysine N-Methyltransferase / chemistry. Leukemia / metabolism. Myeloid-Lymphoid Leukemia Protein / chemistry. Neoplasm Proteins / chemistry

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(PMID = 16990798.001).

[ISSN] 0261-4189

[Journal-full-title] The EMBO journal

[ISO-abbreviation] EMBO J.

[Language] eng

[Grant] United Kingdom / Medical Research Council / / MC/ U105161083; United Kingdom / Medical Research Council / / MC/ U105459896

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

[Publication-country] England

[Chemical-registry-number] 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Solutions; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 9007-49-2 / DNA; EC 2.1.1.- / Protein Methyltransferases; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase

[Other-IDs] NLM/ PMC1589984

   

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

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

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

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[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

   

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RESULTS: In order to analyse the function of the nuclear form of FLRG, we performed a yeast two-hybrid screen, in which we identified AF10 [ALL1 (acute lymphoblastic leukaemia) fused gene from chromosome 10], a translocation partner of the MLL (mixed-lineage leukaemia) oncogene in human leukaemia, as a FLRG-interacting protein.

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(PMID = 17868029.001).

[ISSN] 1768-322X

[Journal-full-title] Biology of the cell

[ISO-abbreviation] Biol. Cell

[Language] ENG

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

[Publication-country] England

[Chemical-registry-number] 0 / Follistatin-Related Proteins; 0 / MLLT10 protein, human; 0 / Protein Isoforms; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors

   

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[Title] Force microscopy of nonadherent cells: a comparison of leukemia cell deformability.

We apply this technique to compare the deformability of human myeloid and lymphoid leukemia cells and neutrophils at low deformation rates, and we find that the cells are well described by an elastic model based on Hertzian mechanics.

Myeloid (HL60) cells were measured to be a factor of 18 times stiffer than lymphoid (Jurkat) cells and six times stiffer than human neutrophils on average (E(infinity) = 855 +/- 670 Pa for HL60 cells, E(infinity) = 48 +/- 35 Pa for Jurkat cells, E(infinity) = 156 +/- 87 for neutrophils, mean +/- SD).

This work demonstrates a simple method for extending AFM mechanical property measurements to nonadherent cells and characterizes properties of human leukemia cells that may contribute to leukostasis, a complication associated with acute leukemia.

[MeSH-major] Leukemia, Myeloid / pathology. Neutrophils / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

[MeSH-minor] Acute Disease. Cell Adhesion. Cell Line, Tumor. Cells, Cultured. Elasticity. Humans. Micromanipulation. Microscopy, Atomic Force. Models, Biological. Viscosity

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(PMID = 16443660.001).

[ISSN] 0006-3495

[Journal-full-title] Biophysical journal

[ISO-abbreviation] Biophys. J.

[Language] eng

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

[Publication-country] United States

[Other-IDs] NLM/ PMC1414579

   

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[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

   

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

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

[MeSH-minor] Adolescent. Humans. Male. Phenotype. Prognosis

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(PMID = 20338638.001).

[ISSN] 1873-5835

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] England

   

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

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

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

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

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

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

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

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

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

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(PMID = 16403255.001).

[ISSN] 1009-2137

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

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

[Language] ENG

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

[Publication-country] China

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

   

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[Title] [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

   

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[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

   

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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

   

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[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

   

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[Title] Mixed phenotype acute leukaemia with giant inclusions.

[MeSH-major] Inclusion Bodies / ultrastructure. Leukemia, Biphenotypic, Acute / pathology

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(PMID = 20015299.001).

[ISSN] 1365-2141

[Journal-full-title] British journal of haematology

[ISO-abbreviation] Br. J. Haematol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

   

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[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)

   

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

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

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

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

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

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(PMID = 20505276.001).

[ISSN] 1880-9952

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

[ISO-abbreviation] J Clin Exp Hematop

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

   

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[Title] 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

   

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[Title] Biphenotypic acute leukemia treated with acute myeloid leukemia regimens: a case series.

This study retrospectively analyzed 8 cases of biphenotypic acute leukemia (BAL) in respect of morphology, immune phenotype, karyotype, and clinical manifestations.

Six patients had myeloid plus T lymphoid, and 2 cases had myeloid plus B-lymphoid immune phenotypic markers.

Because selection of an antileukemic chemotherapy regimen for acute leukemia is largely based on whether a case is classified as myeloid or lymphoid, the presence of markers for both lineages may have important implications for treatment.

All of our patients were treated with regimens designed for acute myeloid leukemia (AML).

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

[MeSH-minor] Adult. Antibiotics, Antineoplastic / therapeutic use. Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Agents / therapeutic use. Biomarkers. Case-Control Studies. Cytarabine / therapeutic use. Female. Humans. Idarubicin / therapeutic use. Immunophenotyping. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / physiopathology. Male. Middle Aged. Mitoxantrone / therapeutic use. Retrospective Studies

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(PMID = 19331261.001).

[ISSN] 1943-4693

[Journal-full-title] Journal of the National Medical Association

[ISO-abbreviation] J Natl Med Assoc

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Biomarkers; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; ZRP63D75JW / Idarubicin

   

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[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

   

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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

   

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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)

   

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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

   

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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

   

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

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

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

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

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

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(PMID = 16026782.001).

[ISSN] 0014-4800

[Journal-full-title] Experimental and molecular pathology

[ISO-abbreviation] Exp. Mol. Pathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

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

   

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[Title] 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

   

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The t(10;11)(p13;q14-21) is found in T-ALL and acute myeloid leukemia and fuses CALM (Clathrin-Assembly protein-like Lymphoid-Myeloid leukaemia gene) to AF10.

Microarray results were validated by quantitative RT-PCR on an independent group of T-ALL and compared to mixed lineage leukemia-translocated acute leukemias (MLL-t AL).

We propose to define a HOXA+ leukemia group composed of at least MLL-t, CALM-AF10 and HOXA-t AL, which may benefit from adapted management.

[MeSH-major] Homeodomain Proteins / biosynthesis. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Repressor Proteins / biosynthesis

[MeSH-minor] Adolescent. Adult. Cell Proliferation. Cell Transformation, Neoplastic. Child. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Polycomb Repressive Complex 1. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Up-Regulation

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(PMID = 16107895.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 157907-48-7 / HoxA protein; EC 6.3.2.19 / Polycomb Repressive Complex 1

   

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

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

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(PMID = 19458630.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] England

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