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1. Jurcic JG: Ab therapy of AML: native anti-CD33 Ab and drug conjugates. Cytotherapy; 2008;10(1):7-12
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  • [Title] Ab therapy of AML: native anti-CD33 Ab and drug conjugates.
  • While the humanized anti-CD33MAb lintuzumab has only modest single-agent activity against overt AML, it can eliminate minimal residual disease detectable by reverse transcription-PCR in acute promyelocytic leukemia.
  • Targeted chemotherapy with the anti−CD33−calicheamicin construct gemtuzumab ozogamicin has produced remissions in patients with relapsed AML and appears promising when used in combination with standard chemotherapy in the treatment of newly diagnosed AML.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD / therapeutic use. Antigens, Differentiation, Myelomonocytic / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 17917880.001).
  • [ISSN] 1477-2566
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 0 / lintuzumab
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2. Lo-Coco F, Ammatuna E, Montesinos P, Sanz MA: Acute promyelocytic leukemia: recent advances in diagnosis and management. Semin Oncol; 2008 Aug;35(4):401-9
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  • [Title] Acute promyelocytic leukemia: recent advances in diagnosis and management.
  • Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia (AML) characterized by a specific genetic alteration, affecting the retinoic acid receptor-alpha (RARalpha), and leading to a blockage in the differentiation of the granulocytic cells.
  • The body of available biological information on APL establishes this leukemia as a unique entity that has to be promptly recognized and clearly distinguished from all other acute leukemias, especially in light of its striking response to treatment with anthracyclines and differentiating agents such as all-trans retinoic acid (ATRA) or arsenic trioxide (ATO).
  • Current state-of-the-art treatments, which include simultaneous administration of ATRA and anthracycline-based chemotherapy for induction and consolidation, as well as ATRA-based maintenance, have dramatically transformed APL into the most curable acute leukemia in adults, with approximately 80% of long-term survivors.
  • Given the high anti-leukemic efficacy observed with ATO in patients who relapse, this agent is currently regarded as the best treatment option in this setting.
  • We also highlight other aspects that can be crucial for the outcome of individual patients, including supportive care, recognition and treatment of life-threatening complications, management of ATRA- and ATO-associated adverse events, and the role of minimal residual disease (MRD) monitoring.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / therapy

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  • (PMID = 18692690.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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3. Tallman MS: The expanding role of arsenic in acute promyelocytic leukemia. Semin Hematol; 2008 Jul;45(3 Suppl 2):S25-9
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  • [Title] The expanding role of arsenic in acute promyelocytic leukemia.
  • Ten percent to 15% of adults in the United States with acute myeloid leukemia (AML) are diagnosed with acute promyelocytic leukemia (APL) each year, which amounts to approximately 1,200 newly diagnosed patients.
  • In almost all APL patients, the retinoic acid receptor-alpha (RARalpha) gene on chromosome 17 is involved in a reciprocal translocation with the promyelocytic leukemia gene (PML) on chromosome 15, denoted as t(15;17)(q22;q12).
  • Identification of this fusion transcript is important for both diagnosis and for detection of minimal residual disease.
  • All-trans retinoic acid (ATRA) causes cells to differentiate and arsenic trioxide (ATO) induces both differentiation and apoptosis.
  • Curative treatments that avoid conventional chemotherapeutic agents and/or extended maintenance strategies for low- and intermediate-risk patients appear possible.
  • High-risk patients continue to present a challenge, but a number of innovative agents and strategies are currently under active study.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 18760708.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 32
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4. Horikoshi A, Takei K, Iriyama N, Uenogawa K, Ishizuka H, Shiraiwa H, Hosokawa Y, Sawada S, Kitoh T: Effect of L-asparaginase combined with vincristine and prednisolone on acute myeloblastic leukemia (M0) associated with non-Hodgkin lymphoma. Acta Haematol; 2009;122(1):54-7
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  • [Title] Effect of L-asparaginase combined with vincristine and prednisolone on acute myeloblastic leukemia (M0) associated with non-Hodgkin lymphoma.
  • She was eventually diagnosed as having acute myeloblastic leukemia (AML;.
  • M0) with non-Hodgkin lymphoma (NHL).
  • We investigated the therapeutic efficacy of L-asparaginase (L-Asp), vincristine and prednisolone for both her AML and NHL.
  • Asparagine synthetase (AS) activity in her AML blast cells was undetectable.
  • A lymph node biopsy specimen revealed NHL of the marginal zone B cell type.
  • Complete remission (CR) of AML and NHL was achieved.
  • CR of the AML lasted for 18 months without further consolidation therapy.
  • We conclude that L-Asp can be an effective drug for the treatment of AML in which blasts are negative for AS.
  • [MeSH-major] Asparaginase / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Lymphoma, Non-Hodgkin / drug therapy. Prednisolone / therapeutic use. Vincristine / therapeutic use

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  • [Copyright] 2009 S. Karger AG, Basel
  • (PMID = 19816010.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 9PHQ9Y1OLM / Prednisolone; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase
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5. Candoni A, Martinelli G, Toffoletti E, Chiarvesio A, Tiribelli M, Malagola M, Piccaluga PP, Michelutti A, Simeone E, Damiani D, Russo D, Fanin R: Gemtuzumab-ozogamicin in combination with fludarabine, cytarabine, idarubicin (FLAI-GO) as induction therapy in CD33-positive AML patients younger than 65 years. Leuk Res; 2008 Dec;32(12):1800-8
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  • [Title] Gemtuzumab-ozogamicin in combination with fludarabine, cytarabine, idarubicin (FLAI-GO) as induction therapy in CD33-positive AML patients younger than 65 years.
  • INTRODUCTION: The addition of gemtuzumab-ozogamicin (GO) to an induction regimen including synergistic drugs, such as intermediate dose of cytarabine (Ara-C), idarubicin and fludarabine (FLAI), could reduce treatment failure in acute myeloid leukemia (AML) patients.
  • Thirty consecutive AML patients were included.
  • Hematopoietic stem cell transplant (HSCT) was planned for all high risk AML patients in first complete remission (CR) after consolidation with intermediate doses of Ara-C and idarubicin (IDAC-IDA).
  • WT1 expression and cytogenetic (in positive cases) analyses were performed after induction to detect and follow minimal residual disease.
  • CONCLUSIONS: These preliminary results suggest that FLAI-GO is an effective and well tolerated induction regimen for CD33 positive AML patients younger than 65 years, with a high complete response rate, favourable safety profile, low DDI.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antigens, CD / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal, Humanized. Cytarabine / administration & dosage. Female. Filgrastim. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Idarubicin / administration & dosage. Male. Middle Aged. Recombinant Proteins. Remission Induction. Sialic Acid Binding Ig-like Lectin 3. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Young Adult

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  • (PMID = 18621416.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Recombinant Proteins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; PVI5M0M1GW / Filgrastim; ZRP63D75JW / Idarubicin
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6. Chen P, Wang J, Hope K, Jin L, Dick J, Cameron R, Brandwein J, Minden M, Reilly RM: Nuclear localizing sequences promote nuclear translocation and enhance the radiotoxicity of the anti-CD33 monoclonal antibody HuM195 labeled with 111In in human myeloid leukemia cells. J Nucl Med; 2006 May;47(5):827-36
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  • [Title] Nuclear localizing sequences promote nuclear translocation and enhance the radiotoxicity of the anti-CD33 monoclonal antibody HuM195 labeled with 111In in human myeloid leukemia cells.
  • Our objective was to evaluate the toxicity of the anti-CD33 monoclonal antibody HuM195 modified with peptides (CGYGPKKKRKVGG) harboring the nuclear localizing sequence (NLS; underlined) of simian virus 40 large T antigen and labeled with (111)In against acute myeloid leukemia (AML) cells.
  • The immunoreactivity of NLS-HuM195 was evaluated by its ability to displace the binding of (111)In-HuM195 to HL-60 leukemia cells.
  • The antiproliferative effects of (111)In-NLS-HuM195 and (111)In-HuM195 on HL-60, U937, or K562 cells with high, intermediate, or minimal CD33 expression, respectively, were studied.
  • The survival of HL-60 cells or patient AML specimens treated with (111)In-NLS-HuM195 or (111)In-HuM195 was studied.
  • The surviving fraction decreased >2-fold in 7 of 9 AML specimens treated with an excess of (111)In-NLS-HuM195 and >10-fold in 2 of these specimens.
  • There was no morphologic damage to the liver or kidneys.
  • CONCLUSION: We conclude that NLS-peptides routed (111)In-HuM195 to the nucleus of AML cells, where the emitted Auger electrons were lethal. (111)In-NLS-HuM195 is a promising targeted radiotherapeutic agent for AML.
  • [MeSH-major] Active Transport, Cell Nucleus. Antibodies, Monoclonal / chemistry. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Indium Radioisotopes / therapeutic use. Leukemia, Myeloid / radionuclide imaging. Leukemia, Myeloid / radiotherapy. Nuclear Localization Signals

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  • [CommentIn] J Nucl Med. 2006 May;47(5):738-9 [16644741.001]
  • (PMID = 16644753.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Cd33 protein, mouse; 0 / Indium Radioisotopes; 0 / Nuclear Localization Signals; 0 / Peptides; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / monoclonal antibody M195
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7. Tsimberidou AM, Giles FJ, Estey E, O'Brien S, Keating MJ, Kantarjian HM: The role of gemtuzumab ozogamicin in acute leukaemia therapy. Br J Haematol; 2006 Feb;132(4):398-409
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  • [Title] The role of gemtuzumab ozogamicin in acute leukaemia therapy.
  • Gemtuzumab ozogamicin (GO) is an immunoconjugate that binds to CD33 on the surface of acute myeloid leukaemia (AML) blasts and, after internalisation, releases a cytotoxic drug, calicheamicin.
  • GO is approved by the US Food and Drug Administration for the treatment of CD33-positive AML at first relapse in patients 60 years and older who are not candidates for other cytotoxic therapy.
  • GO as a single agent has low antileukaemic activity.
  • GO is probably most active in acute promyelocytic leukaemia (APL).
  • It is used for induction regimens in high-risk APL and for the elimination of minimal residual APL.
  • Case reports suggest that GO also has activity in CD33-positive acute lymphoblastic leukaemia.
  • In conclusion, single agent GO can induce responses in patients with CD33-positive AML in first recurrence.
  • The future of GO is its use in combination with other cytotoxic agents.
  • Ongoing clinical trials may better define the role of GO combinations, particularly in untreated AML.
  • [MeSH-major] Aminoglycosides / administration & dosage. Aminoglycosides / therapeutic use. Antibiotics, Antineoplastic / administration & dosage. Antibodies, Monoclonal / therapeutic use. Immunotoxins / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Antibodies, Monoclonal, Humanized. Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance. Enediynes. Humans. Protein Binding. Randomized Controlled Trials as Topic. Recurrence. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 16412015.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Enediynes; 0 / Immunotoxins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 108212-75-5 / calicheamicin gamma(1)I
  • [Number-of-references] 82
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8. Walter RB, Raden BW, Hong TC, Flowers DA, Bernstein ID, Linenberger ML: Multidrug resistance protein attenuates gemtuzumab ozogamicin-induced cytotoxicity in acute myeloid leukemia cells. Blood; 2003 Aug 15;102(4):1466-73
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  • [Title] Multidrug resistance protein attenuates gemtuzumab ozogamicin-induced cytotoxicity in acute myeloid leukemia cells.
  • Gemtuzumab ozogamicin (GO) is a novel immunoconjugate therapy for acute myeloid leukemia (AML).
  • To address whether multidrug resistance protein (MRP) affects GO susceptibility, we characterized Pgp, MRP1, and MRP2 expression in CD33+ cell lines and CD33+ AML samples and analyzed the effect of the Pgp inhibitor cyclosporine (CSA) and the MRP inhibitor MK-571 on GO-induced cytotoxicity.
  • CSA increased GO-induced cytotoxicity in 12 Pgp-positive samples, whereas MK-571 alone was effective in only one sample with minimal Pgp activity.
  • Because MK-571 and CSA failed to affect cytotoxicity in a portion of Pgp-positive/MRP-positive AML samples, additional resistance mechanisms are likely important.
  • [MeSH-major] Aminoglycosides. Anti-Bacterial Agents / pharmacology. Antibodies, Monoclonal / pharmacology. Immunotoxins / pharmacology. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / metabolism. P-Glycoproteins / metabolism
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Cell Survival / drug effects. Cyclosporins / pharmacology. Drug Resistance, Multiple. Drug Resistance, Neoplasm. HL-60 Cells. Humans. Propionates / pharmacology. Quinolines / pharmacology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Sialic Acid Binding Ig-like Lectin 3. Tumor Cells, Cultured

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  • (PMID = 12689934.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA92316
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Anti-Bacterial Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Cyclosporins; 0 / Immunotoxins; 0 / P-Glycoproteins; 0 / Propionates; 0 / Quinolines; 0 / RNA, Messenger; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 5Q9O54P0H7 / verlukast
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9. Chen S, Xue Y, Zhu X, Wu Y, Pan J: Minimally differentiated acute myeloid leukemia with t(12;22)(p13;q11) translocation showing primary multidrug resistance and expressing multiple multidrug-resistant proteins. Acta Haematol; 2007;118(1):38-41
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  • [Title] Minimally differentiated acute myeloid leukemia with t(12;22)(p13;q11) translocation showing primary multidrug resistance and expressing multiple multidrug-resistant proteins.
  • Here we report a rare chromosomal translocation, t(12;22)(p13;q11), which was detected in a 53-year-old female patient diagnosed as having minimally differentiated acute myeloid leukemia (AML-M0) according to the French-American-British classification criteria.
  • As far as we know, this is the first report of t(12;22)(p13;q11) translocation involving TEL and MN1 genes in an AML-M0 patient.
  • [MeSH-major] Drug Resistance, Multiple. Drug Resistance, Neoplasm. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins / analysis. Translocation, Genetic


10. Song JH, Kim HJ, Lee CH, Kim SJ, Hwang SY, Kim TS: Identification of gene expression signatures for molecular classification in human leukemia cells. Int J Oncol; 2006 Jul;29(1):57-64
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  • [Title] Identification of gene expression signatures for molecular classification in human leukemia cells.
  • Although the methods by which leukemia is classified have been improved for effective therapies, leukemia patients occasionally exhibit diverse, sometimes unpredictable, responses to treatment.
  • Consequently, these patients also evidence individually different clinical courses when administered with anti-leukemia drugs.
  • In order to find new, more precise molecular markers for leukemia classification, we have analyzed the gene expression profiles from 65 diagnostic bone marrow specimens of adult patients with AML, ALL, CML or CLL by using high-throughput DNA microarrays harboring approximately 8,300 unique human genes or expression sequence tags.
  • In the present study, we identified a group of leukemia-specific genes, which manifest gene expression profiles distinctly representative of normal bone marrow samples, as determined by a significance analysis of microarray (SAM) and GeneSpring 6.1 programs.
  • We also determined the minimal number of genes showing a difference between acute and chronic leukemia patient groups.
  • Furthermore, the unsupervised cluster analysis revealed a gene subset which can be used to distinguish between AML, ALL, CML and CLL patient groups, based on expression signatures.
  • Our results may provide a novel set of molecular criteria for the classification of leukemia patients, and may also facilitate effects to discovery new targets, allowing for more effective treatment of leukemia patients.
  • [MeSH-major] Biomarkers, Tumor / analysis. Bone Marrow Cells / metabolism. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD / genetics. Antigens, CD / metabolism. Antigens, Differentiation, T-Lymphocyte / genetics. Antigens, Differentiation, T-Lymphocyte / metabolism. Biopsy. Cluster Analysis. Female. Genetic Markers. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Lectins, C-Type. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Phosphatidylinositol 3-Kinases / genetics. Phosphatidylinositol 3-Kinases / metabolism. Transcription Factors / genetics. Transcription Factors / metabolism

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  • (PMID = 16773185.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Biomarkers, Tumor; 0 / CD69 antigen; 0 / Genetic Markers; 0 / HHEX protein, human; 0 / Homeodomain Proteins; 0 / Lectins, C-Type; 0 / Transcription Factors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human
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11. Jankovicová K, Krejsek J, Kopecký O, Voglová J, Novosad J: [Multidrug resistance markers monitoring in acute myeloid leukemia cells]. Cas Lek Cesk; 2004;143(7):471-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Multidrug resistance markers monitoring in acute myeloid leukemia cells].
  • BACKGROUND: P-gp, MRP, LRP, Bcl-2, and Bax proteins play an important role in the multidrug resistance of leukemic cells.
  • P-gp, MRP, and LRP proteins decrease the intracellular drug concentration, Bcl-2 and Bax proteins influence the apoptosis process.
  • The overexpression of some of these proteins is associated with poor prognosis of leukemia.
  • We compare also P-gp expression between acute myeloid leukemia (AML) FAB subgroups M0-M6.
  • METHODS AND RESULTS: With use of flow cytometry we measured the expression of P-gp, MRP, LRP, Bcl-2, and Bax proteins in acute myeloid leukemia patients cells.
  • In AML M0 FAB subgroup of patients the trend to higher P-gp protein expression was observed.
  • Some relations between multidrug resistance markers playing role in acute myeloid leukemia patients prognosis were suggested.
  • [MeSH-major] Leukemia, Myeloid / metabolism. Multidrug Resistance-Associated Proteins / analysis
  • [MeSH-minor] Acute Disease. Female. Flow Cytometry. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 15373290.001).
  • [ISSN] 0008-7335
  • [Journal-full-title] Casopís lékar̆ů c̆eských
  • [ISO-abbreviation] Cas. Lek. Cesk.
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Multidrug Resistance-Associated Proteins
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13. Matsuo Y, Drexler HG, Kaneda K, Kojima K, Ohtsuki Y, Hara M, Yasukawa M, Tanimoto M, Orita K: Megakaryoblastic leukemia cell line MOLM-16 derived from minimally differentiated acute leukemia with myeloid/NK precursor phenotype. Leuk Res; 2003 Feb;27(2):165-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Megakaryoblastic leukemia cell line MOLM-16 derived from minimally differentiated acute leukemia with myeloid/NK precursor phenotype.
  • The megakaryoblastic leukemia cell line MOLM-16 was established at relapse from the peripheral blood of a 77-year-old Japanese woman with minimally differentiated acute myeloid leukemia (AML-M0).
  • Immunophenotyping of the fresh leukemic cells revealed a myeloid/NK precursor phenotype being positive for CD7, CD13, CD33, CD34, and CD56.
  • The extensive immunological, cytogenetic and functional characterization of MOLM-16 suggests that this cell line may represent a scientifically significant in vitro model which could facilitate the evaluation of megakaryocytic differentiation.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / pathology. Tumor Cells, Cultured / cytology
  • [MeSH-minor] Aged. Cell Differentiation. Cell Division / drug effects. Cell Lineage. Chromosomes, Human, Pair 18. Chromosomes, Human, Pair 6. Chromosomes, Human, Pair 8. Chromosomes, Human, Pair 9. Cytogenetic Analysis. Cytokines / pharmacology. Female. Humans. Immunophenotyping. Killer Cells, Natural / immunology. Killer Cells, Natural / pathology. Microscopy, Electron, Scanning. Myeloid Cells / immunology. Myeloid Cells / pathology. Recurrence. Translocation, Genetic


14. Roman E, Cooney E, Harrison L, Militano O, Wolownik K, Hawks R, Foley S, Satwani P, Unal E, Bhatia M, Bradley B, Del Toro G, George D, Garvin J, van de Ven C, Cairo MS: Preliminary results of the safety of immunotherapy with gemtuzumab ozogamicin following reduced intensity allogeneic stem cell transplant in children with CD33+ acute myeloid leukemia. Clin Cancer Res; 2005 Oct 1;11(19 Pt 2):7164s-7170s
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preliminary results of the safety of immunotherapy with gemtuzumab ozogamicin following reduced intensity allogeneic stem cell transplant in children with CD33+ acute myeloid leukemia.
  • PURPOSE: Myeloablative allogeneic stem cell transplantation (SCT) has been successful in the treatment of childhood acute myeloid leukemia (AML), but may be associated with significant toxicity and recurrent disease.
  • Reduced-intensity allogeneic SCT may offer a less toxic approach to patients with AML.
  • Targeted immunotherapy with gemtuzumab ozogamicin has been shown to be safe, well tolerated in children, and, as a single agent, gemtuzumab ozogamicin has induced responses in 30% of patients with recurrent CD33+ AML.
  • Therefore, we explored the feasibility and toxicity of targeted immunotherapy following reduced-intensity allogeneic SCT in children with CD33+ AML.
  • EXPERIMENTAL DESIGN: Eight patients with CD33+ AML received a reduced-intensity allogeneic SCT following fludarabine 30 mg/m2 for 6 days and busulfan 3.2 mg/kg (<4 years, 4 mg/kg/d) for 2 days.
  • CONCLUSIONS: The administration of gemtuzumab ozogamicin post reduced-intensity allogeneic SCT in children with average risk AML is feasible and well tolerated with minimal toxicity.
  • The maximal tolerated dose has yet to be determined for gemtuzumab ozogamicin post reduced-intensity allogeneic SCT in children with CD33+ AML.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Immunotherapy / methods. Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation / methods

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  • (PMID = 16203817.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / T32 HL07968
  • [Publication-type] Clinical Trial; 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 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
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15. Yoshida K, Kusumoto S, Sugahara Y, Yagasaki F, Sakata T, Kawai N, Matsuda A, Suzuki T, Hirashima K, Kayano H, Bessho M: [CD7(+) acute myeloid leukemia (M0) associated with a mediastinal bulky mass lesion]. Rinsho Ketsueki; 2001 Aug;42(8):644-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [CD7(+) acute myeloid leukemia (M0) associated with a mediastinal bulky mass lesion].
  • His symptoms did not improve, despite administration of antibiotics and nonsteroidal anti-inflammatory drugs.
  • We diagnosed the patient as having CD7 (+) acute myeloid leukemia (AML) (M0) with a bulky mediastinal mass based on the surface marker analysis, although the clinical features resembled myeloid/NK precursor acute leukemia.
  • [MeSH-major] Antigens, CD7 / analysis. Leukemia, Myeloid, Acute / diagnosis. Mediastinal Neoplasms / diagnosis. Neoplasms, Multiple Primary

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  • (PMID = 11579505.001).
  • [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, CD7; 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
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16. Iwata H, Kami M, Kishi Y, Oki Y, Tanaka Y, Takeuchi K, Yamazaki I, Suzuki R, Morinaga S, Mutou Y: Limitations of the diagnostic criteria for minimally differentiated acute myeloid leukemia (AML-MO). Leukemia; 2000 Nov;14(11):2013-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Limitations of the diagnostic criteria for minimally differentiated acute myeloid leukemia (AML-MO)
  • [MeSH-major] Leukemia, Myeloid / diagnosis
  • [MeSH-minor] Acute Disease. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Diagnosis, Differential. Humans. Immunophenotyping. Male. Neoplastic Stem Cells / chemistry. Neoplastic Stem Cells / ultrastructure. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Reference Standards. Remission Induction

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  • [CommentIn] Leukemia. 2001 Oct;15(10):1673-4 [11587233.001]
  • (PMID = 11069040.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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17. Nagashima T, Izumi T, Muroi K, Miyasato A, Uchida M, Imagawa S, Komatsu N, Yoshida M, Hatake K, Miura Y, Ozawa K: [Two cases of acute myelogenous leukemia complicated with fatal gastrointestinal tract bleeding after treatment with idarubicin and cytarabine]. Gan To Kagaku Ryoho; 2000 Mar;27(3):487-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Two cases of acute myelogenous leukemia complicated with fatal gastrointestinal tract bleeding after treatment with idarubicin and cytarabine].
  • We describe herein two newly diagnosed patients with acute myelogenous leukemia (AML), who were treated twice with an idarubicin hydrochloride (IDR)-containing regimen as a response-orientated induction therapy.
  • The two patients were as follows: a 35-year-old male, FAB-M4, and a 47-year-old female, FAB-M0.
  • One died of sepsis, and the other of acute respiratory distress syndrome without a recovery in bone marrow.
  • [MeSH-major] Antibiotics, Antineoplastic / adverse effects. Gastrointestinal Hemorrhage / chemically induced. Idarubicin / adverse effects. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adult. Bone Marrow / drug effects. Fatal Outcome. Female. Humans. Male. Middle Aged


18. Shin S, Kahng J, Kim M, Lim J, Kim Y, Han K: [Distribution of antigenic aberration in the bone marrow of acute leukemia in complete remission]. Korean J Lab Med; 2008 Feb;28(1):1-7
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  • [Title] [Distribution of antigenic aberration in the bone marrow of acute leukemia in complete remission].
  • BACKGROUND: The aberrant, leukemia-associated antigen expression patterns allow us to discriminate leukemic blasts from normal precursor cells.
  • Our major goal was to determine a guideline for the detection of minimal residual disease using CD20+/CD34+ and myeloid Ag+/CD19+ combination in the bone marrow of acute leukemia in complete remission (CR) after chemotherapy.
  • METHODS: Bone marrow samples from 117 patients with acute leukemia in complete remission after chemotherapy and from 22 healthy controls were immunophenotyped by triple staining and measured by flow cytometry.
  • % (0.8plusmn;0.82%, P=0.000) in CD20+/CD34+ B-lineage ALL CR (N=31), from 0.03% to 4.2% (0.7plusmn;0.83%, P=0.000) in CD20-/CD34- B-lineage ALL CR (N=66), from 0.1% to 0.96% (0.45plusmn;0.32%, P=0.016) in T-ALL CR (N=10), and from 0.02% to 0.48% (0.18plusmn;0.15%, P=0.776) in AML CR (N=10).
  • The CD13,33+/CD19+ cells in R1 gate ranged from 0% to 2.69% (0.37plusmn;0.48%, P<0.001) in CD13,33+/CD19+ B-lineage ALL CR (N=31), from 0% to 1.8% (0.31plusmn;0.28%, P<0.001) in CD13,33-/CD19+B-lineage ALL CR (N=65), from 0.02% to 0.64% (0.29plusmn;0.22%, P=0.071) in T-ALL CR (N=9), and from 0% to 0.17% (0.07plusmn;0.09%, P=0.341) in AML CR (N=3).
  • CONCLUSIONS: Using an immunophenotypic method for the detection of early relapse or minimal residual disease of B-lineage ALL bone marrow in CR after chemotherapy, different cutoff values should be applied according to antigen combination and gating.
  • [MeSH-major] Antigens, CD / metabolism. Bone Marrow Cells / classification. Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Antigens, CD19 / metabolism. Antigens, CD20 / metabolism. Antigens, CD34 / metabolism. Antigens, Differentiation, Myelomonocytic / analysis. Antigens, Differentiation, Myelomonocytic / metabolism. Biomarkers, Tumor / immunology. Flow Cytometry. Hematopoietic Stem Cells / classification. Hematopoietic Stem Cells / metabolism. Humans. Immunophenotyping. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / drug therapy. Neoplasm, Residual. Remission Induction

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  • (PMID = 18309249.001).
  • [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)
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD19; 0 / Antigens, CD20; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Biomarkers, Tumor
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19. Yamada S, Hongo T, Okada S, Watanabe C, Fujii Y, Ohzeki T: Clinical relevance of in vitro chemoresistance in childhood acute myeloid leukemia. Leukemia; 2001 Dec;15(12):1892-7
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  • [Title] Clinical relevance of in vitro chemoresistance in childhood acute myeloid leukemia.
  • To determine the clinical relevance of in vitro drug chemoresistance in childhood acute myeloid leukemia, we used an MTT assay to test leukemic cells from 132 newly diagnosed children.
  • Patients were diagnosed according to the French-American-British (FAB) classification as follows: M0 (n = 12), M1 (n = 16), M2 (n = 53), M4 (n = 17), M5 (n = 19) and M7 (n = 15).
  • For seven other drugs tested, the median lethal dose of 70% and leukemic cell survival of non-responders were higher than those of complete-responders, but the difference was not statistically significant.
  • We sought correlations between FAB subtypes and in vitro drug resistance.
  • Leukemias of the FAB M4 and M5 subtype were more sensitive to L-asparaginase (P = 0.01, P = 0.0036) than those of the FAB M2 subtype.
  • FAB M5 leukemia was more sensitive to etoposide than were the FAB M2, M4 and M7 subtypes (P = 0.001, P = 0.034, P = 0.023, respectively).
  • By contrast, FAB M5 leukemia was significantly more resistant to prednisolone and dexamethasone than were the FAB M0, M1, M2, M4 and M7 subtypes.
  • We sought correlations between in vitro drug resistance and long-term clinical outcome, but found no associations in this case.
  • Selecting an appropriate anti-cancer drug according to the FAB classification together with drug sensitivity testing may contribute to improved prognoses in childhood acute myeloid leukemia.
  • [MeSH-major] Drug Resistance, Neoplasm. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Antineoplastic Agents / pharmacology. Cell Survival / drug effects. Child. Child, Preschool. Female. Humans. Infant. Male. Prognosis. Remission Induction. Time Factors. Treatment Outcome






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