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1. Jurcic JG, DeBlasio T, Dumont L, Yao TJ, Scheinberg DA: Molecular remission induction with retinoic acid and anti-CD33 monoclonal antibody HuM195 in acute promyelocytic leukemia. Clin Cancer Res; 2000 Feb;6(2):372-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular remission induction with retinoic acid and anti-CD33 monoclonal antibody HuM195 in acute promyelocytic leukemia.
  • Despite achieving complete remission with retinoic acid (RA), most patients with acute promyelocytic leukemia (APL) have minimal residual disease detectable by reverse transcription-PCR (RT-PCR) amplification.
  • HuM195, a humanized monoclonal antibody reactive with the cell surface antigen CD33, specifically targets and kills myeloid leukemia cells.
  • We studied whether HuM195 could eliminate minimal residual disease in patients with APL by using RT-PCR.
  • Among similar patients treated on earlier studies, 7 of 34 patients (21%) induced into remission with RA and then maintained on the drug for 1 month were RT-PCR negative before chemotherapy (P = 0.07).
  • These data suggest that HuM195 has activity against minimal residual disease in APL, particularly in newly diagnosed patients.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Disease-Free Survival. Female. Humans. Male. Middle Aged. Remission Induction. Sialic Acid Binding Ig-like Lectin 3. Time Factors

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  • (PMID = 10690513.001).
  • [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 / FDA HHS / FD / FD-R-000925-01; United States / FDA HHS / FD / FD-R-00764; United States / NCI NIH HHS / CA / R01 CA55349; etc
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / monoclonal antibody M195; 5300-03-8 / alitretinoin; 5688UTC01R / Tretinoin
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2. Barbaric D, Alonzo TA, Gerbing RB, Meshinchi S, Heerema NA, Barnard DR, Lange BJ, Woods WG, Arceci RJ, Smith FO: Minimally differentiated acute myeloid leukemia (FAB AML-M0) is associated with an adverse outcome in children: a report from the Children's Oncology Group, studies CCG-2891 and CCG-2961. Blood; 2007 Mar 15;109(6):2314-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Minimally differentiated acute myeloid leukemia (FAB AML-M0) is associated with an adverse outcome in children: a report from the Children's Oncology Group, studies CCG-2891 and CCG-2961.
  • To assess the impact of minimally differentiated acute myeloid leukemia (AML-M0) morphology in children, we analyzed 2 sequential Children's Cancer Group AML clinical trials.
  • We compared presenting characteristics and outcomes of 82 CCG-2891 and CCG-2961 patients with de novo, non-Down syndrome (DS) AML-M0 with those of 1620 patients with non-M0 AML, and of 10 CCG-2891 patients with DS-associated AML-M0 with those of 179 with DS-associated non-M0 AML.
  • The non-DS AML-M0 children had a lower white blood cell (WBC) count (P = .001) than their non-M0 counterparts and a higher incidence of chromosome 5 deletions (P = .002), nonconstitutional trisomy 21 (P = .027), and hypodiploidy (P = .002).
  • Outcome analyses considering all children with non-DS AML demonstrated no significant differences between M0 and non-M0 patients.
  • Analyses restricted to intensive-timing CCG-2891 and CCG-2961 demonstrated comparable complete response (CR) rates (79% and 78%) between non-DS M0 and non-M0 patients.
  • OS from end of induction (45% +/- 17% versus 63% +/- 3%; P = .038), event-free survival (EFS; 23% +/- 11% versus 41% +/- 3%; P = .018), and disease-free survival (DFS; 31% +/- 14% versus 52% +/- 3%; P = .009) were inferior in the M0 group.
  • There was no significant outcome difference between DS-associated AML-M0 and non-M0 children.
  • This study suggests that intensively treated non-DS-associated AML-M0 children have an inferior outcome compared with children with non-M0 AML.

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  • (PMID = 17158236.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 98413; United States / NCI NIH HHS / CA / CA 98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1852193
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3. 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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4. 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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5. 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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6. Bayard-Mc Neeley M, Bansal A, Chowdhury I, Girao G, Small CB, Seiter K, Nelson J, Liveris D, Schwartz I, Mc Neeley DF, Wormser GP, Aguero-Rosenfeld ME: In vivo and in vitro studies on Anaplasma phagocytophilum infection of the myeloid cells of a patient with chronic myelogenous leukaemia and human granulocytic ehrlichiosis. J Clin Pathol; 2004 May;57(5):499-503
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  • [Title] In vivo and in vitro studies on Anaplasma phagocytophilum infection of the myeloid cells of a patient with chronic myelogenous leukaemia and human granulocytic ehrlichiosis.
  • AIMS: The occurrence of human granulocytic ehrlichiosis (HGE) in a patient with chronic myelogenous leukaemia (CML) provided an opportunity to study whether Anaplasma phagocytophilum, the aetiological agent of HGE, infects mature or immature cells, both in vivo and in vitro.
  • The infection rates of different myelogenous stages of granulocytic differentiation were determined by microscopy.
  • In addition, the in vitro growth of A phagocytophilum in the patient's granulocytes and in HL-60 cells (a promyelocytic leukaemia cell line) was compared.
  • RESULTS: Pretreatment blood smears showed that mature granulocytic cells had a higher infection rate with A phagocytophilum than did immature cells.
  • The higher infection rate of the patient's mature versus immature granulocytes before treatment and the minimal level of infection of the patient's bone marrow support this.
  • It is possible that the primary site of infection in HGE is the peripheral mature granulocytic population.
  • [MeSH-major] Anaplasma phagocytophilum / pathogenicity. Ehrlichiosis / complications. Granulocytes / microbiology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications
  • [MeSH-minor] Acute Disease. Aged. HL-60 Cells. Humans. Male


7. 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.
  • RESULTS: NLS-HuM195 exhibited relatively preserved CD33 binding affinity (dissociation constant [K(d)] = 4.3 +/- 1.7 x 10(-9) mol/L to 6.9 +/- 1.3 x 10(-9) mol/L).
  • 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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8. 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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  • (PMID = 11753610.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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9. 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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10. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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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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  • [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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12. 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

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  • [Copyright] Copyright 2007 S. Karger AG, Basel.
  • (PMID = 17476096.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins
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13. Veselská R, Zitterbart K, Auer J, Neradil J: Differentiation of HL-60 myeloid leukemia cells induced by all-trans retinoic acid is enhanced in combination with caffeic acid. Int J Mol Med; 2004 Aug;14(2):305-10
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  • [Title] Differentiation of HL-60 myeloid leukemia cells induced by all-trans retinoic acid is enhanced in combination with caffeic acid.
  • We investigated a possible enhancement of all-trans retinoic acid (ATRA)-induced differentiation of HL-60 human myeloid leukemia cells by caffeic acid (CA), a widely distributed plant phenolic compound.
  • Our results showed that CA, in the concentration of 13 or 52 micro M, had no or minimal influence on cell differentiation, whereas the differentiating activity of ATRA was potentiated by CA treatment.
  • NBT-assay confirmed that this additive effect of CA on ATRA-induced differentiation.
  • The possibility to enhance the differentiation potential of ATRA by CA may improve outcomes in the therapy of acute promyelocytic leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Caffeic Acids / administration & dosage. Drug Synergism. Tretinoin / administration & dosage
  • [MeSH-minor] Antigens, CD. Antigens, Neoplasm / biosynthesis. Cell Adhesion Molecules / biosynthesis. Cell Differentiation. Cell Proliferation. Coloring Agents / pharmacology. Dose-Response Relationship, Drug. Flow Cytometry. GPI-Linked Proteins. HL-60 Cells. Humans. Immunophenotyping. Leukemia, Promyelocytic, Acute / drug therapy. Models, Chemical. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology. Time Factors

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  • (PMID = 15254783.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CEACAM8 protein, human; 0 / Caffeic Acids; 0 / Cell Adhesion Molecules; 0 / Coloring Agents; 0 / GPI-Linked Proteins; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; 5688UTC01R / Tretinoin; U2S3A33KVM / caffeic acid
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14. Ferrara F, Schiavone EM, Palmieri S, Mele G, Pocali B, Scalia G, Morabito P, Sebastio L, Del Vecchio L: Complete remission induced by G-CSF in a patient with acute myeloid leukemia with t(8;21)(q22;q22). Hematol J; 2003;4(3):218-21
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  • [Title] Complete remission induced by G-CSF in a patient with acute myeloid leukemia with t(8;21)(q22;q22).
  • We describe a case of acute myeloid leukemia (AML) with t(8;21) in which complete remission (CR) was obtained with G-CSF given at 10 microg/kg in the absence of concomitant cytotoxic chemotherapy.
  • CR was achieved following 2 weeks of therapy and confirmed by investigating minimal residual disease by four-color flow cytometry analysis.
  • During treatment with G-CSF, maturing cells with cytoplasmic Auer Rods were observed in the peripheral blood, suggesting a differentiation effect.
  • This case adds further evidence for a specific role of G-CSF in the treatment of AML with t(8;21), namely in patients who are not eligible for aggressive chemotherapy.

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  • (PMID = 12764355.001).
  • [ISSN] 1466-4860
  • [Journal-full-title] The hematology journal : the official journal of the European Haematology Association
  • [ISO-abbreviation] Hematol. J.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
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15. Popov AM, Verzhbitskaia TIu, Tsaur GA, Shorikov EV, Savel'ev LI, Tsvirenko SV, Fechina LG: [Minimal residual disease monitoring by flow cytometry in children with acute lymphoblastic leukemia]. Klin Lab Diagn; 2010 Aug;(8):36-41
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  • [Title] [Minimal residual disease monitoring by flow cytometry in children with acute lymphoblastic leukemia].
  • The cells that have avoided the action of antitumor drugs may be retained after remission achievement during induction therapy and consolidation.
  • A combination of these cells is given the name minimal residual disease (MRD).
  • This technique is based on the detection of the so-called leukemia-associated immunophenotype (LAIP), i.e., a tumor-specific combination of the expression of membrane and cytoplasmic markers.
  • Flow cytometry may be successfully used to monitor MRD in 90-95% cases of acute lymphoblastic leukemia (ALL) and in 80-85% of patients with acute myelocytic leukemia.
  • The monoclonal antibody panels recommended by different groups of investigators for MRD monitoring in B-lineage ALL include antibodies to the pan-B-cell antigen CD19, markers of different stages of differentiation of B-lineage precursors of CD10, CD34, and CD20 and leukemia-associated markers different for each panel, such as CD22, CD38, CD58, CD45, TdT, CD13, CD33.
  • The hyperexpression of CD10, CD34, CD19, TdT, the decreased expression of CD38, CD45, CD22, CD19, the simultaneous expression of markers of different stages of differentiation of B lymphocytes, such as CD10 and CD20, and the lymphoblast coexpression of myeloid markers of CD13, CD33, CDS15 are the most frequently described immunophenotype aberrations in B-lineage ALL.
  • The selection of combinations of markers for MRD monitoring in children with T-ALL is based on the simultaneous expression of combinations of the antigens characteristic for early stages of differentiation of normal T lymphocytes, namely TdT and cytoplasmic CD3.
  • [MeSH-major] Flow Cytometry / methods. Neoplasm, Residual / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 20886718.001).
  • [ISSN] 0869-2084
  • [Journal-full-title] Klinicheskaia laboratornaia diagnostika
  • [ISO-abbreviation] Klin. Lab. Diagn.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antigens, CD
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16. Amadori S, Stasi R: Integration of monoclonal antibodies and immunoconjugates into the treatment of acute myeloid leukemia. Curr Opin Hematol; 2008 Mar;15(2):95-100
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Integration of monoclonal antibodies and immunoconjugates into the treatment of acute myeloid leukemia.
  • PURPOSE OF REVIEW: This review addresses use of monoclonal antibodies and immunoconjugates to treat acute myeloid leukemia.
  • RECENT FINDINGS: Monoclonal antibodies used in acute myeloid leukemia have been directed against the antigens CD33, CD45, and CD66.
  • Unconjugated monoclonal antibodies such as lintuzumab have modest activity against overt acute myeloid leukemia but can eliminate minimal residual disease in acute promyelocytic leukemia.
  • Gemtuzumab ozogamicin has shown activity both singly, particularly in acute promyelocytic leukemia, and combined with conventional cytotoxic chemotherapy.
  • Antibodies reactive with CD66 have been used to deliver targeted radiation to hematopoietic tissues in patients with advanced myeloid malignancies.
  • SUMMARY: Both unlabeled monoclonal antibodies and immunoconjugates appear to have a limited role if used as single agents to treat acute myeloid leukemia.
  • These agents hold promise as potentially useful additions to conventional therapy, but the optimal dosing and timing remain to be defined.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Immunoconjugates / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Antigens, Differentiation, Myelomonocytic / drug effects. Antigens, Differentiation, Myelomonocytic / immunology. Clinical Trials as Topic. Humans

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  • (PMID = 18300754.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Immunoconjugates
  • [Number-of-references] 49
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17. 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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  • [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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18. Grimwade D, Mistry AR, Solomon E, Guidez F: Acute promyelocytic leukemia: a paradigm for differentiation therapy. Cancer Treat Res; 2010;145:219-35
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  • [Title] Acute promyelocytic leukemia: a paradigm for differentiation therapy.
  • Acute promyelocytic leukemia(APL) is characterized by the t(15;17) chromosomal translocation leading to the formation of the PML-RARalpha oncoprotein.
  • This leukemia has attracted considerable interest in recent years, being the first in which therapies that specifically target the underlying molecular lesion, i.e., all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), leading to induction of differentiation and apoptosis have been successfully used in clinical practice.
  • The advent of ATRA therapy has transformed APL from being a disease with a poor outlook to one of the most prognostically favorable subsets of acute myeloid leukemia.
  • This raises the possibility that some patients can be cured using differentiation therapies alone, without the need for chemotherapy, thereby potentially reducing treatment-related toxicity.
  • It is clear that the success of such an approach is critically dependent upon molecular diagnostics and monitoring for minimal residual disease (MRD) to distinguish those patients who can potentially be cured with differentiation therapy from those requiring additional myelosuppressive agents.
  • This represents an exciting new phase in the treatment of acute leukemia, highlighting the potential of molecularly targeted and MRD-directed therapies to achieve an individualized approach to patient management.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use. Tretinoin / therapeutic use
  • [MeSH-minor] Apoptosis / drug effects. Cell Differentiation / drug effects. Dyspnea / chemically induced. Fever / chemically induced. Gene Expression Regulation, Leukemic. Humans. Leukocytosis / chemically induced. Models, Biological. Neoplasm, Residual. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / physiology. Transcription, Genetic. Treatment Outcome

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  • (PMID = 20306254.001).
  • [ISSN] 0927-3042
  • [Journal-full-title] Cancer treatment and research
  • [ISO-abbreviation] Cancer Treat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 77
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19. 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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20. Feldman E, Kalaycio M, Weiner G, Frankel S, Schulman P, Schwartzberg L, Jurcic J, Velez-Garcia E, Seiter K, Scheinberg D, Levitt D, Wedel N: Treatment of relapsed or refractory acute myeloid leukemia with humanized anti-CD33 monoclonal antibody HuM195. Leukemia; 2003 Feb;17(2):314-8
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  • [Title] Treatment of relapsed or refractory acute myeloid leukemia with humanized anti-CD33 monoclonal antibody HuM195.
  • Fifty adult patients with relapsed or refractory AML were randomized to receive HuM195 at a dose of 12 or 36 mg/m(2) by intravenous infusion over 4 h on days 1-4 and 15-18.
  • HuM195 as a single agent has minimal, but observable, anti-leukemic activity in patients with relapsed or refractory AML and activity is confined to patients with low burden disease.
  • Meaningful clinical efficacy of this unconjugated monoclonal antibody may be realized only in patients with minimal residual disease, or in combination with chemotherapy.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Dose-Response Relationship, Drug. Female. Humans. Infusions, Intravenous. Male. Middle Aged. Salvage Therapy. Sialic Acid Binding Ig-like Lectin 3. Treatment Outcome

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  • (PMID = 12592328.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3
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21. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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22. 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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23. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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24. 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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25. Claus R, Lübbert M: Epigenetic targets in hematopoietic malignancies. Oncogene; 2003 Sep 29;22(42):6489-96
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  • Frequent genetic alterations in hematopoietic neoplasias (chromosomal translocations, point mutations, etc.) have provided biologic targets for the development of effective novel therapies.
  • Gene inactivation ('silencing') of tumor suppressor and growth inhibitory genes (e.g. the cyclin-dependent kinase inhibitors p16, p15, p21) is frequently mediated by DNA methylation of gene promoters.
  • Therapeutic reversal strategies are being developed for acute leukemias, myelodysplastic syndromes and malignant lymphomas.
  • Since the discovery of the DNA methyltransferase (Dnmt) inhibitory activity of two azanucleosides (5-azacytidine, 5-aza-2'-deoxycytidine/decitabine) even at doses with minimal nonhematologic toxicity, both have been clinically studied in several myeloid neoplasias, particularly in elderly patients unable to tolerate aggressive treatment.
  • Further development of agents counteracting aberrant methylation is directed at more targeted approaches, for example, antisense molecules against Dnmts.
  • Impressive effects of HDAC inhibition in acute promyelocytic leukemia models (PML/RARA expression) translate the finding of HDAC recruitment by this chimeric transcription factor to its target genes.
  • Thus, resensitization to biological agents such as retinoids, colony-stimulating factors and other differentiation inducers may be envisioned.
  • [MeSH-minor] DNA Methylation. Dinucleoside Phosphates / genetics. Gene Silencing. Humans. Leukemia, Myeloid / genetics. Leukemia, Myeloid / therapy. Point Mutation. Promoter Regions, Genetic / genetics. Translocation, Genetic

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  • (PMID = 14528273.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dinucleoside Phosphates; 2382-65-2 / cytidylyl-3'-5'-guanosine
  • [Number-of-references] 93
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26. Shiohara M, Uskokovic M, Hisatake J, Hisatake Y, Koike K, Komiyama A, Koeffler HP: 24-Oxo metabolites of vitamin D3 analogues: disassociation of their prominent antileukemic effects from their lack of calcium modulation. Cancer Res; 2001 Apr 15;61(8):3361-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The seco-steroid hormone, 1alpha,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] inhibits proliferation and induces differentiation of malignant cells including those of the hematopoietic system.
  • We chemically synthesized five novel 24-oxo vitamin D(3) analogues and evaluated their abilities both to inhibit clonal growth and induce differentiation of myeloid leukemia cells and to cause hypercalcemia.
  • The synthetic analogues also had greater potency than 1,25(OH)(2)D(3) to induce differentiation of HL-60 and NB4 cells as measured by generation of superoxide, nonspecific esterase production, and induction of CD11b and CD14 cell surface antigens and to increase the proportion of these cells in the G(0)-G(1) phase of the cell cycle.
  • Expression of p27(KIP1), a cyclin-dependent kinase inhibitor that plays an important role in blocking the cell cycle, was found by Western blot analysis to be induced by the analogues and their 24-oxo metabolites in both HL-60 and U937 cells, suggesting a possible mechanism by which these analogues inhibit leukemic growth.
  • Taken together, chemically synthesized 24-oxo metabolites of 1alpha,25(OH)(2)-16-ene-D(3) and 1alpha,25(OH)(2)-16-ene-19-nor-D(3) irreversibly inhibited proliferation and induced differentiation of acute myeloid leukemia cells with minimal toxicity; these compounds may have a role in the maintenance phase of therapy for acute myeloid leukemia.
  • [MeSH-major] Calcium / blood. Cell Cycle Proteins. Cholecalciferol / analogs & derivatives. Cholecalciferol / pharmacology. Leukemia, Myeloid / drug therapy. Tumor Suppressor Proteins
  • [MeSH-minor] Cell Cycle / drug effects. Cell Differentiation / drug effects. Cell Division / drug effects. Cyclin-Dependent Kinase Inhibitor p21. Cyclin-Dependent Kinase Inhibitor p27. Cyclins / biosynthesis. Dihydroxycholecalciferols / metabolism. Dihydroxycholecalciferols / pharmacology. Dose-Response Relationship, Drug. Growth Inhibitors / metabolism. Growth Inhibitors / pharmacology. HL-60 Cells / drug effects. Humans. Microtubule-Associated Proteins / biosynthesis

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  • (PMID = 11309293.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Dihydroxycholecalciferols; 0 / Growth Inhibitors; 0 / Microtubule-Associated Proteins; 0 / Tumor Suppressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 1C6V77QF41 / Cholecalciferol; 60965-80-2 / 1 alpha,24-dihydroxyvitamin D3; SY7Q814VUP / Calcium
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27. Mistry AR, Pedersen EW, Solomon E, Grimwade D: The molecular pathogenesis of acute promyelocytic leukaemia: implications for the clinical management of the disease. Blood Rev; 2003 Jun;17(2):71-97

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The molecular pathogenesis of acute promyelocytic leukaemia: implications for the clinical management of the disease.
  • Acute promyelocytic leukaemia (APL) is characterised by chromosomal rearrangements of 17q21, leading to fusion of the gene encoding retinoic acid receptor alpha (RARalpha) to a number of alternative partner genes (X), the most frequent of which are PML (>95%), PLZF (0.8%) and NPM (0.5%).
  • Over the last few years, it has been established that the X-RARalpha fusion proteins play a key role in the pathogenesis of APL through recruitment of co-repressors and the histone deacetylase (HDAC)-complex to repress genes implicated in myeloid differentiation.
  • Paradoxically, the X-RARalpha fusion protein has the potential to mediate myeloid differentiation at pharmacological doses of its ligand (all trans-retinoic acid (ATRA)), which is dependent on the dissociation of the HDAC/co-repressor complex.
  • Arsenic compounds have also been shown to be promising therapeutic agents, leading to differentiation and apoptosis of APL blasts.
  • Patients at high risk of relapse can be identified by minimal residual disease monitoring.
  • The challenge for future studies is to improve complete remission rates through reduction of induction deaths, particularly due to haemorrhage, identification of patients at high risk of relapse who would benefit from additional therapy, and identification of a favourable-risk group, for which treatment intensity could be reduced, thereby reducing risks of treatment toxicity and development of secondary leukaemia/myelodysplasia.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / pathology
  • [MeSH-minor] Animals. Gene Rearrangement. Humans. Models, Biological. Mutation. Neoplasm, Residual / genetics. Neoplasm, Residual / pathology. Receptors, Retinoic Acid / genetics. Receptors, Retinoic Acid / metabolism. Translocation, Genetic

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  • [Copyright] Copyright 2003 Elsevier Science Ltd.
  • (PMID = 12642121.001).
  • [ISSN] 0268-960X
  • [Journal-full-title] Blood reviews
  • [ISO-abbreviation] Blood Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha
  • [Number-of-references] 265
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28. Countouriotis A, Moore TB, Sakamoto KM: Cell surface antigen and molecular targeting in the treatment of hematologic malignancies. Stem Cells; 2002;20(3):215-29
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Currently, monoclonal antibodies are being evaluated for their cytotoxic effects as well as their ability to deliver toxic agents or radiation.
  • Rituximab, a chimeric anti-CD20 antibody, has shown response rates of approximately 50% with minimal toxicity in patients with refractory indolent lymphoma.
  • Campath-1H (anti-CD52) has shown encouraging results in patients previously treated for chronic lymphocytic leukemia, with response rates up to 33%, although with significant toxicity.
  • Anti-CD33 antibodies are being used to deliver cytotoxic agents, such as calicheamicin to patients with acute myeloid leukemia with response rates up to 30%.
  • Lastly, the therapeutic agent STI571 (signal transduction inhibitor 571) has demonstrated the capability of targeting specific molecular abnormalities seen in hematologic malignancies.
  • STI571 targets the tyrosine kinase activity of the bcr-abl fusion protein seen in chronic myeloid leukemia.
  • [MeSH-minor] Animals. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antigens, CD / immunology. Antigens, CD45 / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Antineoplastic Agents / therapeutic use. Benzamides. Humans. Imatinib Mesylate. Leukemia / therapy. Lymphoma, B-Cell / therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Rituximab. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 12004080.001).
  • [ISSN] 1066-5099
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA068821
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antigens, Surface; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / CD33 protein, human; 0 / Piperazines; 0 / Pyrimidines; 0 / Sialic Acid Binding Ig-like Lectin 3; 4F4X42SYQ6 / Rituximab; 8A1O1M485B / Imatinib Mesylate; EC 3.1.3.48 / Antigens, CD45
  • [Number-of-references] 106
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29. 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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  • [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


30. Behre G, Singh SM, Liu H, Bortolin LT, Christopeit M, Radomska HS, Rangatia J, Hiddemann W, Friedman AD, Tenen DG: Ras signaling enhances the activity of C/EBP alpha to induce granulocytic differentiation by phosphorylation of serine 248. J Biol Chem; 2002 Jul 19;277(29):26293-9
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  • [Title] Ras signaling enhances the activity of C/EBP alpha to induce granulocytic differentiation by phosphorylation of serine 248.
  • The transcription factor C/EBP alpha regulates early steps of normal granulocyte differentiation since mice with a disruption of the C/EBP alpha gene do not express detectable levels of the granulocyte colony-stimulating factor receptor and produce no neutrophils.
  • We have recently shown that C/EBP alpha function is also impaired in acute myeloid leukemias.
  • The current study demonstrates that activated Ras enhances the ability of C/EBP alpha to transactivate the granulocyte colony-stimulating factor receptor promoter and a minimal promoter containing only C/EBP DNA binding sites.
  • Finally, mutation of serine 248 to alanine obviates the ability of C/EBP alpha to induce granulocytic differentiation.
  • These data suggest a model where Ras signaling enhances the activity of C/EBP alpha to induce granulocytic differentiation by phosphorylation of serine 248.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / metabolism. Granulocytes / cytology. Serine / metabolism. ras Proteins / physiology
  • [MeSH-minor] Acute Disease. Alanine / metabolism. Amino Acid Substitution. Cell Differentiation / drug effects. Cell Line. Humans. Leukemia, Myeloid / metabolism. Phosphorylation. Point Mutation. Promoter Regions, Genetic. Protein Kinase C / metabolism. Receptors, Granulocyte Colony-Stimulating Factor / genetics. Signal Transduction. Transcriptional Activation

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  • (PMID = 11978795.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 72009; United States / NHLBI NIH HHS / HL / HL 56745
  • [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 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 452VLY9402 / Serine; EC 2.7.11.13 / Protein Kinase C; EC 3.6.5.2 / ras Proteins; OF5P57N2ZX / Alanine
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31. Koyama N, Koschmieder S, Tyagi S, Nürnberger H, Wagner S, Böcker U, Hoelzer D, Gerhard Ottmann O, Kalina U: Differential effects of histone deacetylase inhibitors on interleukin-18 gene expression in myeloid cells. Biochem Biophys Res Commun; 2002 Apr 12;292(4):937-43
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  • [Title] Differential effects of histone deacetylase inhibitors on interleukin-18 gene expression in myeloid cells.
  • Histone deacetyrase (HDAC) inhibitors induce growth arrest and differentiation of leukemia cell lines and tumor cells derived from a large variety of human tissues.
  • Here we showed that HDAC inhibitors sodium butyrate, TSA, and valproate regulated the expression of Interleukin-18 (IL-18), a cytokine with antitumor and proinflammatory properties, in human acute myeloid leukemia cell lines U937 and HEL.
  • While sodium butyrate or TSA stimulated the 108-bp IL-18 minimal promoter, valproate failed to activate it, indicating that valproate may use a distinct mechanism from sodium butyrate and TSA to activate IL-18 gene expression.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Gene Expression / drug effects. Histone Deacetylase Inhibitors. Interleukin-18 / metabolism. Myeloid Cells / drug effects
  • [MeSH-minor] Blotting, Northern. Blotting, Western. Butyrates / pharmacology. Cell Differentiation / drug effects. Cell Division / drug effects. Cell Line. Cell Survival / drug effects. Growth Inhibitors / pharmacology. Humans. Hydroxamic Acids / pharmacology. Leukemia, Erythroblastic, Acute / drug therapy. Leukemia, Erythroblastic, Acute / metabolism. Promoter Regions, Genetic / drug effects. RNA, Messenger / metabolism. U937 Cells. Valproic Acid / pharmacology

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  • [Copyright] (c)2002 Elsevier Science (USA).
  • (PMID = 11944905.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Butyrates; 0 / Enzyme Inhibitors; 0 / Growth Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Interleukin-18; 0 / RNA, Messenger; 3X2S926L3Z / trichostatin A; 614OI1Z5WI / Valproic Acid
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32. Panoskaltsis N, Belanger TJ, Liesveld JL, Abboud CN: Optimal cytokine stimulation for the enhanced generation of leukemic dendritic cells in short-term culture. Leuk Res; 2002 Feb;26(2):191-201
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Dendritic cells (DCs) are professional antigen presenting cells derived from myeloid or lymphoid precursors.
  • Herein, we describe the generation of DCs from different leukemias and determine the optimal culture conditions with minimal manipulation.
  • Optimal growth and DC characteristics were obtained with GM-CSF, FL, and SCF in 3-5 day cultures, suggesting a practical strategy for the immunotherapy of leukemia.
  • [MeSH-major] Cytokines / pharmacology. Dendritic Cells / cytology. Leukemia / pathology. Neoplastic Stem Cells / drug effects
  • [MeSH-minor] Acute Disease. Aged. Cell Count. Cell Differentiation / drug effects. Child, Preschool. Female. Flow Cytometry. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. In Situ Hybridization, Fluorescence. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myeloid / pathology. Leukemia, Myelomonocytic, Chronic / pathology. Male. Microscopy, Phase-Contrast. Middle Aged. Phenotype. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Proto-Oncogene Proteins / pharmacology. Receptor Protein-Tyrosine Kinases / pharmacology. Recombinant Fusion Proteins / pharmacology. Stem Cell Factor / pharmacology. T-Lymphocytes / immunology. Tumor Cells, Cultured / drug effects. Vascular Endothelial Growth Factor Receptor-1

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  • [CommentIn] Leuk Res. 2002 Apr;26(4):409-10 [11839387.001]
  • (PMID = 11755469.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Proto-Oncogene Proteins; 0 / Recombinant Fusion Proteins; 0 / Stem Cell Factor; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1
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33. 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

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  • (PMID = 10740646.001).
  • [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
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; ZRP63D75JW / Idarubicin
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34. Ward JO, McConnell MJ, Carlile GW, Pandolfi PP, Licht JD, Freedman LP: The acute promyelocytic leukemia-associated protein, promyelocytic leukemia zinc finger, regulates 1,25-dihydroxyvitamin D(3)-induced monocytic differentiation of U937 cells through a physical interaction with vitamin D(3) receptor. Blood; 2001 Dec 1;98(12):3290-300
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The acute promyelocytic leukemia-associated protein, promyelocytic leukemia zinc finger, regulates 1,25-dihydroxyvitamin D(3)-induced monocytic differentiation of U937 cells through a physical interaction with vitamin D(3) receptor.
  • Monocyte differentiation induced by 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) is interrupted during the course of acute promyelocytic leukemia (APL).
  • One form of APL is associated with the translocation t(11;17), which joins the promyelocytic leukemia zinc finger (PLZF) and retinoic acid receptor alpha (RARalpha) genes.
  • Because PLZF is coexpressed in the myeloid lineage with the vitamin D(3) receptor (VDR), the interplay between PLZF and VDR was examined.
  • Overexpression of PLZF in a monocytic cell line abrogated 1,25(OH)(2)D(3) activation from both a minimal VDR responsive reporter and the promoter of p21(WAF1/CIP1), a target gene of VDR.
  • Deletion of the BTB/POZ domain significantly relieved PLZF-mediated repression of 1,25(OH)(2)D(3)-dependent activation.
  • In addition, stable, inducible expression of PLZF in U937 cells inhibited the ability of 1,25(OH)(2)D(3) to induce surface expression of the monocytic marker CD14 and morphologic changes associated with differentiation.
  • These results suggest that PLZF may play an important role in regulating the process by which 1,25(OH)(2)D(3) induces monocytic differentiation in hematopoietic cells.
  • [MeSH-major] Calcitriol / pharmacology. Cell Differentiation / drug effects. DNA-Binding Proteins / pharmacology. Monocytes / drug effects. Receptors, Calcitriol / drug effects. Transcription Factors / pharmacology
  • [MeSH-minor] Binding Sites. Cell Nucleus / chemistry. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / genetics. DNA / metabolism. Gene Expression. Humans. Kruppel-Like Transcription Factors. Lymphoma, Large B-Cell, Diffuse. Promoter Regions, Genetic. Transcription, Genetic / drug effects. Transfection. U937 Cells. Zinc Fingers

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  • (PMID = 11719366.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA59936; United States / NIDDK NIH HHS / DK / DK52621
  • [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 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / DNA-Binding Proteins; 0 / Kruppel-Like Transcription Factors; 0 / Receptors, Calcitriol; 0 / Transcription Factors; 147855-37-6 / ZBTB16 protein, human; 9007-49-2 / DNA; FXC9231JVH / Calcitriol
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35. Eibl M, Auner HW, Zinke-Cerwenka W, Sill H, Dornbusch HJ, Linkesch W: High-risk AML complicated by pulmonary aspergillosis: successful treatment with nonmyeloablative stem cell transplantation and long-term administration of voriconazole. Ann Hematol; 2004 Feb;83(2):133-6
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  • [Title] High-risk AML complicated by pulmonary aspergillosis: successful treatment with nonmyeloablative stem cell transplantation and long-term administration of voriconazole.
  • Acute myeloid leukemia (AML) associated with central diabetes insipidus (DI) and chromosomal aberrations is characterised by a very poor prognosis.
  • We present a 28-year-old female with AML FAB M0, preceding DI and cytogenetic abnormalities (monosomy 7 and inversion of chromosome 9).
  • The presented case study thus demonstrates that high-risk AML with concomitant invasive fungal infection may be safely and effectively treated by nonmyeloablative stem cell transplantation and long-term administration of voriconazole.
  • [MeSH-major] Antifungal Agents / administration & dosage. Aspergillosis / drug therapy. Leukemia, Myeloid, Acute / microbiology. Leukemia, Myeloid, Acute / therapy. Lung Diseases, Fungal / drug therapy. Pyrimidines / administration & dosage. Stem Cell Transplantation. Triazoles / administration & dosage

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  • (PMID = 14530879.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Myeloablative Agonists; 0 / Pyrimidines; 0 / Triazoles; JFU09I87TR / Voriconazole
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36. 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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