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1. Strick R, Zhang Y, Emmanuel N, Strissel PL: Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias. Hum Genet; 2006 Jun;119(5):479-95
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  • [Title] Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias.
  • The t(9;22) BCR/ABL fusion is associated with over 90% of chronic myelogenous and 25% of acute lymphocytic leukemia.
  • Chromosome 11q23 translocations in acute myeloid and lymphoid leukemia cells demonstrate myeloid lymphoid leukemia (MLL) fusions with over 40 gene partners, like AF9 and AF4 on chromosomes 9 and 4, respectively.
  • Therapy-related leukemia is associated with the above gene rearrangements following the treatment with topoisomerase II (topo II) inhibitors.
  • In this report, using cell lines and primary cells, chromatin structural elements were analyzed in BCR, ABL and AF4 and, for comparison, in MLL2, which is a homolog to MLL, but not associated with chromosome translocations.
  • Although MLL2 was expressed in all cell lines tested, except for the presence of one DNAse I site in the promoter, no other structural elements were found in MLL2.
  • A NHR model presented demonstrates the importance of chromatin structure in chromosome translocations involved with leukemia.
  • [MeSH-major] Chromatin / chemistry. Chromosome Breakage. Chromosomes, Human / genetics. Leukemia / genetics. Leukemia / metabolism. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Cells, Cultured. Chronic Disease. Humans. K562 Cells. Proto-Oncogene Proteins c-bcr / chemistry. Proto-Oncogene Proteins c-bcr / genetics. Recombination, Genetic

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  • (PMID = 16572268.001).
  • [ISSN] 0340-6717
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Chromatin; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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2. Zhao XF, Gojo I, York T, Ning Y, Baer MR: Diagnosis of biphenotypic acute leukemia: a paradigmatic approach. Int J Clin Exp Pathol; 2009;3(1):75-86
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  • [Title] Diagnosis of biphenotypic acute leukemia: a paradigmatic approach.
  • Biphenotypic acute leukemia (BAL), or acute leukemia with a single population of blasts coexpressing markers of two different lineages, is a rare clinical entity.
  • To define BAL, a scoring system was proposed by the European Group of Immunological Markers for Leukemias (EGIL) in 1995.
  • However, increasing evidence suggests that this system has limitations, as acknowledged by the 2008 World Health Organization (WHO) Classification of Tumors of Hematopoietic and Lymphoid Tissues.
  • We propose a new paradigmatic approach to defining BAL based on recent clinical studies of BAL and advances in immunologic marker definition and cytogenetics, and applied our new approach to 8 cases of "BAL" among a cohort of 742 new acute leukemias in our Cancer Center.
  • By our new criteria, 6 cases were reclassified as acute lymphoblastic leukemia (ALL), while only 2 were still classified as BAL.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis
  • [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
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3. Dixon N, Kishnani PS, Zimmerman S: Clinical manifestations of hematologic and oncologic disorders in patients with Down syndrome. Am J Med Genet C Semin Med Genet; 2006 Aug 15;142C(3):149-57
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  • Increased erythrocyte mean corpuscular volume (MCV) is frequently found among DS infants and remains elevated throughout life in two-thirds of patients, making interpretation of red cell indices for diagnosis of nutritional anemias or bone marrow failure disorders more challenging.
  • Transient myeloproliferative disorder (TMD) associated with pancytopenia, hepatosplenomegaly, and circulating immature WBCs, is found almost exclusively in DS infants with an incidence of approximately 10%.
  • Despite the high rate of spontaneous regression, TMD can be a preleukemic disorder in 20-30% of children with DS.
  • There is an increased risk of leukemia with an equal incidence of lymphoid and myeloid leukemia.
  • Acute megakaryocytic leukemia (AMKL) subtype is the most common form of acute myeloid leukemia (AML) in this setting, and is uncommon in children without DS.
  • Children with DS and leukemia are more sensitive to some chemotherapeutic agents such as methotrexate than other children which requires careful monitoring for toxicity.
  • Although the risk for leukemia is higher in individuals with DS, these patients have a lower risk of developing solid tumors, with the exception of germ cell tumors, and perhaps retinoblastoma and lymphoma.
  • [MeSH-major] Down Syndrome / complications. Hematologic Diseases / diagnosis. Hematologic Diseases / etiology. Neoplasms / diagnosis. Neoplasms / etiology
  • [MeSH-minor] Child. Female. Humans. Infant. Leukemia / diagnosis. Leukemia / etiology. Male. Myeloproliferative Disorders / diagnosis. Myeloproliferative Disorders / etiology

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  • (PMID = 17048354.001).
  • [ISSN] 1552-4868
  • [Journal-full-title] American journal of medical genetics. Part C, Seminars in medical genetics
  • [ISO-abbreviation] Am J Med Genet C Semin Med Genet
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 2T32 CA 09307
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 72
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4. Hatoum HA, Mahfouz RA, Otrock ZK, Hudaib AR, Taher AT, Shamseddine AI: Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report. Am J Hematol; 2007 Jan;82(1):69-72
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  • [Title] Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report.
  • The association of chronic lymphocytic leukemia (CLL) and acute leukemia, either lymphoid or myeloid is a rare event.
  • Our review of the medical literature revealed only 6 cases of CLL transformation to acute myeloid leukemia (AML) (M0, M1 and M2) with no other associated malignancy.
  • We report a similar case but with occurrence of AML-M4 associated with normal cytogenetic analysis and molecular testing but with positive T-cell receptor gamma gene rearrangement rather than the usual Vbeta rearrangement.
  • [MeSH-major] Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics


5. Scolnik MP, Aranguren PN, Cuello MT, Palacios MF, Sanjurjo J, Giunta M, Bracco MM, Acevedo S: Biphenotypic acute leukemia with t(15;17). Leuk Lymphoma; 2005 Apr;46(4):607-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biphenotypic acute leukemia with t(15;17).
  • Biphenotypic acute leukemias (BAL) represent 5% of all acute leukemias.
  • Immunophenotype revealed the compromise of myeloid and B-lymphoid lineages.
  • This report describes a BAL case with an unfrequent cytogenetic abnormality, and highlights the importance of correlating the results of multiple diagnostic methods in order to establish a correct diagnosis and treatment in BAL patients.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Child. Chromosome Aberrations. Chromosomes, Human, Pair 8 / genetics. Female. Flow Cytometry / methods. Gene Rearrangement. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence / methods. Neoplasm, Residual / diagnosis. Neoplasm, Residual / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Trisomy

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  • (PMID = 16019491.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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6. Yin B, Delwel R, Valk PJ, Wallace MR, Loh ML, Shannon KM, Largaespada DA: A retroviral mutagenesis screen reveals strong cooperation between Bcl11a overexpression and loss of the Nf1 tumor suppressor gene. Blood; 2009 Jan 29;113(5):1075-85
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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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7. Buckley O, Reardon M: A young male with bone pain. Eur J Intern Med; 2005 Sep;16(5):366-8
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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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8. Coche D, Bergues B, Harrivel V, Guillaume N: [Biphenotypic acute leukaemia with Burkitt-like cytology]. Ann Biol Clin (Paris); 2009 Jul-Aug;67(4):437-40
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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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9. Murase K, Iyama S, Sato T, Takimoto R, Kobune M, Kato J: [Therapeutic results in patients with biphenotypic acute leukemia at Sapporo Medical University Hospital]. Gan To Kagaku Ryoho; 2010 Oct;37(10):2011-3
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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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10. Thavaraj V, Seth R: Prophylaxis of central nervous system leukemia: a case of chronic myeloid leukemia with lymphoid blast crisis treated with imatinib mesylate. World J Pediatr; 2008 May;4(2):145-7
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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
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11. Shen Q, Chen Z, Liu XP, Xing HY, Wang M, Wang JX: [Expression of PTEN mRNA in acute leukemia and its clinical significance]. Zhonghua Xue Ye Xue Za Zhi; 2005 Aug;26(8):493-6
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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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12. Ara AI, Xia M, Ramani K, Mato JM, Lu SC: S-adenosylmethionine inhibits lipopolysaccharide-induced gene expression via modulation of histone methylation. Hepatology; 2008 May;47(5):1655-66
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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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13. Mohan AV, Ramnath VR, Patalas E, Attar EC: Non-specific interstitial pneumonia as the initial presentation of biphenotypic acute leukemia: a case report. Cases J; 2009;2:8217
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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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14. Choi HW, Shin MG, Kim HJ, Lee IK, Yun JH, Kim HR, Kim YK, Yun HK, Cho D, Kee SJ, Shin JH, Suh SP, Ryang DW: [Biphenotypic Acute Leukemia with BCR-ABL mRNA Transcript b3a2 Type: A Case Report with Review of the Literature.]. Korean J Lab Med; 2006 Aug;26(4):249-54
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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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15. Gujral S, Badrinath Y, Kumar A, Subramanian PG, Raje G, Jain H, Pais A, Amre Kadam PS, Banavali SD, Arora B, Kumar P, Hari Menon VG, Kurkure PA, Parikh PM, Mahadik S, Chogule AB, Shinde SC, Nair CN: Immunophenotypic profile of acute leukemia: critical analysis and insights gained at a tertiary care center in India. Cytometry B Clin Cytom; 2009 May;76(3):199-205
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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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16. Zhang J, Mi YC, Wang Y, Lin D, Li W, Sun XM, Zhou K, Bian SG, Wang JX: [Study on the clinical characteristics of adult biphenotypic acute leukaemia]. Zhonghua Xue Ye Xue Za Zhi; 2009 Jan;30(1):18-21
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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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17. Kakihana K, Ohashi K, Sakai F, Kamata N, Hosomi Y, Nishiwaki M, Yokoyama R, Kobayashi T, Yamashita T, Akiyama H, Sakamaki H: Leukemic infiltration of the lung following allogeneic hematopoietic stem cell transplantation. Int J Hematol; 2009 Jan;89(1):118-22
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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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18. Xu XQ, Wang JM, Lü SQ, Chen L, Yang JM, Zhang WP, Song XM, Hou J, Ni X, Qiu HY: 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. Haematologica; 2009 Jul;94(7):919-27
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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


19. Carretta A, Ciriaco P, Melloni G, Bandiera A, Libretti L, Puglisi A, Giovanardi M, Zannini P: Surgical treatment of multiple primary adenocarcinomas of the lung. Thorac Cardiovasc Surg; 2009 Feb;57(1):30-4
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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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20. Daser A, Rabbitts TH: The versatile mixed lineage leukaemia gene MLL and its many associations in leukaemogenesis. Semin Cancer Biol; 2005 Jun;15(3):175-88
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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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21. Liu Z, Liu XL, Du QF, Xu N, Zhong M, Song LL, Yi ZS, Liu QF, Meng FY, Zhou SY: [Clinical characteristics and outcomes of 59 patients with acute lymphoblastic leukemia positive for BCR/ABL]. Nan Fang Yi Ke Da Xue Xue Bao; 2009 Mar;29(3):512-5
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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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22. Gozzetti A, Calabrese S, Raspadori D, Crupi R, Tassi M, Bocchia M, Fabbri A, Lauria F: Concomitant t(4;11) and t(1;19) in a patient with biphenotypic acute leukemia. Cancer Genet Cytogenet; 2007 Aug;177(1):81-2
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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


23. Cano F, Drynan LF, Pannell R, Rabbitts TH: Leukaemia lineage specification caused by cell-specific Mll-Enl translocations. Oncogene; 2008 Mar 20;27(13):1945-50
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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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24. Schwartz CM, Cheng A, Mughal MR, Mattson MP, Yao PJ: Clathrin assembly proteins AP180 and CALM in the embryonic rat brain. J Comp Neurol; 2010 Sep 15;518(18):3803-18
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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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25. Nishiuchi T, Ohnishi H, Kamada R, Kikuchi F, Shintani T, Waki F, Kitanaka A, Kubota Y, Tanaka T, Ishida T: Acute leukemia of ambiguous lineage, biphenotype, without CD34, TdT or TCR-rearrangement. Intern Med; 2009;48(16):1437-41
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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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26. Allen MD, Grummitt CG, Hilcenko C, Min SY, Tonkin LM, Johnson CM, Freund SM, Bycroft M, Warren AJ: Solution structure of the nonmethyl-CpG-binding CXXC domain of the leukaemia-associated MLL histone methyltransferase. EMBO J; 2006 Oct 04;25(19):4503-12
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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

  • MedlinePlus Health Information. consumer health - Leukemia.
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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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27. Nakada S, Katsuki Y, Imoto I, Yokoyama T, Nagasawa M, Inazawa J, Mizutani S: Early G2/M checkpoint failure as a molecular mechanism underlying etoposide-induced chromosomal aberrations. J Clin Invest; 2006 Jan;116(1):80-9
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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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  • (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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28. Forissier S, Razanajaona D, Ay AS, Martel S, Bartholin L, Rimokh R: AF10-dependent transcription is enhanced by its interaction with FLRG. Biol Cell; 2007 Oct;99(10):563-71
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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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29. Rosenbluth MJ, Lam WA, Fletcher DA: Force microscopy of nonadherent cells: a comparison of leukemia cell deformability. Biophys J; 2006 Apr 15;90(8):2994-3003
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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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30. Takasaki H, Tachibana T, Tanaka M, Maruta A, Ishigatsubo Y, Kanamoari H: [Successful selection of chemotherapy based on cell surface antigens in a patient with mixed phenotype acute leukemia]. Rinsho Ketsueki; 2010 May;51(5):339-44
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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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31. Marques-Salles Tde J, Barros JE, Soares-Ventura EM, Cartaxo Muniz MT, Santos N, Ferreira da Silva E, Silva ML, Liehr T, Mkrtchyan H: Unusual childhood biphenotypic acute leukemia with a yet unreported t(3;13)(p25.1;q13). Leuk Res; 2010 Aug;34(8):e206-7
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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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32. Ning BT, Tang YM, Chen YH, Shen HQ, Qian BQ: Comparison between CD19 and CD20 expression patterns on acute leukemic cells. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Dec;13(6):943-7
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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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33. Hu XX, Gong SL, Song XM, Chen L, Qiu HY, Gao L, Wang JM: [Report of a case of hybrid acute leukemia with t (12; 22) and literature review]. Zhonghua Xue Ye Xue Za Zhi; 2006 May;27(5):331-4
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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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34. Jeha S, Kantarjian H: Clofarabine for the treatment of acute lymphoblastic leukemia. Expert Rev Anticancer Ther; 2007 Feb;7(2):113-8
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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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35. Kinjo K, Sandoval S, Sakamoto KM, Shankar DB: The role of CREB as a proto-oncogene in hematopoiesis. Cell Cycle; 2005 Sep;4(9):1134-5
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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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36. Ohe M, Hashino S: [Successful treatment with clarithromycin for Mixed phenotype acute leukemia, T/myeloid, NOS]. Rinsho Ketsueki; 2010 Apr;51(4):297-9
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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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37. Shi M, Cui F, Li B, Li SY, Ma HJ: Mixed phenotype acute leukaemia with giant inclusions. Br J Haematol; 2010 Apr;149(1):2
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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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38. Suh B, Song J, Kim J, Park TS, Choi JR: Constitutional pericentric inversion 9 in Korean patients with chronic myelogenous leukemia. Korean J Lab Med; 2010 Jun;30(3):218-23
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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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39. Amakawa R, Hiramoto N, Kawano S, Hyo A, Nakamichi N, Tajima K, Ito T, Mori S, Kishimoto Y, Fukuhara S: Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia. J Clin Exp Hematop; 2010;50(1):51-8
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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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40. Yamamoto K, Sada A, Kawano Y, Katayama Y, Shimoyama M, Matsui T: Therapy-related, mixed phenotype acute leukemia with t(1;21)(p36;q22) and RUNX1 rearrangement. Cancer Genet Cytogenet; 2010 Sep;201(2):122-7
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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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41. Serefhanoglu S, Buyukasik Y, Goker H, Sayinalp N, Ozcebe OI: Biphenotypic acute leukemia treated with acute myeloid leukemia regimens: a case series. J Natl Med Assoc; 2009 Mar;101(3):270-2
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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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42. Shildkrot Y, Onciu M, Hoehn ME, Wilson MW: Mixed-phenotype acute leukemia relapse in the iris. J AAPOS; 2010 Oct;14(5):453-4
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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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43. Michaud J, Simpson KM, Escher R, Buchet-Poyau K, Beissbarth T, Carmichael C, Ritchie ME, Schütz F, Cannon P, Liu M, Shen X, Ito Y, Raskind WH, Horwitz MS, Osato M, Turner DR, Speed TP, Kavallaris M, Smyth GK, Scott HS: Integrative analysis of RUNX1 downstream pathways and target genes. BMC Genomics; 2008 Jul 31;9:363
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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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44. Kim MK, Mun YC, Seong CM, Chung WS, Huh J: [Variant Philadelphia chromosome identified by interphase fluorescence in situ hybridization (FISH) without evidence on G-banded karyotyping and metaphase FISH]. Korean J Lab Med; 2010 Dec;30(6):711-7
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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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45. Liu H, Yu H, Jia HY, Zhang W, Guo CJ: [Detection of FLT3 gene mutation in hematologic malignancies and its clinical significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):709-13
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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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46. Xia ZB, Popovic R, Chen J, Theisler C, Stuart T, Santillan DA, Erfurth F, Diaz MO, Zeleznik-Le NJ: The MLL fusion gene, MLL-AF4, regulates cyclin-dependent kinase inhibitor CDKN1B (p27kip1) expression. Proc Natl Acad Sci U S A; 2005 Sep 27;102(39):14028-33
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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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47. Papenhausen PR, Griffin S, Tepperberg J: Oncogene amplification in transforming myelodysplasia. Exp Mol Pathol; 2005 Oct;79(2):168-75
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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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48. Costantini AS, Benvenuti A, Vineis P, Kriebel D, Tumino R, Ramazzotti V, Rodella S, Stagnaro E, Crosignani P, Amadori D, Mirabelli D, Sommani L, Belletti I, Troschel L, Romeo L, Miceli G, Tozzi GA, Mendico I, Maltoni SA, Miligi L: Risk of leukemia and multiple myeloma associated with exposure to benzene and other organic solvents: evidence from the Italian Multicenter Case-control study. Am J Ind Med; 2008 Nov;51(11):803-11
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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


49. Dik WA, Brahim W, Braun C, Asnafi V, Dastugue N, Bernard OA, van Dongen JJ, Langerak AW, Macintyre EA, Delabesse E: CALM-AF10+ T-ALL expression profiles are characterized by overexpression of HOXA and BMI1 oncogenes. Leukemia; 2005 Nov;19(11):1948-57
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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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50. Lee JC, Yang S, Zou Y, Joseph L: Erythroid/B-cell biphenotypic acute leukemia first case report. Leukemia; 2009 Oct;23(10):1920-3
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  • [Title] Erythroid/B-cell biphenotypic acute leukemia first case report.
  • [MeSH-major] B-Lymphocytes / pathology. Erythroid Cells / pathology. Leukemia, Biphenotypic, Acute / pathology

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  • (PMID = 19458630.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD
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56. Archangelo LF, Gläsner J, Krause A, Bohlander SK: The novel CALM interactor CATS influences the subcellular localization of the leukemogenic fusion protein CALM/AF10. Oncogene; 2006 Jul 6;25(29):4099-109
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  • The Clathrin Assembly Lymphoid Myeloid leukemia gene (CALM or PICALM) was first identified as the fusion partner of AF10 in the t(10;11)(p13;q14) translocation, which is observed in acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL) and malignant lymphoma.
  • Using the N-terminal half of CALM as a bait in a yeast two-hybrid screen, a novel protein named CATS (CALM interacting protein expressed in thymus and spleen) was identified.
  • [MeSH-major] Active Transport, Cell Nucleus. Carrier Proteins / metabolism. Cell Nucleolus / metabolism. Monomeric Clathrin Assembly Proteins / metabolism. Oncogene Proteins, Fusion / metabolism
  • [MeSH-minor] 3T3 Cells. Animals. Base Sequence. Cell Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 10 / metabolism. Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 13 / metabolism. Gene Expression Regulation / genetics. Humans. Mice. Molecular Sequence Data. Organ Specificity. Protein Binding / genetics. Translocation, Genetic / genetics

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • SciCrunch. HGNC: Data: Gene Annotation .
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  • (PMID = 16491119.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / Carrier Proteins; 0 / FAM64A protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human
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57. Hinrichsen L, Meyerholz A, Groos S, Ungewickell EJ: Bending a membrane: how clathrin affects budding. Proc Natl Acad Sci U S A; 2006 Jun 6;103(23):8715-20
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  • We have found that domains containing the adapter complex 2 (AP2)-coated vesicle adapter and the endocytic accessory proteins CALM (clathrin assembly lymphoid myeloid leukemia protein), epsin, and eps15/eps15R (EGF receptor pathway substrate 15-related) nevertheless persist at the plasma membrane.
  • [MeSH-major] Cell Membrane / metabolism. Cell Surface Extensions / metabolism. Clathrin / metabolism

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  • (PMID = 16735469.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Protein Complex 2; 0 / Adaptor Proteins, Vesicular Transport; 0 / Clathrin; 0 / epsin
  • [Other-IDs] NLM/ PMC1482644
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58. Gujral S, Polampalli S, Badrinath Y, Kumar A, Subramanian PG, Raje G, Amare P, Arora B, Banavali SD, Nair CN: Clinico-hematological profile in biphenotypic acute leukemia. Indian J Cancer; 2009 Apr-Jun;46(2):160-8
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  • [Title] Clinico-hematological profile in biphenotypic acute leukemia.
  • BACKGROUND: We present a clinico-hematological profile and treatment outcome of Biphenotypic Acute Leukemia (BAL).
  • MATERIAL AND METHODS: Diagnosis was based on WHO classification, including clinical details, morphology, cytochemistry, immunophenotyping, and molecular genetics.
  • We included those cases, which fulfilled the European Group for the Immunological Characterization of Acute Leukemia's (EGIL's) scoring system criteria for the diagnosis of BAL, as per recommendation of the WHO classification.
  • B-Myeloid (14 cases) followed by T-Myeloid BAL (13 cases) were the commonest subtypes.
  • Polymorphous population of blasts (16 cases) was commonly associated with T-Myeloid BAL (10 cases).
  • BCR ABL fusion positivity was a common cytogenetic abnormality (seven cases).
  • CONCLUSIONS: Pediatric BAL and T-B lymphoid BAL have a better prognosis.
  • BCR-ABL expression is an important prognostic factor, as these cases will be labeled as Chronic myeloid leukemia (CML) in blast crisis with biphenotypic expression and treated accordingly.
  • [MeSH-major] Immunophenotyping. Leukemia, Biphenotypic, Acute / blood. Leukemia, Biphenotypic, Acute / diagnosis
  • [MeSH-minor] Adolescent. Adult. Case-Control Studies. Child. Child, Preschool. Disease Progression. Female. Hematologic Tests. Humans. Incidence. Male. Middle Aged. Phenotype. Retrospective Studies. Young Adult

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  • (PMID = 19346652.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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59. Saitoh T, Matsushima T, Iriuchishima H, Yamane A, Irisawa H, Handa H, Tsukamoto N, Karasawa M, Nojima Y, Murakami H: Presentation of extramedullary Philadelphia chromosome-positive biphenotypic acute leukemia as testicular mass: Response to imatinib-combined chemotherapy. Leuk Lymphoma; 2006 Dec;47(12):2667-9
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  • [Title] Presentation of extramedullary Philadelphia chromosome-positive biphenotypic acute leukemia as testicular mass: Response to imatinib-combined chemotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Piperazines / pharmacology. Pyrimidines / pharmacology. Testicular Neoplasms / diagnosis
  • [MeSH-minor] Benzamides. Bone Marrow Cells / cytology. Flow Cytometry. Humans. Imatinib Mesylate. Male. Middle Aged. Philadelphia Chromosome. Stem Cell Transplantation. Transplantation, Homologous


60. Balgobind BV, Hollink IH, Reinhardt D, van Wering ER, de Graaf SS, Baruchel A, Stary J, Beverloo HB, de Greef GE, Pieters R, Zwaan CM, van den Heuvel-Eibrink MM: Low frequency of MLL-partial tandem duplications in paediatric acute myeloid leukaemia using MLPA as a novel DNA screenings technique. Eur J Cancer; 2010 Jul;46(10):1892-9
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  • [Title] Low frequency of MLL-partial tandem duplications in paediatric acute myeloid leukaemia using MLPA as a novel DNA screenings technique.
  • Mixed-lineage leukaemia (MLL)-partial tandem duplications (PTDs) are found in 3-5% of adult acute myeloid leukaemia (AML), and are associated with poor prognosis.
  • [MeSH-major] Gene Duplication. Genetic Testing / methods. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Tandem Repeat Sequences / genetics

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20233657.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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61. Leung J, Pang A, Yuen WH, Kwong YL, Tse EW: Relationship of expression of aquaglyceroporin 9 with arsenic uptake and sensitivity in leukemia cells. Blood; 2007 Jan 15;109(2):740-6
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  • [Title] Relationship of expression of aquaglyceroporin 9 with arsenic uptake and sensitivity in leukemia cells.
  • Arsenic trioxide (As2O3) is highly efficacious in acute promyelocytic leukemia (APL).
  • In 10 of 11 myeloid and lymphoid leukemia lines, quantitative polymerase chain reaction (Q-PCR) and Western blotting showed that AQP9 expression correlated positively with As2O3-induced cytotoxicity.
  • Similarly, the chronic myeloid leukemia line K562 expressed low levels of AQP9 and was As2O3 insensitive.
  • Pretreatment of the myeloid leukemia line HL-60 with all-trans retinoic acid (ATRA) up-regulated AQP9, leading to a significantly increased arsenic uptake and As2O3-induced cytotoxicity on incubation with As2O3, which might explain the synergism between ATRA and As2O3.
  • Q-PCR showed that primary APL cells expressed AQP9 significantly (2-3 logs) higher than other acute myeloid leukemias (AMLs), which might explain their exquisite As2O3 sensitivity.
  • [MeSH-major] Aquaporins / metabolism. Arsenicals / pharmacology. Leukemia, Myeloid / metabolism. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / metabolism. Oxides / pharmacology
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Cell Proliferation / drug effects. Gene Expression Profiling. Humans. K562 Cells. Point Mutation. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity. Tretinoin / pharmacology. Up-Regulation / drug effects

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  • (PMID = 16968895.001).
  • [ISSN] 0006-4971
  • [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 / AQP9 protein, human; 0 / Aquaporins; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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62. Han X, Bueso-Ramos CE: Precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma and acute biphenotypic leukemias. Am J Clin Pathol; 2007 Apr;127(4):528-44
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  • [Title] Precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma and acute biphenotypic leukemias.
  • Session 4 of the 2005 Society of Hematopathology/European Association for Haematopathology Workshop focused on case presentations of precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma (pre-T ALL/LBL) and acute biphenotypic leukemia.
  • Acute biphenotypic leukemias are characterized by a single population of blasts that express myeloid, T- or B-lineage antigens in various combinations and account for fewer than 4% of all acute leukemias.
  • An accurate diagnosis of pre-T ALL/LBL and acute biphenotypic leukemia requires a multiparametric approach, including examination of morphologic features, immunophenotype, clinical characteristics, and cytogenetic and molecular findings.
  • [MeSH-major] Biomarkers, Tumor / analysis. Leukemia, Lymphoid / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Chromosome Aberrations. Diagnosis, Differential. Gene Expression Profiling. Humans. Immunohistochemistry


63. Xavier MO, Oliveira Fde M, Almeida Vd, Prolla G, Severo LC: Invasive Aspergillus flavus sinusitis: case report in a patient with biphenotypic acute leukemia. Rev Inst Med Trop Sao Paulo; 2009 Jan-Feb;51(1):57-8
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  • [Title] Invasive Aspergillus flavus sinusitis: case report in a patient with biphenotypic acute leukemia.
  • Here we report a case of invasive pansinusitis with proptosis of the right eye caused by Aspergillus flavus in an immunocompromised patient with acute biphenotypic leukemia without aggressive therapy response.
  • [MeSH-major] Aspergillosis / diagnosis. Aspergillus flavus / isolation & purification. Immunocompromised Host. Leukemia, Biphenotypic, Acute / immunology. Sinusitis / microbiology

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  • (PMID = 19229393.001).
  • [ISSN] 1678-9946
  • [Journal-full-title] Revista do Instituto de Medicina Tropical de São Paulo
  • [ISO-abbreviation] Rev. Inst. Med. Trop. Sao Paulo
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
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64. Liu B, Li R, Wu HJ, Chen Y: [Clinical study on prognosis of acute leukemia subtypes Ly + AML and My + ALL]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Apr;15(2):421-4
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  • [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
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65. Alvarado Y, Welch MA, Swords R, Bruzzi J, Schlette E, Giles FJ: Nelarabine activity in acute biphenotypic leukemia. Leuk Res; 2007 Nov;31(11):1600-3
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  • [Title] Nelarabine activity in acute biphenotypic leukemia.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use. Leukemia / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cyclophosphamide / administration & dosage. Dexamethasone / administration & dosage. Doxorubicin / administration & dosage. Flow Cytometry. Humans. Middle Aged. Phenotype. Vincristine / administration & dosage

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  • (PMID = 17512588.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 5J49Q6B70F / Vincristine; 60158CV180 / nelarabine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; CVAD protocol
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66. Asgarian Omran H, Shabani M, Shahrestani T, Sarafnejad A, Khoshnoodi J, Vossough P, Faranoush M, Sharifian RA, Jeddi-Tehrani M, Rabbani H, Shokri F: Immunophenotypic subtyping of leukemic cells from Iranian patients with acute lymphoblastic leukaemia: association to disease outcome. Iran J Immunol; 2007 Mar;4(1):15-25
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  • [Title] Immunophenotypic subtyping of leukemic cells from Iranian patients with acute lymphoblastic leukaemia: association to disease outcome.
  • BACKGROUND: Immunophenotypic characterization of the leukemic cells has been widely used as a tool for diagnosis, classification, stratification and prognosis of leukaemia.
  • OBJECTIVE: To investigate the immunophenotypic subtype profiles of Iranian patients with acute lymphoblastic leukemia (ALL) and its association to disease outcome.
  • RESULTS: The samples were initially categorized into T-ALL (n=9), B-ALL (n=50) and mixed lineage (n=1) based on the expression patterns of CD3 and CD19 molecules.
  • B-ALL patients could further be classified into four subtypes, including Pro-B (n=7, 11.7%), Pre-B I (n=28, 46.7%), Pre-B II (n=13, 21.7%) and immature/mature B cells (n=2, 3.3%) on the basis of expression of CD10, CD19, CD20, HLA-DR and TdT.
  • Clinical manifestations and laboratory findings of the patients did not reveal association with immunophenotypic subtypes of ALL, with the exception of mediastinal mass and WBC count at the time of diagnosis which were found to be significantly higher in patients with T-ALL compared with B-ALL (p=0.001 and 0.014), respectively.
  • CONCLUSION: Our results indicate that overall the immunophenotypic profile of Iranian ALL patients is similar to previous reports and it might be used for monitoring of minimal residual disease and prognosis.
  • [MeSH-major] Immunophenotyping. Leukemia, B-Cell / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Adult. Child. Disease Progression. Humans. Iran / epidemiology. Predictive Value of Tests. Recurrence

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  • (PMID = 17652839.001).
  • [ISSN] 1735-1383
  • [Journal-full-title] Iranian journal of immunology : IJI
  • [ISO-abbreviation] Iran J Immunol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Iran
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67. Liu Y, Tang SQ, Yang G, Feng C, Liu LZ, Lei Q: [Skin lesions and myelodysplastic syndrome as initial manifestations of biphenotypic acute leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Oct;15(5):961-6
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  • [Title] [Skin lesions and myelodysplastic syndrome as initial manifestations of biphenotypic acute leukemia].
  • The aim of this study was to investigate the clinical, pathological and biological features of biphenotypic acute leukemia.
  • The results showed that extramedullary skin lesions and myelodysplasia occurred before the onset of overt disease.
  • At the time of diagnosis, this case had more than 30% blasts in bone marrow with meningeal involvement.
  • Flow cytometry revealed the co-expression of myeloid antigens (cMPO, CD33 and CD117) and T-lymphoid antigens (cCD3, CD5, CD7, dual expression of CD4 and CD8).
  • All above-mentioned results led to the diagnosis of biphenotypic acute leukemia.
  • It is concluded that the biphenotypic acute leukemia is an uncommon type of leukemia which may be preceded by myelodysplastic syndrome and has aggressive clinical and biological behavior.
  • Immunophenotype, cytogenetics and molecular analysis can contribute to early diagnosis of BAL and evaluation of prognosis.


68. Kuroda N, Mizobuchi M, Shimamura Y, Daibata M, Miyoshi I, Ohara M, Hirouchi T, Mizuno K, Lee GH: Bridging necrosis and reticulin bridging fibrosis induced by intrahepatic involvement of acute biphenotypic leukemia. APMIS; 2006 Dec;114(12):908-11
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  • [Title] Bridging necrosis and reticulin bridging fibrosis induced by intrahepatic involvement of acute biphenotypic leukemia.
  • A 47-year-old Japanese woman was diagnosed as having acute biphenotypic leukemia with association of t(9;22)(q34;q11).
  • In conclusion, extensive intrahepatic involvement by neoplastic cells in adult acute biphenotypic leukemia may cause the unusual "disorganized" hepatic fibrosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Liver Cirrhosis / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 17207092.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins c-sis; 0 / Reticulin; 0 / Transforming Growth Factor beta1; 0 / platelet-derived growth factor BB; 9007-34-5 / Collagen
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69. Kong CT, Sham MH, So CW, Cheah KS, Chen SJ, Chan LC: The Mll-Een knockin fusion gene enhances proliferation of myeloid progenitors derived from mouse embryonic stem cells and causes myeloid leukaemia in chimeric mice. Leukemia; 2006 Oct;20(10):1829-39
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  • [Title] The Mll-Een knockin fusion gene enhances proliferation of myeloid progenitors derived from mouse embryonic stem cells and causes myeloid leukaemia in chimeric mice.
  • Rearrangement of the mixed lineage leukaemia (MLL) gene with extra eleven nineteen (EEN) was previously identified in an infant with acute myeloid leukaemia.
  • Using homologous recombination, we have created a mouse equivalent of the human MLL-EEN allele and showed that when Mll(Een/+) embryonic stem (ES) cells were induced to differentiate in vitro into haemopoietic cells, there was increased proliferation of myeloid progenitors with self-renewal property.
  • We also generated Mll(Een/+) chimeric mice, which developed leukaemia displaying enlarged livers, spleens, thymuses and lymph nodes owing to infiltration of Mll(Een/+)-expressing leukemic cells.
  • Immunophenotyping of cells from enlarged organs and bone marrow (BM) of the Mll(Een/+) chimeras revealed an accumulation of Mac-1+/Gr-1- immature myeloid cells and a reduction in normal B- and T-cell populations.
  • We observed differential regulation of Hox genes between myeloid cells derived from Mll(Een/+) ES cells and mouse BM leukemic cells which suggested different waves of Hox expression may be activated by MLL fusion proteins for initiation (in ES cells) and maintenance (in leukemic cells) of the disease.
  • We believe studies of MLL fusion proteins in ES cells combined with in vivo animal models offer new approaches to the dissection of molecular events in multistep pathogenesis of leukaemia.
  • [MeSH-major] Hematopoietic Stem Cells / pathology. Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Myeloid Cells / pathology. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] Amino Acid Sequence. Animals. Base Sequence. Cell Division / physiology. Chimera. Disease Models, Animal. Female. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Genes, Homeobox / physiology. Humans. Infant. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Molecular Sequence Data. Translocation, Genetic

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  • (PMID = 16888613.001).
  • [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 / Intracellular Signaling Peptides and Proteins; 0 / SH3GL1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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70. Royer-Bégyn M, Teira P, Deybach JC, Mas E, Mazereeuw-Hautier J: [Porphyria cutanea tarda in a child undergoing bone marrow grafting]. Ann Dermatol Venereol; 2010 Oct;137(10):640-4
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  • [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


71. Matsumoto Y, Taki T, Fujimoto Y, Taniguchi K, Shimizu D, Shimura K, Uchiyama H, Kuroda J, Nomura K, Inaba T, Shimazaki C, Horiike S, Taniwaki M: Monosomies 7p and 12p and FLT3 internal tandem duplication: possible markers for diagnosis of T/myeloid biphenotypic acute leukemia and its clonal evolution. Int J Hematol; 2009 Apr;89(3):352-8
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  • [Title] Monosomies 7p and 12p and FLT3 internal tandem duplication: possible markers for diagnosis of T/myeloid biphenotypic acute leukemia and its clonal evolution.
  • Biphenotypic acute leukemia co-expressing T-lymphoid and myeloid markers is rare, accounting for less than 1% of acute leukemias.
  • Recurrence of monosomies 7p and/or 12p in T/myeloid biphenotypic acute leukemia has been reported.
  • We treated a patient with T/myeloid biphenotypic acute leukemia showing clonal chromosomal and genetic abnormalities including dic(7;12)(p11;p11) and Fms-like tyrosine kinase 3 (FLT3)-internal tandem duplication.
  • Cytogenetic analysis of both bone marrow and lymph node cells disclosed that the patient's lymph node leukemia cells had chromosomal abnormalities in addition to dic(7;12).
  • Our findings suggest that the leukemia cells of systemic lymphadenopathy had evolved as secondary cells from marrow leukemia cells.
  • The patient was successfully treated with induction chemotherapy for acute myeloid leukemia followed by allogeneic bone marrow transplantation.
  • [MeSH-major] Biomarkers, Tumor / genetics. Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 7 / genetics. Gene Duplication. Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / enzymology. fms-Like Tyrosine Kinase 3 / metabolism

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  • (PMID = 19308660.001).
  • [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
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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72. Zheng C, Wu J, Liu X, Ding K, Cai X, Zhu W: What is the optimal treatment for biphenotypic acute leukemia? Haematologica; 2009 Dec;94(12):1778-80; author reply 1780
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] What is the optimal treatment for biphenotypic acute leukemia?
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Biphenotypic, Acute / drug therapy

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  • (PMID = 19996120.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] Italy
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  • [Other-IDs] NLM/ PMC2791943
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73. Batinić D, Dubravcić K, Rajić L, Mikulić M, Labar B: [Biphenotypic and bilineal acute leukemias]. Acta Med Croatica; 2008 Oct;62(4):387-90
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  • [Title] [Biphenotypic and bilineal acute leukemias].
  • Human acute leukemias (AL) are classified as myeloid or lymphoid according to cytomorphology and the expression of leukocyte differentiation antigens/CD-markers.
  • However, in the minority of cases leukemic cells express markers of more than one lineage, which has led to the introduction of a new subgroup of acute leukemias termed mixed or biphenotypic acute leukemias (BAL).
  • In an effort to distinguish between BAL and those AL with aberrant expression of markers of other lineage, the European Group for the Immunological Characterization of Acute Leukemias (EGIL) has proposed a scoring system in which CD-markers are assigned a score of 0.5, 1.0 or 2.0, depending on the specificity of a particular antigen for myeloid, B- and/or T-lymphoid lineage, respectively.
  • The new WHO classification of hematologic tumors has adopted the EGIL criteria for BAL and introduced a new group of AL termed 'AL of ambiguous lineage'.
  • In addition to BAL in which a single cell population expresses both myeloid and lymphoid differentiation markers, this new group of leukemias also comprises cases that present with two separate blast populations (acute bilineal leukemia, aBLL).
  • In general, BAL accounts for less than 5% of all AL cases, whereas aBLL is a rare disease constituting 1%-2% of AL cases that contains B- or T-lymphoid along with myeloid blasts.
  • Chromosome abnormalities are frequent in both entities with a relatively high incidence of Philadelphia chromosome and rearrangements involving 11q23, especially in cases with B- and myeloid involvement.
  • Unfortunately, optimal therapy is not known, although regimens designed for acute lymphoblastic leukemia may result in a better response rate.
  • [MeSH-major] Leukemia, Biphenotypic, Acute

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  • (PMID = 19209464.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Croatia
  • [Number-of-references] 30
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74. Sárová I, Brezinová J, Zemanová Z, Izáková S, Lizcová L, Malinová E, Berková A, Cermák J, Maaloufová J, Nováková L, Michalová K: Cytogenetic manifestation of chromosome 11 duplication/amplification in acute myeloid leukemia. Cancer Genet Cytogenet; 2010 Jun;199(2):121-7
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  • [Title] Cytogenetic manifestation of chromosome 11 duplication/amplification in acute myeloid leukemia.
  • Gene amplification is a frequent genetic abnormality in solid tumors, and many oncogenes are activated in this way.
  • In acute myeloid leukemia (AML), a frequent target of gene amplification is chromosome 11, particularly chromosome region 11q23, including the MLL (myeloid/lymphoid leukemia) gene.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Gene Amplification. Gene Duplication. Leukemia, Myeloid, Acute / genetics. Trisomy

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20471515.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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75. Al-Seraihy AS, Owaidah TM, Ayas M, El-Solh H, Al-Mahr M, Al-Ahmari A, Belgaumi AF: Clinical characteristics and outcome of children with biphenotypic acute leukemia. Haematologica; 2009 Dec;94(12):1682-90
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  • [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
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76. Tsutsumi Y, Tanaka J, Minami H, Musashi M, Fukushima A, Ehira N, Kanamori H, Yamato H, Sasaki J, Funaki C, Hasegawa S, Obara S, Ogura N, Asaka M, Imamura M, Masauzi N: Acute biphenotypic leukemia and an acquired X chromosome. Cancer Genet Cytogenet; 2005 Feb;157(1):94-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute biphenotypic leukemia and an acquired X chromosome.
  • [MeSH-major] Chromosomes, Human, X. Leukemia / genetics. Sex Chromosome Aberrations
  • [MeSH-minor] Acute Disease. Aged. Humans. Male

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  • (PMID = 15676158.001).
  • [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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77. Georgy M, Yonescu R, Griffin CA, Batista DA: Acute mixed lineage leukemia and a t(6;14)(q25;q32) in two adults. Cancer Genet Cytogenet; 2008 Aug;185(1):28-31
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  • [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
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78. Oka S, Yokote T, Akioka T, Hara S, Kobayashi K, Hirata Y, Hiraoka N, Tsuji M, Hanafusa T: Trisomy 21 as the sole acquired karyotypic abnormality in biphenotypic acute leukemia. Int J Hematol; 2007 Apr;85(3):270-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trisomy 21 as the sole acquired karyotypic abnormality in biphenotypic acute leukemia.
  • [MeSH-major] Chromosome Aberrations. Down Syndrome / blood. Down Syndrome / pathology. Leukemia / genetics
  • [MeSH-minor] Acute Disease / classification. Acute Disease / therapy. Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Dexamethasone / therapeutic use. Doxorubicin / therapeutic use. Humans. Male. Treatment Outcome. Vincristine / therapeutic use


79. Nakagawa Y, Hasegawa M, Kurata M, Yamamoto K, Abe S, Inoue M, Takemura T, Hirokawa K, Suzuki K, Kitagawa M: Expression of IAP-family proteins in adult acute mixed lineage leukemia (AMLL). Am J Hematol; 2005 Mar;78(3):173-80
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  • [Title] Expression of IAP-family proteins in adult acute mixed lineage leukemia (AMLL).
  • To determine the apoptosis-resistant mechanism in adult acute mixed lineage leukemia (AMLL) with biphenotypic blasts responsible for resistance against chemotherapy, the expression levels of IAP-family proteins in AMLL bone marrow cells were analyzed by quantitative RT-PCR.
  • These findings suggest that higher expression of various IAPs is associated with the chemotherapy-resistant nature of this specific type of leukemia.
  • [MeSH-major] Apoptosis. Biomarkers, Tumor / metabolism. Bone Marrow Cells / metabolism. Leukemia, Biphenotypic, Acute / metabolism. Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Flow Cytometry. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Inhibitor of Apoptosis Proteins. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / metabolism. Leukemia, Monocytic, Acute / pathology. Male. Microtubule-Associated Proteins / analysis. Microtubule-Associated Proteins / metabolism. Middle Aged. Neoplasm Proteins. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15726601.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proteins; 0 / RNA, Messenger
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80. Dimou J, Jithoo R, Tsui A, Morokoff AP: Spinal cord compression as the initial presentation of acute biphenotypic leukaemia. J Clin Neurosci; 2009 Dec;16(12):1696-8
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  • [Title] Spinal cord compression as the initial presentation of acute biphenotypic leukaemia.
  • Acute biphenotypic leukaemia (BAL) is an uncommon haematological malignancy with features of myeloid and lymphoid origin and poor overall prognosis.
  • Histopathology confirmed the diagnosis of acute biphenotypic (B/myeloid) leukaemia.
  • He succumbed to the disease three months post-diagnosis after failing induction chemotherapy.
  • While central nervous system involvement with acute leukaemia is well recognised, this is the first reported patient with spinal cord compression secondary to this leukaemia subtype.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / etiology. Spinal Cord Compression / complications

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  • (PMID = 19815414.001).
  • [ISSN] 1532-2653
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antigens, CD79; EC 1.11.1.7 / Peroxidase
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81. Kim HR, Hong JH, Yoon CH, Lee SH, Park SH, Kim HY: Arthritis preceding acute biphenotypic leukemia. Clin Rheumatol; 2006 May;25(3):380-1
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  • [Title] Arthritis preceding acute biphenotypic leukemia.
  • [MeSH-major] Arthritis / etiology. Leukemia / complications
  • [MeSH-minor] Acute Disease. Adult. Ankle / pathology. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Antineoplastic Agents / therapeutic use. Female. Humans. Magnetic Resonance Imaging. Pain / drug therapy. Phenotype

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  • [Cites] Acta Haematol. 1999 Mar;101(1):1-6 [10085431.001]
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  • (PMID = 16220224.001).
  • [ISSN] 0770-3198
  • [Journal-full-title] Clinical rheumatology
  • [ISO-abbreviation] Clin. Rheumatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents
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82. Ramamoorthy SK, Pandita R, Prakash A, Ramaswamy NV, Al Bahar S: Safety of imatinib in chronic myeloid leukemia in blastic crisis presenting as cholestatic jaundice. Acta Haematol; 2007;118(3):141-5
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  • [Title] Safety of imatinib in chronic myeloid leukemia in blastic crisis presenting as cholestatic jaundice.
  • Acute leukemia presenting as cholestatic jaundice is rare.
  • It can occur due to granulocytic sarcoma compressing the bile ducts in case of acute myeloid leukemia.
  • We report a case of chronic myeloid leukemia in lymphoid blast cell crisis presenting with severe cholestatic jaundice due to diffuse infiltration of the liver sinusoids with lymphoblasts.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Blast Crisis / drug therapy. Jaundice, Obstructive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Liver Neoplasms / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Adult. Benzamides. Diagnosis, Differential. Drug-Related Side Effects and Adverse Reactions. Humans. Imatinib Mesylate. Male


83. Mandal C, Dutta A, Mallick A, Chandra S, Misra L, Sangwan RS, Mandal C: Withaferin A induces apoptosis by activating p38 mitogen-activated protein kinase signaling cascade in leukemic cells of lymphoid and myeloid origin through mitochondrial death cascade. Apoptosis; 2008 Dec;13(12):1450-64
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  • [Title] Withaferin A induces apoptosis by activating p38 mitogen-activated protein kinase signaling cascade in leukemic cells of lymphoid and myeloid origin through mitochondrial death cascade.
  • Here we demonstrate how WA exhibits a strong growth-inhibitory effect on several human leukemic cell lines and on primary cells from patients with lymphoblastic and myeloid leukemia in a dose-dependent manner, showing no toxicity on normal human lymphocytes and primitive hematopoietic progenitor cells.
  • WA-mediated decrease in cell viability was observed through apoptosis as demonstrated by externalization of phosphatidylserine, a time-dependent increase in Bax/Bcl-2 ratio; loss of mitochondrial transmembrane potential, cytochrome c release, caspases 9 and 3 activation; and accumulation of cells in sub-G0 region based on DNA fragmentation.
  • WA caused increased levels of Bax in response to MAPK signaling, which resulted in the initiation of mitochondrial death cascade, and therefore it holds promise as a new, alternative, inexpensive chemotherapeutic agent for the treatment of patients with leukemia of both lymphoid and myeloid origin.
  • [MeSH-major] Apoptosis / drug effects. Ergosterol / analogs & derivatives. Leukemia. MAP Kinase Signaling System / physiology. Mitochondria. Tumor Cells, Cultured / drug effects. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Animals. Caspase Inhibitors. Caspases / metabolism. Cell Survival / drug effects. Dose-Response Relationship, Drug. Enzyme Activation. Humans. Medicine, Traditional. Membrane Potential, Mitochondrial / drug effects. Mice. Molecular Structure. Plants, Medicinal / chemistry. Poly(ADP-ribose) Polymerases / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Withanolides. bcl-2-Associated X Protein / metabolism

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  • (PMID = 18987975.001).
  • [ISSN] 1573-675X
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Caspase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Small Interfering; 0 / Withanolides; 0 / bcl-2-Associated X Protein; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspases; L6DO3QW4K5 / withaferin A; Z30RAY509F / Ergosterol
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84. Cerveira N, Meyer C, Santos J, Torres L, Lisboa S, Pinheiro M, Bizarro S, Correia C, Norton L, Marschalek R, Teixeira MR: A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia. BMC Cancer; 2010;10:518
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  • [Title] A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia.
  • BACKGROUND: Abnormalities of 11q23 involving the MLL gene are found in approximately 10% of human leukemias.
  • In this work we present the identification of a novel MLL fusion partner in a pediatric patient with de novo biphenotypic acute leukemia.
  • METHODS: Cytogenetics, fluorescence in situ hybridization (FISH), molecular studies (RT-PCR and LDI-PCR), and bioinformatic sequence analysis were used to characterize the CT45A2 gene as novel MLL fusion partner in pediatric acute leukemia.
  • CONCLUSION: We have identified CT45A2 as a novel spliced MLL fusion partner in a pediatric patient with de novo biphenotypic acute leukemia, as a result of a cryptic insertion of 11q23 in Xq26.3.
  • Since CT45A2 is the first Cancer/Testis antigen family gene found fused with MLL in acute leukemia, future studies addressing its biologic relevance for leukemogenesis are warranted.
  • [MeSH-major] Antigens, Neoplasm / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 20920256.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / CT45A1 protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC2956734
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85. Jin ZX, Zhang SL, Wang XM, Bi SH, Xin M, Zhou JJ, Cui Q, Duan WX, Wang HB, Yi DH: The myocardial protective effects of a moderate-potassium adenosine-lidocaine cardioplegia in pediatric cardiac surgery. J Thorac Cardiovasc Surg; 2008 Dec;136(6):1450-5
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  • 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
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86. Boatsman EE, Fu CH, Song SX, Moore TB: Graft-versus-leukemia effect on infant lymphoblastic leukemia relapsed after sibling hematopoietic stem cell transplantation. J Pediatr Hematol Oncol; 2010 Mar;32(2):e57-60
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  • [Title] Graft-versus-leukemia effect on infant lymphoblastic leukemia relapsed after sibling hematopoietic stem cell transplantation.
  • INTRODUCTION: Infant acute lymphoblastic leukemia (ALL) is considered a high-risk entity.
  • By morphology, infant ALL is classified as a lymphoid lineage leukemia; however, its physiologic behavior has brought many to consider it a pathologic hybrid between lymphoid leukemia and myeloid leukemias.
  • As such, standard of care currently employs the use of chemotherapeutic agents used commonly in ALL protocols and agents typically reserved for the treatment of myelogenous lineage leukemias.
  • The role of hematopoietic stem cell transplantation and graft-versus-leukemia effect in these patients has not been well studied.
  • CASE PRESENTATION: An earlier healthy 9-week-old Hispanic male diagnosed with precursor B-cell lymphoblastic leukemia was treated with protocol P9407 and matched sibling hematopoietic stem cell transplantation.
  • The sole antigraft-versus-host disease (GVHD) agent, cyclosporine, was discontinued.
  • He remains disease free more than 2 years posttransplant.
  • CONCLUSION: Traditionally, graft-versus-leukemia effect was thought to contribute therapeutically little to the treatment of ALL by hematopoietic stem cell transplantation (HSCT).
  • The effects of graft-versus-leukemia immunologic phenomenon in our patient with infant acute lymphoblastic leukemia underscore the potential that infant ALL may not be entirely the same biologic entity as standard pediatric ALL and may be more responsive than understood earlier.
  • Therapeutic response and appearance of GVHD after the withdrawal of immunosuppression in this patient provides evidence that graft-versus-leukemia effect may play a role in disease control in infant ALL after HSCT.
  • This suggests that other immunotherapeutic interventions in the context of relapse may offer potential clinical benefit in this disease.
  • [MeSH-major] Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 20168246.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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87. Di Croce L: Chromatin modifying activity of leukaemia associated fusion proteins. Hum Mol Genet; 2005 Apr 15;14 Spec No 1:R77-84
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  • [Title] Chromatin modifying activity of leukaemia associated fusion proteins.
  • The leukaemias, which are divided into chronic and acute forms, are malignant diseases of haematopoietic cells in which the proper balance between proliferation, differentiation and apoptosis is no longer operative.
  • Genes, such as those of mixed-lineage leukaemia, AML1 and retinoic acid receptor alpha, have been found to be aberrantly fused to different partners, which often encode transcription factors or other chromatin modifying enzymes, in numerous types of acute lymphoid and myeloid leukaemias.
  • These chimeric fusion oncoproteins, generated by reciprocal chromosomal translocations, are responsible for chromatin alterations on target genes whose expression is critical to stem cell development or lineage specification in haematopoiesis.
  • [MeSH-major] Chromatin / metabolism. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Neoplastic. Leukemia / metabolism. Proto-Oncogene Proteins / metabolism. Receptors, Retinoic Acid / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Differentiation. Core Binding Factor Alpha 2 Subunit. DNA Methylation. Epigenesis, Genetic. Gene Silencing. Hematopoiesis. Humans. Models, Biological. Molecular Sequence Data. Oncogene Proteins, Fusion / chemistry

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  • (PMID = 15809276.001).
  • [ISSN] 0964-6906
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromatin; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / retinoic acid receptor alpha
  • [Number-of-references] 64
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88. Gluzman DF, Nadgornaya VA, Sklyarenko LM, Ivanovskaya TS, Poludnenko LY, Ukrainskaya NI: Immunocytochemical markers in acute leukaemias diagnosis. Exp Oncol; 2010 Sep;32(3):195-9
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  • [Title] Immunocytochemical markers in acute leukaemias diagnosis.
  • The study included 1742 patients with acute myeloblastic leukaemias (AML) and acute lymphoblastic leukaemias (ALL), Kyiv city residents and patients from 20 regions of Ukraine.
  • Bone marrow and blood smears were sent at diagnosis to Reference Center.
  • Immunocytochemical techniques (APAAP, LSAB) and broad panel of monoclonal antibodies (MoAbs) against lineage specific and differentiation antigens of leukocytes were employed for immunophenotyping of leukemic blast cells directly in blood and bone marrow smears.
  • Different types of AML were defined by the expression of the cell surface and cytoplasmic antigens.
  • Immunocytochemical study was required especially in diagnosing of AML with minimal differentiation, acute megakaryoblastic leukaemia, acute erythroid leukaemia and acute leukaemias of ambiguous lineage.
  • Acute lymphoblastic leukaemias was broadly classified into B-lineage and T-lineage ALL.
  • According to the degree of B-lymphoid differentiation of the blast cells four subtypes of B-lineage ALL were established.
  • T-lineage ALL observed in patients were also divided into four subtypes.
  • Immunocytochemical examination was required to diagnose AL of ambiguous lineage with no clear evidence of lineage differentiation (acute undifferentiated leukaemia) or those with blasts that express markers of more than one lineage (mixed phenotype acute leukaemias).
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Acute Disease. Biomarkers, Tumor / immunology. Humans. Immunohistochemistry. Immunophenotyping. Lymphocyte Subsets / immunology. Lymphocyte Subsets / pathology

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  • (PMID = 21403617.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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89. Gibaud S, Zirar SB, Mutzenhardt P, Fries I, Astier A: Melarsoprol-cyclodextrins inclusion complexes. Int J Pharm; 2005 Dec 8;306(1-2):107-21
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  • Melarsoprol, a water-insoluble drug, is mainly used in the treatment of trypanosomiasis and has demonstrated an in vitro activity on myeloid and lymphoid leukemia derived cell lines.
  • However, the cytotoxic properties of melarsoprol on K562 and U937 human leukemia cell lines was not modified by complexation.
  • [MeSH-minor] Cell Line, Tumor. Cell Survival / drug effects. Drug Compounding. Drug Stability. Humans. Kinetics. Magnetic Resonance Spectroscopy. Molecular Structure. Solubility

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  • (PMID = 16253447.001).
  • [ISSN] 0378-5173
  • [Journal-full-title] International journal of pharmaceutics
  • [ISO-abbreviation] Int J Pharm
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclodextrins; ZF3786Q2E8 / Melarsoprol
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90. Lou Z, Zhang CC, Tirado CA, Slone T, Zheng J, Zaremba CM, Oliver D, Chen W: Infantile mixed phenotype acute leukemia (bilineal and biphenotypic) with t(10;11)(p12;q23);MLL-MLLT10. Leuk Res; 2010 Aug;34(8):1107-9
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  • [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
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91. Park AH, Muntz HR, Smith ME, Afify Z, Pysher T, Pavia A: Pediatric invasive fungal rhinosinusitis in immunocompromised children with cancer. Otolaryngol Head Neck Surg; 2005 Sep;133(3):411-6
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  • RESULTS: Seventeen consecutive pediatric immunocompromised patients with hematologic and lymphoid neoplasms underwent nasal endoscopy and biopsy for possible FS.
  • Eight patients had acute myelogenous leukemia (AML); 6 patients had acute lymphoblastic leukemia (ALL); 1 patient had Burkitt's lymphoma, 1 patient had undifferentiated leukemia; and 1 patient had biphenotypic acute leukemia.

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  • (PMID = 16143192.001).
  • [ISSN] 0194-5998
  • [Journal-full-title] Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery
  • [ISO-abbreviation] Otolaryngol Head Neck Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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92. El-Ziny MA, Al-Tonbary YA, Salama OS, Bakr AA, Al-Marsafawy H, Elsharkawy AA: Low turnover bone disease in Egyptian children with acute leukemia. Hematology; 2005 Aug;10(4):327-33
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  • [Title] Low turnover bone disease in Egyptian children with acute leukemia.
  • The aim of this work was to study bone turnover markers, calcium homeostasis and bone mineral density (BMD) in children with acute leukemia at diagnosis, after induction chemotherapy, and during maintenance therapy to delineate abnormalities present.
  • After evaluation of L2-L4 BMD using dual-energy X-ray absorptiometry in patients with acute myeloid and lymphoid leukemia at presentation and after treatment, the results were compared to 352 healthy age- and sex-matched Egyptian controls.
  • Osteopenia was observed at diagnosis and during treatment in patients with acute leukemia.
  • At diagnosis osteopenia was observed in 27 patients (62.8%): 10 (23.3%) had non severe osteopenia and 17 (39.5%) had severe osteopenia.
  • Parathyroid hormone (PTH) (pg/ml) levels demonstrated non significant differences between children with acute leukemia at different stages of therapy and controls, while, 25 (OH) D3 (ng/ml) was significantly lower in acute leukemia patients at different stages of therapy compared to controls (p<0.001).
  • Osteocalcin (ng/ml) is significantly lower in patients at different stages of the disease compared to controls (p<0.001) but there was no significant difference between patients at different stages of therapy.
  • Deoxy-pyridoline cross links showed non-significant difference between the different types of acute leukemia and with controls.
  • Osteopenia is a significant problem in children with acute leukemia at presentation and after chemotherapy.
  • Osteopenia in acute leukemia appears to be of the low turnover type (decreased osteoblastic activity and decreased bone mineralization).
  • [MeSH-major] Bone Density. Bone Diseases, Metabolic / blood. Bone Remodeling. Leukemia / blood
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Cholecalciferol / blood. Egypt. Humans. Infant. Male. Osteoblasts / metabolism. Osteocalcin / blood. Parathyroid Hormone / blood

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  • (PMID = 16085546.001).
  • [ISSN] 1024-5332
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Parathyroid Hormone; 104982-03-8 / Osteocalcin; 1C6V77QF41 / Cholecalciferol
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93. Vanura K, Vrsalovic MM, Le T, Marculescu R, Kusec R, Jäger U, Nadel B: V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2009 Aug;48(8):725-36
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  • [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
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94. Pullarkat V, Veliz L, Chang K, Mohrbacher A, Teotico AL, Forman SJ, Slovak ML: Therapy-related, mixed-lineage leukaemia translocation-positive, monoblastic myeloid sarcoma of the uterus. J Clin Pathol; 2007 May;60(5):562-4
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  • [Title] Therapy-related, mixed-lineage leukaemia translocation-positive, monoblastic myeloid sarcoma of the uterus.
  • Myeloid sarcomas are tumour masses of myeloid leukaemic cells at extramedullary sites.
  • These tumours can, on occasion, occur without concurrent or antecedent leukaemia.
  • Myeloid sarcomas have been described at unusual locations including the female genital tract.
  • An unusual case of therapy-related acute myeloid leukaemia (t-AML) presenting as isolated monoblastic myeloid sarcoma of the uterus in a patient who had received adjuvant chemotherapy for breast cancer is presented.
  • Fluorescence in situ hybridisation analysis performed on paraffin-wax-embedded tumour tissue revealed a mixed-lineage leukaemia (MLL) gene rearrangement, supporting the association of this malignancy with prior chemotherapy.
  • This case illustrates that t-AML can rarely present as isolated extramedullary tumours, and the detection of specific chromosomal abnormalities in these myeloid sarcomas can be useful for risk assessment and guiding definitive therapy.

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  • [Cites] Am J Clin Pathol. 2000 Nov;114(5):807-11 [11068557.001]
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  • (PMID = 17513515.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA030206; United States / NCI NIH HHS / CA / 2 P01 CA030206-24A1; United States / NCI NIH HHS / CA / 5P30 CA33572
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1994540
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95. Iacobucci I, Storlazzi CT, Cilloni D, Lonetti A, Ottaviani E, Soverini S, Astolfi A, Chiaretti S, Vitale A, Messa F, Impera L, Baldazzi C, D'Addabbo P, Papayannidis C, Lonoce A, Colarossi S, Vignetti M, Piccaluga PP, Paolini S, Russo D, Pane F, Saglio G, Baccarani M, Foà R, Martinelli G: Identification and molecular characterization of recurrent genomic deletions on 7p12 in the IKZF1 gene in a large cohort of BCR-ABL1-positive acute lymphoblastic leukemia patients: on behalf of Gruppo Italiano Malattie Ematologiche dell'Adulto Acute Leukemia Working Party (GIMEMA AL WP). Blood; 2009 Sep 3;114(10):2159-67
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  • [Title] Identification and molecular characterization of recurrent genomic deletions on 7p12 in the IKZF1 gene in a large cohort of BCR-ABL1-positive acute lymphoblastic leukemia patients: on behalf of Gruppo Italiano Malattie Ematologiche dell'Adulto Acute Leukemia Working Party (GIMEMA AL WP).
  • The BCR-ABL1 fusion gene defines the subgroup of acute lymphoblastic leukemia (ALL) with the worst clinical prognosis.
  • The IKZF1 deletion also was identified in the progression of chronic myeloid leukemia to lymphoid blast crisis (66%) but never in myeloid blast crisis or chronic-phase chronic myeloid leukemia or in patients with acute myeloid leukemia.
  • [MeSH-major] Base Sequence / genetics. Chromosomes, Human, Pair 7 / genetics. Fusion Proteins, bcr-abl / genetics. Ikaros Transcription Factor / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Deletion
  • [MeSH-minor] Adolescent. Adult. Aged. Blast Crisis / genetics. Blast Crisis / metabolism. Cell Line, Tumor. Codon, Initiator / genetics. Codon, Initiator / metabolism. Cohort Studies. Exons / genetics. Female. Gene Expression Regulation, Leukemic / genetics. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Male. Microarray Analysis. Middle Aged. Polymorphism, Single Nucleotide

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  • [ErratumIn] Blood. 2010 Sep 23;116(12):2196
  • (PMID = 19589926.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon, Initiator; 0 / IKZF1 protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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96. Pieters R, Schrappe M, De Lorenzo P, Hann I, De Rossi G, Felice M, Hovi L, LeBlanc T, Szczepanski T, Ferster A, Janka G, Rubnitz J, Silverman L, Stary J, Campbell M, Li CK, Mann G, Suppiah R, Biondi A, Vora A, Valsecchi MG: A treatment protocol for infants younger than 1 year with acute lymphoblastic leukaemia (Interfant-99): an observational study and a multicentre randomised trial. Lancet; 2007 Jul 21;370(9583):240-50
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  • [Title] A treatment protocol for infants younger than 1 year with acute lymphoblastic leukaemia (Interfant-99): an observational study and a multicentre randomised trial.
  • BACKGROUND: Acute lymphoblastic leukaemia in infants younger than 1 year is rare, and infants with the disease have worse outcomes than do older children.
  • We initiated an international study to investigate the effects of a new hybrid treatment protocol with elements designed to treat both acute lymphoblastic leukaemia and acute myeloid leukaemia, and to identify any prognostic factors for outcome in infants.
  • Eligible patients were stratified for risk according to their peripheral blood response to a 7-day prednisone prophase, and then given a hybrid regimen based on the standard protocol for acute lymphoblastic leukaemia, with some elements designed for treatment of acute myeloid leukaemia.
  • The primary outcomes were event-free survival (EFS) for the initial cohort of patients and disease-free survival (DFS) for the patients randomly assigned to a treatment group.
  • FINDINGS: In the 482 enrolled patients who underwent hybrid treatment, 260 (58%) were in complete remission at a median follow-up of 38 (range 1-78) months, and EFS at 4 years was 47.0% (SE 2.6, 95% CI 41.9-52.1).
  • At a median follow-up of 42 (range 1-73) months, 60 patients in the treatment group and 57 controls were disease-free.
  • All types of rearrangements in the (mixed lineage leukaemia) MLL gene, very high white blood cell count, age of younger than 6 months, and a poor response to the prednisone prophase were independently associated with inferior outcomes.
  • INTERPRETATION: Patients treated with our hybrid protocol, and especially those who responded poorly to prednisone, had higher EFS than most reported outcomes for treatment of infant ALL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [CommentIn] Lancet. 2007 Jul 21;370(9583):198-200 [17658376.001]
  • (PMID = 17658395.001).
  • [ISSN] 1474-547X
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00015873; ISRCTN/ ISRCTN24251487
  • [Grant] United Kingdom / Medical Research Council / / G0300130
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate
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97. Okada Y, Jiang Q, Lemieux M, Jeannotte L, Su L, Zhang Y: Leukaemic transformation by CALM-AF10 involves upregulation of Hoxa5 by hDOT1L. Nat Cell Biol; 2006 Sep;8(9):1017-24
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  • 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
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98. Naghashpour M, Lancet J, Moscinski L, Zhang L: Mixed phenotype acute leukemia with t(11;19)(q23;p13.3)/ MLL-MLLT1(ENL), B/T-lymphoid type: A first case report. Am J Hematol; 2010 Jun;85(6):451-4
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  • [Title] Mixed phenotype acute leukemia with t(11;19)(q23;p13.3)/ MLL-MLLT1(ENL), B/T-lymphoid type: A first case report.
  • The majority of cases of acute leukemia belong to a specific lineage origin, either lymphoid or myeloid, and therefore are classified as acute lymphoblastic leukemia (ALL) or acute myelogenous leukemia (AML), based on morphologic features and cytochemical and immunophenotypic profile of the blast cells.
  • A minority of acute leukemias however, show no clear evidence of differentiation along a single lineage.
  • These are now classified under acute leukemias of ambiguous lineage by the most recent WHO classification and account for <4% of all cases of acute leukemia [1].
  • They include leukemias with no lineage specific antigens (acute undifferentiated leukemias) and those with blasts that express antigens of more than one lineage to such degree that it is not possible to assign the leukemia to any one particular lineage with certainty (mixed phenotype acute leukemias).
  • The latter can either be leukemias with two distinct populations of blasts, each expressing antigens of a different lineage (historically referred to as "bilineal" leukemias) or a single blast population expressing antigens of multiple lineages (historically referred to as "biphenotypic" acute leukemias) [2].
  • Acute leukemias of ambiguous lineage may harbor a variety of genetic lesions.
  • Those with t(9;22)(q34;q11) or translocations associated with mixed lineage leukemias (MLL) gene, i.e., t(11;V)(q23;V), occur frequently enough and are associated with distinct features, that are considered as separate entities according to the recent WHO classification.
  • Co-expression of myeloid and B-lymphoid antigens is most common in mixed phenotype acute leukemia (MPAL), followed by co-expression of myeloid and T-lymphoid antigens, accounting for 66-70% and 23-24% of MLLs, respectively.
  • Coexpression of B- and T-lineage associated antigens or antigens of all three lineages is exceedingly rare, accounting for <5% of MLLs [3,4].
  • The requirements for assigning more than one lineage to a single blast population has been established by current WHO classification [1].
  • [MeSH-major] Antigens, Neoplasm / blood. Chromosomes, Human, Pair 11 / ultrastructure. Chromosomes, Human, Pair 19 / ultrastructure. Immunophenotyping. Leukemia / classification. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / analysis. Bone Marrow / pathology. Cell Lineage. Gene Rearrangement. Humans. In Situ Hybridization, Fluorescence. Male. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 20513125.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / MLL-ENL oncoprotein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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99. Wang L, Lin D, Zhang X, Chen S, Wang M, Wang J: Analysis of FLT3 internal tandem duplication and D835 mutations in Chinese acute leukemia patients. Leuk Res; 2005 Dec;29(12):1393-8
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  • [Title] Analysis of FLT3 internal tandem duplication and D835 mutations in Chinese acute leukemia patients.
  • Genomic aberrations of Fms-like tyrosine kinase 3 (FLT3), including internal tandem duplication (ITD) and point mutations, have been demonstrated in 25-30% of adults acute myeloid leukemia (AML) and are markers of poor prognosis.
  • FLT3/ITD and D835 mutations were analyzed in 194 Chinese patients with acute leukemia and myelodysplastic syndromes (MDS) by polymerase chain reaction (PCR).
  • However, neither aberrations was found in 25 patients with acute lymphoblastic leukemia (ALL), 2 acute hybrid leukemia, 17 MDS and 7 chronic myeloid leukemia in blast crisis (CML-BC).
  • [MeSH-major] Leukemia / genetics. Mutation, Missense. Tandem Repeat Sequences. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Amino Acid Sequence. Asian Continental Ancestry Group / genetics. DNA Mutational Analysis. Female. Humans. Leukocytosis. Male. Middle Aged. Molecular Sequence Data. Myelodysplastic Syndromes / genetics. Prognosis. Remission Induction


100. Dickson GJ, Lappin TR, Thompson A: Complete array of HOX gene expression by RQ-PCR. Methods Mol Biol; 2009;538:369-93
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  • Many of the chromosomal translocations associated with acute leukemias involve HOX genes directly or some of their regulatory factors, e.g., mixed lineage leukaemia (MLL), leading to inappropriate expression of certain subsets of the genes.
  • Defining the roles for HOX in hematopoiesis should help to elucidate the mechanisms of deregulation in leukemia and eventually identify targets for therapeutic intervention.

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  • (PMID = 19277582.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Homeodomain Proteins
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