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1. Lindner D, Raghavan D: Intra-tumoural extra-cellular pH: a useful parameter of response to chemotherapy in syngeneic tumour lines. Br J Cancer; 2009 Apr 21;100(8):1287-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intra-tumoural extra-cellular pH: a useful parameter of response to chemotherapy in syngeneic tumour lines.
  • Reliable surrogate markers of response to anticancer therapy remain a desirable tool for preclinical modelling and clinical practice in oncology.
  • Clinical evaluation is relatively unreliable when attempting to assess rapidly and prospectively the outcome of treatment.
  • Because tissue breakdown is associated with release of nucleic acids and other cellular products, we reasoned that serial measurement of intra-tumoural pH may correlate with the extent of tumour lysis, and thus with outcomes of cytotoxic chemotherapy.
  • Doxorubicin-sensitive and doxorubicin-resistant sublines of P388 murine monocytic leukaemia in C57BL/6 mice were treated with increasing concentrations of doxorubicin.
  • Serial sampling of pH in tumour masses may provide a useful surrogate of long-term response to chemotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / analysis. Hydrogen-Ion Concentration. Leukemia P388 / drug therapy
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Line, Tumor. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Drug Resistance, Neoplasm. Drug Tolerance. Humans. Kinetics. Mice. Mice, Inbred C57BL

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  • (PMID = 19367285.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide
  • [Other-IDs] NLM/ PMC2676543
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2. Laurenzana A, Petruccelli LA, Pettersson F, Figueroa ME, Melnick A, Baldwin AS, Paoletti F, Miller WH Jr: Inhibition of DNA methyltransferase activates tumor necrosis factor alpha-induced monocytic differentiation in acute myeloid leukemia cells. Cancer Res; 2009 Jan 1;69(1):55-64
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  • [Title] Inhibition of DNA methyltransferase activates tumor necrosis factor alpha-induced monocytic differentiation in acute myeloid leukemia cells.
  • We find that clinically achievable levels of 5-aza-2'-deoxycytidine (5-AZA-dC), a potent inhibitor of DNA methylation, can modify chromatin and restore the ability of tumor necrosis factor alpha (TNFalpha) to induce monocytic differentiation of the acute myeloid leukemia cells NB4 and U937.
  • Our results support the concept of low doses of 5-AZA-dC acting in combination with other agents to target epigenetic changes that drive malignant growth in leukemic cells.
  • [MeSH-major] Azacitidine / analogs & derivatives. DNA (Cytosine-5-)-Methyltransferase / antagonists & inhibitors. Leukemia, Myeloid / drug therapy. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Acetylation / drug effects. Acute Disease. Cell Differentiation / drug effects. Cell Differentiation / physiology. Chromatin / drug effects. DNA Methylation / drug effects. Enzyme Inhibitors / pharmacology. Histones / metabolism. Humans. Monocytes / drug effects. Monocytes / enzymology. Monocytes / pathology. NF-kappa B / metabolism. NF-kappa B p50 Subunit / metabolism. Promoter Regions, Genetic. Receptors, Tumor Necrosis Factor, Type I / metabolism. Receptors, Tumor Necrosis Factor, Type II / metabolism. Transcription Factor RelA / metabolism. U937 Cells

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  • (PMID = 19117987.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromatin; 0 / Enzyme Inhibitors; 0 / Histones; 0 / NF-kappa B; 0 / NF-kappa B p50 Subunit; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha; 776B62CQ27 / decitabine; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA (cytosine-5-)-methyltransferase 1; M801H13NRU / Azacitidine
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3. Chung J, Koyama T, Ohsawa M, Shibamiya A, Hoshi A, Hirosawa S: 1,25(OH)(2)D(3) blocks TNF-induced monocytic tissue factor expression by inhibition of transcription factors AP-1 and NF-kappaB. Lab Invest; 2007 Jun;87(6):540-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 1,25(OH)(2)D(3) blocks TNF-induced monocytic tissue factor expression by inhibition of transcription factors AP-1 and NF-kappaB.
  • An essential coagulation factor, tissue factor (TF), is rapidly expressed by human monocytes when exposed to a variety of agonists, such as lipopolysaccharide or tumor necrosis factor (TNF).
  • We previously found that 1alpha,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) and its potent synthetic analogs downregulate TF and upregulate thrombomodulin expression on monocytic cells, counteracting the effects of TNF at the level of transcription.
  • In this study, we investigated the regulatory mechanisms by which 1,25(OH)(2)D(3) inhibits TNF-induced TF expression in human monocytic cells.
  • 1,25(OH)(2)D(3) inhibited TNF-induced phosphorylation of c-Jun without affecting phosphorylation of the other pathways.
  • On the other hand, 1,25(OH)(2)D(3) directly inhibited nuclear binding and activities of NF-kappaB in the nucleus without affecting phosphorylation of the NF-kappaB activation pathway.
  • These results indicate that 1,25(OH)(2)D(3) suppresses basal and TNF-induced TF expression in monocytic cells by inhibition of AP-1 and NF-kappaB activation pathways, but not of Egr-1.
  • Our results may help to elucidate the regulatory mechanisms of 1,25(OH)(2)D(3) in TF induction, and may have physiological significance in the clinical challenge to use potential 1,25(OH)(2)D(3) analogs in antithrombotic therapy as well as immunomodulation and antineoplastic therapy of leukemia.
  • [MeSH-minor] Cells, Cultured. Gene Expression Regulation / drug effects. Humans

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  • (PMID = 17401435.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Transcription Factor AP-1; 0 / Tumor Necrosis Factor-alpha; 65878-49-1 / 1,25-dihydroxydihydrotachysterol(3); 9035-58-9 / Thromboplastin; R5LM3H112R / Dihydrotachysterol
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4. Studzinski GP, Wang X, Ji Y, Wang Q, Zhang Y, Kutner A, Harrison JS: The rationale for deltanoids in therapy for myeloid leukemia: role of KSR-MAPK-C/EBP pathway. J Steroid Biochem Mol Biol; 2005 Oct;97(1-2):47-55
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  • [Title] The rationale for deltanoids in therapy for myeloid leukemia: role of KSR-MAPK-C/EBP pathway.
  • The evidence for the promising potential for derivatives of Vitamin D (deltanoids) in the treatment of myeloid leukemias is increasing, but currently is not matched by the understanding of the precise mechanisms by which these anti-neoplastic effects are achieved.
  • Unlike solid tumors in which growth retardation by deltanoids appears to result from inhibition of cell proliferation and the promotion of cell death by apoptosis, control of myeloid leukemia proliferation by deltanoids results from the induction of differentiation of the immature myelo-monocytic cells towards functional monocytic cells.
  • We present here the accumulating evidence that a pathway that is initiated by deltanoid activation of Vitamin D receptor (VDR) and leads to monocytic differentiation of human myeloblastic HL60 cells, includes the MEK-ERK and JNK mitogen-activated protein kinases (MAPKs), their positive and negative regulators and a downstream effector C/EBPbeta.
  • As in other cells, the abundance of VDR protein increases shortly after an exposure of HL60 cells to 1alpha,25-dihydroxyvitamin D(3) (1alpha,25(OH)(2) D(3)).
  • Other early events include a parallel upregulation of kinase suppressor of Ras (KSR-1) and the activation of the ERK MAPK pathway and data suggest that KSR-1 acts to amplify the signal provided by low concentrations of 1alpha,25(OH)(2) D(3).
  • Maintenance of monocytic differentiation may be enhanced by JNK, but diminished by p38, MAPK signaling.
  • Importantly, in freshly obtained acute myeloid leukemia (AML)-M2 cells exposed to PRI-2191, a novel deltanoid with a modified side chain, upregulation of C/EBPbeta paralleled the induction of monocytic differentiation.
  • These data provide a basis for the hypothesis that deltanoid-induced upregulation of C/EBPbeta bypasses the block to granulocytic differentiation in myeloid leukemia cells by redirecting the cells to monocytic differentiation.

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  • (PMID = 16046262.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA044722-15; United States / NCI NIH HHS / CA / R01 CA044722; United States / NCI NIH HHS / CA / R01 CA044722-15; United States / NCI NIH HHS / CA / R01 CA44722
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CCAAT-Enhancer-Binding Protein-beta; 0 / Retinoblastoma Protein; 1406-16-2 / Vitamin D; EC 2.7.- / Protein Kinases; EC 2.7.1.- / KSR-1 protein kinase; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS169830; NLM/ PMC2814418
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5. Aikawa Y, Katsumoto T, Zhang P, Shima H, Shino M, Terui K, Ito E, Ohno H, Stanley ER, Singh H, Tenen DG, Kitabayashi I: PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2. Nat Med; 2010 May;16(5):580-5, 1p following 585
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  • [Title] PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2.
  • Leukemias and other cancers possess self-renewing stem cells that help to maintain the cancer.
  • Cancer stem cell eradication is thought to be crucial for successful anticancer therapy.
  • Using an acute myeloid leukemia (AML) model induced by the leukemia-associated monocytic leukemia zinc finger (MOZ)-TIF2 fusion protein, we show here that AML can be cured by the ablation of leukemia stem cells.
  • Cells expressing high amounts of CSF1R (CSF1R(high) cells), but not those expressing low amounts of CSF1R (CSF1R(low) cells), showed potent leukemia-initiating activity.
  • Using transgenic mice expressing a drug-inducible suicide gene controlled by the CSF1R promoter, we cured AML by ablation of CSF1R(high) cells.
  • Moreover, induction of AML was suppressed in CSF1R-deficient mice and CSF1R inhibitors slowed the progression of MOZ-TIF2-induced leukemia.
  • Thus, in this subtype of AML, leukemia stem cells are contained within the CSF1R(high) cell population, and we suggest that targeting of PU.1-mediated upregulation of CSF1R expression might be a useful therapeutic approach.

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  • (PMID = 20418886.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA041456-24; United States / NCI NIH HHS / CA / R01 CA032551; United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / 5P30-CA13330; United States / NCI NIH HHS / CA / CA041456-24; United States / NCI NIH HHS / CA / R01-CA41456; United States / NCI NIH HHS / CA / CA32551; United States / NCI NIH HHS / CA / R01 CA041456; United States / NCI NIH HHS / CA / P30 CA013330; United States / NHLBI NIH HHS / HL / R01 HL112719
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Colony-Stimulating Factors; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Proto-Oncogene Proteins; 0 / Receptors, Colony-Stimulating Factor; 0 / Recombinant Fusion Proteins; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1; 81627-83-0 / Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS265702; NLM/ PMC3039870
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6. Contractor R, Samudio IJ, Estrov Z, Harris D, McCubrey JA, Safe SH, Andreeff M, Konopleva M: A novel ring-substituted diindolylmethane,1,1-bis[3'-(5-methoxyindolyl)]-1-(p-t-butylphenyl) methane, inhibits extracellular signal-regulated kinase activation and induces apoptosis in acute myelogenous leukemia. Cancer Res; 2005 Apr 1;65(7):2890-8
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  • [Title] A novel ring-substituted diindolylmethane,1,1-bis[3'-(5-methoxyindolyl)]-1-(p-t-butylphenyl) methane, inhibits extracellular signal-regulated kinase activation and induces apoptosis in acute myelogenous leukemia.
  • We investigated the antileukemic activity and molecular mechanisms of action of a newly synthesized ring-substituted diindolylmethane derivative, 1,1-bis[3'-(5-methoxyindolyl)]-1-(p-t-butylphenyl) methane (DIM #34), in acute myelogenous leukemia (AML) cells.
  • Because other methylene-substituted diindolylmethane analogues have been shown to transactivate the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma), we studied the role of PPARgamma in apoptosis induction.
  • Cotreatment of cells with a selective PPARgamma antagonist or with retinoid X receptor and retinoic acid receptor ligands partially modulated apoptosis when combined with DIM #34, suggesting PPARgamma receptor-dependent and receptor-independent cell death.
  • [MeSH-major] Apoptosis / drug effects. Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors. Indoles / pharmacology. Leukemia, Myeloid / drug therapy. Protein Kinase Inhibitors / pharmacology
  • [MeSH-minor] Acute Disease. Caspases / metabolism. Enzyme Activation / drug effects. HL-60 Cells. Humans. Jurkat Cells. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / enzymology. Leukemia, Monocytic, Acute / pathology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / enzymology. Leukemia, Myeloid, Acute / pathology. Leukemia, Myelomonocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / enzymology. Leukemia, Myelomonocytic, Acute / pathology. MAP Kinase Signaling System / drug effects. PPAR gamma / metabolism. Proto-Oncogene Proteins c-bcl-2 / physiology. U937 Cells

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  • (PMID = 15805291.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / CA16654; United States / NCI NIH HHS / CA / CA19639; United States / NCI NIH HHS / CA / CA55164; United States / NIEHS NIH HHS / ES / ES09106
  • [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 / 1,1-bis(3'-(5-methoxyindolyl))-1-(p-t-butylphenyl)indolesmethane; 0 / Indoles; 0 / PPAR gamma; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.22.- / Caspases
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7. Tamayose K, Sugimoto K, Ando M, Oshimi K: Mononucleosis syndrome and acute monocytic leukemia. Eur J Haematol; 2002 Apr;68(4):236-8
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  • [Title] Mononucleosis syndrome and acute monocytic leukemia.
  • The association of infectious mononucleosis and an immunocompromised host such as occurs in acute leukemia is reported.
  • Patients with mononucleosis syndrome caused by other agents are rare.
  • We report a case of acute monocytic leukemia (AMoL) who developed varicella zoster virus (VZV) mononucleosis syndrome in the bone marrow recovery phase after myelosuppression due to high-dose cytarabine.
  • [MeSH-major] Cytarabine / adverse effects. Herpes Zoster / etiology. Herpesvirus 3, Human. Immunosuppressive Agents / adverse effects. Infectious Mononucleosis / etiology. Leukemia, Monocytic, Acute / complications. Leukemia, Monocytic, Acute / drug therapy

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  • (PMID = 12071940.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 04079A1RDZ / Cytarabine
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8. Ji YY, Zhang WG, Chen YX, Zhao XM, He AL, Liu J, Wang JL, Wang FX, Zhang PY, Zhang WJ: [Efficiency of GHA priming therapy on patients with acute monocytic leukemia and its mechanism]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Feb;18(1):213-8
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  • [Title] [Efficiency of GHA priming therapy on patients with acute monocytic leukemia and its mechanism].
  • The aim of this study was to explore the clinical efficiency and side effects of GHA-priming therapy on patients with acute monocytic leukemia, and to analyze its mechanism.
  • 37 patients with refractory, relapse, hypocellular acute monocytic leukemia and elderly patients with AML-M(5) were treated with GHA-priming therapy (G-CSF, homoharringtonine and low dosage of cytarabine).
  • Clinical efficiency, side effects, and therapy-relevant mortality were observed.
  • The expression of MLAA34 on U937 before or after treating with chemotherapy was analyzed by immunohistochemical method.
  • The incidence of granulocyte deficiency was 18.92% (2/37) with median time of 4 days.
  • Other non-hematological toxicities were low in vitro when incubated with G-CSF for 24 hours, the S-phase cells obviously increased.
  • It is concluded that the GHA priming therapy can be used to treat patients with refractory, relapse, senile and hypocellular acute monocytic leukemia with satisfied response rate and low hematological and non-hematological toxicities.
  • G-CSF can enhance cytotoxicity of drugs such as Ara-C and HHT by promoting G(0) phase cells into the reproductive cycle.
  • GHA and HA therapy can inhibit cell proliferation, induce apoptosis, and the former has a more significant function.
  • GHA priming therapy can down regulate the expression of MLAA 34.
  • MLAA-34 is a novel anti-apoptotic factor of acute monocytic leukemia.

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  • (PMID = 20137150.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Harringtonines; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 6FG8041S5B / homoharringtonine
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9. Hijiya N, Metzger ML, Pounds S, Schmidt JE, Razzouk BI, Rubnitz JE, Howard SC, Nunez CA, Pui CH, Ribeiro RC: Severe cardiopulmonary complications consistent with systemic inflammatory response syndrome caused by leukemia cell lysis in childhood acute myelomonocytic or monocytic leukemia. Pediatr Blood Cancer; 2005 Jan;44(1):63-9
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  • [Title] Severe cardiopulmonary complications consistent with systemic inflammatory response syndrome caused by leukemia cell lysis in childhood acute myelomonocytic or monocytic leukemia.
  • BACKGROUND: Life-threatening pulmonary complications that coincide with cell lysis during early chemotherapy and that mimic systemic inflammatory response syndrome (SIRS) have been reported in patients with acute myeloid leukemia (AML).
  • Severe SIRS was significantly more common in myelomonocytic or monocytic AML (M4/M4eo/M5) than in other subtypes (P = 0.010) and significantly more common in M4eo than in M4/M5 (P = 0.008).
  • Among 112 cases for which information was available, leukocyte reduction was significantly greater in patients with M4/M4eo/M5 than among others during the first 4 days of chemotherapy (P = 0.015).
  • [MeSH-major] Cell Death. Leukemia, Monocytic, Acute / complications. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / complications. Leukemia, Myelomonocytic, Acute / drug therapy. Systemic Inflammatory Response Syndrome / etiology
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Humans. Male. Retrospective Studies. Risk Factors

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15368547.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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10. Sunnaram BL, Gandemer V, Sebillot M, Grandgirard N, Amiot L, Leray E, Goasguen JE: LRP overexpression in monocytic lineage. Leuk Res; 2003 Aug;27(8):755-9
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  • [Title] LRP overexpression in monocytic lineage.
  • The failure to chemotherapy is a multi factorial phenomenon and lung resistance protein (LRP) overexpression has already been discussed as implicated in drug resistance.
  • In 1996, we studied the expression of LRP and P170 (MDR) in a series of leukemias, at the time of diagnosis, by immunocytochemical (ICC) method.
  • The observation of a strong and unusual expression of LRP in acute myeloid leukemia (AML) with monocytic component led us to test (for P170 and LRP) a new series of 47 AML with different FAB subtypes.
  • Code 5 reaction was found in 10/13 M5 versus the other FAB subtypes (P<10(-3)).
  • The strongest LRP overexpression was also found in chronic myelomonocytic leukemia (four cases), reactive monocytosis (three cases) and in a dendritic cell line.
  • In conclusion, we report that LRP is rather a marker of monocytic lineage than a prognostic index for MDR and we suggest that detection of LRP by ICC could be an argument for the diagnosis of monoblastic and monocytic leukemias.
  • [MeSH-major] Leukemia, Myeloid / pathology. Monocytes / chemistry. Neoplasm Proteins / analysis

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  • (PMID = 12801535.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Glycoproteins; 0 / Neoplasm Proteins; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 0 / p-170 glycoprotein, human
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11. Meng A, Luberto C, Meier P, Bai A, Yang X, Hannun YA, Zhou D: Sphingomyelin synthase as a potential target for D609-induced apoptosis in U937 human monocytic leukemia cells. Exp Cell Res; 2004 Jan 15;292(2):385-92
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  • [Title] Sphingomyelin synthase as a potential target for D609-induced apoptosis in U937 human monocytic leukemia cells.
  • Using U937 human monocytic leukemia cells, we examined the ability of D609 to inhibit sphingomyelin synthase (SMS), since inhibition of SMS may contribute to D609-induced tumor cell cytotoxicity via modulating the cellular levels of ceramide and diacylglycerol (DAG).
  • The results showed that D609 is capable of inducing U937 cell death by apoptosis in a dose- and time-dependent manner.
  • In addition, incubation of U937 cells with C(6)-ceramide and/or H7 (a selective PKC inhibitor) reduced U937 cell viability; whereas pretreatment of the cells with a PKC activator, PMA or 1-oleoyl-2-acetylglycerol (OAG), attenuated D609-induced U937 cell apoptosis.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Bridged Compounds / pharmacology. Leukemia, Monocytic, Acute / drug therapy. Thiones / pharmacology. Transferases (Other Substituted Phosphate Groups) / antagonists & inhibitors
  • [MeSH-minor] Ceramides / metabolism. Ceramides / pharmacology. Cytotoxins / pharmacology. Diglycerides / metabolism. Diglycerides / pharmacology. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Down-Regulation / physiology. Enzyme Inhibitors / pharmacology. Humans. Protein Kinase C / antagonists & inhibitors. Protein Kinase C / metabolism. Reaction Time / drug effects. Reaction Time / physiology. Tetradecanoylphorbol Acetate / pharmacology. U937 Cells. Up-Regulation / drug effects. Up-Regulation / physiology

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  • (PMID = 14697345.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL43707
  • [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 / Antineoplastic Agents; 0 / Bridged Compounds; 0 / Ceramides; 0 / Cytotoxins; 0 / Diglycerides; 0 / Enzyme Inhibitors; 0 / Thiones; 038753E78J / N-caproylsphingosine; 83373-60-8 / tricyclodecane-9-yl-xanthogenate; 86390-77-4 / 1-oleoyl-2-acetylglycerol; EC 2.7.11.13 / Protein Kinase C; EC 2.7.8.- / Transferases (Other Substituted Phosphate Groups); EC 2.7.8.- / phosphatidylcholine-ceramide phosphocholine transferase; NI40JAQ945 / Tetradecanoylphorbol Acetate
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12. Xu WL, Jin J, Chen ZM, Lou JY, Yu YB: [Clinical and experimental study of 38 cases with trisomy 8]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2003 Dec;20(6):528-31
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  • RESULTS: Thirty-two of 38(84.2%) cases with trisomy 8, and fourteen of 17(82.4%) cases with trisomy 8 as the sole chromosome aberration were myeloid disorders such as myelodysplastic syndrome (MDS), acute myelocytic leukemia (AML), chronic myelocytic leukemia (CML).
  • The incidence of trisomy 8 was higher in myeloid disease than in lymphocytic disease (5% vs 1.3%); the incidence of trisomy 8 was higher in acute monocytic leukemia than in other AML (6.1% vs 2.4%), and the incidence of trisomy 8 in chronic myelomonocytic leukemia( CMML) was higher than that in other myelodysplastic syndrome (MDS) (25% vs 13.2%); 17 cases had trisomy 8 as the sole chromosome aberration, 21 cases had other additional chromosome aberrations.
  • Eleven cases were treated with chemotherapy, among them only 10 cases data were available.
  • Seven cases acquired complete remission but 3 of them were M3, the other 3 cases had no response after two courses of chemotherapy.
  • Trisomy 8 might be related with differentiation abnormality of monocyte.
  • [MeSH-major] Chromosomes, Human, Pair 8. Leukemia / genetics. Myelodysplastic Syndromes / genetics. Trisomy

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  • (PMID = 14669224.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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13. Procházková J, Stixová L, Soucek K, Hofmanová J, Kozubík A: Monocytic differentiation of leukemic HL-60 cells induced by co-treatment with TNF-alpha and MK886 requires activation of pro-apoptotic machinery. Eur J Haematol; 2009 Jul;83(1):35-47
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  • [Title] Monocytic differentiation of leukemic HL-60 cells induced by co-treatment with TNF-alpha and MK886 requires activation of pro-apoptotic machinery.
  • The block of hematopoietic differentiation program in acute myeloid leukemia cells can be overcome by differentiating agent like retinoic acid, but it has several side effects.
  • A study of other differentiation signaling pathways is therefore useful to predict potential targets of anti-leukemic therapy.
  • We demonstrated previously that the co-treatment of HL-60 cells with Tumor necrosis factor-alpha (TNF-alpha) (1 ng/mL) and inhibitor of 5-lipoxygenase MK886 (5 microm) potentiated both monocytic differentiation and apoptosis.
  • In this study, we detected enhanced activation of three main types of mitogen-activated protein kinases (MAPKs) (p38, c-Jun amino-terminal kinase [JNK], extracellular signal-regulated kinase [ERK]), so we assessed their role in differentiation using appropriate pharmacologic inhibitors.
  • The inhibition of pro-apoptotic MAPKs (p38 and JNK) suppressed the effect of MK886 + TNF-alpha co-treatment.
  • On the other hand, down-regulation of pro-survival ERK pathway led to increased differentiation.
  • To conclude, we evidenced that the activation of apoptotic processes and pathways supporting apoptosis (p38 and JNK MAPKs) is required for the monocytic differentiation of HL-60 cells.
  • [MeSH-major] Apoptosis / drug effects. Indoles / pharmacology. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / pathology. Monocytes / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Amino Acid Chloromethyl Ketones / pharmacology. Caspase Inhibitors. Caspases / metabolism. Cell Differentiation / drug effects. Cysteine Proteinase Inhibitors / pharmacology. Enzyme Activation / drug effects. HL-60 Cells. Humans. Lipoxygenase Inhibitors / pharmacology. MAP Kinase Signaling System / drug effects. NF-kappa B / antagonists & inhibitors

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  • (PMID = 19220423.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amino Acid Chloromethyl Ketones; 0 / Caspase Inhibitors; 0 / Cysteine Proteinase Inhibitors; 0 / Indoles; 0 / Lipoxygenase Inhibitors; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 118414-82-7 / L 663536; EC 3.4.22.- / Caspases
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14. Ramos MG, Rabelo FL, Brumatti G, Bueno-da-Silva AE, Amarante-Mendes GP, Alvarez-Leite JI: Butyrate increases apoptosis induced by different antineoplastic drugs in monocytic leukemia cells. Chemotherapy; 2004 Nov;50(5):221-8
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  • [Title] Butyrate increases apoptosis induced by different antineoplastic drugs in monocytic leukemia cells.
  • Cancer including leukemia is usually treated with chemotherapeutic drugs that can be effective, but frequently problems are encountered that impair the success of the treatment.
  • METHODS: The effect of a combination treatment with butyrate and antineoplastic agents Ara-C, etoposide and vincristine is evaluate on the leukemic cell line THP-1.
  • We also demonstrate that the process of apoptosis induced by butyrate and chemotherapeutic drugs involves the participation of caspases and induced activation of caspase-3, -8 and -9.
  • CONCLUSIONS: We believe that butyrate could be a promising therapeutic agent for the treatment of leukemia in combination with other antineoplastic drugs.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Butyrates / pharmacology. Drug Synergism. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / pathology
  • [MeSH-minor] Amino Acid Chloromethyl Ketones / pharmacology. Amino Acid Chloromethyl Ketones / therapeutic use. Apoptosis / drug effects. Apoptosis / physiology. Blotting, Western. Caspase Inhibitors. Caspases / metabolism. Caspases / therapeutic use. Cell Line, Tumor. Cytarabine / pharmacology. Cytarabine / therapeutic use. DNA Replication / drug effects. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor / methods. Drug Therapy, Combination. Etoposide / pharmacology. Etoposide / therapeutic use. Humans. Vincristine / pharmacology. Vincristine / therapeutic use

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  • (PMID = 15528887.001).
  • [ISSN] 0009-3157
  • [Journal-full-title] Chemotherapy
  • [ISO-abbreviation] Chemotherapy
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Amino Acid Chloromethyl Ketones; 0 / Antineoplastic Agents; 0 / Butyrates; 0 / Caspase Inhibitors; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; EC 3.4.22.- / Caspases
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15. Wu HJ, Chen Y: [Biological characteristics of hyperleukocytic acute leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Jun;14(3):450-4
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  • [Title] [Biological characteristics of hyperleukocytic acute leukemia].
  • The study was to investigate the biological characteristics of hyperleucocyte acute leukemia (HAL) and its clinical significance.
  • In AML, monocytic leukemia is easier to become into HAL than other leukemias.
  • In ALL, T-lineage antigens of HAL group are more easily expressed than those of NHAL group; the leukemia cells of HAL group are naiver than those of NHAL group, meanwhile the prognosis of HAL is poor.

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  • (PMID = 16800918.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Antigens, CD79; 0 / Antigens, CD8; 0 / Sialic Acid Binding Ig-like Lectin 2
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16. Gadhoum Z, Delaunay J, Maquarre E, Durand L, Lancereaux V, Qi J, Robert-Lezenes J, Chomienne C, Smadja-Joffe F: The effect of anti-CD44 monoclonal antibodies on differentiation and proliferation of human acute myeloid leukemia cells. Leuk Lymphoma; 2004 Aug;45(8):1501-10
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  • [Title] The effect of anti-CD44 monoclonal antibodies on differentiation and proliferation of human acute myeloid leukemia cells.
  • Acute myeloid leukemia (AML) is a clonal malignant disease characterized by an increasing number of immature myeloid cells arrested at various stages of granulocytic and monocytic differentiation.
  • Contrarily to chemotherapy alone, which is still unable to cure most AML patients, the differentiation therapy, which consists in releasing the differentiation blockage of leukemic blasts, has succeeded, when it is combined with chemotherapy, to greatly improve the survival of AML3 patients, using retinoic acid as differentiating agent.
  • However, this molecule is ineffective in other AML subtypes, which are the most frequent.
  • These results have raised the perspective of developing a CD44-targeted differentiation therapy in most AML cases.
  • The challenges of an anti-CD44 based differentiation therapy in AML, and its importance in relation to the new other therapies developed in this malignancy, are discussed in this review.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, CD44 / immunology. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Apoptosis. Cell Differentiation / drug effects. Cell Proliferation / drug effects. Humans


17. Rots MG, Pieters R, Jansen G, Kaspers GJ, Van Zantwijk CH, Noordhuis P, Voorn DA, Van Wering ER, Creutzig U, Veerman AJ, Peters GJ: A possible role for methotrexate in the treatment of childhood acute myeloid leukaemia, in particular for acute monocytic leukaemia. Eur J Cancer; 2001 Mar;37(4):492-8
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  • [Title] A possible role for methotrexate in the treatment of childhood acute myeloid leukaemia, in particular for acute monocytic leukaemia.
  • Acute myeloid leukaemia (AML) is thought to be methotrexate (MTX)-resistant.
  • However, a small study suggested that acute monocytic leukemia (AML-M5) is sensitive to MTX.
  • We measured MTX accumulation/polyglutamylation in 20 AML-nonM5, 37 AML-M5 and 83 common/preB-acute lymphoblastic leukaemia (c/preB-ALL) samples.
  • In both AML-nonM5 and AML-M5 cells, MTX resistance was circumvented by continuous MTX exposure (median TSI(50) values: 0.052 and 0.041 microM, respectively) compared with a c/preB-ALL value of 0.066 microM.
  • In conclusion, AML-M5 is relatively sensitive to MTX compared with other AML-subtypes even though polyglutamylation of MTX is poor.
  • This report suggests that MTX might be an overlooked drug in the treatment of childhood AML.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Leukemia, Monocytic, Acute / drug therapy. Methotrexate / therapeutic use
  • [MeSH-minor] Biological Transport. Child. Drug Resistance, Neoplasm. Humans. Thymidylate Synthase / antagonists & inhibitors. Tumor Cells, Cultured

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  • (PMID = 11267859.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; EC 2.1.1.45 / Thymidylate Synthase; YL5FZ2Y5U1 / Methotrexate
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18. Stasik C, Ganguly S, Cunningham MT, Hagemeister S, Persons DL: Infant acute lymphoblastic leukemia with t(11;16)(q23;p13.3) and lineage switch into acute monoblastic leukemia. Cancer Genet Cytogenet; 2006 Jul 15;168(2):146-9
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  • [Title] Infant acute lymphoblastic leukemia with t(11;16)(q23;p13.3) and lineage switch into acute monoblastic leukemia.
  • Rearrangements of the mixed-lineage leukemia (MLL) gene have been associated with a poor prognosis in infant acute lymphoblastic leukemia (ALL).
  • Previously, MLL translocations involving the CREP-binding protein (CREBBP) gene at chromosome band 16p13.3 have primarily been reported in treatment-related acute myeloid leukemia, after chemotherapy for other primary malignancies using topoisomerase II inhibitors.
  • We report a case of de novo infant ALL with t(11;16)(q23;p13.3).
  • After chemotherapy, this patient developed an acute monoblastic leukemia (M5b) with retention of the t(11;16)(q23;p13.3), indicating that this is a lineage switch of the original leukemic clone.
  • [MeSH-major] Cell Lineage. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 16 / genetics. Leukemia, Monocytic, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics

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  • (PMID = 16843104.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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19. Lai YY, Qiu JY, Jiang B, Lu XJ, Huang XJ, Zhang Y, Liu YR, Shi HL, Lu DP: Characteristics and prognostic factors of acute myeloid leukemia with t (8; 21) (q22; q22). Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Oct;13(5):733-40
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  • [Title] Characteristics and prognostic factors of acute myeloid leukemia with t (8; 21) (q22; q22).
  • Clinically, this type of AML usually shows some specific characteristics and has a good response to chemotherapy with a high remission rate and a relatively long median survival.
  • On the other hand, some reports also showed poor prognosis in AML patients with t (8; 21), and the associated bad-prognosis factors have not been strongly established to date.
  • 21) AML in China, 75 Chinese AML patients with t (8;.
  • After conventional induction therapy, 62 patients attained complete remission (CR) resulting in the CR rate 82.7%.
  • With a follow-up of 1 to 96 months, 19 cases relapsed at a median time of 10.5 months (range 3 to 42 months).
  • In multivariate analyses of prognostic factors, karyotype, extramedullary leukemia, age and post-remission therapy were of prognostic value for OS.
  • Patients with additional chromosomal anomalies had shorter survival compared to those with t (8;.
  • Extramedullary leukemia was an adverse prognostic factor (P = 0.012).
  • Patients accepted HSCT in post-remission therapy had better outcome compared to those with chemotherapy only.
  • It is concluded that Chinese AML patients with t (8;.
  • 21) had some different characteristics as compared with patients from other countries, a relatively poor outcome was observed in our patients, especially in those with extramedullary leukemia or additional chromosomal abnormalities.

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  • (PMID = 16277833.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] China
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20. Okoshi Y, Shimizu S, Kojima H, Obara N, Mukai HY, Komeno T, Hasegawa Y, Mori N, Nagasawa T: Detection of minimal residual disease in a patient having acute myelogenous leukemia with t(16;21)(p11;q22) treated by allogeneic bone marrow transplantation. Acta Haematol; 2001;105(1):45-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of minimal residual disease in a patient having acute myelogenous leukemia with t(16;21)(p11;q22) treated by allogeneic bone marrow transplantation.
  • A 29-year-old woman having acute myelogeneous leukemia-M1 subtype with the chromosomal abnormality t(16;21)(p11;q22) is presented.
  • Complete blood count at onset showed a hemoglobin level of 7.2 g/dl, a platelet count of 48 x 10(9)/l, and a white blood cell count of 161.2 x 10(9)/l with 99% blasts and 1% lymphocytes.
  • Bone marrow aspiration revealed massive proliferation of blasts that were positive for CD13, CD33, CD34, CD56 and myeloperoxidase, and negative for other T-cell, B-cell and monocytic markers.
  • After achieving complete remission following conventional chemotherapy, she received an HLA-matched bone marrow transplantation (BMT) from her sibling after conditioning with busulfan, etoposide and cyclophosphamide.
  • However, 9 months later, the leukemia relapsed as a painful extramedullary mass in her left femur.
  • In spite of intensive re-induction chemotherapy, she died of progressive disease and sepsis.
  • We consider that even high-dose chemotherapy with BMT may not be effective in the eradication of this type of leukemia, and that the detection of minimal residual disease possibly contributes to the better planning of the therapeutic strategy.
  • [MeSH-major] Bone Marrow Transplantation. Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Leukemia, Myeloid, Acute / genetics. Neoplasm, Residual / diagnosis. Translocation, Genetic
  • [MeSH-minor] Adult. Antigens, CD / analysis. Antigens, CD13 / analysis. Antigens, CD34 / analysis. Antigens, CD56 / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow / pathology. Fatal Outcome. Female. Hemoglobins / analysis. Humans. Karyotyping. Leukocyte Count. Peroxidase / analysis. Platelet Count. Radiotherapy. Recurrence. Remission Induction. Reverse Transcriptase Polymerase Chain Reaction. Sialic Acid Binding Ig-like Lectin 3. Transplantation, Homologous. Treatment Failure

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  • [Copyright] Copyright 2001 S. Karger AG, Basel
  • (PMID = 11340253.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, CD56; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Hemoglobins; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 1.11.1.7 / Peroxidase; EC 3.4.11.2 / Antigens, CD13
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21. Lestringant GG, Masouyé I, El-Hayek M, Girardet C, Révész T, Frossard PM: Diffuse calcinosis cutis in a patient with congenital leukemia and leukemia cutis. Dermatology; 2000;200(2):147-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diffuse calcinosis cutis in a patient with congenital leukemia and leukemia cutis.
  • We report an unusual case of congenital leukemia with leukemia cutis (LC) and diffuse calcinosis cutis.
  • Bone marrow morphology was consistent with the diagnosis of acute monocytic leukemia of the FAB M5 type.
  • Calcinosis was diffuse in the whole skin but spared other organs.
  • The patient responded to chemotherapy but, following consolidation treatment, developed sepsis and died at 120 days of age.
  • Congenital leukemia is rare and LC is uncommon.
  • Hypercalcemia may be a complication of leukemia, which leads to multiorgan metastatic calcification.
  • Despite the absence of frank hypercalcemia, the presence of bone lesions suggests that the patient's calcinosis cutis was of the metastatic type.
  • [MeSH-major] Calcinosis / congenital. Leukemia, Myeloid / congenital. Skin Neoplasms / congenital

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  • [Copyright] Copyright 2000 S. Karger AG, Basel.
  • (PMID = 10773706.001).
  • [ISSN] 1018-8665
  • [Journal-full-title] Dermatology (Basel, Switzerland)
  • [ISO-abbreviation] Dermatology (Basel)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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22. Hall RE, Agarwal S, Kestler DP: Induction of leukemia cell differentiation and apoptosis by recombinant P48, a modulin derived from Mycoplasma fermentans. Biochem Biophys Res Commun; 2000 Mar 5;269(1):284-9
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  • [Title] Induction of leukemia cell differentiation and apoptosis by recombinant P48, a modulin derived from Mycoplasma fermentans.
  • P48 is a 48-kDa monocytic differentiation/activation factor which was originally identified in the conditioned medium of the Reh and other leukemia cell lines and has recently been shown to be a Mycoplasma fermentans gene product.
  • Previously, conditioned medium P48 has been shown to induce differentiation of HL-60 (human promyelocytic leukemia) cells.
  • We show that rP48-MBP induces differentiation of HL-60, U937 (human histiocytic lymphoma), and M1 (mouse myeloid leukemia) cell lines.
  • [MeSH-major] Apoptosis / drug effects. Bacterial Proteins / pharmacology. Cell Differentiation / drug effects. Cytokines / pharmacology. Leukemia / drug therapy. Leukemia / pathology. Membrane Proteins / pharmacology. Mycoplasma fermentans / chemistry

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  • [Copyright] Copyright 2000 Academic Press.
  • (PMID = 10694514.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-58205; United States / NCI NIH HHS / CA / CA-72591
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / Cytokines; 0 / Macrophage-1 Antigen; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / polypeptide 48
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23. Wang Q, Harrison JS, Uskokovic M, Kutner A, Studzinski GP: Translational study of vitamin D differentiation therapy of myeloid leukemia: effects of the combination with a p38 MAPK inhibitor and an antioxidant. Leukemia; 2005 Oct;19(10):1812-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translational study of vitamin D differentiation therapy of myeloid leukemia: effects of the combination with a p38 MAPK inhibitor and an antioxidant.
  • Human myeloid leukemia cell lines are induced to terminal differentiation into monocyte lineage by 1,25-dihydroxyvitamin D3 (1,25D3) or its analogs (deltanoids).
  • Strategies to overcome this problem include combination of deltanoids with other compounds to induce differentiation at lower, noncalcemic, deltanoid concentrations.
  • Our studies suggest that patients with CML or AML subtypes M2 and M4, but not M1, M3 or M4eo, are particularly suitable for this combination therapy.
  • We conclude that the established cell line HL60 presents a good model for some, but not all, subtypes of myeloid leukemia, and that the JNK pathway plays an important role in monocytic differentiation of human leukemic cells ex vivo, as well as in vitro.
  • [MeSH-major] Antioxidants / therapeutic use. Cell Differentiation / drug effects. Enzyme Inhibitors / therapeutic use. Leukemia, Myeloid / drug therapy. Vitamin D / analogs & derivatives. p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Calcium / metabolism. Cell Lineage. Drug Therapy, Combination. Female. Humans. Male. Middle Aged. Monocytes / metabolism

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  • (PMID = 16107889.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Enzyme Inhibitors; 1406-16-2 / Vitamin D; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; SY7Q814VUP / Calcium
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24. Vural F, Ozcan MA, Ozsan GH, Demirkan F, Piskin O, Ates H, Kargi A, Undar B: Gingival involvement in a patient with CD56+ chronic myelomonocytic leukemia. Leuk Lymphoma; 2004 Feb;45(2):415-8
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  • [Title] Gingival involvement in a patient with CD56+ chronic myelomonocytic leukemia.
  • Leukemic infiltration of the gingiva is most commonly reported to be associated with monocytic subtypes of acute myeloblastic leukemia (AML) but rarely with myelodysplastic syndromes (MDS).
  • Here we report a case of CD56+ chronic myelomonocytic leukemia (CMML) who developed gingival involvement simultaneously when the leukocyte count elevated.
  • At that time no increase in peripheral or bone marrow blasts were observed.
  • Gingival hypertrophy regressed with the treatment of hydroxyurea.
  • Three months later, bone marrow blast count elevated and the patient was treated with two courses of AML-like regimen and then one course of consolidation therapy.
  • Similar to other extramedullary involvements, gingival hypertrophy in CMML can be a harbinger of the disease entering a more aggressive phase requiring systemic chemotherapy.
  • [MeSH-major] Antigens, CD56 / biosynthesis. Gingival Neoplasms / pathology. Leukemia, Myelomonocytic, Chronic / metabolism

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  • (PMID = 15101735.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD56; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD68 antigen, human
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25. Ishii Y, Kiyota H, Sakai S, Honma Y: Induction of differentiation of human myeloid leukemia cells by jasmonates, plant hormones. Leukemia; 2004 Aug;18(8):1413-9
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  • [Title] Induction of differentiation of human myeloid leukemia cells by jasmonates, plant hormones.
  • Some regulators of plant growth and differentiation have been shown to induce the differentiation of several human myeloid leukemia cells, and might be effective as differentiation inducers to control acute myelogenous leukemia cells.
  • In this study, the growth-inhibiting and differentiation-inducing effects of jasmonates on human myeloid leukemia cells were examined.
  • Several myeloid leukemia cells were cultured with methyl jasmonate (MJ) and its derivatives.
  • MJ induced both monocytic and granulocytic differentiation of HL-60 cells.
  • MJ also induced the differentiation of other human leukemia cell lines.
  • MJ and its derivatives potently induce the differentiation of some myelomonocytic leukemia cells.
  • One novel derivative is a particularly promising therapeutic agent for the treatment of leukemia.
  • [MeSH-major] Cell Differentiation / drug effects. Cyclopentanes / pharmacology. Leukemia, Myeloid / drug therapy. Plant Growth Regulators / pharmacology
  • [MeSH-minor] Cell Division / drug effects. Cell Line, Tumor. Cell Size / drug effects. Enzyme Activation. Granulocytes / cytology. Humans. Immunophenotyping. Mitogen-Activated Protein Kinases / metabolism. Monocytes / cytology. Oxylipins. Structure-Activity Relationship. Tumor Cells, Cultured

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  • (PMID = 15229618.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclopentanes; 0 / Oxylipins; 0 / Plant Growth Regulators; 6RI5N05OWW / jasmonic acid; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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26. Barnes BJ, Izydore RA, Hall IH: Cytotoxicity and mode of action of 1-(1-cyclohexenyl) and 1-unsubstituted 3,5-pyrazolidinediones in human Molt4 T cell leukemia. Anticancer Res; 2001 May-Jun;21(3B):1857-68
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  • [Title] Cytotoxicity and mode of action of 1-(1-cyclohexenyl) and 1-unsubstituted 3,5-pyrazolidinediones in human Molt4 T cell leukemia.
  • The 3,5-pyrazolidinediones proved to be potent cytotoxic agents against the growth of a number of murine and human tumor cell lines, e.g. human THP-I monocytic leukemia, Hut-78 lymphoma, MCF-7 breast effusion, A549 lung carcinoma, U87MG glioma, Hela uterine and A431 epidermoid skin cancer.
  • In human Tmolt4 cell leukemia, the agents substantially suppressed DNA and RNA syntheses after 60 min at 100 microM.
  • Suppression of IMPDH activity was due to the inhibition of both the Type I and II isoforms through an uncompetitive mechanism; however, the Type II isoform was preferentially inhibited at lower concentrations of compounds tested (>50-150 microM).
  • Therefore IMPDH Type II activity, which predominates in cancer cells, was selectively inhibited over the Type I isoform (208-312 microM).
  • The activities of other enzymes examined were inhibited which added to the overall suppression of DNA synthesis, i.e., ribonucleotide reductase, dihydrofolate reductase and nucleoside kinases.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Leukemia / drug therapy. Phenylbutazone / pharmacology
  • [MeSH-minor] Amidophosphoribosyltransferase / antagonists & inhibitors. Animals. DNA / metabolism. HeLa Cells. Humans. IMP Dehydrogenase / antagonists & inhibitors. Inhibitory Concentration 50. Kinetics. Mice. Models, Chemical. Protein Isoforms. Recombinant Proteins / metabolism. Time Factors. Tumor Cells, Cultured

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  • (PMID = 11497269.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Protein Isoforms; 0 / Recombinant Proteins; 9007-49-2 / DNA; EC 1.1.1.205 / IMP Dehydrogenase; EC 2.4.2.14 / Amidophosphoribosyltransferase; GN5P7K3T8S / Phenylbutazone
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27. Niitsu N, Umeda M, Honma Y: Myeloid and monocytoid leukemia cells have different sensitivity to differentiation-inducing activity of deoxyadenosine analogs. Leuk Res; 2000 Jan;24(1):1-9
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  • [Title] Myeloid and monocytoid leukemia cells have different sensitivity to differentiation-inducing activity of deoxyadenosine analogs.
  • The differentiation-inducing effect of clinically applicable analogs of deoxyadenosine on myelomonocytic leukemia cells was examined.
  • Monocytoid leukemia cells were more sensitive to the analogs than were erythroid or myeloid leukemia cells based on the inhibition of cell growth and induction of cell differentiation.
  • Monocytoid leukemia cells were highly sensitive to combined treatment with 2'-deoxycoformycin (dCF) and 9-beta-D-arabinofuranosyladenine (Ara A) for inducing cell differentiation.
  • Ara A induced the differentiation of monocytoid leukemia U937 and THP-1 cells at concentrations which were 1/1000-10000 of that at which it induced the differentiation of other cell lines in the presence of dCF.
  • In combination with a low concentration of 1alpha,25-dihydroxyvitamin D3 (VD3), the induction of the monocytic differentiation was greater in monoblastic U937 cells.
  • Adenosine deaminase-resistant analogs such as fludarabine (FLU) and cladribine (CdA) also induced the differentiation of human myelomonocytic leukemia cells, and these analogs synergistically enhanced the differentiation induced by all-trans retinoic acid (ATRA) or VD3.
  • CdA was the most potent analog for inducing the differentiation of myeloid leukemia NB4 and HL-60 cells in the presence or absence of ATRA.
  • These findings indicate that dCF + Ara A and CdA may be effective for the therapy of acute monocytoid and myeloid leukemia, respectively.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Cladribine / pharmacology. Leukemia, Myeloid / pathology. Monocytes / drug effects. Neoplastic Stem Cells / drug effects. Vidarabine / analogs & derivatives. Vidarabine / pharmacology
  • [MeSH-minor] Acute Disease. Adenosine Deaminase Inhibitors. Calcitriol / pharmacology. Cell Differentiation / drug effects. Deoxyadenosines / pharmacology. Dose-Response Relationship, Drug. Drug Synergism. Enzyme Inhibitors / pharmacology. HL-60 Cells / drug effects. Humans. K562 Cells / drug effects. Neoplasm Proteins / antagonists & inhibitors. Pentostatin / pharmacology. Tretinoin / pharmacology. Tumor Cells, Cultured / drug effects. U937 Cells / drug effects

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  • (PMID = 10634639.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Adenosine Deaminase Inhibitors; 0 / Antimetabolites, Antineoplastic; 0 / Deoxyadenosines; 0 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 14365-44-7 / 5'-amino-5'-deoxyadenosine; 395575MZO7 / Pentostatin; 47M74X9YT5 / Cladribine; 5688UTC01R / Tretinoin; FA2DM6879K / Vidarabine; FXC9231JVH / Calcitriol; P2K93U8740 / fludarabine
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28. Wu XX, Da WM, Li HH, Zhao Y, Wang QS, Wang SH, Zhu HY: [Effects of FLAG regimen in treatment of refractory or relapsed acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Jun;13(3):394-6
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  • [Title] [Effects of FLAG regimen in treatment of refractory or relapsed acute myeloid leukemia].
  • In order to evaluate the effects of FLAG regimen in treatment of refractory and relapsed acute myeloid leukemia (AML), 27 patients with refractory or relapsed acute myeloid leukemia (10 refractory AML patients, 17 relapsed AML patients) were treated with FLAG regimen.
  • It is concluded that FLAG regimen can be employed in treatment of the refractory or relapsed patients who were not respond to other regimen, and the regiment was safe.

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  • (PMID = 15972128.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine
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29. Yu C, Rahmani M, Dai Y, Conrad D, Krystal G, Dent P, Grant S: The lethal effects of pharmacological cyclin-dependent kinase inhibitors in human leukemia cells proceed through a phosphatidylinositol 3-kinase/Akt-dependent process. Cancer Res; 2003 Apr 15;63(8):1822-33
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  • [Title] The lethal effects of pharmacological cyclin-dependent kinase inhibitors in human leukemia cells proceed through a phosphatidylinositol 3-kinase/Akt-dependent process.
  • The impact of disruption of the PI3K (phosphatidylinositol 3-kinase) pathway on the response of human leukemia cells to pharmacological cyclin-dependent kinase (CDK) inhibitors has been examined.
  • Exposure of U937 monocytic leukemia cells to minimally toxic concentrations of flavopiridol (FP), roscovitine, or CGP74514A for 3 h in conjunction with the PI3K inhibitor LY294002 (abbreviated LY in the article) resulted in a marked decrease in Akt phosphorylation.
  • Similar interactions were observed in a variety of other leukemia cell types (e.g., HL-60, Jurkat, Raji, and NB4).
  • Inducible expression of constitutively active (myristolated) Akt significantly, albeit partially, attenuated apoptosis in Jurkat leukemia cells treated with either FP alone or the combination of FP and LY.
  • Finally, cotreatment with LY and FP resulted in a dramatic increase in apoptosis in primary leukemic blasts obtained from a patient with acute myeloblastic leukemia.
  • Together, these findings suggest that the PI3K/Akt pathway plays a major role in regulating the apoptotic response of human leukemia cells to pharmacological CDK inhibitors and raise the possibility that combined interruption of CDK- and PI3K-related pathways may represent a novel therapeutic strategy in hematological malignancies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cyclin-Dependent Kinases / antagonists & inhibitors. Enzyme Inhibitors / pharmacology. Leukemia / drug therapy. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] 2-Aminopurine / analogs & derivatives. 2-Aminopurine / pharmacology. Apoptosis / drug effects. Apoptosis / physiology. Chromones / pharmacology. Drug Synergism. Flavonoids / pharmacology. Humans. Morpholines / pharmacology. Piperidines / pharmacology. Proto-Oncogene Proteins c-akt. Purines / pharmacology. Tumor Cells, Cultured


30. Kumagai T, Shih LY, Hughes SV, Desmond JC, O'Kelly J, Hewison M, Koeffler HP: 19-Nor-1,25(OH)2D2 (a novel, noncalcemic vitamin D analogue), combined with arsenic trioxide, has potent antitumor activity against myeloid leukemia. Cancer Res; 2005 Mar 15;65(6):2488-97
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  • [Title] 19-Nor-1,25(OH)2D2 (a novel, noncalcemic vitamin D analogue), combined with arsenic trioxide, has potent antitumor activity against myeloid leukemia.
  • In this study, we explored if paricalcitol enhanced anticancer effects of other clinically useful drugs in vitro against a large variety of cancer cells.
  • Paricalcitol, when combined with As2O3, showed a markedly enhanced antiproliferative effect against acute myeloid leukemia (AML) cells.
  • This combination induced monocytic differentiation of NB-4 acute promyelocytic leukemia (APL) cells and HL-60 AML cells and caused both to undergo apoptosis associated with down-regulation of Bcl-2 and Bcl-x(L).
  • Paricalcitol induced monocytic differentiation of U937 AML cells, which was partially blocked by inducing expression of APL-related PML-retinoic acid receptor alpha (RARalpha) chimeric protein in the U937 cells containing a Zn2+-inducible expression vector coding for this fusion protein (PR9 cells).
  • Exposure to As2O3 decreased levels of PML-RARalpha in PR9 cells, and the combination of paricalcitol and As2O3 enhanced their monocytic differentiation in parallel with the As2O3-mediated decrease of PML-RARalpha.
  • The combination of both of these Food and Drug Administration-approved drugs should be considered for treatment of all-trans retinoic acid-resistant APL patients as well as those with other types of AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Arsenicals / administration & dosage. Cell Differentiation / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Cytochrome P-450 Enzyme Inhibitors. Cytochrome P-450 Enzyme System / metabolism. Drug Screening Assays, Antitumor. Drug Synergism. Ergocalciferols / administration & dosage. Gene Expression / drug effects. HL-60 Cells. Humans. Mitochondria / drug effects. Neoplasm Proteins / antagonists & inhibitors. Oncogene Proteins, Fusion / antagonists & inhibitors. Oxides / administration & dosage. Steroid Hydroxylases / antagonists & inhibitors. Steroid Hydroxylases / metabolism. Vitamin D3 24-Hydroxylase

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  • (PMID = 15781666.001).
  • [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, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Cytochrome P-450 Enzyme Inhibitors; 0 / Ergocalciferols; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 6702D36OG5 / paricalcitol; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.- / Steroid Hydroxylases; EC 1.14.13.126 / Vitamin D3 24-Hydroxylase; S7V92P67HO / arsenic trioxide
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31. Honma Y: Cotylenin A--a plant growth regulator as a differentiation-inducing agent against myeloid leukemia. Leuk Lymphoma; 2002 Jun;43(6):1169-78
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  • [Title] Cotylenin A--a plant growth regulator as a differentiation-inducing agent against myeloid leukemia.
  • Acute myeloid leukemia (AML) is characterized by the arrest of differentiation leading to the accumulation of immature cells.
  • Although differentiation therapy for patients with acute promyelocytic leukemia (APL) using all-trans retinoic acid (ATRA) has been established, the clinical response of AML patients other than those with APL to ATRA is limited.
  • We must consider novel therapeutic drugs against other forms of AML for the development of a differentiation therapy for leukemia.
  • Regulators that play an important role in the differentiation and development of plants or invertebrates may also affect the differentiation of human leukemia cells through a common signal transduction system, and might be clinically useful for treating AML.
  • Cotylenin A, a plant growth regulator, is a potent and novel inducer of the monocytic differentiation of human myeloid leukemia cell lines and leukemia cells freshly isolated from AML patients.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Cell Differentiation / drug effects. Diterpenes / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Animals. Antigens, Differentiation / biosynthesis. Cholecalciferol / therapeutic use. Drug Screening Assays, Antitumor. Drug Synergism. HL-60 Cells / drug effects. HL-60 Cells / pathology. Humans. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / pathology. Mice. Neoplastic Stem Cells / drug effects. Neoplastic Stem Cells / pathology. Retinoids / pharmacology. Structure-Activity Relationship. Tretinoin / therapeutic use. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / pathology

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  • (PMID = 12152984.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Antineoplastic Agents, Phytogenic; 0 / Diterpenes; 0 / Retinoids; 0 / cotylenin A; 1C6V77QF41 / Cholecalciferol; 5688UTC01R / Tretinoin
  • [Number-of-references] 121
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32. Dai Y, Yu C, Singh V, Tang L, Wang Z, McInistry R, Dent P, Grant S: Pharmacological inhibitors of the mitogen-activated protein kinase (MAPK) kinase/MAPK cascade interact synergistically with UCN-01 to induce mitochondrial dysfunction and apoptosis in human leukemia cells. Cancer Res; 2001 Jul 1;61(13):5106-15
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  • [Title] Pharmacological inhibitors of the mitogen-activated protein kinase (MAPK) kinase/MAPK cascade interact synergistically with UCN-01 to induce mitochondrial dysfunction and apoptosis in human leukemia cells.
  • Interactions between the checkpoint abrogator UCN-01 and several pharmacological inhibitors of the mitogen-activated protein kinase (MAPK) kinase (MEK)/MAPK pathway have been examined in a variety of human leukemia cell lines.
  • Exposure of U937 monocytic leukemia cells to a marginally toxic concentration of UCN-01 (e.g., 150 nM) for 18 h resulted in phosphorylation/activation of p42/44 MAPK.
  • Similar interactions were noted in the case of other MEK inhibitors (e.g., PD98059; U0126) as well as in multiple other leukemia cell types (e.g., HL-60, Jurkat, CCRF-CEM, and Raji).
  • Lastly, although UCN-01 +/- PD184352 did not induce p21(CIP1), stable expression of a p21(CIP1) antisense construct significantly increased susceptibility to this drug combination.
  • [MeSH-major] Alkaloids / pharmacology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Enzyme Inhibitors / pharmacology. Leukemia / drug therapy. MAP Kinase Signaling System / drug effects. Mitochondria / drug effects. Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors
  • [MeSH-minor] Benzamides / administration & dosage. Benzamides / pharmacology. Butadienes / administration & dosage. Butadienes / pharmacology. Caspases / metabolism. Drug Synergism. Enzyme Activation. Flavonoids / administration & dosage. Flavonoids / pharmacology. HL-60 Cells / drug effects. HL-60 Cells / enzymology. Humans. Jurkat Cells / drug effects. Jurkat Cells / enzymology. Nitriles / administration & dosage. Nitriles / pharmacology. Staurosporine / analogs & derivatives. Tumor Cells, Cultured. U937 Cells / drug effects. U937 Cells / enzymology

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  • (PMID = 11431348.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 63753; United States / NCI NIH HHS / CA / CA 77141; United States / NIDDK NIH HHS / DK / DK 52825
  • [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 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / 2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide; 0 / Alkaloids; 0 / Benzamides; 0 / Butadienes; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Nitriles; 0 / U 0126; 7BU5H4V94A / 7-hydroxystaurosporine; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 3.4.22.- / Caspases; H88EPA0A3N / Staurosporine
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33. Danilenko M, Wang Q, Wang X, Levy J, Sharoni Y, Studzinski GP: Carnosic acid potentiates the antioxidant and prodifferentiation effects of 1alpha,25-dihydroxyvitamin D3 in leukemia cells but does not promote elevation of basal levels of intracellular calcium. Cancer Res; 2003 Mar 15;63(6):1325-32
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  • [Title] Carnosic acid potentiates the antioxidant and prodifferentiation effects of 1alpha,25-dihydroxyvitamin D3 in leukemia cells but does not promote elevation of basal levels of intracellular calcium.
  • Differentiation therapy of cancer remains an only partially attained goal.
  • An approach that may obviate this problem is to combine 1,25D(3) or its derivatives with other agents that increase the antineoplastic effects of low, nontoxic concentrations of vitamin D compounds.
  • We have recently used the plant-derived polyphenolic antioxidant, carnosic acid (CA), to demonstrate an increase in the differentiating action of 1,25D(3) on human leukemia cells under these conditions (M.
  • We now show that treatment of HL60-G cells with either CA or 1,25D(3) alone resulted in a decrease in the intracellular levels of reactive oxygen species.
  • Furthermore, the combination of 10 micro M CA and a low concentration of 1,25D(3) (1 nM) produced an enhanced antioxidant effect, which correlated with the potentiation of monocytic differentiation.
  • Other plant antioxidants tested (curcumin, silibinin, and the organoselenium antioxidant ebselen) also potentiated differentiation induced by 1,25D(3), although alone, they had only minor differentiating effects.
  • Cell treatment with a high concentration of 1,25D(3) (100 nM) resulted in a substantial elevation of basal intracellular calcium concentration.
  • These findings suggest that combinations of CA with derivatives of vitamin D should be evaluated for use in differentiation therapy of myeloid leukemias.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Antioxidants / pharmacology. Calcitriol / pharmacology. Calcium / metabolism. Diterpenes / pharmacology. Leukemia, Promyelocytic, Acute / drug therapy. Plant Extracts / pharmacology
  • [MeSH-minor] Cell Differentiation / drug effects. Cell Differentiation / physiology. Cytosol / metabolism. Diterpenes, Abietane. Drug Synergism. HL-60 Cells. Humans. MAP Kinase Signaling System / drug effects. Transcription Factor AP-1 / physiology


34. Muthumani K, Lambert VM, Shanmugam M, Thieu KP, Choo AY, Chung JC, Satishchandran A, Kim JJ, Weiner DB, Ugen KE: Anti-tumor activity mediated by protein and peptide transduction of HIV viral protein R (Vpr). Cancer Biol Ther; 2009 Jan;8(2):180-7
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  • Peptides that are capable of traversing the cell membrane, via protein transduction domains (PTDs), are attractive either directly as drugs or indirectly as carriers for the delivery of therapeutic molecules.
  • There also exists other naturally occurring membrane permeable peptides which have potential as PTDs.
  • Likewise, in in vitro experiments with other tumor cell lines, conjugation of Vpr to the Tat derived PTD and transfection of this construct into cells enhanced the induction of in vitro apoptosis by this protein when compared to the effects of transfection of cells with unconjugated Vpr.
  • These results underscore the potential for Vpr based reagents as well as PTDs to enhance anti-tumor activity, and warrants further examination of Vpr protein and derived peptides as potential therapeutic agents against progressive cell proliferative diseases such as cancer.
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Carcinoma / drug therapy. Cell Line, Tumor. Female. HeLa Cells. Humans. Leukemia, Monocytic, Acute / drug therapy. Male. Melanoma, Experimental / drug therapy. Neuroblastoma / drug therapy. Prostatic Neoplasms / drug therapy. Skin Neoplasms / drug therapy. Transduction, Genetic

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  • [CommentIn] Cancer Biol Ther. 2009 Jan;8(2):188-91 [19182513.001]
  • (PMID = 19029839.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Gene Products, vpr; 0 / Peptides; 0 / Proteins
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35. Drexler HG, Matsuo Y, MacLeod RA: Malignant hematopoietic cell lines: in vitro models for the study of erythroleukemia. Leuk Res; 2004 Dec;28(12):1243-51

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  • A panel of leukemia cell lines has been assembled over the last 30 years representing a spectrum of erythroid cells arrested at various stages of differentiation.
  • Most cell lines have been established from acute myeloid leukemia M6 or chronic myeloid leukemia in blast crisis and generally express immunoprofiles typically seen in immature erythroid cells.
  • It is striking that many cell lines though committed to either the erythroid or megakaryocytic lineage tend to co-express features of the other lineage, consistent with the concept of a common erythroid-megakaryocytic progenitor.
  • Several cell lines may be induced to differentiate along the erythroid, megakaryocytic or monocytic pathway by treatment with pharmacological or physiological reagents.
  • [MeSH-major] Cell Line, Tumor. Erythroid Cells / pathology. Leukemia, Erythroblastic, Acute / pathology
  • [MeSH-minor] Cell Differentiation. Cytogenetic Analysis. Cytokines. Humans. Immunophenotyping. Leukemia, Megakaryoblastic, Acute / pathology

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  • (PMID = 15475063.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
  • [Number-of-references] 67
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36. Pogrebniak A, Hasmann M, Schemainda I, Pelka-Fleischer R, Nuessler V: Cytoprotective features of selenazofurin in hematopoietic cells. Int J Clin Pharmacol Ther; 2002 Aug;40(8):368-75
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  • OBJECTIVES: Antineoplastic activity of tiazofurin (Tz) and selenazofurin (Se) depends on their conversion to substances which are analogs of NAD.
  • The therapeutic potential of modulating intracellular NAD levels and activity of NAD-dependent enzymes by concomitant administration of conventional anticancer agents merits further research.
  • Our aim was to investigate the cytotoxic effects of Tz and Se in hematopoietic cells and to test their ability to potentiate the effects of DNA strand-disrupting agents.
  • MATERIAL: THP-1, a cell line, derived from human acute monoblastic leukemia, was used.
  • METHODS: The WST-l test was used to detect the function of NAD(P)-dependent dehydrogenases after exposure of THP-1 cells to Tz or Se.
  • Cytotoxicity of Tz, Se, MNNG and chlorambucil was assessed using the membrane permeability assay (PI test).
  • RESULTS: THP-1 cells were sensitive to cytotoxic effects of Tz and Se, with IC50 values of 2.5 x 10(-5) M for Tz and 2 x 10(-6) M for Se, as determined with the WST-1 test; 10 microM Se induced cell membrane disruption in more than 20% of THP-1 cells 48 hours after commencement of treatment, whereas the same concentration of Tz failed to increase membrane permeability.
  • Pretreatment of THP-1 cells with 0.5 - 1.5 microM Se had no effect on the time course of cell death, induced by treatment with the DNA-damaging agent 1-methyl-3-nitro-1 - nitrosoguanidinium (MNNG) for 36 hours.
  • However, when incubation of THP-1 cells with MNNG was prolonged (72 hours) without changing the incubation medium, pretreatment with Se had the following effects: the relative number of cells that died spontaneously decreased, and the cytotoxicity of MNNG was diminished.
  • CONCLUSIONS: Contrary to other investigations, we here demonstrate that preincubation with Se may partially protect cells from cell death induced by the alkylating agents MNNG and chlorambucil in the THP-1 cell line and in CLL lymphocytes presumably by affecting spontaneous cell death.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Organoselenium Compounds / pharmacology. Organoselenium Compounds / therapeutic use. Ribavirin / analogs & derivatives. Ribonucleosides / pharmacology. Ribonucleosides / therapeutic use
  • [MeSH-minor] Cell Death / drug effects. Cell Line. Cell Survival / drug effects. Chlorambucil / pharmacology. Dose-Response Relationship, Drug. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Monocytic, Acute / drug therapy. Methylnitronitrosoguanidine / pharmacology

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  • (PMID = 12467305.001).
  • [ISSN] 0946-1965
  • [Journal-full-title] International journal of clinical pharmacology and therapeutics
  • [ISO-abbreviation] Int J Clin Pharmacol Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Organoselenium Compounds; 0 / Ribonucleosides; 12H3O2UGSF / Methylnitronitrosoguanidine; 18D0SL7309 / Chlorambucil; 49717AWG6K / Ribavirin; 83705-13-9 / selenazofurin; ULJ82834RE / tiazofurin
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37. Jones KH, Liu JJ, Roehm JS, Eckel JJ, Eckel TT, Stickrath CR, Triola CA, Jiang Z, Bartoli GM, Cornwell DG: Gamma-tocopheryl quinone stimulates apoptosis in drug-sensitive and multidrug-resistant cancer cells. Lipids; 2002 Feb;37(2):173-84
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  • [Title] Gamma-tocopheryl quinone stimulates apoptosis in drug-sensitive and multidrug-resistant cancer cells.
  • Chemotherapy-induced cell death is linked to apoptosis, and there is increasing evidence that multidrug-resistance in cancer cells may be the result of a decrease in the ability of a cell to initiate apoptosis in response to cytotoxic agents.
  • In previous studies, we synthesized two classes of electrophilic tocopheryl quinones (TQ), nonarylating alpha-TQ and arylating gamma- and delta-TQ, and found that gamma- and delta-TQ, but not alpha-TQ, were highly cytotoxic in human acute lymphoblastic leukemia cells (CEM) and multidrug-resistant (MDR) CEM/VLB100.
  • We have now extended these studies on tumor biology with CEM, HL60 and MDR HL60/MX2 human promyelocytic leukemia, U937 human monocytic leukemia, and ZR-75-1 breast adenocarcinoma cells. gamma-TQ, but not alpha-TQ or tocopherols, showed concentration and incubation time-dependent effects on loss of plasma membrane integrity, diminished viable cell number, and stimulation of apoptosis.
  • The biological properties of arylating TQ electrophiles are closely associated with cytotoxicity and may contribute to other biological effects of these highly active agents.
  • [MeSH-major] Apoptosis / drug effects. Drug Resistance, Multiple. Vitamin E / analogs & derivatives. Vitamin E / pharmacology

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  • (PMID = 11908909.001).
  • [ISSN] 0024-4201
  • [Journal-full-title] Lipids
  • [ISO-abbreviation] Lipids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cytochrome c Group; 1406-18-4 / Vitamin E; 7559-04-8 / tocopherylquinone; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; GAN16C9B8O / Glutathione
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38. Sciacca FL, Canal N, Grimaldi LM: Induction of IL-1 receptor antagonist by interferon beta: implication for the treatment of multiple sclerosis. J Neurovirol; 2000 May;6 Suppl 2:S33-7
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  • [Title] Induction of IL-1 receptor antagonist by interferon beta: implication for the treatment of multiple sclerosis.
  • IFNbeta has been the first drug approved for the treatment of multiple sclerosis patients, but we still lack a full understanding of the mechanisms underlying its clinical effects and the great variability of its therapeutic efficacy among different patients.
  • The amounts of induced IL-1ra were equal or higher than those obtained using other IL-1ra stimuli (LPS, IL-1beta, IFNgamma, IL-4, dexamethasone).
  • [MeSH-major] Adjuvants, Immunologic / pharmacology. Interferon-beta / pharmacology. Multiple Sclerosis / drug therapy. Multiple Sclerosis / immunology. Sialoglycoproteins / genetics. Sialoglycoproteins / immunology
  • [MeSH-minor] Antibodies / pharmacology. Blotting, Northern. Gene Expression / drug effects. Gene Expression / immunology. Humans. Interleukin 1 Receptor Antagonist Protein. Leukemia, Monocytic, Acute. Monocytes / cytology. Monocytes / immunology. RNA, Messenger / metabolism. U937 Cells

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  • (PMID = 10871782.001).
  • [ISSN] 1355-0284
  • [Journal-full-title] Journal of neurovirology
  • [ISO-abbreviation] J. Neurovirol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antibodies; 0 / IL1RN protein, human; 0 / Interleukin 1 Receptor Antagonist Protein; 0 / RNA, Messenger; 0 / Sialoglycoproteins; 77238-31-4 / Interferon-beta
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39. Yuksel S, Saydam G, Uslu R, Sanli UA, Terzioglu E, Buyukececi F, Omay SB: Arsenic trioxide and methylprednisolone use different signal transduction pathways in leukemic differentiation. Leuk Res; 2002 Apr;26(4):391-8
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  • Certain cell lines like HL 60 and K 562 are utilised as leukemic cell models for leukemogenesis research, which differentiate along the granulocytic and/or monocytic pathway when treated with certain inducer molecules.
  • High dose methylprednisolone treatment has been shown to induce in vivo and in vitro differentiation of myeloid leukemia cells to mature granulocytes in patients with acute promyelocytic leukemia (APL) and other subtypes of acute myeloid leukemia (AML).
  • However, there are conflicting results on the effects with other AML subtypes.
  • Unlike As(2)O(3), methylprednisolone induced complete granulocytic and/or monocytic differentiation of HL 60 and K 562 cells via upregulation of PP2A regulatory subunits.
  • Therefore, As(2)O(3) and methylprednisolone are promising agents that have the potential to be used together in myeloid leukemic differentiation therapy.
  • [MeSH-major] Anti-Inflammatory Agents / pharmacology. Antineoplastic Agents / pharmacology. Arsenicals / pharmacology. Leukemia / metabolism. Leukemia / pathology. Methylprednisolone / pharmacology. Oxides / pharmacology. Signal Transduction / drug effects
  • [MeSH-minor] Cell Differentiation / drug effects. Dose-Response Relationship, Drug. HL-60 Cells. Humans. K562 Cells. Phosphoprotein Phosphatases / metabolism

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  • (PMID = 11839383.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; EC 3.1.3.16 / Phosphoprotein Phosphatases; S7V92P67HO / arsenic trioxide; X4W7ZR7023 / Methylprednisolone
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40. Requena L, Kutzner H, Palmedo G, Pascual M, Fernández-Herrera J, Fraga J, García-Díez A, Yus ES: Histiocytoid Sweet syndrome: a dermal infiltration of immature neutrophilic granulocytes. Arch Dermatol; 2005 Jul;141(7):834-42
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  • METHODS: Conventional histopathologic study as well as immunohistochemical investigations were performed using the alkaline phosphatase antialkaline phosphatase technique with a large panel of antibodies.
  • RESULTS: Immunohistochemical studies demonstrated that most cells of the infiltrate showed immunoreactivity for CD15, CD43, CD45, CD68, MAC-386, HAM56, and lysozyme, which is consistent with a monocytic-histiocytic immunoprofile.
  • However, intense myeloperoxidase reactivity was detected in most of the cells with histiocytic appearance, which raised the possibility of specific cutaneous involvement by myelogenous leukemia.
  • We named this histopathologic variant histiocytoid Sweet syndrome, which should not be mistaken with leukemia cutis or other inflammatory dermatoses that are histopathologically characterized by histiocytes interstitially arranged between collagen bundles of the dermis.
  • [MeSH-major] Diclofenac / analogs & derivatives. Histiocytes / pathology. Sweet Syndrome / drug therapy. Sweet Syndrome / pathology
  • [MeSH-minor] Acetaminophen / administration & dosage. Administration, Oral. Adult. Aged. Biopsy, Needle. Cohort Studies. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Prednisone / administration & dosage. Severity of Illness Index. Treatment Outcome

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  • [CommentIn] Int J Dermatol. 2014 Feb;53(2):e80-2 [23330976.001]
  • [CommentIn] Arch Dermatol. 2005 Jul;141(7):893-5 [16027307.001]
  • (PMID = 16027297.001).
  • [ISSN] 0003-987X
  • [Journal-full-title] Archives of dermatology
  • [ISO-abbreviation] Arch Dermatol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 144O8QL0L1 / Diclofenac; 362O9ITL9D / Acetaminophen; RPK779R03H / aceclofenac; VB0R961HZT / Prednisone
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41. Leone G, Voso MT, Sica S, Morosetti R, Pagano L: Therapy related leukemias: susceptibility, prevention and treatment. Leuk Lymphoma; 2001 Apr;41(3-4):255-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy related leukemias: susceptibility, prevention and treatment.
  • Acute leukemia is the most frequent therapy-related malignancy.
  • The tumorigenic action of topoisomerase inhibitors is on the other hand due to the formation of multiple DNA strand breaks, resolved by chromosomal translocations.
  • Among these, chromosome 11, band q23, where the myeloid-lymphoid leukemia (MLL) gene is located, is often involved.
  • Younger age, a mean period of latency of 2 years and monocytic subtypes are characteristic features of this type of leukemia.
  • Among patients at risk for secondary leukemia, those with Hodgkin's disease are the most extensively studied, with the major impact of alkylating agents included in the chemotherapy schedule.
  • The same is true for non-Hodgkin's lymphoma, while in multiple myeloma and acute lymphoblastic leukemia determinants are the dose of melphalan and of epypodophyllotoxin, respectively.
  • According to the EBMT registry, in patients with lymphoma treated with high-dose therapy and autologous stem cell transplantation the cumulative risk of inducing leukemia at 5 years is 2.6%.
  • Among treatment options, supportive therapy is indicated in older patients, while allogeneic stem cell transplantation, related or matched-unrelated, is feasible in younger patients.
  • These data indicate the need for the identification of predisposing factors for secondary leukemia.
  • Whenever possible, the exclusion of drugs known to be leukemogenic from the treatment schedules should be considered, especially in young patients.
  • [MeSH-major] Leukemia. Neoplasms, Second Primary

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  • (PMID = 11378539.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating
  • [Number-of-references] 193
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42. Niedre MJ, Secord AJ, Patterson MS, Wilson BC: In vitro tests of the validity of singlet oxygen luminescence measurements as a dose metric in photodynamic therapy. Cancer Res; 2003 Nov 15;63(22):7986-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro tests of the validity of singlet oxygen luminescence measurements as a dose metric in photodynamic therapy.
  • Singlet oxygen ((1)O(2)) is widely believed to be the major cytotoxic agent involved in photodynamic therapy (PDT).
  • We showed recently that measurement of the weak near infrared luminescence of (1)O(2) is possible in cells in vitro and tissues in vivo.
  • Here, we investigated the relationship between the integrated luminescence signal and the in vitro PDT response of AML5 leukemia cells sensitized with aminolevulinic acid-induced protoporphyrin IX (PpIX).
  • Sensitized cell suspensions were irradiated with pulsed 523 nm laser light at average fluence rates of 10, 25, or 50 mWcm(-2) and, (1)O(2) luminescence measurements were made throughout the treatment.
  • There were large variations in cell survival and (1)O(2) generation in different experiments due to different controlled treatment parameters (fluence and fluence rate) and other uncontrolled factors (PpIX synthesis and oxygenation).
  • [MeSH-major] Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / metabolism. Photochemotherapy / methods. Singlet Oxygen / analysis
  • [MeSH-minor] Aminolevulinic Acid / pharmacokinetics. Aminolevulinic Acid / pharmacology. Cell Line, Tumor. Cell Survival / drug effects. Humans. Luminescent Measurements. Protoporphyrins / pharmacokinetics. Protoporphyrins / pharmacology. Reproducibility of Results. Spectrum Analysis / methods

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  • (PMID = 14633731.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protoporphyrins; 17778-80-2 / Singlet Oxygen; 553-12-8 / protoporphyrin IX; 88755TAZ87 / Aminolevulinic Acid
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43. Jamshidi F, Zhang J, Harrison JS, Wang X, Studzinski GP: Induction of differentiation of human leukemia cells by combinations of COX inhibitors and 1,25-dihydroxyvitamin D3 involves Raf1 but not Erk 1/2 signaling. Cell Cycle; 2008 Apr 1;7(7):917-24
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  • [Title] Induction of differentiation of human leukemia cells by combinations of COX inhibitors and 1,25-dihydroxyvitamin D3 involves Raf1 but not Erk 1/2 signaling.
  • Differentiation therapy of cancer is being explored as a potential modality for treatment of myeloid leukemia, and derivatives of vitamin D are gaining prominence as agents for this form of therapy.
  • Cyclooxygenase (COX) inhibitors have been reported to enhance 1,25-dihydroxyvitamin D(3) (1,25D)-induced monocytic differentiation of promyeloblastic HL60 cells, but the mechanisms of this effect are not fully elucidated, and whether this potentiation can occur in other types of myeloid leukemia is not known.
  • We found that combination treatment with 1,25D and non-specific COX inhibitors acetyl salicylic acid (ASA) or indomethacin can robustly potentiate differentiation of other types of human leukemia cells, i.e., U937, THP-1, and that ASA +/- 1,25D is effective in primary AML cultures.
  • Identification of the strong antiproliferative activity of ASA/1,25D combinations associated with monocytic differentiation has implications for cancer chemoprevention in individuals who have a predisposition to myeloid leukemia.

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  • (PMID = 18414055.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA044722-18A2; United States / NCI NIH HHS / CA / R01 CA044722; United States / NCI NIH HHS / CA / R01 CA044722-18A2; United States / PHS HHS / / R01-44722
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / RNA, Small Interfering; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf; FXC9231JVH / Calcitriol; R16CO5Y76E / Aspirin; XXE1CET956 / Indomethacin
  • [Other-IDs] NLM/ NIHMS169983; NLM/ PMC2843692
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44. Au WY, Ma SK, Wan TS, Man C, Kwong YL: Pentasomy 8q in therapy-related myelodysplastic syndrome due to cyclophosphamide therapy for fibrosing alveolitis. Cancer Genet Cytogenet; 2003 Feb;141(1):79-82
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  • [Title] Pentasomy 8q in therapy-related myelodysplastic syndrome due to cyclophosphamide therapy for fibrosing alveolitis.
  • Trisomy 8/8q is a common cytogenetic event in myelocytic malignancies, ranging from myelodysplastic syndrome (MDS) to acute myelocytic leukemia (AML) to blastic transformation of chronic myelocytic leukemia.
  • A patient with fibrosing alveolitis on prolonged cyclophosphamide treatment developed therapy-related MDS.
  • Karyotyping, FISH, and CGH analysis showed a duplicated i(8q) among other complex abnormalities.
  • The clinical features of 11 cases of myelocytic leukemia with pentasomy and hexasomy 8/8q were summarized.
  • Compared with trisomy and tetrasomy 8, significant features included reduced median survival (90 days), treatment refractoriness (even with transplantation), monocytic differentiation, trilineage dysplasia, and radiation or toxin exposure.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Cyclophosphamide / adverse effects. Cyclophosphamide / therapeutic use. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics. Pulmonary Fibrosis / complications. Pulmonary Fibrosis / drug therapy


45. Wang X, Wang TT, White JH, Studzinski GP: Induction of kinase suppressor of RAS-1(KSR-1) gene by 1, alpha25-dihydroxyvitamin D3 in human leukemia HL60 cells through a vitamin D response element in the 5'-flanking region. Oncogene; 2006 Nov 9;25(53):7078-85
Hazardous Substances Data Bank. 1,25-DIHYDROXYCHOLECALCIFEROL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of kinase suppressor of RAS-1(KSR-1) gene by 1, alpha25-dihydroxyvitamin D3 in human leukemia HL60 cells through a vitamin D response element in the 5'-flanking region.
  • Differentiation therapy is being developed as an additional therapeutic option for the treatment of several forms of cancer, including myeloid leukemia.
  • In model systems, the physiologically active form of vitamin D, 1, alpha25-dihydroxyvitamin D3 (1,25D), induces monocytic differentiation of human myeloid cells, but the mechanism is not clear.
  • We report here, the first direct connection between the signal provided by 1,25D and the molecular circuitry known to be involved in monocytic differentiation.
  • Specifically, we show that 1,25D selectively increases the expression of the gene encoding kinase suppressor of Ras-1 (KSR-1) in HL60 cells, while other differentiation-inducing agents such as 12-O-tetradecanoylphorbol-13-acetate, retinoic acid or dimethyl sulfoxide do not significantly increase KSR-1 expression.
  • Our findings offer a potential mechanism for a signaling pathway that contributes to 1,25D-induced monocytic differentiation of human myeloid leukemia cells.

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  • (PMID = 16732322.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA044722-16; United States / NCI NIH HHS / CA / R01 CA044722; United States / NCI NIH HHS / CA / R01 CA044722-16; United States / NCI NIH HHS / CA / R01-CA44722-16
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Calcitriol; 0 / ZK159222; EC 2.7.- / Protein Kinases; EC 2.7.1.- / KSR-1 protein kinase; FXC9231JVH / Calcitriol
  • [Other-IDs] NLM/ NIHMS170005; NLM/ PMC2843694
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