[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 2336
1. Knipp S, Strupp C, Gattermann N, Hildebrandt B, Schapira M, Giagounidis A, Aul C, Haas R, Germing U: Presence of peripheral blasts in refractory anemia and refractory cytopenia with multilineage dysplasia predicts an unfavourable outcome. Leuk Res; 2008 Jan;32(1):33-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In 1103 patients with these diagnoses, we analysed survival and risk of AML evolution depending on the presence of PB.
  • Cumulative risk of AML was significantly higher in patients showing PB (p<0.00005).
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Anemia, Sideroblastic / pathology. Chromosome Aberrations. Female. Humans. Male. Middle Aged. Pancytopenia / mortality. Prognosis. Risk. Survival Rate


2. Kuchenbauer F, Schnittger S, Look T, Gilliland G, Tenen D, Haferlach T, Hiddemann W, Buske C, Schoch C: Identification of additional cytogenetic and molecular genetic abnormalities in acute myeloid leukaemia with t(8;21)/AML1-ETO. Br J Haematol; 2006 Sep;134(6):616-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of additional cytogenetic and molecular genetic abnormalities in acute myeloid leukaemia with t(8;21)/AML1-ETO.
  • AML1-ETO collaborates with further genetic abnormalities to induce acute myeloid leukaemia (AML).
  • These clinical findings support the model that AML1-ETO collaborates with other genetic alterations, such as mutations of receptor tyrosine kinases, to induce AML.
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Cytogenetics. Female. Humans. In Situ Hybridization, Fluorescence. Leukemia, Myeloid. Male. Middle Aged

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16938118.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
  •  go-up   go-down


3. Reikvam H, Hatfield KJ, Oyan AM, Kalland KH, Kittang AO, Bruserud O: Primary human acute myelogenous leukemia cells release matrix metalloproteases and their inhibitors: release profile and pharmacological modulation. Eur J Haematol; 2010 Mar;84(3):239-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary human acute myelogenous leukemia cells release matrix metalloproteases and their inhibitors: release profile and pharmacological modulation.
  • OBJECTIVES: Angiogenesis seems important for both leukemogenesis and chemosensitivity in acute myelogenous leukemia (AML).
  • We investigated the constitutive release of MMPs and TIMPs for a large group of consecutive AML patients.
  • METHODS: AML cells were cultured in vitro either alone or together with microvascular endothelial cells, and levels of MMPs and TIMPs were determined in culture supernatants.
  • RESULTS: AML cells showed constitutive release of several MMPs and TIMPs.
  • MMP-9 release was higher for AML cells with monocytic differentiation corresponding to the FAB-subtype M4/M5 AML; it was mainly released in its inactive form, but endogenously active MMP-9 could be detected even in the presence of the constitutively released TIMP-1/2.
  • Endothelial cells released relatively high levels of MMP-10, and these levels were further increased by coculture with AML cells.
  • CONCLUSION: We conclude that primary human AML cells show constitutive release of both MMPs and TIMPs, and this release may be important for leukemogenesis and possibly also for chemosensitivity.
  • [MeSH-major] Leukemia, Myeloid / pathology. Matrix Metalloproteinases / secretion. Neoplasm Proteins / secretion. Tissue Inhibitor of Metalloproteinases / secretion
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Angiopoietin-2 / pharmacology. Anthracyclines / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Boronic Acids / pharmacology. Bortezomib. Cells, Cultured / cytology. Chemokines / secretion. Coculture Techniques. Culture Media, Serum-Free / pharmacology. Cytarabine / administration & dosage. Diterpenes / pharmacology. Endothelial Cells / cytology. Female. Humans. Imidazoles / pharmacology. Male. Matrix Metalloproteinase Inhibitors. Middle Aged. NF-kappa B / antagonists & inhibitors. Protease Inhibitors / pharmacology. Pyrazines / pharmacology. Quinoxalines / pharmacology. Receptor, TIE-2 / antagonists & inhibitors. Receptor, TIE-2 / physiology. Recombinant Proteins / pharmacology. Tumor Cells, Cultured / enzymology. Tumor Cells, Cultured / secretion

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19922462.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 3-ingenyl angelate; 0 / 4(2'-aminoethyl)amino-1,8-dimethylimidazo(1,2-a)quinoxaline; 0 / Angiopoietin-2; 0 / Anthracyclines; 0 / Boronic Acids; 0 / Chemokines; 0 / Culture Media, Serum-Free; 0 / Diterpenes; 0 / Imidazoles; 0 / Matrix Metalloproteinase Inhibitors; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Protease Inhibitors; 0 / Pyrazines; 0 / Quinoxalines; 0 / Recombinant Proteins; 0 / Tissue Inhibitor of Metalloproteinases; 04079A1RDZ / Cytarabine; 69G8BD63PP / Bortezomib; EC 2.7.10.1 / Receptor, TIE-2; EC 3.4.24.- / Matrix Metalloproteinases
  •  go-up   go-down


Advertisement
4. Suzuki T, Kiyoi H, Ozeki K, Tomita A, Yamaji S, Suzuki R, Kodera Y, Miyawaki S, Asou N, Kuriyama K, Yagasaki F, Shimazaki C, Akiyama H, Nishimura M, Motoji T, Shinagawa K, Takeshita A, Ueda R, Kinoshita T, Emi N, Naoe T: Clinical characteristics and prognostic implications of NPM1 mutations in acute myeloid leukemia. Blood; 2005 Oct 15;106(8):2854-61
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical characteristics and prognostic implications of NPM1 mutations in acute myeloid leukemia.
  • Recently, somatic mutations of the nucleophosmin gene (NPM1), which alter the subcellular localization of the product, have been reported in acute myeloid leukemia (AML).
  • We analyzed the clinical significance of NPM1 mutations in comparison with cytogenetics, FLT3, NRAS, and TP53 mutations, and a partial tandem duplication of the MLL gene (MLL-TD) in 257 patients with AML.
  • In 190 patients without the M3 French-American-British (FAB) subtype who were treated with the protocol of the Japan Adult Leukemia Study Group, multivariate analyses showed that the NPM1 mutation was a favorable factor for achieving complete remission but was associated with a high relapse rate.
  • These results suggest that the NPM1 mutation is not necessarily an early event during leukemogenesis or that leukemia clones with NPM1 mutations are sensitive to chemotherapy.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Base Sequence. Disease Progression. Exons / genetics. Female. Genotype. Humans. Male. Middle Aged. Molecular Sequence Data. Prognosis. Survival Rate


5. Brixius K, Gross T, Tossios P, Geissler HJ, Mehlhorn U, Schwinger RH, Hekmat K: Increased vascular selectivity and prolonged pharmacological efficacy of the L-type Ca2+ channel antagonist lercanidipine in human cardiovascular tissue. Clin Exp Pharmacol Physiol; 2005 Sep;32(9):708-13
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 1. The present study investigates the vasoselectivity of lercanidipine (LER), a 1,4-dihydropyridine calcium channel blocker, compared with amlodipine (AML) and nifedipine (NIF) in human cardiovascular tissue.
  • 2. The obtained rank order for the L-type Ca2+ channel affinity in human tissue was LER > NIF >or= AML.
  • Lercanidipine had the lowest negative inotropic efficacy (1 micromol/L LER: 60.3% basal < AML: 79.1% basal < NIF: 92.4 basal) and potency (IC50 NIF: 3.5 nmol/L < AML: 48 nmol/L < Ler: 127 nmol/L) in right atrial trabeculae.
  • 3. The vasorelaxant potency of LER (IC50 0.5 nmol/L) and AML (IC50 0.8 nmol/L) was similar and significantly increased compared with that of NIF (IC50 5.9 nmol/L) in arteria mammaria preparations of the very same patients.
  • 4. The following rank order was obtained for vasoselectivity: LER (260) < AML (60) < NIF (0.6).
  • 5. The pharmacological effects of LER and AML were still present 2 h after drug washout.
  • [MeSH-minor] Adolescent. Adult. Aged. Amlodipine / pharmacology. Binding, Competitive. Calcium Channels, L-Type / drug effects. Female. Humans. In Vitro Techniques. Male. Mammary Arteries / drug effects. Middle Aged. Nifedipine / pharmacology. Protein Binding. Stimulation, Chemical

  • Hazardous Substances Data Bank. Nifedipine .
  • Hazardous Substances Data Bank. AMLODIPINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16173926.001).
  • [ISSN] 0305-1870
  • [Journal-full-title] Clinical and experimental pharmacology & physiology
  • [ISO-abbreviation] Clin. Exp. Pharmacol. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; 0 / Calcium Channels, L-Type; 0 / Dihydropyridines; 1J444QC288 / Amlodipine; I9ZF7L6G2L / Nifedipine; V7XTJ4R0BH / lercanidipine
  •  go-up   go-down


6. Ohwada C, Nakaseko C, Tanaka H, Abe D, Oda K, Ozawa S, Takeuchi M, Shimizu N, Cho R, Saito Y, Nishimura M: Successful matched unrelated BMT for secondary AML which developed simultaneously with relapsed Hodgkin's lymphoma. Bone Marrow Transplant; 2007 May;39(9):569-70
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful matched unrelated BMT for secondary AML which developed simultaneously with relapsed Hodgkin's lymphoma.
  • [MeSH-major] Bone Marrow Transplantation. Hodgkin Disease / therapy. Leukemia, Myeloid, Acute / therapy. Neoplasms, Second Primary / therapy
  • [MeSH-minor] Adult. Asian Continental Ancestry Group. Combined Modality Therapy. Female. Humans. Japan. Recurrence. Transplantation, Homologous


7. Karp JE, Blackford A, Smith BD, Alino K, Seung AH, Bolaños-Meade J, Greer JM, Carraway HE, Gore SD, Jones RJ, Levis MJ, McDevitt MA, Doyle LA, Wright JJ: Clinical activity of sequential flavopiridol, cytosine arabinoside, and mitoxantrone for adults with newly diagnosed, poor-risk acute myelogenous leukemia. Leuk Res; 2010 Jul;34(7):877-82
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical activity of sequential flavopiridol, cytosine arabinoside, and mitoxantrone for adults with newly diagnosed, poor-risk acute myelogenous leukemia.
  • In a Phase II study, flavopiridol 50 mg/m(2) was given by 1-h infusion daily x 3 beginning day 1 followed by 2 g/m(2)/72 h ara-C beginning day 6 and 40 mg/m(2) mitoxantrone on day 9 (FLAM) to 45 adults with newly diagnosed acute myelogenous leukemia (AML) with multiple poor-risk features.

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. Allopurinol .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • [Cites] N Engl J Med. 2009 Sep 24;361(13):1235-48 [19776405.001]
  • [Cites] Blood. 2009 Apr 23;113(17):4063-73 [19144992.001]
  • [Cites] N Engl J Med. 2009 Sep 24;361(13):1249-59 [19776406.001]
  • [Cites] J Natl Cancer Inst. 2000 Mar 1;92(5):376-87 [10699068.001]
  • [Cites] Cell Death Differ. 2001 Jul;8(7):715-24 [11464216.001]
  • [Cites] J Biol Chem. 2001 Aug 24;276(34):31793-9 [11431468.001]
  • [Cites] Genome Biol. 2001;2(10):RESEARCH0041 [11597333.001]
  • [Cites] Clin Cancer Res. 2002 Nov;8(11):3527-38 [12429644.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Leuk Res. 2003 Apr;27(4):313-21 [12531222.001]
  • [Cites] Clin Cancer Res. 2003 Jan;9(1):307-15 [12538483.001]
  • [Cites] Cancer Res. 2003 Apr 15;63(8):1822-33 [12702569.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4642-9 [14673054.001]
  • [Cites] Am J Med. 1969 Sep;47(3):351-66 [5258033.001]
  • [Cites] Ann Intern Med. 1975 Jan;82(1):54-7 [16553.001]
  • [Cites] Medicine (Baltimore). 1980 Nov;59(6):409-25 [7003298.001]
  • [Cites] Blood. 1989 Oct;74(5):1499-506 [2676014.001]
  • [Cites] Biochem Pharmacol. 1993 Nov 17;46(10):1831-40 [8250970.001]
  • [Cites] Cancer Res. 1996 Jul 1;56(13):2973-8 [8674031.001]
  • [Cites] Cancer Res. 1996 Nov 1;56(21):4856-61 [8895733.001]
  • [Cites] Cancer Res. 1997 Aug 15;57(16):3375-80 [9269999.001]
  • [Cites] Cancer Res. 1999 Sep 15;59(18):4634-41 [10493518.001]
  • [Cites] Clin Cancer Res. 2005 Dec 1;11(23):8403-12 [16322302.001]
  • [Cites] Mol Cancer Ther. 2006 Jan;5(1):138-48 [16432172.001]
  • [Cites] Blood. 2006 May 1;107(9):3481-5 [16455952.001]
  • [Cites] Leuk Lymphoma. 2006 Apr;47(4):697-706 [16690529.001]
  • [Cites] Blood. 2007 Jan 15;109(2):399-404 [17003373.001]
  • [Cites] Blood. 2007 Mar 1;109(5):1810-6 [17095617.001]
  • [Cites] J Clin Oncol. 2007 May 10;25(14):1908-15 [17488990.001]
  • [Cites] Clin Cancer Res. 2007 Aug 1;13(15 Pt 1):4467-73 [17671131.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]
  • [Cites] Blood. 2009 Mar 19;113(12):2637-45 [18981292.001]
  • [Cites] Blood. 2009 Apr 23;113(17):4052-62 [19144991.001]
  • [CommentIn] Leuk Res. 2010 Jul;34(7):856-7 [20378170.001]
  • (PMID = 19962759.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P30 CA06973-44; United States / NCI NIH HHS / CA / U01 CA069854; United States / NCRR NIH HHS / RR / M01-RR0052; United States / NCI NIH HHS / CA / U01 CA70095; United States / NCI NIH HHS / CA / CA069854-05; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCRR NIH HHS / RR / M01 RR000052; United States / NCI NIH HHS / CA / U01 CA069854-05
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Piperidines; 0 / Polyamines; 04079A1RDZ / Cytarabine; 45AD6X575G / alvocidib; 63CZ7GJN5I / Allopurinol; 9YCX42I8IU / Sevelamer; BZ114NVM5P / Mitoxantrone
  • [Other-IDs] NLM/ NIHMS158765; NLM/ PMC2875369
  •  go-up   go-down


8. Rogers BB: Advances in the management of acute myeloid leukemia in older adult patients. Oncol Nurs Forum; 2010 May;37(3):E168-79
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advances in the management of acute myeloid leukemia in older adult patients.
  • PURPOSE/OBJECTIVES: To update oncology nurses on new developments in the care of older adult patients with acute myeloid leukemia (AML).
  • DATA SYNTHESIS: Therapies for older adult patients with AML include cytarabine-based intensive-induction chemotherapy, investigational therapy, and supportive care.
  • CONCLUSIONS: Survival outcomes have not improved significantly for older adult patients with AML.
  • Efforts to improve transplantation safety may increase use in the older adult patient population.
  • Knowledge of the key management issues for older adult patients with AML is critical in fulfilling this role.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Oncology Nursing / methods

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. AZACITIDINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20439202.001).
  • [ISSN] 1538-0688
  • [Journal-full-title] Oncology nursing forum
  • [ISO-abbreviation] Oncol Nurs Forum
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
  •  go-up   go-down


9. van Rhenen A, Moshaver B, Ossenkoppele GJ, Schuurhuis GJ: New approaches for the detection of minimal residual disease in acute myeloid leukemia. Curr Hematol Malig Rep; 2007 May;2(2):111-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New approaches for the detection of minimal residual disease in acute myeloid leukemia.
  • The detection of minimal residual disease (MRD) in patients with acute leukemia has been studied for about 15 years by different groups in both the United States and Europe.
  • When informative, we compare literature on MRD in acute myeloid leukemia (AML) with information from MRD studies in acute lymphoblastic leukemia.
  • Finally, we address the promising detection of AML stem cells, the likely cells of origin in AML, for prediction of clinical outcome and guidance of future therapies.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / genetics. Bone Marrow Examination. Child. Clinical Trials as Topic. Clone Cells / chemistry. Clone Cells / pathology. DNA Mutational Analysis. Flow Cytometry. Forecasting. Humans. Immunophenotyping. Multicenter Studies as Topic. Neoplasm Proteins / genetics. Neoplasm, Residual. Neoplastic Stem Cells / chemistry. Neoplastic Stem Cells / pathology. Polymerase Chain Reaction / methods

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cytometry. 1997 Dec 1;29(4):328-39 [9415416.001]
  • [Cites] Leukemia. 1999 Dec;13(12):1901-28 [10602411.001]
  • [Cites] Crit Rev Oncol Hematol. 2005 Nov;56(2):283-309 [16213150.001]
  • [Cites] Blood. 2003 Apr 1;101(7):2521-8 [12468436.001]
  • [Cites] Nat Med. 1997 Dec;3(12 ):1337-45 [9396603.001]
  • [Cites] Blood. 2000 Dec 1;96(12):3948-52 [11090082.001]
  • [Cites] Blood. 1998 Jun 15;91(12):4480-8 [9616142.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2746-55 [12842988.001]
  • [Cites] Blood. 2001 Aug 15;98 (4):1166-73 [11493466.001]
  • [Cites] Blood. 2004 Nov 15;104(10):3078-85 [15284114.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1416-23 [15920493.001]
  • [Cites] Br J Haematol. 2006 Aug;134(3):273-82 [16848770.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3574-80 [11369653.001]
  • [Cites] Leukemia. 2006 Jan;20(1):87-94 [16281071.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1674-7 [12886261.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1380-90 [15201848.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2691-6 [11023499.001]
  • [Cites] Leukemia. 2006 Mar;20(3):451-7 [16424875.001]
  • [Cites] Cancer Res. 2000 Aug 15;60(16):4403-11 [10969785.001]
  • [Cites] Leukemia. 2005 Mar;19(3):367-72 [15674426.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2399-402 [12239148.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2003;:82-101 [14633778.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1103-8 [16541144.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1217-20 [16642044.001]
  • [Cites] Cancer Genet Cytogenet. 2002 Mar;133(2):118-23 [11943337.001]
  • [Cites] Clin Cancer Res. 2005 Sep 15;11(18):6520-7 [16166428.001]
  • [Cites] Am J Clin Pathol. 2004 Dec;122 Suppl:S47-57 [15690642.001]
  • [Cites] Br J Haematol. 2005 Mar;128(6):774-82 [15755280.001]
  • [Cites] Br J Haematol. 2001 Aug;114(2):313-8 [11529849.001]
  • [Cites] Leuk Lymphoma. 2007 Jan;48(1):80-8 [17325851.001]
  • [Cites] Br J Haematol. 2003 Oct;123(2):243-52 [14531905.001]
  • [Cites] J Clin Oncol. 1988 May;6(5):802-12 [3163363.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Leukemia. 2002 May;16(5):846-54 [11986946.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1746-51 [11535507.001]
  • [Cites] Leukemia. 2000 Oct;14(10):1777-84 [11021753.001]
  • [Cites] Haematologica. 2004 Jan;89(1):29-33 [14754603.001]
  • [Cites] Oncogene. 2006 May 25;25(22):3113-22 [16407823.001]
  • [Cites] Lancet. 1998 Nov 28;352(9142):1731-8 [9848348.001]
  • [Cites] Blood. 2003 Feb 1;101(3):837-45 [12393383.001]
  • [Cites] Haematologica. 2003 Jun;88(6):646-53 [12801840.001]
  • [Cites] Clin Cancer Res. 2005 Apr 1;11(7):2540-6 [15814631.001]
  • [Cites] Med Oncol Tumor Pharmacother. 1987;4(1):23-31 [3600054.001]
  • [Cites] Br J Haematol. 2006 Jul;134(1):54-7 [16803567.001]
  • [Cites] J Exp Med. 1996 Apr 1;183(4):1797-806 [8666936.001]
  • [Cites] Nat Med. 2003 Sep;9(9):1158-65 [12897778.001]
  • [Cites] Cancer Res. 2004 Nov 15;64(22):8443-50 [15548716.001]
  • [Cites] Am J Hematol. 2005 Aug;79(4):257-61 [16044453.001]
  • [Cites] Blood. 2003 Mar 15;101(6):2125-31 [12424199.001]
  • [Cites] Leukemia. 2001 May;15(5):716-27 [11368431.001]
  • [Cites] Leukemia. 2002 Jun;16(6):1176-81 [12040450.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Jul 15;168(2):172-4 [16843110.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2659-66 [17609428.001]
  • [Cites] Blood. 2003 Jun 15;101(12):4695-700 [12586618.001]
  • [Cites] Blood. 2003 May 1;101(9):3398-406 [12506020.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4086-92 [16131573.001]
  • [Cites] Leukemia. 2002 Aug;16(8):1432-6 [12145681.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] Blood. 2002 Jul 1;100(1):59-66 [12070009.001]
  • (PMID = 20425359.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
  • [Number-of-references] 66
  •  go-up   go-down


10. Buck AK, Bommer M, Juweid ME, Glatting G, Stilgenbauer S, Mottaghy FM, Schulz M, Kull T, Bunjes D, Möller P, Döhner H, Reske SN: First demonstration of leukemia imaging with the proliferation marker 18F-fluorodeoxythymidine. J Nucl Med; 2008 Nov;49(11):1756-62
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] First demonstration of leukemia imaging with the proliferation marker 18F-fluorodeoxythymidine.
  • Acute myeloid leukemia (AML) is a neoplasm of hematopoietic stem cells with partial or complete loss of the ability to differentiate but with preserved proliferation capacity.
  • The aim of our study was to evaluate if the in vivo proliferation marker 3'-deoxy-3'-18F-fluorothymidine (FLT) is suitable for visualizing leukemia manifestation sites and if 18F-FLT is a surrogate marker for disease activity.
  • METHODS: In this pilot study, 10 patients with AML underwent pretherapeutic imaging with 18F-FLT PET or 18F-FLT PET/CT.
  • RESULTS: Retention of 18F-FLT was observed predominantly in bone marrow and spleen and was significantly higher in AML patients than in controls (mean 18F-FLT SUV in bone marrow, 11.5 and 6.6, P < 0.05; mean 18F-FLT SUV in spleen, 6.1 and 1.8, P < 0.05).
  • Outside bone marrow, focal 18F-FLT uptake showed extramedullary manifestation sites of leukemia in 4 patients (meningeal disease, pericardial, abdominal, testicular, and lymph node), proven by other diagnostic procedures.
  • CONCLUSION: This pilot study indicated that PET using 18F-FLT is able to visualize extramedullary manifestation sites of AML and reflects disease activity.
  • [MeSH-major] Dideoxynucleosides. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / radionuclide imaging
  • [MeSH-minor] Adult. Aged. Bone Marrow / metabolism. Case-Control Studies. Cell Proliferation. Female. Humans. Male. Middle Aged. Positron-Emission Tomography. Tissue Distribution. Young Adult

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18927328.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dideoxynucleosides; PG53R0DWDQ / alovudine
  •  go-up   go-down


11. Kim YK, Kim HN, Lee SR, Ahn JS, Yang DH, Lee JJ, Lee IK, Shin MG, Kim HJ: Prognostic significance of nucleophosmin mutations and FLT3 internal tandem duplication in adult patients with cytogenetically normal acute myeloid leukemia. Korean J Hematol; 2010 Mar;45(1):36-45
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of nucleophosmin mutations and FLT3 internal tandem duplication in adult patients with cytogenetically normal acute myeloid leukemia.
  • BACKGROUND: Nucleophosmin (NPM1) gene and fms-like tyrosine kinase 3 gene-internal tandem duplication (FLT3-ITD) mutations are the most frequent mutations in patients with cytogenetically normal (CN)-AML.
  • We analyzed the prognostic impact of these mutations and their interactions in adults with CN-AML.
  • METHODS: NPM1 mutation (NPM1mut) and FLT3-ITD mutation (FLT3-ITD+) were analyzed by GeneScan and PCR assays of bone marrow samples obtained from 121 adult patients with CN-AML (age≤60 years at diagnosis).
  • CONCLUSION: Adult patients with CN-AML carrying isolated NPM1mut and isolated FLT3-ITD+ exhibit different clinical outcomes than those with NPM1mut/FLT3-ITD+ or NPM1wt/FLT3-ITD-.
  • Although isolated NPM1mut leads to favorable clinical outcomes of CN-AML, the role of alloSCT in such patients remains to be considered.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21120161.001).
  • [ISSN] 2092-9129
  • [Journal-full-title] The Korean journal of hematology
  • [ISO-abbreviation] Korean J Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2983002
  • [Keywords] NOTNLM ; Acute myeloid leukemia / FLT3-ITD / NPM1 / Normal karyotype
  •  go-up   go-down


12. Graham RP, Coard KC: Angiomyolipoma of the kidney: the experience at the University Hospital of the West Indies. West Indian Med J; 2009 Dec;58(6):556-60
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Angiomyolipoma (AML) of the kidney is an uncommon tumour that, until recently, was often misdiagnosed preoperatively as renal cell carcinoma (RCC).
  • METHODS: All cases of AML diagnosed during the period 1980 to 2007 were retrospectively identified from the files of the Department of Pathology.
  • The total number of primary renal tumours diagnosed in adults during the same period was also determined for comparison.
  • RESULTS: Eleven cases of AML were identified among 149 primary renal tumours in adults.
  • CONCLUSIONS: These data confirm that AML is uncommon at the University Hospital of the West Indies.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Carcinoma, Renal Cell / diagnosis. Diagnosis, Differential. Female. Hospitals, University. Humans. Jamaica. Male. Middle Aged. Retrospective Studies. Sex Factors. Tuberous Sclerosis / complications. Young Adult

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20583682.001).
  • [ISSN] 0043-3144
  • [Journal-full-title] The West Indian medical journal
  • [ISO-abbreviation] West Indian Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Jamaica
  •  go-up   go-down


13. Liu LB, Liu L, Wang XB, Xiao J, Zou P: Cytobiological and clinicobiological features of AML with 11q23 chromosome abnormalities. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Dec;13(6):932-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytobiological and clinicobiological features of AML with 11q23 chromosome abnormalities.
  • To investigate the interrelationship among morphology, immunology and clinical features in adult acute myeloid leukemia cases with 11q23 chromosome abnormalities, 210 newly diagnosed AML patients were retrospectively analyzed by cell morphology, immunophenotyping, G-banding or R-bamding analysis and clinical features.
  • Immunophenotyping tests indicated that AML cases with 11q23 abnormalities usually expressed the marker molecules of hematopoietic stem or progenitor cells, monocytic lineage cells, such as CD34, CD117, CD14, CD15 and CD11b.
  • It is concluded that the category AML with 11q23 abnormalities accounts for 6.19% of all the newly diagnosed AML cases, that seems to be closely associated with monocytic differentiation blocking with a dismal prognosis.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16403253.001).
  • [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
  •  go-up   go-down


14. Kim J, Park TS, Song J, Lee KA, Hong DJ, Min YH, Cheong JW, Choi JR: Detection of FUS-ERG chimeric transcript in two cases of acute myeloid leukemia with t(16;21)(p11.2;q22) with unusual characteristics. Cancer Genet Cytogenet; 2009 Oct 15;194(2):111-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of FUS-ERG chimeric transcript in two cases of acute myeloid leukemia with t(16;21)(p11.2;q22) with unusual characteristics.
  • Reciprocal t(16;21)(p11;q22) is a rare chromosomal abnormality in acute myeloid leukemia (AML).
  • Here we report two cases of AML with t(16;21)(p11.2;q22) showing unusual characteristics, and address the clinical, hematological, and molecular aspects of leukemia with t(16;21), along with a review of the literature.
  • [MeSH-major] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Aged. Base Sequence. Cytogenetic Analysis. DNA Mutational Analysis. Female. Humans. Male. RNA, Messenger / genetics. RNA, Messenger / isolation & purification

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19781443.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human
  •  go-up   go-down


15. Sazawal S, Kumar B, Hasan SK, Dutta P, Kumar R, Chaubey R, Mir R, Saxena R: Haematological & molecular profile of acute myelogenous leukaemia in India. Indian J Med Res; 2009 Mar;129(3):256-61
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Haematological & molecular profile of acute myelogenous leukaemia in India.
  • BACKGROUND & OBJECTIVE: Recurrent balanced translocations are generally recognized to be a major parameter for prognostication in acute myeloid leukaemia (AML).
  • Therefore, we screened the AmL patients for known specific genetic abnormalities that could lead to more definitive prognoses.
  • METHODS: A total of 113 AML patients were evaluated at diagnosis based on routine morphology and cytochemistry and classified according to the WHO criteria.
  • The distribution of AML subtypes was M1(1), M2(32), M3(57), M4(14), M5(1), M6(1) and seven cases where morphological subtype could not be classified.
  • FLT3 internal tandem duplication (ITD) mutations were more frequent in patients with APL than in other AML subtypes (17.5 vs. 8.9%), the frequency greater in patients with bcr3 isoform (70%) than in those with in bcr1 isoform (30%).
  • FLT3 internal tandem duplication (ITD) mutation was predominant in acute promyelocytic leukaemia patients with bcr3 isoform.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Child. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Duplication. Genetic Predisposition to Disease / epidemiology. Humans. India / epidemiology. Male. Middle Aged. Oncogene Proteins, Fusion / genetics. Prevalence. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors. Young Adult. fms-Like Tyrosine Kinase 3 / genetics

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19491417.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  •  go-up   go-down


16. Li R, Chen Y: [Clinical characteristics and immunophenotype of aged patients with acute leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Dec;14(6):1221-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical characteristics and immunophenotype of aged patients with acute leukemia].
  • In order to analyze the clinical characteristics and biological features of acute leukemia in elderly, 104 acute leukemia patients in elderly were retrospectively analyzed and compared with 71 acute leukemia patients below 60 years old.
  • (1) the proportion of AML in the aged group (73%) was higher than that in the young group (54.9%), and the difference was statistically significant (P < 0.05), but AML (M3) was absent in the aged group;.
  • (3) in AML, the frequently of CD14 expression was higher in the aged group (18.8%) than that in the young group (2.6%), while the expression frequencies of CD15 (37.5%), CD117 (62.5%), and CD38 (59.4%) were respectively lower in the aged group than that in the young group which were (69.2%) for CD15, (89.7%) for CD17, and (84.6%) for CD38 respectively, and the difference was also statistically significant (P < 0.05). (4) CD19 was most frequently expressed in ALL of the aged group and the positive rate was 100%;.
  • The CR rate of acute leukemia in elderly is low, thus the patients in elderly often have unfavorable prognosis.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17204198.001).
  • [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; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
  •  go-up   go-down


17. Wang Y, Xue Y, Chen S, Wu Y, Pan J, Zhang J, Shen J: [A clinical and laboratory study on acute myeloid leukemia with t(6;9)(p23;q34)]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2010 Feb;27(1):34-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A clinical and laboratory study on acute myeloid leukemia with t(6;9)(p23;q34)].
  • OBJECTIVE: To explore the clinical and laboratory features of 6 cases of acute myeloid leukemia (AML) with t(6;9)(p23;q34).
  • AML with t(6;9)(p23;q34) has unique clinical and laboratory features and its prognosis is poor in most cases.
  • [MeSH-major] Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Antigens, CD / genetics. Antigens, CD13 / genetics. Antigens, CD34 / genetics. Antigens, Differentiation, Myelomonocytic / genetics. Female. Humans. Male. Middle Aged. Proto-Oncogene Proteins c-kit / genetics. Sialic Acid Binding Ig-like Lectin 3

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20140864.001).
  • [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
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.4.11.2 / Antigens, CD13
  •  go-up   go-down


18. Marcucci G, Baldus CD, Ruppert AS, Radmacher MD, Mrózek K, Whitman SP, Kolitz JE, Edwards CG, Vardiman JW, Powell BL, Baer MR, Moore JO, Perrotti D, Caligiuri MA, Carroll AJ, Larson RA, de la Chapelle A, Bloomfield CD: Overexpression of the ETS-related gene, ERG, predicts a worse outcome in acute myeloid leukemia with normal karyotype: a Cancer and Leukemia Group B study. J Clin Oncol; 2005 Dec 20;23(36):9234-42
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of the ETS-related gene, ERG, predicts a worse outcome in acute myeloid leukemia with normal karyotype: a Cancer and Leukemia Group B study.
  • PURPOSE: To test the prognostic significance of ETS-related gene (ERG) expression in cytogenetically normal primary acute myeloid leukemia (AML).
  • PATIENTS AND METHODS: Pretreatment blood samples from 84 cytogenetically normal AML patients aged less than 60 years, who were characterized for BAALC expression, FLT3 internal tandem duplication (ITD), and MLL partial tandem duplication (PTD) and uniformly treated on Cancer and Leukemia Group B 9621 protocol, were analyzed for ERG expression by real-time reverse transcriptase polymerase chain reaction.
  • CONCLUSION: ERG overexpression in AML patients with normal cytogenetics predicts an adverse clinical outcome and seems to be associated with a specific molecular signature.
  • [MeSH-major] DNA-Binding Proteins / biosynthesis. Gene Expression Profiling. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Trans-Activators / biosynthesis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Expressed Sequence Tags. Female. Humans. Karyotyping. Male. Middle Aged. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Up-Regulation

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16275934.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA09512; United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / CA102031; United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA31946; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / CA90469
  • [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 / DNA-Binding Proteins; 0 / ERG protein, human; 0 / Trans-Activators
  •  go-up   go-down


19. Chen L, Wang JM, Xu XP, Li Y, Xu H, Ju XP, Ni X, Yang JM, Xu YQ: [A pilot study of spectrum of gene expression of acute leukemia]. Zhonghua Yi Xue Za Zhi; 2005 Apr 27;85(16):1089-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A pilot study of spectrum of gene expression of acute leukemia].
  • OBJECTIVE: To investigate the gene expression of acute leukemia so as to study the pathogenesis of leukemia.
  • METHODS: Five ml of bone marrow was collected from 22 patients with leukemia, 15 males and 7 females, aged 15-86, 17 with acute myelocytic leukemia, 4 with acute lymphocytic leukemia, and 1 with AHL.
  • RESULTS: The predicted 45 genes were enormously expressed in 21 patients with acute leukemia, which were consistent with the ALL and AML classification standards reported by Golub and others.
  • 7 genes which were overexpressed in multiple-resistant cell line K562-n/VCR were also overexpressed in 6 cases of refractory acute leukemia.
  • Further analysis showed that 31 genes were upregulated in AML (M(4)-M(6)) and ALL but downregulated in AML (M(1)-M(3)).
  • The reason that adult patients with ALL and subtypes of AML (M(4)-M(6)) have poorer prognosis in comparison with AMLM(1)-M(3) is attributed to alterations in gene expression.
  • Primary drug resistance may be the major characteristics of refractory leukemia.
  • Analysis of gene expression profile in acute leukemia is significant for classification and prognosis.
  • [MeSH-major] Gene Expression Profiling. Leukemia, Myeloid, Acute / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Female. Gene Expression. Humans. Male. Middle Aged. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Oligonucleotide Array Sequence Analysis. Pilot Projects. Prognosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16029563.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Messenger
  •  go-up   go-down


20. Westerlund H, Nyberg A, Bernin P, Hyde M, Oxenstierna G, Jäppinen P, Väänänen A, Theorell T: Managerial leadership is associated with employee stress, health, and sickness absence independently of the demand-control-support model. Work; 2010;37(1):71-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We therefore investigated the associations between a measure of Attentive Managerial Leadership (AML), and perceived stress, age-relative self-rated health, and sickness absence due to overstrain/fatigue, adjusting for the dimensions of the Demand-Control-Support model.
  • RESULTS: AML was associated with perceived stress, age-relative self-rated health, and sickness absence due to overstrain/fatigue after controlling for the Demand-Control-Support model.
  • Lack of AML was significantly associated with a high stress level in all subgroups (OR=1.68-2.67).
  • Associations with age-relative self-rated health and sickness absence due to overstrain/fatigue were weaker, but still significant, and in the expected direction for several of the subgroups studied, suggesting an association between lack of AML and negative health consequences.
  • [MeSH-minor] Adult. Age Factors. Aged. Confidence Intervals. Cross-Sectional Studies. Female. Finland. Germany. Humans. Internationality. Logistic Models. Male. Middle Aged. Occupations. Odds Ratio. Reference Values. Risk Assessment. Sex Factors. Sickness Impact Profile. Surveys and Questionnaires. Sweden. Workplace / psychology

  • MedlinePlus Health Information. consumer health - Stress.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20858989.001).
  • [ISSN] 1875-9270
  • [Journal-full-title] Work (Reading, Mass.)
  • [ISO-abbreviation] Work
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  •  go-up   go-down


21. Cornely OA, Böhme A, Reichert D, Reuter S, Maschmeyer G, Maertens J, Buchheidt D, Paluszewska M, Arenz D, Bethe U, Effelsberg J, Lövenich H, Sieniawski M, Haas A, Einsele H, Eimermacher H, Martino R, Silling G, Hahn M, Wacker S, Ullmann AJ, Karthaus M, Multinational Case Registry of the Infectious Diseases Working Party of the German Society for Hematology and Oncology: Risk factors for breakthrough invasive fungal infection during secondary prophylaxis. J Antimicrob Chemother; 2008 Apr;61(4):939-46
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: From 25 European cancer centres, 166 consecutive patients with acute myelogenous leukaemia (AML) and a recent history of proven or probable pulmonary IFI were included.
  • Multiple logistic regressions yielded predisposing factors: duration of neutropenia [per additional day; odds ratio (OR) 1.043, confidence interval (CI) 1.008-1.078], high-dose cytarabine (OR 3.920, CI 1.120-12.706), number of antibiotics (per antibiotic; OR 1.504, CI 1.089-2.086), partial response as outcome of prior IFI (OR 4.037, CI 1.301-12.524) and newly diagnosed AML (OR 3.823, CI 0.953-15.340).
  • CONCLUSIONS: Duration of neutropenia, high-dose cytarabine, prior antibiotic therapy and a partial response to the first IFI therapy were risk factors for recurrent IFI and should be considered in AML patients with prior pulmonary IFI undergoing further chemotherapy.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Chemoprevention. Child. Child, Preschool. Female. Humans. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Logistic Models. Male. Middle Aged. Recurrence. Risk Factors. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Fungal Infections.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18272515.001).
  • [ISSN] 1460-2091
  • [Journal-full-title] The Journal of antimicrobial chemotherapy
  • [ISO-abbreviation] J. Antimicrob. Chemother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents
  •  go-up   go-down


22. Jin L, Lee EM, Ramshaw HS, Busfield SJ, Peoppl AG, Wilkinson L, Guthridge MA, Thomas D, Barry EF, Boyd A, Gearing DP, Vairo G, Lopez AF, Dick JE, Lock RB: Monoclonal antibody-mediated targeting of CD123, IL-3 receptor alpha chain, eliminates human acute myeloid leukemic stem cells. Cell Stem Cell; 2009 Jul 2;5(1):31-42
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monoclonal antibody-mediated targeting of CD123, IL-3 receptor alpha chain, eliminates human acute myeloid leukemic stem cells.
  • Leukemia stem cells (LSCs) initiate and sustain the acute myeloid leukemia (AML) clonal hierarchy and possess biological properties rendering them resistant to conventional chemotherapy.
  • The poor survival of AML patients raises expectations that LSC-targeted therapies might achieve durable remissions.
  • We report that an anti-interleukin-3 (IL-3) receptor alpha chain (CD123)-neutralizing antibody (7G3) targeted AML-LSCs, impairing homing to bone marrow (BM) and activating innate immunity of nonobese diabetic/severe-combined immunodeficient (NOD/SCID) mice.
  • 7G3 treatment profoundly reduced AML-LSC engraftment and improved mouse survival.
  • Mice with pre-established disease showed reduced AML burden in the BM and periphery and impaired secondary transplantation upon treatment, establishing that AML-LSCs were directly targeted.
  • 7G3 inhibited IL-3-mediated intracellular signaling of isolated AML CD34(+)CD38(-) cells in vitro and reduced their survival.
  • These results provide clear validation for therapeutic monoclonal antibody (mAb) targeting of AML-LSCs and for translation of in vivo preclinical research findings toward a clinical application.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Interleukin-3 Receptor alpha Subunit / antagonists & inhibitors. Leukemia, Myeloid, Acute / therapy. Neoplastic Stem Cells / drug effects
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Antigens, CD34 / metabolism. Bone Marrow / metabolism. Cell Line. Cell Movement / drug effects. Cell Proliferation / drug effects. Female. Hematopoietic Stem Cells / metabolism. Humans. Intracellular Signaling Peptides and Proteins / metabolism. Male. Mice. Mice, Inbred NOD. Mice, SCID. Middle Aged. Stem Cell Transplantation. Transplantation, Heterologous. Tumor Burden

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19570512.001).
  • [ISSN] 1875-9777
  • [Journal-full-title] Cell stem cell
  • [ISO-abbreviation] Cell Stem Cell
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD34; 0 / Interleukin-3 Receptor alpha Subunit; 0 / Intracellular Signaling Peptides and Proteins
  •  go-up   go-down


23. Stone RM: Targeted agents in AML: much more to do. Best Pract Res Clin Haematol; 2007 Mar;20(1):39-48
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted agents in AML: much more to do.
  • To what degree has targeted therapy succeeded in acute myeloid leukemia (AML)?
  • In chronic myeloid leukemia (CML), gastrointestinal stromal cell tumor, and a small subset of patients with non-small cell lung cancer, a validated target has been identified and a highly specific therapeutic agent has been developed.
  • Are similar "drugable" targets available in AML?
  • While our understanding of the pathophysiology of AML has advanced over the past decade, and some potential targets have been identified, no single agent will likely produce a significant proportion of remissions.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Leukemia, Myeloid / drug therapy. Oncogenes / drug effects
  • [MeSH-minor] Acute Disease. Clinical Trials as Topic. Farnesyltranstransferase / antagonists & inhibitors. Gene Expression Regulation, Leukemic / drug effects. Humans. Translocation, Genetic / drug effects. Translocation, Genetic / genetics. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors. fms-Like Tyrosine Kinase 3 / genetics

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17336253.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 45
  •  go-up   go-down


24. Grafone T, Palmisano M, Nicci C, Martelli AM, Emanuela O, Storti S, Baccarani M, Martinelli G: Monitoring of FLT3 phosphorylation status and its response to drugs by flow cytometry in AML blast cells. Hematol Oncol; 2008 Sep;26(3):159-66
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monitoring of FLT3 phosphorylation status and its response to drugs by flow cytometry in AML blast cells.
  • FLT3 mutation and overexpression in most acute myeloid leukaemia (AML) patients make this tyrosine kinase receptor an attractive therapeutic target.
  • FLT3 kinase inhibitors are actually in clinical trials, thus it is critical to develop a reproducible and standardized method for screening of FLT3 activation and for monitoring its inhibition in response to drug in AML patients.
  • The method also proved to be reproducible in AML patient samples.
  • [MeSH-major] Flow Cytometry / methods. Leukemia, Myeloid, Acute / metabolism. fms-Like Tyrosine Kinase 3 / metabolism
  • [MeSH-minor] Adult. Aged. Cell Line, Tumor. Female. Humans. Male. Middle Aged. Phosphorylation. Protein Kinase Inhibitors / therapeutic use

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2008 John Wiley & Sons, Ltd.
  • (PMID = 18383555.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  •  go-up   go-down


25. Soupir CP, Vergilio JA, Dal Cin P, Muzikansky A, Kantarjian H, Jones D, Hasserjian RP: Philadelphia chromosome-positive acute myeloid leukemia: a rare aggressive leukemia with clinicopathologic features distinct from chronic myeloid leukemia in myeloid blast crisis. Am J Clin Pathol; 2007 Apr;127(4):642-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Philadelphia chromosome-positive acute myeloid leukemia: a rare aggressive leukemia with clinicopathologic features distinct from chronic myeloid leukemia in myeloid blast crisis.
  • We performed a multi-institutional retrospective analysis of the morphologic features, immunophenotype, cytogenetics, and BCR-ABL transcript characterization of cases of Philadelphia chromosome-positive acute myeloid leukemia (Ph+ AML).
  • We compared these cases with cases of documented chronic myelogenous leukemia in myeloid blast crisis (CML-MBC).
  • Patients with Ph+ AML were less likely to have splenomegaly or peripheral basophilia and had lower bone marrow cellularity and myeloid/erythroid ratios than patients with CML-MBC.
  • Additional specific cytogenetic abnormalities that typically occur in CML-MBC were less common in Ph+ AML.
  • Of 7 patients with Ph+ AML treated with imatinib mesylate, 6 showed at least a partial hematologic response, but the responses were of a short duration (median, 2.5 months).
  • The median survival of patients with Ph+ AML was 9 months, similar to that of patients with CML-MBC (7 months).
  • Ph+ AML is a rare aggressive acute leukemia with some features distinct from CML-MBC.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Antigens, CD / metabolism. Female. Fusion Proteins, bcr-abl / metabolism. Humans. Immunophenotyping. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis


26. Al-Badriyeh D, Slavin M, Liew D, Thursky K, Downey M, Grigg A, Bajel A, Stewart K, Kong DC: Pharmacoeconomic evaluation of voriconazole versus posaconazole for antifungal prophylaxis in acute myeloid leukaemia. J Antimicrob Chemother; 2010 May;65(5):1052-61
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacoeconomic evaluation of voriconazole versus posaconazole for antifungal prophylaxis in acute myeloid leukaemia.
  • BACKGROUND: Voriconazole and posaconazole are used prophylactically against invasive fungal infection (IFI) in patients with acute myeloid leukaemia (AML).
  • The current study attempted to evaluate the economics of voriconazole versus posaconazole for prophylaxis in AML.
  • METHODS: A 6 year (2003-09) retrospective chart review of AML patients was performed at a major Australian tertiary hospital.
  • CONCLUSIONS: This is the first economic evaluation of voriconazole versus posaconazole; where posaconazole appears to be more cost-beneficial than voriconazole as antifungal prophylaxis in AML.
  • [MeSH-major] Antifungal Agents / therapeutic use. Chemoprevention / economics. Chemoprevention / methods. Leukemia, Myeloid, Acute / complications. Mycoses / prevention & control. Pyrimidines / therapeutic use. Triazoles / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Australia. Cost-Benefit Analysis. Female. Hospitals. Humans. Male. Middle Aged. Retrospective Studies. Treatment Outcome. Voriconazole

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Fungal Infections.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20237074.001).
  • [ISSN] 1460-2091
  • [Journal-full-title] The Journal of antimicrobial chemotherapy
  • [ISO-abbreviation] J. Antimicrob. Chemother.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Pyrimidines; 0 / Triazoles; 6TK1G07BHZ / posaconazole; JFU09I87TR / Voriconazole
  •  go-up   go-down


27. Liu L, Ma JZ, O'Quigley J: Joint analysis of multi-level repeated measures data and survival: an application to the end stage renal disease (ESRD) data. Stat Med; 2008 Nov 29;27(27):5679-91
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To simplify the estimation procedure, we adopt the Gaussian quadrature technique with a piecewise log-linear baseline hazard for the death process, which can be conveniently implemented in the freely available software aML.
  • [MeSH-minor] Adolescent. Adult. Female. Hematocrit. Humans. Kidney Transplantation. Linear Models. Male. Middle Aged. Proportional Hazards Models. Renal Dialysis

  • MedlinePlus Health Information. consumer health - Kidney Failure.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2008 John Wiley & Sons, Ltd.
  • (PMID = 18693300.001).
  • [ISSN] 0277-6715
  • [Journal-full-title] Statistics in medicine
  • [ISO-abbreviation] Stat Med
  • [Language] eng
  • [Grant] United States / AHRQ HHS / HS / R03 HS016543
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  •  go-up   go-down


28. Kawakami K, Nishii K, Hyou R, Watanabe Y, Nakao M, Mitani H, Murata T, Monma F, Yamamori S, Hosokai N, Miura I: A case of acute myeloblastic leukemia with a novel variant of t(8;21)(q22;q22). Int J Hematol; 2008 Jan;87(1):78-82
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of acute myeloblastic leukemia with a novel variant of t(8;21)(q22;q22).
  • We encountered a case of acute myeloblastic leukemia (AML), with extramedullary leukemia (EML) and a masked type of the variant translocation t(8;21)(q22;q22).
  • Morphologically, the AML M2 subtype according to the French-American-British (FAB) classification was present.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Hematopoiesis, Extramedullary / genetics. Humans. Male. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18224418.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
  •  go-up   go-down


29. Gorello P, Cazzaniga G, Alberti F, Dell'Oro MG, Gottardi E, Specchia G, Roti G, Rosati R, Martelli MF, Diverio D, Lo Coco F, Biondi A, Saglio G, Mecucci C, Falini B: Quantitative assessment of minimal residual disease in acute myeloid leukemia carrying nucleophosmin (NPM1) gene mutations. Leukemia; 2006 Jun;20(6):1103-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitative assessment of minimal residual disease in acute myeloid leukemia carrying nucleophosmin (NPM1) gene mutations.
  • Mutations in exon 12 of the nucleophosmin (NPM1) gene occur in about 60% of adult AML with normal karyotype.
  • In all 13 AML patients carrying NPM1 mutations at diagnosis, cDNA RQ-PCR showed >30 000 copies of NPM1-mutated transcript.
  • Thus, reliable, sensitive RQ-PCR assays for NPM1 mutations can now monitor and quantify MRD in AML patients with normal karyotype and NPM1 gene mutations.
  • [MeSH-major] Gene Dosage. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / genetics. Neoplasm, Residual / diagnosis. Neoplasm, Residual / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Acute Disease. DNA Mutational Analysis / methods. Gene Expression Profiling. Humans. Mutation. Predictive Value of Tests. Reverse Transcriptase Polymerase Chain Reaction / methods

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16541144.001).
  • [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 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  •  go-up   go-down


30. Jeddi R, Gouider E, Benneji H, Mnif S, Ben Abid H, Belhadjali Z, Meddeb B: Secondary chronic myelomonocytic leukemia with monosomy 7 after successful treatment of acute promyelocytic leukemia. Pathol Biol (Paris); 2008 May;56(3):162-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary chronic myelomonocytic leukemia with monosomy 7 after successful treatment of acute promyelocytic leukemia.
  • In the last years, several case reports of myelodysplastic syndrome (MDS) or AML (different from APL), occurring during the course of APL have been made.
  • [MeSH-major] Chromosomes, Human, Pair 7. Leukemia, Myelomonocytic, Chronic / genetics. Leukemia, Promyelocytic, Acute / drug therapy. Monosomy
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Karyotyping. Male. Translocation, Genetic


31. Yalcintepe L, Frankel AE, Hogge DE: Expression of interleukin-3 receptor subunits on defined subpopulations of acute myeloid leukemia blasts predicts the cytotoxicity of diphtheria toxin interleukin-3 fusion protein against malignant progenitors that engraft in immunodeficient mice. Blood; 2006 Nov 15;108(10):3530-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of interleukin-3 receptor subunits on defined subpopulations of acute myeloid leukemia blasts predicts the cytotoxicity of diphtheria toxin interleukin-3 fusion protein against malignant progenitors that engraft in immunodeficient mice.
  • The interleukin-3 receptor (IL-3R) subunits are overexpressed on acute myeloid leukemia (AML) blasts compared with normal hematopoietic cells and are thus potential targets for novel therapeutic agents.
  • Both fluorescence-activated cell sorter (FACS) analysis and quantitative real-time reverse transcription-polymerase chain reaction (QRT-PCR) were used to quantify expression of the IL-3Ralpha and beta(c) subunits on AML cells.
  • QRT-PCR for both subunits was most predictive of killing of AML colony-forming cells (AML-CFCs) by diphtheria toxin-IL-3 fusion protein (DT(388)IL3).
  • Among 19 patient samples, the relative level of the IL-3Ralpha was higher than the IL-3Rbeta(c) and highest in CD34(+)CD38(-)CD71(-) cells, enriched for candidate leukemia stem cells, compared with cell fractions depleted of such progenitors.
  • However, expression of both subunits varied by more than 10-fold among different AML samples for all subpopulations studied.
  • The level of IL-3Rbeta(c) expression versus glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (set at 1000) ranged from 0.14 to 13.56 in CD34(+)CD38(-)CD71(-) cells from different samples; this value was correlated (r = .76, P = .05) with the ability of DT(388)IL3 to kill AML progenitors that engraft in beta(2)-microglobin-deficient nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice (n = 7).
  • Thus, quantification of IL-3R subunit expression on AML blasts predicts the effectiveness IL-3R-targeted therapy in killing primitive leukemic progenitors.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Diphtheria Toxin / therapeutic use. Drug Delivery Systems. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / pathology. Predictive Value of Tests. Receptors, Interleukin-3 / analysis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Animals. Blast Crisis / pathology. Cytokine Receptor Common beta Subunit / analysis. Female. Humans. Immunophenotyping. Interleukin-3 Receptor alpha Subunit / analysis. Male. Mice. Mice, SCID. Middle Aged. Neoplasm Proteins / analysis. Neoplasms, Experimental. Neoplastic Stem Cells / transplantation. Prognosis. Recombinant Fusion Proteins / therapeutic use

  • Genetic Alliance. consumer health - Diphtheria.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16882709.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytokine Receptor Common beta Subunit; 0 / Diphtheria Toxin; 0 / IL3RA protein, human; 0 / Interleukin-3 Receptor alpha Subunit; 0 / Neoplasm Proteins; 0 / Receptors, Interleukin-3; 0 / Recombinant Fusion Proteins
  •  go-up   go-down


32. Sohn SK, Kim JG, Kim DH: Tailored strategy for AML patients receiving allogeneic peripheral blood stem cell transplantation. J Clin Apher; 2006 Oct;21(3):207-13
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tailored strategy for AML patients receiving allogeneic peripheral blood stem cell transplantation.
  • Considering the heterogeneity of acute myelogenous leukemia (AML), along with the pros and cons of allogeneic peripheral blood stem cell transplantation (PBSCT), a tailored strategy is needed to minimize the transplant-related mortality and maximize the transplant outcomes in AML patients exhibiting certain factors that have an impact on the post-transplant quality of life and outcomes.
  • The factors that need to be considered when tailoring a strategy in an allogeneic PBSCT setting include the recipient's performance status and co-morbid disease include AML risk stratification, disease status, expected severity of graft-versus-host disease, and the necessity of a graft-versus-leukemia effect.
  • Accordingly, this review article describes a possible tailoring strategy for AML patients receiving allogeneic PBSCT based on certain factors influencing the transplant outcome.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Peripheral Blood Stem Cell Transplantation / methods. Stem Cells / cytology
  • [MeSH-minor] Adult. Aged. Graft vs Leukemia Effect. Humans. Middle Aged. Risk. Transplantation, Homologous. Treatment Outcome


33. Ersvaer E, Liseth K, Skavland J, Gjertsen BT, Bruserud Ø: Intensive chemotherapy for acute myeloid leukemia differentially affects circulating TC1, TH1, TH17 and TREG cells. BMC Immunol; 2010;11:38
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intensive chemotherapy for acute myeloid leukemia differentially affects circulating TC1, TH1, TH17 and TREG cells.
  • BACKGROUND: Several observations suggest that immunological events early after chemotherapy, possibly during the period of severe treatment-induced cytopenia, are important for antileukemic immune reactivity in acute myeloid leukemia (AML).
  • We therefore investigated the frequencies of various T cell subsets (TC1, TH1, TH17) and CD25+ FoxP3+ TREG cells in AML patients with untreated disease and following intensive chemotherapy.
  • Increased levels of regulatory CD25+ FoxP3+ T cells were detected in AML patients with untreated disease, during chemotherapy-induced cytopenia and during regeneration after treatment.
  • Finally, exogenous IL17-A usually had no or only minor effects on proliferation of primary human AML cells.
  • CONCLUSIONS: We conclude that the effect of intensive AML chemotherapy differ between circulating T cell subsets, relative frequencies of TH17 cells are not affected by chemotherapy and this subset may affect AML cells indirectly through their immunoregulatory effects but probably not through direct effects of IL17-A.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cell Movement / immunology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / immunology. T-Lymphocyte Subsets / drug effects. T-Lymphocytes, Helper-Inducer / drug effects. T-Lymphocytes, Regulatory / drug effects
  • [MeSH-minor] Adult. Antigens, CD3 / metabolism. CD8-Positive T-Lymphocytes / drug effects. CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / pathology. Female. Forkhead Transcription Factors / metabolism. Health. Humans. Interleukin-2 Receptor alpha Subunit / metabolism. Leukopenia / chemically induced. Leukopenia / immunology. Male. Middle Aged. Sex Characteristics. Tumor Cells, Cultured. Young Adult

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Immunol. 1999 Nov 15;163(10):5211-8 [10553041.001]
  • [Cites] Clin Exp Immunol. 2009 Nov;158(2):199-204 [19737137.001]
  • [Cites] Cell Immunol. 2000 Nov 25;206(1):36-50 [11161436.001]
  • [Cites] J Immunol. 2001 Aug 1;167(3):1137-40 [11466326.001]
  • [Cites] Microbes Infect. 2001 Sep;3(11):911-8 [11564439.001]
  • [Cites] J Cell Biochem Suppl. 2002;38:88-95 [12046855.001]
  • [Cites] Leukemia. 2002 Jul;16(7):1311-8 [12094255.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2292-302 [12239137.001]
  • [Cites] J Hematother Stem Cell Res. 2003 Oct;12(5):525-35 [14594509.001]
  • [Cites] Haematologica. 2004 Apr;89(4):391-402 [15075072.001]
  • [Cites] Crit Rev Oncol Hematol. 2004 Jun;50(3):197-222 [15182826.001]
  • [Cites] Cell. 2004 Jul 23;118(2):217-28 [15260991.001]
  • [Cites] Leukemia. 1987 Jan;1(1):52-7 [2444829.001]
  • [Cites] Hematol Oncol Clin North Am. 1993 Feb;7(1):47-64 [8449864.001]
  • [Cites] Scand J Immunol. 1998 Jan;47(1):54-62 [9467659.001]
  • [Cites] Blood. 2005 Apr 15;105(8):3206-13 [15618466.001]
  • [Cites] Bone Marrow Transplant. 2005 May;35(9):835-57 [15778723.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1362-8 [15845901.001]
  • [Cites] Eur J Haematol. 2005 Dec;75(6):468-76 [16313258.001]
  • [Cites] Leukemia. 2006 Jan;20(1):29-34 [16281063.001]
  • [Cites] Nature. 2006 May 11;441(7090):231-4 [16648837.001]
  • [Cites] Nature. 2006 May 11;441(7090):235-8 [16648838.001]
  • [Cites] Bone Marrow Transplant. 2006 Jun;37(11):1037-42 [16708062.001]
  • [Cites] Bone Marrow Transplant. 2006 Jun;37(12):1119-28 [16699530.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 Sep;12(9):919-27 [16920557.001]
  • [Cites] Cancer Immunol Immunother. 2007 Jan;56(1):13-24 [16612597.001]
  • [Cites] Nat Med. 2007 Feb;13(2):139-45 [17290272.001]
  • [Cites] Cancer Immunol Immunother. 2007 Jun;56(6):913-25 [17115221.001]
  • [Cites] J Immunol. 2007 Jun 1;178(11):6730-3 [17513719.001]
  • [Cites] Hematology. 2007 Jun;12(3):199-207 [17558695.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3192-201 [17616639.001]
  • [Cites] Immunol Rev. 2007 Dec;220:22-34 [17979837.001]
  • [Cites] Leukemia. 2007 Dec;21(12):2495-505 [17898786.001]
  • [Cites] Semin Immunol. 2007 Oct;19(5):318-30 [18023361.001]
  • [Cites] Gut. 2008 Jun;57(6):772-9 [17965063.001]
  • [Cites] Immunol Res. 2008;41(2):87-102 [18172584.001]
  • [Cites] J Clin Immunol. 2008 Nov;28(6):660-70 [18810613.001]
  • [Cites] Curr Cancer Drug Targets. 2008 Dec;8(8):666-75 [19075589.001]
  • [Cites] Clin Cancer Res. 2009 May 15;15(10):3325-32 [19417016.001]
  • [Cites] Genes Immun. 2009 Jul;10(5):509-16 [19279650.001]
  • [Cites] J Interferon Cytokine Res. 2000 Nov;20(11):947-54 [11096451.001]
  • (PMID = 20618967.001).
  • [ISSN] 1471-2172
  • [Journal-full-title] BMC immunology
  • [ISO-abbreviation] BMC Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Antineoplastic Agents; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Interleukin-2 Receptor alpha Subunit
  • [Other-IDs] NLM/ PMC2912832
  •  go-up   go-down


34. Brown JR, Yeckes H, Friedberg JW, Neuberg D, Kim H, Nadler LM, Freedman AS: Increasing incidence of late second malignancies after conditioning with cyclophosphamide and total-body irradiation and autologous bone marrow transplantation for non-Hodgkin's lymphoma. J Clin Oncol; 2005 Apr 1;23(10):2208-14
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increasing incidence of late second malignancies after conditioning with cyclophosphamide and total-body irradiation and autologous bone marrow transplantation for non-Hodgkin's lymphoma.
  • We report the incidence and outcome of solid tumors at 10-year follow-up in a large cohort of uniformly treated patients who underwent ABMT for non-Hodgkin's lymphoma (NHL).
  • RESULTS: Forty-two solid tumors, six non-MDS hematologic malignancies, 39 nonmelanoma skin cancers, and 68 cases of MDS/acute myelogenous leukemia (AML) were observed at a median follow-up of 9.5 years.
  • A cumulative incidence model using death as a competing risk found that the 10-year incidence of second malignancy is 21%, with 10.0% non-MDS malignancies.
  • Although the incidence of MDS/AML starts to plateau, the incidence of solid tumors continues to rise.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Alkylating / therapeutic use. Bone Marrow Transplantation. Cyclophosphamide / adverse effects. Cyclophosphamide / therapeutic use. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / radiotherapy. Neoplasms / epidemiology. Neoplasms / etiology. Neoplasms, Second Primary / epidemiology. Neoplasms, Second Primary / etiology. Whole-Body Irradiation / adverse effects
  • [MeSH-minor] Adult. Cohort Studies. Female. Follow-Up Studies. Humans. Incidence. Male. Middle Aged. Risk Factors. Transplantation, Autologous

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Clin Oncol. 2005 Nov 1;23(31):8120-1; author reply 8121-2 [16258113.001]
  • (PMID = 15753460.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide
  •  go-up   go-down


35. Wu Y, Slovak ML, Snyder DS, Arber DA: Coexistence of inversion 16 and the Philadelphia chromosome in acute and chronic myeloid leukemias : report of six cases and review of literature. Am J Clin Pathol; 2006 Feb;125(2):260-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Coexistence of inversion 16 and the Philadelphia chromosome in acute and chronic myeloid leukemias : report of six cases and review of literature.
  • We report 5 cases of chronic myelogenous leukemia (CML) and 1 case of acute myeloid leukemia (AML) with the dual presence of t(9;22) and inv(16).
  • All cases were BCR-ABL+ with p210 products detected in all CML cases and a p190 product detected in the AML case.
  • The CBFbeta-MYH11 fusion gene was confirmed in all 3 CML cases and the 1 AML case tested, and this correlated with the presence of abnormal eosinophils with coarse basophilic granules.
  • Of 5 patients with CML, 4 had a rapid transformation to myeloid accelerated phase of blast crisis.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 16. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid, Acute / genetics. Philadelphia Chromosome
  • [MeSH-minor] Adult. Core Binding Factor beta Subunit / genetics. Female. Humans. Male. Middle Aged. Myosin Heavy Chains / genetics. Recombinant Fusion Proteins / genetics. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Chromosome 16.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16393682.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFB protein, human; 0 / Core Binding Factor beta Subunit; 0 / Recombinant Fusion Proteins; EC 3.6.4.1 / Myosin Heavy Chains
  •  go-up   go-down


36. Cheng CK, Li L, Cheng SH, Lau KM, Chan NP, Wong RS, Shing MM, Li CK, Ng MH: Transcriptional repression of the RUNX3/AML2 gene by the t(8;21) and inv(16) fusion proteins in acute myeloid leukemia. Blood; 2008 Oct 15;112(8):3391-402
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcriptional repression of the RUNX3/AML2 gene by the t(8;21) and inv(16) fusion proteins in acute myeloid leukemia.
  • In this study on 73 acute myeloid leukemia (AML) patients (44 children and 29 adults), we first showed that high RUNX3 expression among childhood AML was associated with a shortened event-free survival, and RUNX3 was significantly underexpressed in the prognostically favorable subgroup of AML with the t(8;21) and inv(16) translocations.
  • Taken together, RUNX3 was the first transcriptional target found to be commonly repressed by the t(8;21) and inv(16) fusion proteins and might have an important role in core-binding factor AML.
  • [MeSH-major] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 3 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Transcription, Genetic. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Female. Humans. Infant. Male. Middle Aged

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18663147.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 3 Subunit; 0 / Runx3 protein, human
  •  go-up   go-down


37. Schlenk RF, Germing U, Hartmann F, Glasmacher A, Fischer JT, del Valle y Fuentes F, Götze K, Pralle H, Nerl C, Salwender H, Grimminger W, Petzer A, Hensel M, Benner A, Zick L, Döhner K, Fröhling S, Döhner H, AML Study Group (AMLSG): High-dose cytarabine and mitoxantrone in consolidation therapy for acute promyelocytic leukemia. Leukemia; 2005 Jun;19(6):978-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-dose cytarabine and mitoxantrone in consolidation therapy for acute promyelocytic leukemia.
  • The objective of our study was to evaluate high-dose cytarabine in consolidation therapy in patients with newly diagnosed acute promyelocytic leukemia (APL).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cytarabine / administration & dosage. Idarubicin / administration & dosage. Leukemia, Promyelocytic, Acute / drug therapy. Mitoxantrone / administration & dosage. Tretinoin / administration & dosage
  • [MeSH-minor] Adolescent. Adult. Female. Humans. Male. Middle Aged. Prognosis. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics. Remission Induction. fms-Like Tyrosine Kinase 3

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Leukemia. 2005 Jun;19(6):913-5 [15843820.001]
  • (PMID = 15843821.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; BZ114NVM5P / Mitoxantrone; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; ZRP63D75JW / Idarubicin; AIDA protocol; MAC chemotherapy protocol
  •  go-up   go-down


38. Robin M, Porcher R, De Castro Araujo R, de Latour RP, Devergie A, Rocha V, Larghero J, Adès L, Ribaud P, Mary JY, Socié G: Risk factors for late infections after allogeneic hematopoietic stem cell transplantation from a matched related donor. Biol Blood Marrow Transplant; 2007 Nov;13(11):1304-12
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Patients transplanted for aplastic anemia, chronic myelogenous leukemia (CML), and acute myelogenous leukemia (AML) were included.
  • Extensive cGVHD was the only risk factor for non-HCV viral infections in patients transplanted for AML or CML (HR: 2.7, 95%CI: 1.4-5.1, P = .002).
  • [MeSH-minor] Adolescent. Adult. Anemia, Aplastic / therapy. Female. France / epidemiology. Graft vs Host Disease. Humans. Incidence. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / therapy. Male. Retrospective Studies. Risk Factors. Transplantation, Homologous / adverse effects


39. Mazur G, Wróbel T, Butrym A, Kapelko-Słowik K, Poreba R, Kuliczkowski K: Increased monocyte chemoattractant protein 1 (MCP-1/CCL-2) serum level in acute myeloid leukemia. Neoplasma; 2007;54(4):285-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased monocyte chemoattractant protein 1 (MCP-1/CCL-2) serum level in acute myeloid leukemia.
  • Acute myeloid leukaemia (AML) is an aggressive malignancy with accumulation of blasts in bone marrow.
  • The aim of the study was to evaluate plasma level of CCL2 in patients with AML.
  • Plasma samples from 65 adult patients with AML taken before chemotherapy and in complete remission were measured by enzyme linked immunoassay to evaluate CCL2 levels.
  • In AML patients mean baseline CCL2 level (+/- SEM standard error of measurement) was significantly higher than in normal control: 365,26 +/- 5,62 pg/ml vs 265,56 +/- 5,48 pg/ml respectively (p<0.01).
  • We demonstrate increased mean CCL2 plasma level in untreated patients with AML.
  • Significantly lower plasma level of CCL2 was observed in patients with M4 and M5 AML subtypes according to FAB classification.
  • In AML group chemotherapy did not reduce CCL2 plasma level.
  • [MeSH-major] Chemokine CCL2 / blood. Leukemia, Myeloid / blood
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Case-Control Studies. Enzyme-Linked Immunosorbent Assay. Female. Humans. Male. Middle Aged. Remission Induction

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17822317.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Chemokine CCL2
  •  go-up   go-down


40. Tosios KI, Koutlas IG, Kyriakopoulos VF, Balta M, Theologie-Lygidakis N, Vardas E, Iatrou I: Time to abandon the term angiomyolipoma for non-PEComatous angiomyomatous (or angiomatous) oral tumors with adipocytes. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2010 Oct;110(4):492-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Time to abandon the term angiomyolipoma for non-PEComatous angiomyomatous (or angiomatous) oral tumors with adipocytes.
  • Angiomyolipoma (AML) is the most common benign mesenchymal neoplasm of the kidneys with well-established clinical and morphological features.
  • Herein, through review of the pertinent oral pathology literature and the detailed description of 2 lesions, one an oral angiomyoma with an adipocytic component and the other an apparently hamartomatous angioleiomyomatous proliferation with adipocytes, we provide, in our opinion, a solid argument against the use of the term AML for non-PEComatous oral tumors.
  • [MeSH-minor] Actins / analysis. Adipocytes / pathology. Aged. Desmin / analysis. Female. Humans. Immunoenzyme Techniques. Male. S100 Proteins / analysis. Young Adult. von Willebrand Factor / analysis

  • MedlinePlus Health Information. consumer health - Oral Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Mosby, Inc. All rights reserved.
  • (PMID = 20674420.001).
  • [ISSN] 1528-395X
  • [Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
  • [ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Desmin; 0 / S100 Proteins; 0 / von Willebrand Factor
  •  go-up   go-down


41. Zhang XH, Huang XJ, Liu KY, Xu LP, Liu DH, Lu DP: [Pharmacokinetics of antithymocyte globulin in recipients under-going HLA partially matched hematopoietic stem cell transplantation]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Feb;15(1):152-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • All patients including 5 cases of AML, 6 cases of CML, 3 cases of ALL, 1 case of AA were consecutively enrolled in the present study after providing written informed consent.

  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17490543.001).
  • [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 / Antilymphocyte Serum
  •  go-up   go-down


42. Deng YF, Lin Q, Zhang SH, Ling YM, He JK, Chen XF: Malignant angiomyolipoma in the liver: a case report with pathological and molecular analysis. Pathol Res Pract; 2008;204(12):911-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Malignant angiomyolipoma (AML) of the liver is rare.
  • We report a case of AML with malignant transformation and metastases.
  • Microscopically, the periphery of the tumor showed components of classic hepatic AML, but the central region contained atypical epithelioid components with extremely pleomorphic and hyperchromatic nuclei with frequent mitotic figures.
  • Markedly atypical epithelioid cells with vascular invasion, distant metastasis, and fatal outcome were interpreted as malignant characteristics of hepatic AML.
  • It is suggested that large tumor size, pleomorphic nuclei with high proliferation activity, and P53 immunoreactivity may predict the existence of malignant transformation of hepatic AML.
  • [MeSH-minor] Actins / metabolism. Adult. Antigens, Neoplasm / metabolism. Base Sequence. Cell Transformation, Neoplastic. DNA Mutational Analysis. Epithelioid Cells / pathology. Humans. Immunohistochemistry. Male. Melanoma-Specific Antigens. Molecular Sequence Data. Mutation. Neoplasm Proteins / metabolism. Polymerase Chain Reaction. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18723294.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Actins; 0 / Antigens, Neoplasm; 0 / Melanoma-Specific Antigens; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53
  •  go-up   go-down


43. Roti G, Rosati R, Bonasso R, Gorello P, Diverio D, Martelli MF, Falini B, Mecucci C, Gruppo Italiano Malattie Ematologiche dell' Adulto Working Party: Denaturing high-performance liquid chromatography: a valid approach for identifying NPM1 mutations in acute myeloid leukemia. J Mol Diagn; 2006 May;8(2):254-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Denaturing high-performance liquid chromatography: a valid approach for identifying NPM1 mutations in acute myeloid leukemia.
  • NPM1 gene mutations are the most frequent genetic lesion in the 60% of adult acute myeloid leukemias (AMLs) with normal karyotype and no evidence of typical fusion genes (BCR/ABL1, PML/RARA, AML1/ETO, CBFB/MYH11, DEK/CAN).
  • To assess specificity, sensitivity, reliability, and reproducibility, we analyzed DNA from 120 primary adult AMLs and compared DHPLC results with immunohistochemistry and sequencing.
  • Our results suggest that DHPLC detects NPM1mutations as well as direct sequencing and immunohistochemistry, providing a helpful approach in the diagnosis of NPMc+ AML.
  • [MeSH-major] Chromatography, High Pressure Liquid / methods. Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 1999 Dec;13(12):1901-28 [10602411.001]
  • [Cites] Blood Rev. 2004 Jun;18(2):115-36 [15010150.001]
  • [Cites] Hum Mutat. 2001 Jun;17(6):439-74 [11385705.001]
  • [Cites] Methods Mol Med. 2004;92:45-66 [14733306.001]
  • [Cites] Science. 1995 Jan 20;267(5196):316-7 [7824924.001]
  • [Cites] Blood. 1996 Feb 1;87(3):882-6 [8562957.001]
  • [Cites] Oncogene. 1996 Jan 18;12(2):265-75 [8570204.001]
  • [Cites] Mol Cell Biol. 1996 Aug;16(8):4207-14 [8754820.001]
  • [Cites] Genomics. 1998 Aug 15;52(1):44-9 [9740670.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Blood. 1999 Jan 15;93(2):632-42 [9885226.001]
  • [Cites] Curr Opin Hematol. 2005 Jan;12(1):68-75 [15604894.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1819-20; author reply 1819-20 [15858195.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1419-22 [15870172.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2854-61 [15994285.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3618-20 [16046528.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3733-9 [16076867.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3747-54 [16109776.001]
  • [Cites] Cancer Genet Cytogenet. 2000 Jul 1;120(1):25-9 [10913673.001]
  • (PMID = 16645213.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  • [Other-IDs] NLM/ PMC1867590
  •  go-up   go-down


44. Oktay MF, Cureoglu S, Schachern PA, Gulbahce E, Paparella MM, Hayasi H: Histologic changes in the anterior mallear ligament and the head of the malleus in otosclerosis. Otolaryngol Head Neck Surg; 2006 Feb;134(2):232-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To determine ossicular and anterior mallear ligament (AML) changes in otosclerosis.
  • STUDY DESIGN AND SETTING: Hyalinization of AML was graded as follows: none, patchy, or diffuse in 95 temporal bones (TBs) with otosclerosis: 52 with stapedial fixation (SF); 43 without fixation (NSF); and 52 age-matched controls.
  • CONCLUSION: Based on our findings, we do not believe that there is a relationship between hyalinization of the AML and otosclerosis; however, otosclerosis with SF seems to be a predisposing factor for fixation of the head of the malleus.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged

  • Genetic Alliance. consumer health - Otosclerosis.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16455369.001).
  • [ISSN] 0194-5998
  • [Journal-full-title] Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery
  • [ISO-abbreviation] Otolaryngol Head Neck Surg
  • [Language] eng
  • [Grant] United States / NIDCD NIH HHS / DC / P30 DC04660
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


45. Gari M, Abuzenadah A, Chaudhary A, Al-Qahtani M, Banni H, Ahmad W, Al-Sayes F, Lary S, Damanhouri G: Detection of FLT3 oncogene mutations in acute myeloid leukemia using conformation sensitive gel electrophoresis. Int J Mol Sci; 2008 Nov;9(11):2194-204
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of FLT3 oncogene mutations in acute myeloid leukemia using conformation sensitive gel electrophoresis.
  • FLT3 is also expressed on leukemia blasts in most cases of acute myeloid leukemia (AML).
  • In order to determine the frequency of FLT3 oncogene mutations, we analyzed genomic DNA of adult de novo acute myeloid leukemia (AML).
  • The high frequency of the flt3 proto-oncogene mutations in acute myeloid leukemia AML suggests a key role for the receptor function.
  • The association of FLT3 mutations with chromosomal abnormalities invites speculation as to the link between these two changes in the pathogenesis of acute myeloid leukemiaAML.
  • Finally, this study reports, for the first time in Saudi Arabia, mutations in the human FLT3 gene in acute myeloid leukemia AML patients.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Haematologica. 2007 Apr;92(4):550-3 [17488667.001]
  • [Cites] Hum Mutat. 2002 Apr;19(4):334-42 [11933188.001]
  • [Cites] Leuk Res. 2005 Dec;29(12):1393-8 [15996732.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Oct 15;162(2):127-34 [16213360.001]
  • [Cites] Leukemia. 1998 Sep;12(9):1333-7 [9737679.001]
  • [Cites] Blood. 1999 May 1;93(9):3074-80 [10216104.001]
  • [Cites] Br J Haematol. 1999 Apr;105(1):155-62 [10233379.001]
  • [Cites] Leukemia. 1997 Oct;11(10):1605-9 [9324277.001]
  • [Cites] Leukemia. 1997 Sep;11(9):1442-6 [9305595.001]
  • [Cites] Br J Haematol. 1999 Mar;104(4):915-8 [10192459.001]
  • [Cites] Thromb Haemost. 1998 Apr;79(4):723-6 [9569180.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Leukemia. 1996 Apr;10(4):588-99 [8618433.001]
  • [Cites] Leukemia. 1995 Aug;9(8):1368-72 [7643626.001]
  • [Cites] Annu Rev Immunol. 1995;13:369-98 [7612228.001]
  • [Cites] Blood. 1993 Aug 15;82(4):1110-9 [8394751.001]
  • [Cites] Blood. 1992 Nov 15;80(10):2584-93 [1384791.001]
  • [Cites] Cell. 1991 Jun 28;65(7):1143-52 [1648448.001]
  • [Cites] Annu Rev Biochem. 1988;57:443-78 [3052279.001]
  • [Cites] Cell. 1990 Apr 20;61(2):203-12 [2158859.001]
  • [Cites] Br J Haematol. 1976 Aug;33(4):451-8 [188440.001]
  • [Cites] Blood. 2002 Jan 1;99(1):310-8 [11756186.001]
  • [Cites] Blood. 2001 Aug 1;98(3):885-7 [11468194.001]
  • [Cites] Leukemia. 2001 Jul;15(7):1001-10 [11455967.001]
  • [Cites] Br J Haematol. 2001 Jun;113(4):983-8 [11442493.001]
  • [Cites] Blood. 2001 Apr 15;97(8):2434-9 [11290608.001]
  • [Cites] Thromb Haemost. 2000 Jun;83(6):844-8 [10896236.001]
  • [Cites] Br J Haematol. 2000 Oct;111(1):190-5 [11091200.001]
  • [Cites] Br J Haematol. 2000 Feb;108(2):322-30 [10691863.001]
  • [Cites] Leukemia. 2000 Mar;14(3):374-8 [10720129.001]
  • [Cites] Clin Cancer Res. 2003 Nov 15;9(15):5465-76 [14654525.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2763-7 [12843001.001]
  • [Cites] Cancer Cell. 2002 Jun;1(5):433-43 [12124173.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8283-8 [12060771.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3674-81 [16902153.001]
  • (PMID = 19330068.001).
  • [ISSN] 1422-0067
  • [Journal-full-title] International journal of molecular sciences
  • [ISO-abbreviation] Int J Mol Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Keywords] NOTNLM ; AML / CSGE / Flt3 / ITD / Mutational analysis
  •  go-up   go-down


46. Bug G, Atta J, Klein SA, Hertenstein B, Bergmann L, Boehrer S, Mousset S, Hoelzer D, Martin H: High-dose melphalan is an effective salvage therapy in acute myeloid leukaemia patients with refractory relapse and relapse after autologous stem cell transplantation. Ann Hematol; 2005 Oct;84(11):748-54
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-dose melphalan is an effective salvage therapy in acute myeloid leukaemia patients with refractory relapse and relapse after autologous stem cell transplantation.
  • In a pilot study high-dose melphalan (HD-Mel, 200 mg/m2) and autologous stem cell transplantation (ASCT) were administered to 14 patients (median age 52, range 29-60 years) with acute myeloid leukaemia (AML) in first relapse after a previous ASCT in first complete remission (n=11) or chemotherapy (n=3).
  • Three MTC-refractory patients, but none of the upfront HD-Mel patients, died due to an allograft-related non-relapse cause.
  • Our results highly encourage to further investigate HD-Mel and ASCT as a promising salvage regimen for relapsed AML patients for whom autologous peripheral blood stem cells are available.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Melphalan / therapeutic use. Salvage Therapy / methods. Stem Cell Transplantation
  • [MeSH-minor] Adult. Antineoplastic Agents, Alkylating / therapeutic use. Female. Humans. Karyotyping. Male. Middle Aged. Recurrence. Transplantation, Autologous

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. MELPHALAN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16001243.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; Q41OR9510P / Melphalan
  •  go-up   go-down


47. Gorini G, Stagnaro E, Fontana V, Miligi L, Ramazzotti V, Nanni O, Rodella S, Tumino R, Crosignani P, Vindigni C, Fontana A, Vineis P, Costantini AS: Alcohol consumption and risk of leukemia: A multicenter case-control study. Leuk Res; 2007 Mar;31(3):379-86
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alcohol consumption and risk of leukemia: A multicenter case-control study.
  • A population-based case-control study of 649 leukemia cases and 1771 controls carried out in 11 Italian areas, offered the opportunity to evaluate the relationship between alcohol consumption and leukemia risk.
  • For all leukemias, acute lymphocytic leukemia (ALL), acute myeloid leukemia (AML), and chronic lymphocytic leukemia (CLL), we found a non-significantly inverse association for moderate levels of total alcohol and wine intake, but increased risks at high levels, with, in most cases, significant trend effects (odd ratios (OR) for all leukemias in the lowest quartile of total alcohol consumption [0.1-9.0 g/day of ethanol] versus never-drinker = 0.73; 95% confidence intervals (95% CI) = 0.51-1.03; OR in the highest quartile [> 31.7 g/day] = 1.15; 95% CI = 0.82-1.63; p of the linear trend test = 0.007).
  • For chronic myeloid leukemia (CML), we found a non-significantly positive association for all levels of total alcohol and wine intake, and a significant positive linear trend effect (p = 0.03) for wine intake (OR for 0.1-9.0 g/day of ethanol intake from wine = 1.34; 95% CI = 0.61-2.94; OR in the highest quartile of wine intake [> 27.7 g/day] = 2.13; 95% CI = 1.01-4.50).
  • No consistent dose-response was detected analysing duration of alcohol consumption for any leukemia subtypes.
  • In conclusion, even though our study did not show a clear association between alcohol intake and leukemia risk, some of the patterns of the risk estimates (a possible J-shaped dose-response curve between alcohol intake and ALL, AML, and CLL risks, and the positive association between alcohol and CML), may be suggestive.
  • [MeSH-major] Alcohol Drinking / adverse effects. Leukemia / etiology
  • [MeSH-minor] Adult. Aged. Case-Control Studies. Causality. Female. Humans. Italy / epidemiology. Male. Middle Aged. Predictive Value of Tests. Regression Analysis. Risk Factors

  • MedlinePlus Health Information. consumer health - Alcohol.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16919329.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA51086
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


48. Corless CL, Harrell P, Lacouture M, Bainbridge T, Le C, Gatter K, White C Jr, Granter S, Heinrich MC: Allele-specific polymerase chain reaction for the imatinib-resistant KIT D816V and D816F mutations in mastocytosis and acute myelogenous leukemia. J Mol Diagn; 2006 Nov;8(5):604-12
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allele-specific polymerase chain reaction for the imatinib-resistant KIT D816V and D816F mutations in mastocytosis and acute myelogenous leukemia.
  • Oncogenic mutations of the receptor tyrosine kinase KIT contribute to the pathogenesis of gastrointestinal stromal tumors, systemic mastocytosis (SM), and some cases of acute myelogenous leukemia (AML).
  • Because this mutation occurs in 80 to 95% of adult SM, its detection has diagnostic and predictive significance.
  • There were no amplifications among 64 KIT wild-type tumors and cell lines, whereas all D816V-mutant samples (eight AML and 11 mast cell disease) were positive.
  • [MeSH-major] Alleles. Leukemia, Myeloid, Acute / diagnosis. Mastocytosis / diagnosis. Mutation. Piperazines / therapeutic use. Polymerase Chain Reaction / methods. Pyrimidines / therapeutic use. Receptor Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Adult. Aged. Animals. Benzamides. Cell Line. Female. Genes, ras. Humans. Imatinib Mesylate. Male. Mice. Middle Aged. Protein Kinase Inhibitors / therapeutic use. Sensitivity and Specificity

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • Genetic Alliance. consumer health - Mast cell disease.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Carcinogenesis. 2002 Jun;23(6):943-8 [12082015.001]
  • [Cites] Blood. 2004 Nov 15;104(10):3038-45 [15284118.001]
  • [Cites] Oncogene. 2003 Feb 6;22(5):660-4 [12569358.001]
  • [Cites] Am J Pathol. 2003 Mar;162(3):737-46 [12598308.001]
  • [Cites] N Engl J Med. 2003 Mar 27;348(13):1201-14 [12660384.001]
  • [Cites] Lancet. 2003 Aug 16;362(9383):535-6 [12932387.001]
  • [Cites] Hematol Oncol Clin North Am. 2003 Oct;17(5):1227-41 [14560784.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4342-9 [14645423.001]
  • [Cites] Curr Opin Hematol. 2004 Jan;11(1):58-64 [14676628.001]
  • [Cites] Am J Pathol. 2004 Jan;164(1):305-13 [14695343.001]
  • [Cites] Annu Rev Med. 2004;55:419-32 [14746529.001]
  • [Cites] Eur J Cancer. 2004 Mar;40(5):689-95 [15010069.001]
  • [Cites] Leuk Res. 2004 May;28 Suppl 1:S47-52 [15036941.001]
  • [Cites] Leukemia. 2004 Apr;18(4):864-71 [14973502.001]
  • [Cites] Leuk Lymphoma. 2005 Jan;46(1):35-48 [15621779.001]
  • [Cites] Gastroenterology. 2005 Feb;128(2):270-9 [15685537.001]
  • [Cites] Leuk Res. 2005 Apr;29(4):397-400 [15725473.001]
  • [Cites] Lancet Oncol. 2005 Apr;6(4):249-51 [15811621.001]
  • [Cites] J Mol Diagn. 2005 May;7(2):252-7 [15858149.001]
  • [Cites] Clin Cancer Res. 2005 Jun 1;11(11):4182-90 [15930355.001]
  • [Cites] Blood. 2005 Jul 15;106(2):721-4 [15790786.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1536-42 [16015387.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2865-70 [15972446.001]
  • [Cites] Oncogene. 2005 Oct 13;24(45):6830-4 [16116485.001]
  • [Cites] Cancer Res. 2006 Jan 1;66(1):473-81 [16397263.001]
  • [Cites] Blood. 2006 Jan 15;107(2):752-9 [16189265.001]
  • [Cites] Cancer. 2006 Jul 15;107(2):345-51 [16779792.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2366-72 [16741248.001]
  • [Cites] Exp Hematol. 2000 Feb;28(2):140-7 [10706069.001]
  • [Cites] Hematol Oncol Clin North Am. 2000 Jun;14(3):697-701, viii [10909047.001]
  • [Cites] Leuk Res. 2004 Apr;28(4):421-2 [15109544.001]
  • [Cites] Br J Cancer. 2004 Jun 1;90(11):2059-61 [15150562.001]
  • [Cites] Haematologica. 2004 Aug;89(8):920-5 [15339674.001]
  • [Cites] J Clin Oncol. 2004 Sep 15;22(18):3813-25 [15365079.001]
  • [Cites] Am J Hematol. 2004 Nov;77(3):209-14 [15495258.001]
  • [Cites] J Clin Invest. 1993 Oct;92(4):1736-44 [7691885.001]
  • [Cites] Leuk Res. 2001 Jul;25(7):577-82 [11377683.001]
  • [Cites] Br J Haematol. 2001 May;113(2):357-64 [11380399.001]
  • [Cites] Blood. 2002 Mar 1;99(5):1741-4 [11861291.001]
  • [Cites] J Clin Oncol. 2002 Mar 15;20(6):1692-703 [11896121.001]
  • [Cites] Am J Pathol. 2002 May;160(5):1567-72 [12000708.001]
  • [Cites] Mutat Res. 2002 May 27;517(1-2):209-20 [12034322.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Nov 7;92(23):10560-4 [7479840.001]
  • [Cites] Cancer. 1998 Nov 15;83(10):2120-9 [9827716.001]
  • [Cites] J Invest Dermatol. 1998 Dec;111(6):1227-31 [9856847.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1609-14 [9990072.001]
  • [Cites] Mol Cancer Ther. 2002 Oct;1(12):1115-24 [12481435.001]
  • (PMID = 17065430.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ PMC1876167
  •  go-up   go-down


49. Shin HJ, Kim HJ, Sohn SK, Min YH, Won JH, Kim I, Yoon HJ, Lee JH, Jo DY, Joo YD, Jung CW, Lee KH, Korean Society of Hematology, AML/MDS Working Party, Chung JS, Ahn JS, Kim SJ, Lee JH, Choi SJ, Lee JH, Bae SH, Hong DS, Zang DY, Kim SH, Lee JL, Bang SM: Re-analysis of the outcomes of post-remission therapy for acute myeloid leukemia with core binding factor according to years of patient enrollment. Jpn J Clin Oncol; 2010 Jun;40(6):556-66
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Re-analysis of the outcomes of post-remission therapy for acute myeloid leukemia with core binding factor according to years of patient enrollment.
  • OBJECTIVE: The purpose of this study was to re-evaluate post-remission therapy outcomes after first remission according to years of patient enrollment in patients with core binding factor acute myeloid leukaemia.
  • METHODS: We conducted a retrospective study on 138 patients aged less than 60 years diagnosed with core binding factor acute myeloid leukaemia between 1994 and 2006, comparing allogeneic stem cell transplantation and high-dose cytarabine chemotherapy as post-remission treatment options after the first remission.
  • Especially, 3-year probabilities of disease-free survival (95.2% vs. 59.3%, P = 0.008) and overall survival (95.2% vs. 59.6%, P = 0.032) of allogeneic stem cell transplantation group were significantly better than high-dose cytarabine group in cohort after 2003 of acute myeloid leukaemia patients with t(8;21).
  • CONCLUSIONS: Allogeneic stem cell transplantation is currently the more effective post-remission therapy than it was prior to 2003 for core binding factor acute myeloid leukaemia achieving first remission.
  • On the contrary to previous findings, allogeneic stem cell transplantation provides significantly improved outcomes than high-dose cytarabine chemotherapy in acute myeloid leukaemia with t(8;21).
  • [MeSH-major] Core Binding Factors / metabolism. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cohort Studies. Cytarabine / administration & dosage. Cytarabine / therapeutic use. Daunorubicin / administration & dosage. Disease-Free Survival. Female. Humans. Male. Middle Aged. Remission Induction. Stem Cell Transplantation. Survival Rate. Young Adult

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20185460.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factors; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin; HDAC protocol
  •  go-up   go-down


50. Shi J, Shao ZH, Liu H, Jia HR, Sun J, Bai J, Cao YR, Wang XL, Tu MF: [Expression of cell cycle control genes in myelodysplastic syndromes]. Zhonghua Xue Ye Xue Za Zhi; 2005 Jan;26(1):10-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Reverse transcription polymerase chain reaction (RT-PCR) was used to investigate the expression of cell cycle control genes (cyclin D2, cyclin D3, cyclin A1, cyclin E, CDK2, CDK4, CDK6, p21, p27, p57, Rb and E2F1) in bone marrow mononuclear cells (BMMNCs) from 29 normal control, 27 MDS and 19 de novo acute myeloid leukemia (AML).
  • RESULTS: The expression levels of cyclin D3 (0.65 +/- 0.17, P < 0.05) and cyclin A1 (0.48 +/- 0.04, P < 0.05) in MDS were higher than those in normal control and significantly lower than those in AML.
  • The expression rates and levels of cyclin D2 (40.7% and 0.78 +/- 0.21) and cyclin E (51.9% and 0.52 +/- 0.10) in MDS were statistically higher than those in normal control and AML.
  • There was no significant difference of the expression rates and levels of CDK4 in MDS, AML and normal control.
  • The expression rates and levels of p21 (77.8% and 1.18 +/- 0.21) and p27 (48.1% and 1.14 +/- 0.40) in MDS were statistically higher than those in normal control and AML.
  • The expression level of p57 in MDS (0.69 +/- 0.06) was higher than that (0.53 +/- 0.05, P < 0.01) in normal control but lower than in AML (0.96 +/- 0.16, P < 0.01).
  • The expression rate (55.6%) and level (0.85 +/- 0.17) of Rb in MDS were significantly higher than those in normal control and AML.
  • The expression rate (7.4%) and level (0.39 +/- 0.04) of E2F1 in MDS were comparable to those in normal control but lower than those in AML.
  • [MeSH-minor] Adolescent. Adult. Child. E2F1 Transcription Factor / genetics. Female. Humans. Male. Middle Aged. Retinoblastoma Protein / genetics. Reverse Transcriptase Polymerase Chain Reaction. Young Adult


51. Verheyden S, Ferrone S, Mulder A, Claas FH, Schots R, De Moerloose B, Benoit Y, Demanet C: Role of the inhibitory KIR ligand HLA-Bw4 and HLA-C expression levels in the recognition of leukemic cells by Natural Killer cells. Cancer Immunol Immunother; 2009 Jun;58(6):855-65
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Transplantation of acute myeloid leukemia (AML) patients with grafts from related haploidentical donors has been shown to result in a potent graft-versus-leukemia effect.
  • Therefore in the present study, utilizing a large panel of human monoclonal antibodies we have measured the level of expression of HLA-A, -B and -C alleles on 20 B-chronic lymphoid leukemic (B-CLL) cell preparations, on 16 B-acute lymphoid leukemic (B-ALL) cell preparations and on 19 AML cell preparations.
  • Comparison of the level of HLA class I antigen expression on leukemic cells and autologous normal T cells identified selective downregulation of HLA-A and HLA-B alleles on 15 and 14 of the 20 B-CLL, on 2 and 5 of the 16 B-ALL and on 7 and 11 of the 19 AML patients tested, respectively.
  • Most interestingly HLA-C alleles were markedly downregulated on all three types of leukemic cells; the downregulation was most pronounced on AML cells.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2004 Apr 15;103(8):3122-30 [15070694.001]
  • [Cites] Leukemia. 2008 Feb;22(2):249-57 [18046448.001]
  • [Cites] Immunol Today. 1990 Jul;11(7):237-44 [2201309.001]
  • [Cites] Science. 1993 May 21;260(5111):1121-4 [8493555.001]
  • [Cites] Cancer Res. 1993 Jul 15;53(14):3349-54 [7686817.001]
  • [Cites] J Exp Med. 1993 Aug 1;178(2):597-604 [8340759.001]
  • [Cites] J Immunol Methods. 1993 Nov 5;166(1):45-54 [8228287.001]
  • [Cites] J Exp Med. 1995 Mar 1;181(3):1133-44 [7532677.001]
  • [Cites] J Exp Med. 1995 Aug 1;182(2):605-9 [7629517.001]
  • [Cites] Hum Immunol. 1997 Aug-Sep;56(1-2):106-13 [9455499.001]
  • [Cites] Hum Immunol. 1998 Aug;59(8):524-8 [9712358.001]
  • [Cites] Tissue Antigens. 1998 Oct;52(4):393-6 [9820605.001]
  • [Cites] Eur J Cancer. 1998 Sep;34(10):1618-22 [9893639.001]
  • [Cites] Blood. 1999 Jul 1;94(1):333-9 [10381530.001]
  • [Cites] J Exp Med. 1999 Jul 19;190(2):205-15 [10432284.001]
  • [Cites] Blood. 2005 Mar 1;105(5):2066-73 [15536144.001]
  • [Cites] Leukemia. 2001 Jan;15(1):128-33 [11243380.001]
  • [Cites] Hum Immunol. 2002 Mar;63(3):200-10 [11872238.001]
  • [Cites] Science. 2002 Mar 15;295(5562):2097-100 [11896281.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3825-7 [12393440.001]
  • [Cites] Cancer Res. 2002 Nov 1;62(21):6178-86 [12414645.001]
  • [Cites] Br J Haematol. 2003 Mar;120(6):1000-8 [12648070.001]
  • [Cites] Leuk Res. 2003 Jul;27(7):643-8 [12681364.001]
  • [Cites] Hum Immunol. 2003 Oct;64(10):941-50 [14522091.001]
  • [Cites] Tissue Antigens. 2004 Mar;63(3):204-11 [14989709.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2860-1; author reply 2862 [15033884.001]
  • [Cites] Exp Hematol. 2005 Mar;33(3):344-52 [15730858.001]
  • [Cites] Curr Opin Immunol. 2005 Oct;17(5):553-9 [16085405.001]
  • [Cites] J Immunol. 2006 Nov 15;177(10):6904-10 [17082605.001]
  • [Cites] Cancer Sci. 2007 Jan;98(1):102-8 [17083564.001]
  • [Cites] Blood. 2007 Jul 1;110(1):433-40 [17371948.001]
  • [Cites] Transplantation. 2004 Oct 15;78(7):1081-5 [15480179.001]
  • (PMID = 18841361.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA138188; United States / NCI NIH HHS / CA / R01CA110249; United States / NCI NIH HHS / CA / R01 CA110249; United States / NCI NIH HHS / CA / P01 CA109688; United States / NCI NIH HHS / CA / R01CA113861; United States / NCI NIH HHS / CA / R01 CA113861
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / HLA-A Antigens; 0 / HLA-B Antigens; 0 / HLA-Bw4 antigen; 0 / HLA-C Antigens; 0 / Ligands; 0 / Receptors, KIR
  • [Other-IDs] NLM/ NIHMS395042; NLM/ PMC3426282
  •  go-up   go-down


52. Zhang YL, Ren JH, Guo XN, Zhang JN, Wang Y, Qiao SK, Lin FR: [Expression of c-fes gene in leukemia cells and its clinical significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Dec;17(6):1429-33
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of c-fes gene in leukemia cells and its clinical significance].
  • This study was purposed to investigate the expression of c-fes gene in leukemia patients and its clinical significance.
  • The expression of c-fes mRNA in bone marrow cells from 121 cases of acute and chronic leukemia patients, and the expression of c-fes mRNA in peripheral blood mononuclear cells of 20 normal persons were detected by real time-quantitative reverse transcription polymerase chain reaction (RQ-PCR).
  • The results showed that the level of c-fes mRNA in AML patients was higher than that in normal controls [(48.017 +/- 57.170) x 10(-3) vs (0.152 +/- 0.398) x 10(-3)] (p < 0.0001); but there was no significant differences of level of c-fes mRNA between samples of ALL and normal controls(0.047 +/- 0.068) x 10(-3) vs(0.152 +/- 0.398) x 10(-3) (p>0.05); the level of c-fes mRNA in CML patients was higher than that in normal persons (21.605 +/- 24.818) x 10(-3) vs (0.152 +/- 0.398) x 10(-3) (p < 0.0001).
  • In AML patients, c-fes gene was expressed higher in M(2) (80.77%) and M(3) (92.86%) patients.
  • The remission rate of AML (except M(3))patients who had expression of c-fes gene was 81.08%, which was higher than that of patients with no expression of c-fes gene (40.00%).
  • It is concluded that c-fes gene expression was found in myeloid leukemias, whereas low or no expression in lymphocytic leukemias.
  • The differentiation of myelocytic cells may be related to c-fes gene.
  • All AML (except M(3))patients with high level of c-fes mRNA may get good prognosis.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20030920.001).
  • [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 / RNA, Messenger; EC 2.7.10.2 / FES protein, human; EC 2.7.10.2 / Proto-Oncogene Proteins c-fes
  •  go-up   go-down


53. Okamoto M, Hayakawa F, Miyata Y, Watamoto K, Emi N, Abe A, Kiyoi H, Towatari M, Naoe T: Lyn is an important component of the signal transduction pathway specific to FLT3/ITD and can be a therapeutic target in the treatment of AML with FLT3/ITD. Leukemia; 2007 Mar;21(3):403-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lyn is an important component of the signal transduction pathway specific to FLT3/ITD and can be a therapeutic target in the treatment of AML with FLT3/ITD.
  • An internal tandem duplication (ITD) of FLT3 (FLT3/ITD) is the most frequent mutation in human adult acute myeloid leukemia (AML).
  • These results demonstrate that Lyn is an important component of the signal transduction pathway specific to FLT3/ITD and can be a therapeutic target in the treatment of AML with FLT3/ITD.
  • [MeSH-major] Leukemia, Myeloid / enzymology. Mutant Proteins / metabolism. Neoplasm Proteins / metabolism. Protein Processing, Post-Translational. Signal Transduction. fms-Like Tyrosine Kinase 3 / metabolism. src-Family Kinases / metabolism
  • [MeSH-minor] Acute Disease. Amino Acid Sequence. Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Line / drug effects. Cell Line / transplantation. Drug Design. Drug Screening Assays, Antitumor. Female. Hematopoietic Stem Cells / drug effects. Membrane Proteins / pharmacology. Mice. Mice, Inbred C3H. Molecular Sequence Data. Phosphorylation. Phosphotyrosine / metabolism. Protein Binding. Protein Interaction Mapping. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / pharmacology. Pyrimidines / therapeutic use. RNA Interference. RNA, Small Interfering / pharmacology. Recombinant Fusion Proteins / physiology. STAT5 Transcription Factor / metabolism. Tandem Repeat Sequences. Transfection

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17230226.001).
  • [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 / AG 1879; 0 / Antineoplastic Agents; 0 / Membrane Proteins; 0 / Mutant Proteins; 0 / Neoplasm Proteins; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / RNA, Small Interfering; 0 / Recombinant Fusion Proteins; 0 / STAT5 Transcription Factor; 0 / flt3 ligand protein; 21820-51-9 / Phosphotyrosine; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / lyn protein-tyrosine kinase; EC 2.7.10.2 / src-Family Kinases
  •  go-up   go-down


54. Powell JA, Thomas D, Barry EF, Kok CH, McClure BJ, Tsykin A, To LB, Brown A, Lewis ID, Herbert K, Goodall GJ, Speed TP, Asou N, Jacob B, Osato M, Haylock DN, Nilsson SK, D'Andrea RJ, Lopez AF, Guthridge MA: Expression profiling of a hemopoietic cell survival transcriptome implicates osteopontin as a functional prognostic factor in AML. Blood; 2009 Nov 26;114(23):4859-70
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression profiling of a hemopoietic cell survival transcriptome implicates osteopontin as a functional prognostic factor in AML.
  • We now show that Ser585 phosphorylation is constitutive in 20 (87%) of 23 acute myeloid leukemia (AML) patient samples, indicating that this survival-only pathway is frequently deregulated in leukemia.
  • We show that one such gene, osteopontin (OPN), is a functionally relevant target of the Ser585-survival pathway as shown by siRNA-mediated knockdown of OPN expression that induces cell death in both AML blasts and CD34(+)CD38(-)CD123(+) leukemic progenitors.
  • Increased expression of OPN at diagnosis is associated with poor prognosis with multivariate analysis indicating that it is an independent predictor of overall patient survival in normal karyotype AML (n = 60; HR = 2.2; P = .01).
  • These results delineate a novel cytokine-regulated Ser585/PI3-kinase signaling network that is deregulated in AML and identify OPN as a potential prognostic and therapeutic target.
  • [MeSH-major] Gene Expression Profiling. Hematopoietic Stem Cells / metabolism. Leukemia, Myeloid / genetics. Neoplasm Proteins / physiology. Osteopontin / physiology
  • [MeSH-minor] Adult. Aged. Cell Survival. Cytokine Receptor Common beta Subunit / metabolism. Female. Gene Expression Regulation, Leukemic. Gene Knockdown Techniques. Gene Regulatory Networks. Humans. Male. Middle Aged. Neoplastic Stem Cells / drug effects. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / physiology. Phosphoserine / metabolism. Prognosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / genetics. RNA, Small Interfering / pharmacology. Signal Transduction / genetics. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / metabolism. Tumor Cells, Cultured / pathology

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • PhosphoSitePlus. gene/protein/disease-specific - PhosphoSitePlus® - comprehensive post-translational modification resource .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19805619.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CSF2RB protein, human; 0 / Cytokine Receptor Common beta Subunit; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 106441-73-0 / Osteopontin; 17885-08-4 / Phosphoserine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
  •  go-up   go-down


55. Lu SH, Hou YY, Tan YS, Xu JF, Zeng HY, Sujie AK, Wang XD, Bai CX: Clinical and histopathological alterations of lymphangioleiomyomatosis in 14 Chinese patients. Chin Med J (Engl); 2009 Aug 20;122(16):1895-900
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Extrapulmonary findings such as renal angiomyolipoma (AML), enlarged abdominal lymph nodes, liver AML and retroperitoneal lymphangioleiomyoma were seen in 21.4%, 14.3%, 7.14% and 7.14% in 14 cases respectively, which is remarkably lower than in the previously reported.
  • [MeSH-minor] Adolescent. Adult. Aged. Contraceptives, Oral, Synthetic. Female. Humans. Immunohistochemistry. Medroxyprogesterone / therapeutic use. Middle Aged. Ovariectomy. Progesterone / therapeutic use. Progestins / therapeutic use. Young Adult

  • Genetic Alliance. consumer health - Lymphangioleiomyomatosis.
  • Hazardous Substances Data Bank. MEDROXYPROGESTERONE .
  • Hazardous Substances Data Bank. PROGESTERONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19781367.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Contraceptives, Oral, Synthetic; 0 / Progestins; 4G7DS2Q64Y / Progesterone; HSU1C9YRES / Medroxyprogesterone
  •  go-up   go-down


56. Vehreschild JJ, Rüping MJ, Wisplinghoff H, Farowski F, Steinbach A, Sims R, Stollorz A, Kreuzer KA, Hallek M, Bangard C, Cornely OA: Clinical effectiveness of posaconazole prophylaxis in patients with acute myelogenous leukaemia (AML): a 6 year experience of the Cologne AML cohort. J Antimicrob Chemother; 2010 Jul;65(7):1466-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical effectiveness of posaconazole prophylaxis in patients with acute myelogenous leukaemia (AML): a 6 year experience of the Cologne AML cohort.
  • METHODS: We prospectively evaluated the epidemiology of IFDs in acute myelogenous leukaemia (AML) patients undergoing first remission-induction chemotherapy before and after posaconazole prophylaxis had been introduced as a standard of care.
  • CONCLUSIONS: After introduction of posaconazole prophylaxis for patients with AML, the number of febrile days, the incidence rate of IFDs and aspergillosis and the duration of hospitalization decreased significantly.
  • [MeSH-major] Antifungal Agents / therapeutic use. Chemoprevention / methods. Leukemia, Myeloid, Acute / complications. Mycoses / prevention & control. Triazoles / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Germany. Humans. Incidence. Length of Stay / statistics & numerical data. Male. Middle Aged. Polyenes / therapeutic use. Retrospective Studies. Treatment Outcome. Young Adult

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Fungal Infections.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20410061.001).
  • [ISSN] 1460-2091
  • [Journal-full-title] The Journal of antimicrobial chemotherapy
  • [ISO-abbreviation] J. Antimicrob. Chemother.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Polyenes; 0 / Triazoles; 6TK1G07BHZ / posaconazole
  •  go-up   go-down


57. Babatunde AS, Tan DC, Heng KK, Lee JJ, Loh YS, Hwang WY, Koh MB, Goh YT, Linn YC: Characterization of hemopoietic engraftment kinetics and development of secondary cytopenia in AML post auto-SCT and its correlation with survival outcome. Bone Marrow Transplant; 2009 Aug;44(3):175-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of hemopoietic engraftment kinetics and development of secondary cytopenia in AML post auto-SCT and its correlation with survival outcome.
  • We performed a single center retrospective analysis of 84 autologous hemopoietic stem cell transplants done for AML to characterize the pattern of hemopoietic engraftment, post-transplant cytopenia and their impact on survival outcome.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Graft Rejection. Graft Survival. Hematopoiesis. Hematopoietic Stem Cell Mobilization. Humans. Male. Middle Aged. Retrospective Studies. Thrombocytopenia / blood. Thrombocytopenia / etiology. Transplantation Conditioning. Treatment Outcome. Young Adult

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19204715.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


58. Minami J, Abe C, Akashiba A, Takahashi T, Kameda T, Ishimitsu T, Matsuoka H: Long-term efficacy of combination therapy with losartan and low-dose hydrochlorothiazide in patients with uncontrolled hypertension. Int Heart J; 2007 Mar;48(2):177-86
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We enrolled 15 Japanese hypertensive outpatients whose 24-hour ambulatory blood pressure was >or= 135/80 mmHg after candesartan 8 mg (CND group; n = 10) monotherapy or amlodipine 5 mg (AML group; n = 5) monotherapy for 2 months or more.
  • In the AML group, 24-hour blood pressure decreased significantly from 137 +/- 11/81 +/- 7 to 125 +/- 12/75 +/- 6 mmHg after 3 months (P < 0.05/P < 0.05) and to 124 +/- 9/77 +/- 7 mmHg after 12 months (P < 0.05/NS).
  • [MeSH-minor] Adult. Aged. Amlodipine / therapeutic use. Benzimidazoles / therapeutic use. Drug Administration Schedule. Drug Therapy, Combination. Female. Follow-Up Studies. Humans. Male. Middle Aged. Tetrazoles / therapeutic use. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Blood Pressure Medicines.
  • MedlinePlus Health Information. consumer health - High Blood Pressure.
  • Hazardous Substances Data Bank. Losartan .
  • Hazardous Substances Data Bank. CANDESARTAN .
  • Hazardous Substances Data Bank. HYDROCHLOROTHIAZIDE .
  • Hazardous Substances Data Bank. AMLODIPINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17409583.001).
  • [ISSN] 1349-2365
  • [Journal-full-title] International heart journal
  • [ISO-abbreviation] Int Heart J
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antihypertensive Agents; 0 / Benzimidazoles; 0 / Tetrazoles; 0J48LPH2TH / Hydrochlorothiazide; 1J444QC288 / Amlodipine; JMS50MPO89 / Losartan; S8Q36MD2XX / candesartan
  •  go-up   go-down


59. Peniket A, Wainscoat J, Side L, Daly S, Kusec R, Buck G, Wheatley K, Walker H, Chatters S, Harrison C, Boultwood J, Goldstone A, Burnett A: Del (9q) AML: clinical and cytological characteristics and prognostic implications. Br J Haematol; 2005 Apr;129(2):210-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Del (9q) AML: clinical and cytological characteristics and prognostic implications.
  • Del (9q) is a recurrent cytogenetic abnormality in acute myeloid leukaemia (AML).
  • We report an analysis of 81 patients with del(9q) as a diagnostic karyotypic abnormality entered into the Medical Research Council AML trials 10, 11 and 12.
  • It is likely that the deletion of single or multiple tumour suppressor genes located in this region may underlie the pathogenesis of del (9q) AML.
  • [MeSH-major] Gene Deletion. Genes, Tumor Suppressor. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Bone Marrow Cells / pathology. Child. Child, Preschool. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Cytogenetic Analysis. Disease-Free Survival. Female. Genetic Markers. Humans. Male. Middle Aged. Survival Rate. Translocation, Genetic

  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Br J Haematol. 2005 Sep;130(6):969; author reply 969 [16156871.001]
  • (PMID = 15813849.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Genetic Markers
  •  go-up   go-down


60. Kokate P, Ahmad F, Dalvi R, Das BR, Mandava S: Molecular cytogenetic investigations in a novel complex variant of t(8;21)(q22;q22) with ins(15;21)(q15;q22.2q22.3) in a patient with AML-M2 subtype. Cancer Genet Cytogenet; 2008 Jul;184(1):52-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular cytogenetic investigations in a novel complex variant of t(8;21)(q22;q22) with ins(15;21)(q15;q22.2q22.3) in a patient with AML-M2 subtype.
  • Acute myeloid leukemia (AML) is a clinically and molecularly heterogeneous disease characterized by the aberrant proliferation of myeloid stem cells, reduced apoptosis and blockage in cellular differentiation.
  • The present report describes the results of hematological, cytogenetic, and fluorescence in situ hybridization (FISH) analysis in a 25-year-old man diagnosed with AML-M2.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18558290.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


61. Brooks TA, O'Loughlin KL, Minderman H, Bundy BN, Ford LA, Vredenburg MR, Bernacki RJ, Priebe W, Baer MR: The 4'-O-benzylated doxorubicin analog WP744 overcomes resistance mediated by P-glycoprotein, multidrug resistance protein and breast cancer resistance protein in cell lines and acute myeloid leukemia cells. Invest New Drugs; 2007 Apr;25(2):115-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The 4'-O-benzylated doxorubicin analog WP744 overcomes resistance mediated by P-glycoprotein, multidrug resistance protein and breast cancer resistance protein in cell lines and acute myeloid leukemia cells.
  • We compared its uptake and cytotoxicity with those of doxorubicin and daunorubicin in cell lines overexpressing Pgp, MRP-1 or breast cancer resistance protein (BCRP) and in acute myeloid leukemia (AML) cells.
  • METHODS: Cellular uptake was studied by flow cytometry and cytotoxicity in 96-h 96-well cultures in cell lines overexpressing Pgp, MRP-1 or wild type (BCRP(R482)) or mutant (BCRP(R482T), BCRP(R482G)) BCRP and in pre-treatment AML marrow cells.
  • RESULTS: Uptake and cytotoxicity of WP744 were consistently greater than those of doxorubicin and daunorubicin at equimolar concentrations in all cell lines studied and in AML cells.
  • CONCLUSION: WP744 overcomes transport by Pgp, MRP-1 and BCRP in cell lines and AML cells and is a promising agent for clinical development in AML and other malignancies with broad-spectrum multidrug resistance.
  • [MeSH-major] ATP-Binding Cassette Transporters / physiology. ATP-Binding Cassette, Sub-Family B, Member 1 / physiology. Anthracyclines / pharmacology. Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm / drug effects. Leukemia, Myeloid / pathology. Neoplasm Proteins / physiology
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Adult. Aged. Antibiotics, Antineoplastic / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Daunorubicin / metabolism. Doxorubicin / metabolism. Female. Fluorescence. Humans. Male. Middle Aged

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Cancer Res. 2005 Mar 15;11(6):2320-6 [15788683.001]
  • [Cites] Br J Haematol. 2004 Nov;127(4):392-8 [15521915.001]
  • [Cites] Clin Cancer Res. 2004 Dec 1;10 (23 ):7896-902 [15585622.001]
  • [Cites] Clin Cancer Res. 2003 Aug 15;9(9):3320-8 [12960118.001]
  • [Cites] Br J Haematol. 2001 Nov;115(2):257-62 [11703319.001]
  • [Cites] Leukemia. 2004 Jul;18(7):1252-7 [15208643.001]
  • [Cites] Mol Cancer Ther. 2003 Nov;2(11):1195-205 [14617793.001]
  • [Cites] NeuroRx. 2005 Jan;2(1):86-98 [15717060.001]
  • [Cites] Cancer Res. 2001 Sep 15;61(18):6635-9 [11559526.001]
  • [Cites] J Surg Res. 2004 Oct;121(2):187-96 [15501458.001]
  • [Cites] J Surg Res. 2004 Dec;122(2):231-9 [15555623.001]
  • [Cites] Leukemia. 2002 Aug;16(8):1443-7 [12145683.001]
  • [Cites] Clin Cancer Res. 2003 Nov 1;9(14 ):5171-7 [14613996.001]
  • [Cites] Biochem Pharmacol. 2004 Jan 15;67(2):353-64 [14698047.001]
  • [Cites] Cytometry. 2002 Jun 1;48(2):59-65 [12116365.001]
  • [Cites] Anticancer Res. 2001 Nov-Dec;21(6A):3777-84 [11911247.001]
  • [Cites] Nat Rev Cancer. 2002 Jan;2(1):48-58 [11902585.001]
  • (PMID = 17072745.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA16056; United States / NCI NIH HHS / CA / R01 CA 73872; United States / NCI NIH HHS / CA / R21 CA 98457; United States / NCI NIH HHS / CA / T32 CA 09072-28
  • [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 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Anthracyclines; 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / WP 744; 80168379AG / Doxorubicin; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


62. Shimada A, Ichikawa H, Taki T, Kubota C, Hongo T, Sako M, Morimoto A, Tawa A, Tsukimoto I, Hayashi Y: Low frequency of KIT gene mutation in pediatric acute myeloid leukemia with inv(16)(p13q22): a study of the Japanese Childhood AML Cooperative Study Group. Int J Hematol; 2007 Oct;86(3):289-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low frequency of KIT gene mutation in pediatric acute myeloid leukemia with inv(16)(p13q22): a study of the Japanese Childhood AML Cooperative Study Group.
  • [MeSH-major] Chromosome Inversion. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins c-kit / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease-Free Survival. Female. Follow-Up Studies. Humans. Infant. Male. Survival Rate


63. Batzios C, Hayes LA, He SZ, Quach H, McQuilten ZK, Wall M, Campbell LJ: Secondary clonal cytogenetic abnormalities following successful treatment of acute promyelocytic leukemia. Am J Hematol; 2009 Nov;84(11):715-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary clonal cytogenetic abnormalities following successful treatment of acute promyelocytic leukemia.
  • To identify patients who developed secondary clonal cytogenetic aberrations (CCA) following therapy for acute promyelocytic leukemia (APL), we retrospectively analyzed cytogenetic results from 123 patients diagnosed with APL between 1995 and 2007, who had ongoing cytogenetic analysis undertaken in our laboratory.
  • To date, four patients with CCA have been diagnosed with therapy-related myelodysplastic syndrome (t-MDS)/acute myeloid leukemia (t-AML), giving a median t-MDS/AML free survival of 78 months, with follow-up ranging between 20 and 136 months from APL diagnosis.
  • Three patients have died: two patients died of t-AML and another developed relapsed APL with persistence of his secondary clone but no diagnosis of t-MDS/AML and died from transplant-related complications.
  • [MeSH-major] Chromosome Aberrations / chemically induced. Leukemia, Promyelocytic, Acute / genetics. Neoplasms, Second Primary / chemically induced. Tretinoin / therapeutic use
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols. Female. Humans. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics. Remission Induction / methods. Retrospective Studies. Survival Rate. Treatment Outcome. Young Adult

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Am J Hematol. 2010 Jul;85(7):550
  • (PMID = 19806661.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5688UTC01R / Tretinoin
  •  go-up   go-down


64. Haouas H, Haouas S, Uzan G, Hafsia A: Identification of new markers discriminating between myeloid and lymphoid acute leukemia. Hematology; 2010 Aug;15(4):193-203
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of new markers discriminating between myeloid and lymphoid acute leukemia.
  • BACKGROUND: The heterogeneity of acute myeloid leukemia (AML) with respect to biology and clinical course resides in the fact that patients belonging to the same group show marked differences in their response to chemotherapy, necessitating a refinement of AML classification.
  • METHODS: In order to define molecular markers for AML, we performed microarray analysis on peripheral blood cells from two M5 AML patients, and selected four differentially expressed genes to validate their expression by real-time quantitative PCR (RT-PCR).
  • RESULTS: We have shown that two downregulated genes in AML, those encoding guanine nucleotide-binding protein gamma11 (GNG11) and amphiregulin (AREG), are also downregulated in B-lineage acute lymphoblastic leukemia (B-ALL) and T-lineage acute lymphoblastic leukemia (T-ALL) patients.
  • A second gene, that encoding ceruloplasmin (CP), is upregulated in AML but not in B-ALL and T-ALL.
  • CONCLUSION: Since the number of patients studied is limited, further studies are needed with a larger series of patients to evaluate the potential utility of GNG11, AREG and CP as molecular markers for AML subtype classification.
  • Our study is the first to analyze these genes in AML, B-ALL, T-ALL and chronic leukemia (myeloid and lymphoid) patients by RT-PCR.
  • This rapid and sensitive method could be used to screen these genes in different types of leukemia.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Amphiregulin. Cell Line, Tumor. Ceruloplasmin / genetics. Ceruloplasmin / metabolism. Diagnosis, Differential. EGF Family of Proteins. Female. GTP-Binding Protein alpha Subunits, Gq-G11 / genetics. GTP-Binding Protein alpha Subunits, Gq-G11 / metabolism. Gene Expression Profiling. Glycoproteins / genetics. Glycoproteins / metabolism. Humans. Intercellular Signaling Peptides and Proteins / genetics. Intercellular Signaling Peptides and Proteins / metabolism. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20670477.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AREG protein, human; 0 / Amphiregulin; 0 / Biomarkers, Tumor; 0 / EGF Family of Proteins; 0 / Glycoproteins; 0 / Intercellular Signaling Peptides and Proteins; EC 1.16.3.1 / Ceruloplasmin; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gq-G11
  •  go-up   go-down


65. Hardwick N, Chan L, Ingram W, Mufti G, Farzaneh F: Lytic activity against primary AML cells is stimulated in vitro by an autologous whole cell vaccine expressing IL-2 and CD80. Cancer Immunol Immunother; 2010 Mar;59(3):379-88
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lytic activity against primary AML cells is stimulated in vitro by an autologous whole cell vaccine expressing IL-2 and CD80.
  • Despite being of the myeloid lineage, acute myeloid leukaemia (AML) blasts are of low immunogenicity, probably because they lack the costimulatory molecule CD80 and secrete immunosuppressive factors.
  • We have previously shown that in vitro stimulation of autologous peripheral blood mononuclear cells (PBMCs) with primary AML cells modified to express CD80 and IL-2 promotes proliferation, secretion of Th1 cytokines and expansion of activated CD8(+) T cells.
  • In this study, we show that allogeneic effector cells (from a healthy donor or AML patients) when stimulated with IL-2/CD80 modified AML blasts were able to induce the lysis of unmodified AML blasts.
  • Effector cells stimulated with IL-2/CD80AML blasts had higher lytic activity than cells stimulated with AML cells expressing CD80 or IL-2 alone.
  • Similarly, AML patient PBMCs primed with autologous IL-2/CD80 AML cells had a higher frequency of IFN-gamma secreting cells and show cytotoxicity against autologous, unmodified blasts.
  • Crucially, the response appears to be leukaemia specific, since stimulated patient PBMCs show higher frequencies of IFN-gamma secreting effector cells in response to AML blasts than to remission bone marrow cells from the same patients.
  • Although studied in a small number of heterogeneous patient samples, the data are encouraging and support the continuing development of vaccination for poor prognosis AML patients with autologous cells genetically modified to express IL-2/CD80.
  • [MeSH-major] Antigens, CD80 / genetics. Interleukin-2 / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / immunology
  • [MeSH-minor] Adult. Aged. Cells, Cultured. Female. Genetic Therapy / methods. Humans. Male. Middle Aged. Neutrophils / immunology. Transduction, Genetic

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19711075.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/D014301/1; United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/E005896/1; United Kingdom / Department of Health / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Interleukin-2
  •  go-up   go-down


66. Atsuta Y, Suzuki R, Nagamura-Inoue T, Taniguchi S, Takahashi S, Kai S, Sakamaki H, Kouzai Y, Kasai M, Fukuda T, Azuma H, Takanashi M, Okamoto S, Tsuchida M, Kawa K, Morishima Y, Kodera Y, Kato S, Japan Cord Blood Bank Network: Disease-specific analyses of unrelated cord blood transplantation compared with unrelated bone marrow transplantation in adult patients with acute leukemia. Blood; 2009 Feb 19;113(8):1631-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disease-specific analyses of unrelated cord blood transplantation compared with unrelated bone marrow transplantation in adult patients with acute leukemia.
  • We made a disease-specific comparison of unrelated cord blood (CB) recipients and human leukocyte antigen allele-matched unrelated bone marrow (BM) recipients among 484 patients with acute myeloid leukemia (AML; 173 CB and 311 BM) and 336 patients with acute lymphoblastic leukemia (ALL; 114 CB and 222 BM) who received myeloablative transplantations.
  • In multivariate analyses, among AML cases, lower overall survival (hazard ratio [HR]=1.5; 95% confidence interval [CI], 1.0-2.0, P= .028) and leukemia-free survival (HR=1.5; 95% CI, 1.1-2.0, P= .012) were observed in CB recipients.
  • The relapse rate did not differ between the 2 groups of AML (HR=1.2; 95% CI, 0.8-1.9, P= .38); however, the treatment-related mortality rate showed higher trend in CB recipients (HR=1.5; 95% CI, 1.0-2.3, P= .085).
  • In ALL, there was no significant difference between the groups for relapse (HR=1.4, 95% CI, 0.8-2.4, P= .19) and treatment-related mortality (HR=1.0; 95% CI, 0.6-1.7, P= .98), which contributed to similar overall survival (HR=1.1; 95% CI, 0.7-1.6, P= .78) and leukemia-free survival (HR=1.2; 95% CI, 0.9-1.8, P= .28).
  • For patients with AML, decreasing mortality, especially in the early phase of transplantation, is required to improve the outcome for CB recipients.
  • [MeSH-major] Bone Marrow Transplantation / mortality. Cord Blood Stem Cell Transplantation / mortality. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Blood Platelets / cytology. Cause of Death. Disease-Free Survival. Female. Follow-Up Studies. Graft vs Host Disease / epidemiology. Histocompatibility Testing. Humans. Incidence. Male. Middle Aged. Multivariate Analysis. Neutrophils / cytology. Recurrence. Risk Factors. Treatment Outcome. Young Adult

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19104080.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Investigator] Yoshida M; Sato K; Kohda K; Kobayashi N; Kobayashi R; Fukuhara T; Masauji N; Suzuki N; Ishida T; Matsunaga T; Imamura M; Kaneda M; Nishio M; Sasaki S; Ogura K; Ishida Y; Endo M; Okuda M; Kameoka J; Sasahara Y; Mitsui T; Tajima K; Fujishima N; Ogawa K; Kikuta A; Takayama N; Okamoto S; Shimada H; Waki A; Mori S; Hagiwara S; Kumagai M; Hamano Y; Yanagisawa K; Tashiro H; Fukuda T; Kajiwara M; Kimura Y; Yano S; Yoshinaga K; Takahashi S; Takita J; Akiyama H; Kaneko T; Ueno H; Tajika K; Suzuki K; Hatta Y; Chin M; Sakai R; Fujita H; Goto H; Kanamori H; Kigasawa H; Inoue Y; Onizuka M; Yabe H; Takeuchi M; Tanaka H; Okimoto Y; Yokota A; Nakaseko C; Ishiwada N; Katayama T; Kawai N; Watabe R; Maseki N; Kikuchi A; Ohshima K; Kimura F; Kogawa K; Koike K; Kamoshita M; Hasegawa Y; Muroi K; Sasaki K; Sugita K; Sakura T; Saito T; Kanazawa T; Sugita K; Asami K; cho T; Furukawa T; Koike T; Ito T; Yanagisawa R; Ishii E; Kobayashi H; Naito K; Yagyu T; Takashima Y; Ikeda T; Yago K; Taguchi J; Shigeno K; Okada S; Mihara H; Morishima Y; Morishita Y; Sawa M; Hamaguchi M; Kusumoto S; Murata M; Kojima S; Kato K; Miyamura K; Kasai M; Shimokawa T; Sao H; Kawakami K; Nakase K; Azuma E; Tamaki S; Oka K; Yoshida T; Kanegane H; Fukushima T; Nishimura R; Takami A; Ymaguchi M; Tanizawa A; Kasahara S; Kito K; Doi S; Ito M; Kuroda H; Ichinohe T; Adachi S; Nakagawa H; Taniwaki M; Hatanaka K; Kishimoto Y; Ashida T; Sakata N; Ishida H; Yonetani N; Hara J; Yamane T; Tsudo M; Maeda T; Ohta H; Hiraoka A; Inoue M; Akasaka H; Usami I; Nagai K; Okamura A; Hayakawa A; Otsuka Y; Okada M; Murayama T; Kosaka Y; Yagi H; Nakamura F; Amano I; Higuchi B; Sonoki T; Endo A; Ago H; Okazaki T; Ueyama J; Maeda Y; Sayama K; Ueda Y; Sunami K; Hamamoto K; Iwato K; Kobayashi M; Niimi H; Yujiri T; Ohnishi H; Abe M; Togitani K; Hara M; Tauchi H; Narumi H; Muta T; Yakushiji K; Matsuzaki A; Nagafuji K; Abe Y; Kamimura T; Eto T; Morimoto H; Miyaji R; Imada K; Imamura Y; Uike N; Nagatoshi Y; Moriuchi Y; Miyazaki Y; Otsuka E; Ogata M; Morinaga S; Hidaka M; Otsuka M; Takatsuka Y; Matsushita K; Okamoto Y; Okamura T; Tomoyose T; Kaneda M; Nishio M; Imamura M; Tanaka J; Kobayashi R; Kobayashi N; Suzuki N; Ishida T; Matsunaga T; Yoshida M; Sato K; Kohda K; Masauji N; Fukuhara T; Sasaki S; Ogura K; Endo M; Ishida Y; Sasahara Y; Kameoka J; Okuda M; Meguro K; Imaizumi M; Watanabe A; Fujishima N; Mitsui T; Tajima K; Kikuta A; Ogawa K; Kimura H; Koike K; Komatsu T; Hasegawa Y; Kamoshita M; Muroi K; Sugita K; Sasaki K; Kanazawa T; Saito T; Sakura T; Kikuchi A; Kimura F; Shibuya A; Kawai N; Maseki N; Hirabayashi K; Watabe R; Ohshima K; Nakaseko C; Ishiwada N; Okimoto Y; Aotsuka N; Tanaka H; Yokota A; Takeuchi M; Katayama T; Ishii A; Takita J; Okamoto S; Shimada H; Mori S; Chin M; Hatta Y; Yano S; Kajiwara M; Fukuda T; Takahashi S; Kaku H; Akiyama H; Kumagai M; Yoshinaga K; Ueno H; Ohara A; Tajika K; Tashiro H; Waki A; Hagiwara S; Kozai Y; Suzuki K; Kikuchi T; Yanagisawa K; Kaneko T; Kimura Y; Hamano Y; Manabe A; Usuki K; Takayama N; Miyakoshi S; Yabe H; Onizuka M; Goto H; Fujita H; Sakai R; Kigasawa H; Kanamori H; Isoyama K; Sano F; Inoue Y; Sugita K; Iino M; Yanagisawa R; Ito T; Ishii E; Kobayashi H; Asami K; cho T; Koike T; Furukawa T; Yoshida T; Kanegane H; Nishimura R; Takami A; Fukushima T; Ymaguchi M; Tanizawa A; Kasahara S; Takao A; Yago K; Takashima Y; Shigeno K; Okada S; Naito K; Taguchi J; Yagyu T; Ikeda T; Kato K; Miyamura K; Kasai M; Hamaguchi M; Murata M; Kojima S; Morishita Y; Sao H; Emi N; Morishima Y; Kusumoto S; Sawa M; Mihara H; Oka K; Tamaki S; Azuma E; Nakase K; Kawakami K; Taga T; Kito K; Kuroda H; Ito M; Nakagawa H; Adachi S; Ichinohe T; Taniwaki M; Doi S; Hiraoka A; Ohta H; Maeda T; Inoue M; Kishimoto Y; Hara J; Teshima H; Ashida T; Sakata N; Ishida H; Uoshima N; Kazumi Y; Yamane T; Hatanaka K; Yonetani N; Ishii K; Tsudo M; Tanaka H; Yamagami T; Arima N; Anzai N; Aoyama Y; Otsuka Y; Okada M; Murayama T; Hayakawa A; Okamura A; Matsushita A; Kosaka Y; Nagai K; Nakamura F; Higuchi B; Amano I; Sawada H; Yagi H; Sonoki T; Nougawa M; Nakahashi T; Ago H; Ueyama J; Okazaki T; Sayama K; Maeda Y; Ueda Y; Imajo K; Sunami K; Wada H; Hamamoto K; Iwato K; Kobayashi M; Hyodo H; Niimi H; Yujiri T; Abe M; Goto T; Ohnishi H; Imai T; Hara M; Muta T; Narumi H; Kaneko M; Togitani K; Matsuzaki A; Nagafuji K; Abe Y; Nagatoshi Y; Uike N; Imamura Y; Eto T; Morimoto H; Miyaji R; Imada K; Okamura S; Yakushiji K; Kamimura T; Takamatsu Y; Ohno Y; Sueoka E; Miyazaki Y; Moriuchi Y; Hidaka M; Morinaga S; Hashiyama M; Ogata M; Otsuka E; Takatsuka Y; Okamoto Y; Matsushita K; Okamura T; Tomoyose T
  •  go-up   go-down


67. Lugthart S, van Drunen E, van Norden Y, van Hoven A, Erpelinck CA, Valk PJ, Beverloo HB, Löwenberg B, Delwel R: High EVI1 levels predict adverse outcome in acute myeloid leukemia: prevalence of EVI1 overexpression and chromosome 3q26 abnormalities underestimated. Blood; 2008 Apr 15;111(8):4329-37
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High EVI1 levels predict adverse outcome in acute myeloid leukemia: prevalence of EVI1 overexpression and chromosome 3q26 abnormalities underestimated.
  • Inappropriate expression of EVI1 (ecotropic virus integration-1), in particular splice form EVI1-1D, through chromosome 3q26 lesions or other mechanisms has been implicated in the development of high-risk acute myeloid leukemia (AML).
  • To validate the clinical relevance of EVI1-1D, as well as of the other EVI1 splice forms and the related MDS1/EVI1 (ME) gene, real-time quantitative polymerase chain reaction was performed in 534 untreated adults with de novo AML.
  • EVI1(+)ME(-) expression predicts an extremely poor prognosis distinguishable from the general EVI1(+) AML patients (overall survival [OS]: P < .001 and event-free survival [EFS]: P = .002).
  • We argue that EVI1/ME quantitative expression analysis should be implemented in the molecular diagnostic procedures of AML.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 3 / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / pathology. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adult. Aged. Alternative Splicing / genetics. Cohort Studies. Cytogenetic Analysis. Female. Gene Expression Regulation, Leukemic. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Multivariate Analysis. Prognosis. Protein Isoforms / genetics. Protein Isoforms / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reproducibility of Results. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18272813.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Transcription Factors
  •  go-up   go-down


68. Schliemann C, Bieker R, Thoennissen N, Gerss J, Liersch R, Kessler T, Büchner T, Berdel WE, Mesters RM: Circulating angiopoietin-2 is a strong prognostic factor in acute myeloid leukemia. Leukemia; 2007 Sep;21(9):1901-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Circulating angiopoietin-2 is a strong prognostic factor in acute myeloid leukemia.
  • We investigated the impact of circulating angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2) and soluble Tie2 (sTie2) on overall survival in patients with acute myeloid leukemia (AML).
  • Ang-1, Ang-2 and sTie2 were measured in plasma samples from 68 AML patients and 11 controls using enzyme-linked immunosorbent assay.
  • Circulating levels of Ang-2 and sTie2 (median (range): 1098.0 (361.4-4147.6) pg/ml and 3.40 (1.21-10.00) ng/ml, respectively) were significantly elevated in AML patients as compared to controls (307.9 (199.7-1225.0) pg/ml and 2.88 (1.71-3.29) ng/ml; P<0.001 and P=0.014).
  • The 3-year survival rate for AML patients with Ang-2 levels>/=1495.6 pg/ml was only 14.7% compared to 64.7% for those with Ang-2 levels<1495.6 pg/ml.
  • These data provide evidence that circulating Ang-2 represents an independent prognostic factor in AML and may be used as a prognostic tool in the risk-adapted management of AML.
  • [MeSH-major] Angiopoietin-2 / blood. Biomarkers, Tumor / blood. Leukemia, Myeloid / blood. Leukemia, Myeloid / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Angiopoietin-1 / blood. Female. Humans. Male. Middle Aged. Prognosis. Proportional Hazards Models. Receptor, TIE-2 / blood. Risk Factors. Solubility

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17597808.001).
  • [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 / ANGPT1 protein, human; 0 / Angiopoietin-1; 0 / Angiopoietin-2; 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor, TIE-2
  •  go-up   go-down


69. Alyea EP, Kim HT, Ho V, Cutler C, DeAngelo DJ, Stone R, Ritz J, Antin JH, Soiffer RJ: Impact of conditioning regimen intensity on outcome of allogeneic hematopoietic cell transplantation for advanced acute myelogenous leukemia and myelodysplastic syndrome. Biol Blood Marrow Transplant; 2006 Oct;12(10):1047-55
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of conditioning regimen intensity on outcome of allogeneic hematopoietic cell transplantation for advanced acute myelogenous leukemia and myelodysplastic syndrome.
  • We reviewed 136 patients with advanced acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS) undergoing allogeneic transplantation to assess the impact of conditioning regimen intensity on outcome.
  • Despite the high-risk features of patients with advanced AML or MDS undergoing NST, OS and PFS in these patients was similar to those in patients receiving myeloablative transplantation.
  • These results suggest that NST is a reasonable alternative for patients with advanced AML and MDS at high risk for complications after myeloablative transplantation.
  • [MeSH-major] Bone Marrow Transplantation. Busulfan / administration & dosage. Cyclophosphamide / administration & dosage. Leukemia, Myeloid / surgery. Myelodysplastic Syndromes / surgery. Peripheral Blood Stem Cell Transplantation. Transplantation Conditioning. Vidarabine / analogs & derivatives. Whole-Body Irradiation
  • [MeSH-minor] Acute Disease. Adult. Aged. Female. Graft Survival. Graft vs Host Disease / epidemiology. Graft vs Host Disease / etiology. Humans. Incidence. Kaplan-Meier Estimate. Male. Middle Aged. Recurrence. Reoperation. Retrospective Studies. Tissue Donors. Transplantation, Homologous / mortality. Treatment Outcome


70. Gurkan E, Patah PA, Saliba RM, Ramos CA, Anderson BS, Champlin R, de Lima M, Lichtiger B: Efficacy of prophylactic transfusions using single donor apheresis platelets versus pooled platelet concentrates in AML/MDS patients receiving allogeneic hematopoietic stem cell transplantation. Bone Marrow Transplant; 2007 Sep;40(5):461-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy of prophylactic transfusions using single donor apheresis platelets versus pooled platelet concentrates in AML/MDS patients receiving allogeneic hematopoietic stem cell transplantation.
  • We studied all transfusions administered to 33 patients with AML/MDS during the first 100 days after busulfan-based, myeloablative HSCT.
  • There were two non-lethal hemorrhage episodes (6%).
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Platelet Transfusion / methods
  • [MeSH-minor] Acute Disease. Adult. Aged. Blood Platelets / cytology. Female. Hemorrhage / prevention & control. Humans. Male. Middle Aged. Platelet Count. Retrospective Studies. Transplantation, Homologous


71. Jóhannsdóttir IM, Hjermstad MJ, Moum T, Wesenberg F, Hjorth L, Schrøder H, Lähteenmäki P, Jónmundsson G, Loge JH: Social outcomes in young adult survivors of low incidence childhood cancers. J Cancer Surviv; 2010 Jun;4(2):110-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Social outcomes in young adult survivors of low incidence childhood cancers.
  • The study objective was to assess social outcomes in early adulthood after successful treatment for childhood acute myeloid leukemia (AML), Wilms tumor (WT) and infratentorial astrocytoma (IA).
  • METHODS: Nordic patients treated for AML, WT and IA from 1985 to 2001 identified from a database administered by NOPHO (Nordic Society of Paediatric Haematology and Oncology) were invited to participate in a postal survey.
  • CONCLUSIONS AND IMPLICATIONS FOR CANCER SURVIVORS: The study revealed important differences in social outcomes between survivors and controls early in adult life.
  • [MeSH-major] Astrocytoma / psychology. Infratentorial Neoplasms / psychology. Leukemia, Myeloid, Acute / psychology. Social Behavior. Survivors / psychology. Wilms Tumor / psychology
  • [MeSH-minor] Adolescent. Adult. Child, Preschool. Female. Follow-Up Studies. Humans. Incidence. Infant. Kidney Neoplasms / mortality. Kidney Neoplasms / psychology. Male. Prognosis. Survival Rate. Young Adult

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Wilms Tumor.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Med Pediatr Oncol. 1999 Jul;33(1):60-3 [10401499.001]
  • [Cites] Pediatr Blood Cancer. 2008 Jan;50(1):104-10 [17554791.001]
  • [Cites] Curr Probl Cancer. 2003 May-Jun;27(3):112-26 [12748581.001]
  • [Cites] Psychooncology. 2003 Apr-May;12(3):213-25 [12673806.001]
  • [Cites] JAMA. 2003 Sep 24;290(12):1583-92 [14506117.001]
  • [Cites] Int J Cancer Suppl. 1999;12:25-31 [10679867.001]
  • [Cites] Pediatr Blood Cancer. 2009 Sep;53(3):417-23 [19479971.001]
  • [Cites] Cancer. 2005 Oct 15;104(8):1751-60 [16130127.001]
  • [Cites] J Pediatr Hematol Oncol. 2008 Nov;30(11):807-14 [18989157.001]
  • [Cites] Med Pediatr Oncol. 1999 Jul;33(1):29-33 [10401494.001]
  • [Cites] Curr Probl Cancer. 2003 Jul-Aug;27(4):177-97 [12855950.001]
  • [Cites] Psychosomatics. 1997 Jan-Feb;38(1):54-62 [8997117.001]
  • [Cites] J Clin Oncol. 2000 Dec 15;18(24):4060-6 [11118467.001]
  • [Cites] J Cancer Surviv. 2008 Sep;2(3):205-14 [18663582.001]
  • [Cites] J Clin Oncol. 2007 Aug 10;25(23):3518-24 [17687156.001]
  • [Cites] J Cancer Surviv. 2008 Sep;2(3):149-58 [18792789.001]
  • [Cites] J Clin Oncol. 2009 May 10;27(14):2374-81 [19364956.001]
  • [Cites] Pediatr Hematol Oncol. 1997 Nov-Dec;14(6):513-24 [9383804.001]
  • [Cites] Pediatr Hematol Oncol. 1999 Jan-Feb;16(1):9-21 [9932269.001]
  • [Cites] Med Pediatr Oncol. 1991;19(6):459-66 [1961132.001]
  • [Cites] N Engl J Med. 2006 Oct 12;355(15):1572-82 [17035650.001]
  • [Cites] Acta Paediatr Scand. 1989 Sep;78(5):728-35 [2596279.001]
  • [Cites] J Clin Oncol. 2009 May 10;27(14):2390-5 [19224833.001]
  • [Cites] Pediatrics. 2007 Mar;119(3):554-68 [17332209.001]
  • [Cites] Br J Cancer. 2004 Aug 31;91(5):923-8 [15292930.001]
  • [Cites] Hum Reprod. 2008 Jan;23(1):178-86 [18024486.001]
  • [Cites] Lancet. 2000 Apr 15;355(9212):1310-4 [10776743.001]
  • [Cites] Lancet Oncol. 2008 Jun;9(6):569-76 [18510988.001]
  • [Cites] Pediatr Hematol Oncol. 1997 May-Jun;14(3):223-32 [9185207.001]
  • [Cites] Cancer. 1993 May 15;71(10 Suppl):3392-9 [8490888.001]
  • [Cites] Pediatr Blood Cancer. 2007 Oct 15;49(5):704-15 [16830322.001]
  • [Cites] Cancer. 2006 Jul 1;107(1):1-11 [16718655.001]
  • [Cites] Psychooncology. 2007 Oct;16(10):920-7 [17279494.001]
  • [Cites] Cancer. 1986 Jul 15;58(2 Suppl):529-33 [3719547.001]
  • [Cites] J Dev Behav Pediatr. 2007 Dec;28(6):448-55 [18091089.001]
  • [Cites] Ann Oncol. 2003;14 Suppl 5:v119-27 [14684502.001]
  • [Cites] Eur J Cancer. 1996 Jul;32A(8):1354-8 [8869099.001]
  • [Cites] J Neurosurg. 2002 Feb;96(2):229-34 [11838795.001]
  • [Cites] J Pediatr Hematol Oncol. 2004 Jun;26(6):354-62 [15167348.001]
  • [Cites] Pediatr Hematol Oncol. 1998 Nov-Dec;15(6):479-88 [9842641.001]
  • [Cites] Pediatr Clin North Am. 2008 Feb;55(1):251-73, xiii [18242324.001]
  • [Cites] Support Care Cancer. 2002 Nov;10(8):579-600 [12436217.001]
  • [Cites] Pediatr Blood Cancer. 2006 Jul;47(1):61-70 [16572415.001]
  • [Cites] Psychooncology. 2002 Mar-Apr;11(2):132-41 [11921329.001]
  • [Cites] CA Cancer J Clin. 2004 Jul-Aug;54(4):208-36 [15253918.001]
  • [Cites] Cancer. 2008 May 1;112(9):2071-9 [18327823.001]
  • [Cites] Pediatr Neurosurg. 2005 Jan-Feb;41(1):15-21 [15886508.001]
  • [Cites] Eur J Cancer. 2001 Aug;37(12):1523-7, discussion 1527-30 [11506960.001]
  • (PMID = 20082150.001).
  • [ISSN] 1932-2267
  • [Journal-full-title] Journal of cancer survivorship : research and practice
  • [ISO-abbreviation] J Cancer Surviv
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


72. Borthakur G, Lin E, Jain N, Estey EE, Cortes JE, O'Brien S, Faderl S, Ravandi F, Pierce S, Kantarjian H: Survival is poorer in patients with secondary core-binding factor acute myelogenous leukemia compared with de novo core-binding factor leukemia. Cancer; 2009 Jul 15;115(14):3217-21
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survival is poorer in patients with secondary core-binding factor acute myelogenous leukemia compared with de novo core-binding factor leukemia.
  • BACKGROUND: Therapy related secondary acute myelogenous leukemia (AML) was commonly associated with prior exposure to alkylating agents or topoisomerase inhibitor.
  • The long-term outcome of such patients with secondary AML was found to be worse than that of patients with de novo AML.
  • Earlier reports suggested similar outcomes for patients with de novo and secondary AML associated with core-binding factor (CBF) abnormalities.
  • METHODS: A total of 188 patients with CBF AML were analyzed.
  • The frequency of secondary CBF AML was 9%.
  • RESULTS: Patients with secondary CBF AML were found to have significantly worse overall (OS) and event-free survival (EFS) compared with patients with de novo CBF AML.
  • Secondary CBF AML status appeared to have only marginal significance in multivariate analysis.
  • CONCLUSIONS: Matched analysis (by age, Eastern Cooperative Oncology Group performance status, and additional cytogenetic abnormality) indicated worse OS and EFS in patients with secondary CBF AML.
  • [MeSH-major] Core Binding Factors / metabolism. Leukemia, Myeloid, Acute / mortality. Neoplasms, Second Primary / mortality
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cytarabine / therapeutic use. Disease-Free Survival. Female. Humans. Male. Middle Aged. Survival Analysis. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 1999 Nov;13(11):1735-40 [10557046.001]
  • [Cites] Leuk Lymphoma. 2008 Mar;49(3):517-23 [18297529.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Apr;33(4):395-400 [11921273.001]
  • [Cites] Br J Haematol. 2002 Aug;118(2):385-400 [12139722.001]
  • [Cites] Eur J Haematol. 2003 Sep;71(3):143-54 [12930314.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4413-22 [14645432.001]
  • [Cites] J Clin Oncol. 2004 Mar 15;22(6):1087-94 [15020610.001]
  • [Cites] J Clin Oncol. 2004 Sep 15;22(18):3741-50 [15289486.001]
  • [Cites] Blood. 1992 Oct 1;80(7):1825-31 [1391946.001]
  • [Cites] Science. 1993 Aug 20;261(5124):1041-4 [8351518.001]
  • [Cites] J Clin Oncol. 1993 Dec;11(12):2370-9 [8246025.001]
  • [Cites] J Clin Oncol. 1998 May;16(5):1890-6 [9586906.001]
  • [Cites] Cancer Res. 1998 Sep 15;58(18):4173-9 [9751631.001]
  • [Cites] Biochim Biophys Acta. 1998 Oct 1;1400(1-3):233-55 [9748598.001]
  • [Cites] Br J Haematol. 2006 Oct;135(2):165-73 [16939487.001]
  • [Cites] Leukemia. 2007 Apr;21(4):725-31 [17287858.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Apr;33(4):379-94 [11921272.001]
  • (PMID = 19441109.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factors; 04079A1RDZ / Cytarabine
  • [Other-IDs] NLM/ NIHMS629439; NLM/ PMC4184418
  •  go-up   go-down


73. Crapanzano JP: Fine-needle aspiration of renal angiomyolipoma: cytological findings and diagnostic pitfalls in a series of five cases. Diagn Cytopathol; 2005 Jan;32(1):53-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Diagnosis of renal angiomyolipoma (AML) by fine-needle aspiration (FNA) may be difficult because cytological and radiological findings sometimes overlap with renal cell carcinoma (RCC) and liposarcoma.
  • Corresponding surgical material showed typical features of AML.
  • In FNA, bland chromatin and inconspicuous nucleoli distinguish renal AML from RCC and liposarcoma.
  • [MeSH-minor] Adenoma, Oxyphilic / diagnosis. Adult. Aged. Carcinoma, Renal Cell / diagnosis. Diagnosis, Differential. Epithelioid Cells / pathology. Female. Humans. Liposarcoma / diagnosis. Male. Middle Aged. Retroperitoneal Neoplasms / diagnosis. Stromal Cells / pathology

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15584043.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


74. Riccioni R, Pasquini L, Mariani G, Saulle E, Rossini A, Diverio D, Pelosi E, Vitale A, Chierichini A, Cedrone M, Foà R, Lo Coco F, Peschle C, Testa U: TRAIL decoy receptors mediate resistance of acute myeloid leukemia cells to TRAIL. Haematologica; 2005 May;90(5):612-24
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TRAIL decoy receptors mediate resistance of acute myeloid leukemia cells to TRAIL.
  • The present study was designed to evaluate the sensitivity to TRAIL-induced apoptosis in acute myeloblastic leukemias (AML).
  • DESIGN AND METHODS: TRAIL/TRAIL receptor (TRAIL-R) expression and sensitivity to TRAIL-mediated apoptosis were explored in 79 AML patients, including 17 patients with acute promyelocytic leukemia (APL).
  • RESULTS: In non-APL AML we observed frequent expression of TRAIL decoy receptors (TRAIL-R3 and TRAIL-R4), while TRAIL-R1 and TRAIL-R2 expression was restricted to AML exhibiting monocytic features.
  • Total leukemic blasts, as well as AML colony-forming units (AML-CFU), were invariably resistant to TRAIL-mediated apoptosis.
  • APL express membrane-bound TRAIL on their surface and exhibit a pattern of TRAIL-R expression similar to that observed in the other types of AML.
  • The induction of granulocytic maturation of APL cells by retinoic acid was associated with a marked decline of TRAIL expression.
  • We suggest that AML blasts, including APL blasts, are resistant to TRAIL-mediated apoptosis, a phenomenon seemingly related to the expression of TRAIL decoy receptors on these cells.
  • [MeSH-major] Apoptosis / drug effects. Drug Resistance, Neoplasm / genetics. Leukemia, Myeloid / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand / physiology. Receptors, Tumor Necrosis Factor / physiology. Tumor Necrosis Factor Decoy Receptors / physiology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antineoplastic Agents / pharmacology. Caspase 3 / analysis. Caspase 8 / analysis. Cell Differentiation / drug effects. Cell Membrane / metabolism. Cytarabine / pharmacology. Etoposide / pharmacology. Female. GPI-Linked Proteins. Granulocytes / drug effects. HL-60 Cells / pathology. Humans. Hydroxyurea / pharmacology. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Male. Middle Aged. Monocytes / drug effects. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / physiology. Recombinant Fusion Proteins / pharmacology. Recombinant Fusion Proteins / physiology. Tretinoin / pharmacology. Tumor Cells, Cultured / drug effects. Tumor Stem Cell Assay. U937 Cells / drug effects

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Hazardous Substances Data Bank. HYDROXYUREA .
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15921376.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / GPI-Linked Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Fusion Proteins; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / TNFRSF10C protein, human; 0 / TNFRSF10D protein, human; 0 / Tumor Necrosis Factor Decoy Receptors; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; 6PLQ3CP4P3 / Etoposide; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; X6Q56QN5QC / Hydroxyurea
  •  go-up   go-down


75. Yang DH, Lee JJ, Mun YC, Shin HJ, Kim YK, Cho SH, Chung IJ, Seong CM, Kim HJ: Predictable prognostic factor of CD56 expression in patients with acute myeloid leukemia with t(8:21) after high dose cytarabine or allogeneic hematopoietic stem cell transplantation. Am J Hematol; 2007 Jan;82(1):1-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Predictable prognostic factor of CD56 expression in patients with acute myeloid leukemia with t(8:21) after high dose cytarabine or allogeneic hematopoietic stem cell transplantation.
  • CD56 expression in acute myeloid leukemia (AML) has been associated with extramedullary leukemia and multidrug resistance, but its clinical and prognostic significance has not been clearly identified.
  • This study examined CD56 expression in 37 adult de novo AML patients with t(8:21).
  • We concluded that CD56 expression correlates to a reduced DFS and survival for AML patients with t(8:21), including those patients who underwent transplantation.
  • [MeSH-major] Antigens, CD56 / biosynthesis. Antimetabolites, Antineoplastic / administration & dosage. Biomarkers, Tumor / biosynthesis. Cytarabine / administration & dosage. Gene Expression Regulation, Leukemic. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Adult. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Disease-Free Survival. Female. Humans. Male. Middle Aged. Predictive Value of Tests. Recurrence. Remission Induction. Retrospective Studies. Survival Rate. Translocation, Genetic. Transplantation, Homologous

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. CYTARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16986129.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Antimetabolites, Antineoplastic; 0 / Biomarkers, Tumor; 04079A1RDZ / Cytarabine
  •  go-up   go-down


76. Hämäläinen S, Kuittinen T, Matinlauri I, Nousiainen T, Koivula I, Jantunen E: Neutropenic fever and severe sepsis in adult acute myeloid leukemia (AML) patients receiving intensive chemotherapy: Causes and consequences. Leuk Lymphoma; 2008 Mar;49(3):495-501
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neutropenic fever and severe sepsis in adult acute myeloid leukemia (AML) patients receiving intensive chemotherapy: Causes and consequences.
  • The objective of this study was to evaluate etiology and consequences of neutropenic fever in AML patients.
  • Two hundred and ninety neutropenic periods following chemotherapy in 84 AML patients were retrospectively evaluated.
  • Severe sepsis is associated with significant mortality in AML patients.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Neutropenia / etiology. Sepsis / microbiology
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. C-Reactive Protein / analysis. Female. Fever / etiology. Gram-Negative Bacteria / isolation & purification. Humans. Male. Middle Aged. Retrospective Studies


77. Li XL, Li R, Chen Y: [Clinical characteristics and immunophenotypes of mixed-lineage acute leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Jun;15(3):636-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical characteristics and immunophenotypes of mixed-lineage acute leukemia].
  • The aim of study was to analyze the clinical, biological features, treatment outcome and prognosis of mixed-lineage acute leukemia (MAL).
  • 48 MAL patients diagnosed according to European Group of International Leukemia (EGIL) scoring system were retrospectively analyzed and the analysis results were compared with that from 68 cases of AML and 61 cases of ALL.
  • The results showed that the incidence of MAL in acute leukemia was 9.6%.
  • Morphologically, the subtypes of M(1) and M(2) were predominant in AML, while L(2) in ALL.
  • The median of white blood cell count in MAL was significantly higher than that of non-mixed-lineage cases (AML and ALL) observed during the same period (P < 0.05).
  • The incidences of enlargement of liver, spleen and lymphonodes in MAL were higher than those in AML.
  • Coexpression of myeloid and B lymphoid antigens in MAL patients was predominant, its rate was 70.9%.
  • The coexpression rate of T lymphoid and myeloid antigens was 20.8%, coexpression of B, T lymphoid and myeloid antigens was 8.3%.
  • CD34 was expressed in 79.2% of MAL cases, it was higher than those expressed in AML (54.4%) and ALL (52.5%) (P < 0.01), which suggests that MAL might originate from malignant transformation of hematopoietic stem cells.
  • In MAL Ph chromosome abnormality incidence was 25% and was significantly higher than that in AML group (0%) (P < 0.01), but was not statistical defference with that in ALL group (16.7%) (P > 0.05).
  • The completed remission rate of MAL was 38.1%, lower than CR rate in AML (70.8%) and ALL (72.2%) respectively (P < 0.01).
  • It is concluded that MAL is supposed to be originated from stem cells, coexpression of lymphoid/myeloid antigens is the major feature of MAL which accompanies many poor prognosis factors and lower CR rate.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17605883.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD34
  •  go-up   go-down


78. Mu QT, Chen ZM, Lou JY, Cheng YZ, Wang YG, Ni WM, Wang HP, Xu H, Yu YB, Jin J: [Cytogenetic analysis of 154 case of acute myeloid leukemia with t(8;21)]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2010 May;39(3):236-40
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Cytogenetic analysis of 154 case of acute myeloid leukemia with t(8;21)].
  • OBJECTIVE: To investigate the cytogenetic features of acute myeloid leukemia (AML) with t(8;21).
  • METHODS: The clinical characteristics of 154 cases of acute myeloid leukemia with t(8;21) in our hospital were analyzed retrospectively.
  • Cytogenetically, 85 (55.2%) AML patients with t(8;21) had additional chromosome abnormalities.
  • In the group of t(8;21) with additional chromosome abnormalities, 11 cases (35.5%) were non-M2 AML, higher than that in single t(8;21) group (17.4%)(P<0.05); however, there was no significant difference between the group of single t(8;21) and the group of t(8;21) with single sex chromosome loss(P>0.05).
  • CONCLUSION: t(8;21) translocation is usually accompanied by additional chromosome abnormalities, particularly in M2; while t(8;21) with additional chromosome abnormalities other than sex chromosome loss is more frequently observed in non-M2 AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Chromosome Aberrations. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Cytogenetic Analysis. Female. Humans. Male. Middle Aged. Prognosis. Retrospective Studies. Translocation, Genetic. Young Adult

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20544983.001).
  • [ISSN] 1008-9292
  • [Journal-full-title] Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
  • [ISO-abbreviation] Zhejiang Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  •  go-up   go-down


79. Jelić-Puskarić B, Ostojić-Kolonić S, Planinc-Peraica A, Obad-Kovacević D, Kardum-Skelin I, Jaksić B: Myeloid sarcoma involving the breast. Coll Antropol; 2010 Jun;34(2):641-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myeloid sarcoma involving the breast.
  • Myeloid sarcoma is a tumor mass with extramedullary growth pattern, composed of myeloblasts or immature myeloid cells.
  • The development of myeloid sarcoma may precede or concur with acute or chronic myeloid leukemia (AML or CML) or other myeloproliferative diseases or myelodysplastic syndromes (MDS).
  • Isolated myeloid sarcoma of the breast is very rare.
  • Based on the morphology, cytochemical characteristics and immature cell immunophenotype, it was considered a case of acute myeloid leukemia without maturation.
  • In cases of isolated breast myeloid sarcoma, the diagnosis can be missed if the possibility of myeloid sarcoma is not remembered on differential diagnosis of a breast neoplasm.
  • [MeSH-major] Breast Neoplasms / pathology. Sarcoma, Myeloid / pathology
  • [MeSH-minor] Adult. Anemia / etiology. Anemia / pathology. Biopsy, Fine-Needle. Bone Marrow / pathology. Fatal Outcome. Female. Humans. Leukemia, Myeloid, Acute / pathology. Leukocytosis / etiology. Leukocytosis / pathology. Recurrence. Thrombocytopenia / etiology. Thrombocytopenia / pathology


80. Heuser M, Wingen LU, Steinemann D, Cario G, von Neuhoff N, Tauscher M, Bullinger L, Krauter J, Heil G, Döhner H, Schlegelberger B, Ganser A: Gene-expression profiles and their association with drug resistance in adult acute myeloid leukemia. Haematologica; 2005 Nov;90(11):1484-92
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene-expression profiles and their association with drug resistance in adult acute myeloid leukemia.
  • BACKGROUND AND OBJECTIVES: From 20-50% of patients with acute myeloid leukemia (AML) are primarily resistant to induction chemotherapy.
  • DESIGN AND METHODS: cDNA microarrays containing approximately 41,000 features were used to compare the gene-expression profile of AML blasts between 33 patients with good or poor response to induction chemotherapy.
  • RESULTS: Using significance analysis of microarrays, we identified a characteristic gene-expression profile which distinguished AML samples from patients with good or poor responses.
  • Using the treatment-response signature to predict the outcome in an independent test set of 104 AML patients, samples were separated into two subgroups with significantly inferior response rate (43.5% vs. 66.7%, p=0.04), significantly shorter event-free and overall survival (p=0.01 and p=0.03, respectively) in the poor-response compared to in the good-response signature group.
  • INTERPRETATION AND CONCLUSIONS: Resistance to chemotherapy in AML can be identified by gene-expression profiling before treatment and seems to be mediated by a transcriptional program active in hematopoietic stem/progenitor cells.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Gene Expression Profiling. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / therapeutic use. Female. Genetic Markers / genetics. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Survival Analysis


81. Sakai R, Fujimaki K, Yamazaki E, Sakamoto H, Kanamori H, Miura I, Ishigatsubo Y: Acute myelomonocytic leukemia with dysplastic bone marrow eosinophils showing t(5;17)(q13;q11) and a secondary chromosomal aberration, inv(16)(p13q22). Int J Hematol; 2006 Dec;84(5):417-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myelomonocytic leukemia with dysplastic bone marrow eosinophils showing t(5;17)(q13;q11) and a secondary chromosomal aberration, inv(16)(p13q22).
  • inv(16)(p13q22) is associated with de novo acute myelomonocytic leukemia with dysplastic bone marrow eosinophils (AMML Eo), which has a relatively favorable clinical course with a longer remission duration and better survival prospects.
  • On the other hand, t(5; 17)(q13;q11), although relatively rare, has been reported to be a component of complex chromosomal abnormalities in myelodysplastic syndromes and secondary acute myeloid leukemia (AML).
  • Accordingly, the primary nature of the leukemic cells in this case differs from the findings for core-binding factor AML with inv(16)(p13q22).
  • [MeSH-major] Bone Marrow Cells / pathology. Chromosome Inversion. Chromosomes, Human / genetics. Eosinophils / pathology. Leukemia, Myelomonocytic, Acute. Translocation, Genetic
  • [MeSH-minor] Adult. Bone Marrow Transplantation. Female. Humans. Recurrence. Remission Induction. Transplantation, Homologous

  • Genetic Alliance. consumer health - Acute Myelomonocytic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncogene. 2005 Apr 14;24(16):2625-34 [15782145.001]
  • [Cites] Oncogene. 1990 Oct;5(10):1557-63 [1701231.001]
  • [Cites] Blood. 1993 Dec 1;82(11):3424-9 [8241509.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5705-17 [16110030.001]
  • [Cites] Cancer Genet Cytogenet. 1992 Mar;59(1):35-8 [1555189.001]
  • [Cites] Leuk Res. 2007 Jan;31(1):39-47 [16687173.001]
  • [Cites] Cancer Genet Cytogenet. 1992 Jul 15;61(2):197-200 [1638503.001]
  • [Cites] N Engl J Med. 1983 Sep 15;309(11):630-6 [6577285.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Leukemia. 1992 May;6(5):381-4 [1593903.001]
  • [Cites] Blood. 1998 Feb 1;91(3):1008-15 [9446663.001]
  • [Cites] Blood. 1986 Feb;67(2):270-4 [3455826.001]
  • [Cites] Leukemia. 1994 Jun;8(6):953-62 [8207990.001]
  • [Cites] Leuk Lymphoma. 1998 Sep;31(1-2):231-6 [9720733.001]
  • [Cites] Cancer. 2005 Dec 15;104(12):2726-34 [16284985.001]
  • [Cites] Cancer Genet Cytogenet. 1989 Oct 1;42(1):43-50 [2790745.001]
  • [Cites] Blood. 2000 Mar 15;95(6):2138-43 [10706886.001]
  • (PMID = 17189222.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


82. van den Heuvel-Eibrink MM, van der Holt B, Sonneveld P: Role of BCRP and its expression with MDR1 in adult AML. Leuk Res; 2005 Jan;29(1):115
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of BCRP and its expression with MDR1 in adult AML.
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Drug Resistance, Multiple. Gene Expression. Humans. Leukemia, Myeloid, Acute

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Leuk Res. 2004 Apr;28(4):367-72 [15109536.001]
  • (PMID = 15541485.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Letter; Comment
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Neoplasm Proteins
  •  go-up   go-down


83. Graf M, Reif S, Hecht K, Pelka-Fleischer R, Pfister K, Schmetzer H: High expression of urokinase plasminogen activator receptor (UPA-R) in acute myeloid leukemia (AML) is associated with worse prognosis. Am J Hematol; 2005 May;79(1):26-35
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High expression of urokinase plasminogen activator receptor (UPA-R) in acute myeloid leukemia (AML) is associated with worse prognosis.
  • We studied the expression of the UPA-R on bone marrow (BM) cells of 93 patients with acute myeloid leukemia at first diagnosis and 8 healthy probands as controls by FACS analysis using phycoerythrin (PE)-conjugated antibodies.
  • Whereas none of the 8 healthy BM samples was positive for the UPA-R, 32 (34%) of the 93 AML samples were UPA-R+.
  • Proportions of UPA-R+ cells varied between 1% and 98% of the mononuclear cell fractions, with the highest proportions in M4/M5 subtypes (on average 27%/40% UPA-R+ cells) and the lowest expression in AML M2 (11% UPA-R+ cells).
  • The density of expressed UPA-R, estimated as mean channel fluorescence activity, was highest in cases with AML M1 (mFI: 124) followed by M4 and M5 (mFI: 78/77) and lowest in AML M2 (mFI: 43).
  • For evaluations of the clinical course of AML, only patients treated by the AML-CG protocol (n = 65) were included.
  • In the group of patients who did not respond to AML-CG therapy, significantly higher proportions of UPA-R+ cells (31% vs. 14%, P = 0.0015, t-test) were found.
  • In summary, our data show a high expression of the UPA-R in AML, especially in (myelo)monocytoid subtypes.
  • Cases with higher proportions of UPA-R+ cells were characterized by a significant lower remission rate after AML-CG therapy and a higher risk for relapse.
  • UPA-R positivity may identify subtypes of AML associated with a more aggressive clinical course.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / immunology. Receptors, Cell Surface / genetics
  • [MeSH-minor] Adult. Aged. Antigens, CD / genetics. Bone Marrow Cells / immunology. Female. Flow Cytometry. Genetic Markers. Humans. Male. Middle Aged. Neoplasm Invasiveness. Prognosis. Receptors, Urokinase Plasminogen Activator

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2005 Wiley-Liss, Inc.
  • (PMID = 15849776.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Genetic Markers; 0 / PLAUR protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Urokinase Plasminogen Activator
  •  go-up   go-down


84. Bang SM, Ahn JY, Park J, Park SH, Park J, Cho EK, Shin DB, Lee JH, Yoo SJ, Jeon IS, Kim YK, Kim HJ, Kim HN, Lee IK, Kang HJ, Shin HY, Ahn HS: Low frequency and variability of FLT3 mutations in Korean patients with acute myeloid leukemia. J Korean Med Sci; 2008 Oct;23(5):833-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low frequency and variability of FLT3 mutations in Korean patients with acute myeloid leukemia.
  • FLT3 mutations are common genetic changes, and are reported to have prognostic significance in acute myeloid leukemia (AML).
  • The FLT3 internal tandem duplication (ITD) and the D835 activating mutation in the tyrosine kinase domain (TKD) were analyzed by polymerase chain reaction (PCR) in the genomic DNA of Korean patients with AML at diagnosis and during follow-up.
  • There were 226 patients with AML enrolled between March 1996 and August 2005.
  • When compared to Western and other Asian patients with AML, Korean patients had a lower frequency by about two-thirds of ITD and TKD.
  • Among the non-M3 cases (N=203), the patients with an ITD had a significantly shorter event-free survival when compared with those without an ITD (p=0.0079).
  • Therefore, effective therapy with FLT3 targeting agents may improve the prognosis of non-M3 AML patients with the FLT3 mutation.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Leukemia, Myeloid, Acute / genetics. Mutation. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Infant, Newborn. Korea. Male. Middle Aged. Prognosis. Recurrence. Remission Induction

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Curr Opin Hematol. 2005 Jan;12(1):7-13 [15604885.001]
  • [Cites] Blood. 1999 May 1;93(9):3074-80 [10216104.001]
  • [Cites] Br J Haematol. 2005 Jul;130(2):196-202 [16029447.001]
  • [Cites] Leuk Res. 2005 Dec;29(12):1393-8 [15996732.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3768-76 [16105978.001]
  • [Cites] Leuk Lymphoma. 2006 Sep;47(9):1788-93 [17064989.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4075-83 [11110676.001]
  • [Cites] Blood. 2001 Apr 15;97(8):2434-9 [11290608.001]
  • [Cites] Br J Haematol. 2001 Jun;113(4):983-8 [11442493.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Blood. 2002 Jul 1;100(1):59-66 [12070009.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1699-704 [12200684.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2387-92 [12239146.001]
  • [Cites] Blood. 2002 Nov 1;100(9):3423-5 [12384447.001]
  • [Cites] Leuk Lymphoma. 2002 Aug;43(8):1541-7 [12400596.001]
  • [Cites] Leuk Lymphoma. 2002 Oct;43(10):2027-9 [12481903.001]
  • [Cites] Hematol J. 2002;3(6):283-9 [12522450.001]
  • [Cites] Haematologica. 2003 Jan;88(1):19-24 [12551822.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):650-65 [12951584.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2387-94 [12816873.001]
  • [Cites] Leuk Res. 2004 Oct;28(10):1069-74 [15289019.001]
  • [Cites] Leukemia. 1996 Dec;10(12):1911-8 [8946930.001]
  • [Cites] Leukemia. 1997 Oct;11(10):1605-9 [9324277.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Br J Haematol. 1999 Mar;104(4):659-64 [10192423.001]
  • [Cites] Leuk Res. 2005 Jun;29(6):617-23 [15863200.001]
  • (PMID = 18955790.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC2580007
  •  go-up   go-down


85. Ahmad F, Dalvi R, Das BR, Mandava S: Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population. Cancer Detect Prev; 2008;32(2):168-77
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population.
  • BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous disease with regard to morphology, immunophenotype, and genetic rearrangements.
  • Multiple recurrent chromosomal aberrations have been identified by conventional cytogenetic analysis, which is now widely recognized as one of the most important diagnostic and prognostic determinants in AML.
  • METHOD: Conventional cytogenetic analysis was done on 200 de novo AML subjects.
  • Furthermore, ongoing cytogenetic studies are warranted in larger groups of AML cases to identify newly acquired chromosomal aberrations that may aid in cloning novel genes involved in the neoplastic process, ultimately helping in the development of targeted therapeutic drugs.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Aged, 80 and over. Child. Child, Preschool. Cytogenetic Analysis. Female. Humans. India. Infant. Karyotyping. Male. Middle Aged

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18639991.001).
  • [ISSN] 1525-1500
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


86. Chen XH, Tong Y, Xu WL, Jin J, Qian WB: [Expression of telomere binding factor 2 (TRF2) on leukemia cell lines and primary leukemia cells]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2008 Mar;37(2):170-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of telomere binding factor 2 (TRF2) on leukemia cell lines and primary leukemia cells].
  • OBJECTIVE: To detect the expression levels of telomere binding factor 2 (TRF2) on leukemia cell lines and primary leukemia cells.
  • METHODS: The expression of TRF2 mRNA was detected with quantitative real-time RT-PCR in leukemia cell lines and primary leukemia cells.
  • RESULT: TRF2 was overexpressed in T-cell leukemia cell lines but not in myelogenous leukemia cell lines.
  • Significant higher expression levels of TRF2 were observed in primary leukemia cells from patients with M0 and M1 subtypes of acute myelogenous leukemia (AML) compared with normal control and other subtypes of AML.
  • CONCLUSION: Increased TRF2 expression levels are found in T-cell leukemia cell lines and AML patients with poor prognosis, which suggests that TRF2 expression might be related to the prognosis of leukemia.
  • [MeSH-major] Leukemia, T-Cell / metabolism. Telomeric Repeat Binding Protein 2 / metabolism
  • [MeSH-minor] Adolescent. Adult. Female. HL-60 Cells. Humans. Jurkat Cells. K562 Cells. Leukemia, Myeloid, Acute / metabolism. Male. Middle Aged. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18422278.001).
  • [ISSN] 1008-9292
  • [Journal-full-title] Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
  • [ISO-abbreviation] Zhejiang Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / TERF2 protein, human; 0 / Telomeric Repeat Binding Protein 2
  •  go-up   go-down


87. Huisman C, Meijer E, Petersen EJ, Lokhorst HM, Verdonck LF: Hematopoietic stem cell transplantation after reduced intensity conditioning in acute myelogenous leukemia patients older than 40 years. Biol Blood Marrow Transplant; 2008 Feb;14(2):181-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hematopoietic stem cell transplantation after reduced intensity conditioning in acute myelogenous leukemia patients older than 40 years.
  • We analyzed the outcome of RIC HSCT in acute myelogenous leukemia (AML) patients over the age of 40 years.
  • Forty-three AML or high-risk myelodysplastic syndrome (MDS) patients were treated with a fludarabine and low-dose total-body irradiation (TBI)-based pretransplantation regimen.
  • All but 2 AML patients were in complete remission (CR) at the time of transplantation.
  • Sixty percent of patients developed acute graft-versus-host disease (aGVHD), which was grade II in 40% and grade III in 12%.
  • In conclusion, fludarabine plus low-dose TBI-based RIC HSCT is effective in AML patients over the age of 40 years without active disease at the time of transplant and is associated with low TRM.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Adult. Age Factors. Aged. Female. Graft Survival. Graft vs Host Disease. Humans. Male. Middle Aged. Myelodysplastic Syndromes. Opportunistic Infections. Survival Rate. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Whole-Body Irradiation


88. Monzo M, Brunet S, Urbano-Ispizua A, Navarro A, Perea G, Esteve J, Artells R, Granell M, Berlanga J, Ribera JM, Bueno J, Llorente A, Guardia R, Tormo M, Torres P, Nomdedéu JF, Montserrat E, Sierra J, CETLAM: Genomic polymorphisms provide prognostic information in intermediate-risk acute myeloblastic leukemia. Blood; 2006 Jun 15;107(12):4871-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic polymorphisms provide prognostic information in intermediate-risk acute myeloblastic leukemia.
  • Current prognostic factors for acute myeloblastic leukemia (AML) are not sufficient to accurately predict the group of patients in the intermediate-risk category who will successfully respond to treatment.
  • We used the allelic discrimination method to identify polymorphisms in GSTT1, SULT1C2, CDA, SXR (drug metabolic pathways), XPD, XPA, XPG, ERCC1, TOP2A (DNA repair), VEGF (angiogenesis), and MDR1 (multidrug resistance) genes in 110 adult patients with intermediate-risk AML, enrolled in the CETLAM-99 prospective trial.
  • These findings might be useful in selecting risk-adapted treatment strategies in intermediate-risk AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality. Neoplasm Proteins / genetics. Polymorphism, Genetic
  • [MeSH-minor] Adult. Alleles. Disease-Free Survival. Female. Heterozygote. Humans. Leukocyte Count. Male. Multivariate Analysis. Prognosis. Prospective Studies. Recurrence. Remission Induction. Risk Factors. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16507781.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  •  go-up   go-down


89. Georgiou G, Karali V, Zouvelou C, Kyriakou E, Dimou M, Chrisochoou S, Greka P, Dufexis D, Vervesou E, Dimitriadou E, Efthymiou A, Petrikkos L, Dima K, Lilakos K, Panayiotidis P: Serial determination of FLT3 mutations in myelodysplastic syndrome patients at diagnosis, follow up or acute myeloid leukaemia transformation: incidence and their prognostic significance. Br J Haematol; 2006 Aug;134(3):302-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serial determination of FLT3 mutations in myelodysplastic syndrome patients at diagnosis, follow up or acute myeloid leukaemia transformation: incidence and their prognostic significance.
  • Forty-two patients progressed to acute myeloid leukaemia (AML), including the three patients with FLT3 mutations at MDS diagnosis.
  • Three additional patients acquired FLT3 mutations and progressed to AML in 1 month.
  • FLT3 mutations seem to be a critical additional genetic event that transforms a minority of MDS patients to AML.
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. DNA Mutational Analysis. Disease Progression. Female. Humans. Leukemia, Myeloid / genetics. Male. Middle Aged. Prognosis. Proportional Hazards Models. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Survival Rate


90. Grandics P: Complete remission achieved in a case of both primary and recurrent adult acute myelogeneous leukemia by a novel nutritional therapy. J Altern Complement Med; 2006 Apr;12(3):311-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complete remission achieved in a case of both primary and recurrent adult acute myelogeneous leukemia by a novel nutritional therapy.
  • OBJECTIVES: The aim of this study was to determine the possible clinical benefit of molasses-based dietary compositions (designated as MSQ 13, MSQ 15, and MSQ 18) in a case of both primary and recurrent adult AML.
  • OUTCOME MEASURES: Clinical improvement and regression of AML were the outcome measures.
  • CONCLUSIONS: Treatment with the MSQ dietary compositions resulted in disease regression and the reversal of clinical manifestations over two episodes of AML.
  • Therefore, further studies are warranted to evaluate the utility of this approach for the clinical management of AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / diet therapy. Molasses. Nutrition Therapy / methods
  • [MeSH-minor] Adult. Female. Humans. Remission Induction. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16646731.001).
  • [ISSN] 1075-5535
  • [Journal-full-title] Journal of alternative and complementary medicine (New York, N.Y.)
  • [ISO-abbreviation] J Altern Complement Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


91. Appelbaum FR: Incorporating hematopoietic cell transplantation (HCT) into the management of adults aged under 60 years with acute myeloid leukemia (AML). Best Pract Res Clin Haematol; 2008 Mar;21(1):85-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incorporating hematopoietic cell transplantation (HCT) into the management of adults aged under 60 years with acute myeloid leukemia (AML).
  • Current strategies for incorporating hematopoietic cell transplantation into the treatment of adults with AML are based predominantly on pre-treatment patient, donor and disease characteristics.
  • Here we review the currently accepted indications for transplantation and raise the possibility that alternative approaches to incorporating transplantation into the management of adults with AML that rely predominantly on the measurement of minimal residual disease (MRD) could save additional lives without any major advance in chemotherapy or transplant technologies.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy


92. Rubnitz JE, Inaba H, Dahl G, Ribeiro RC, Bowman WP, Taub J, Pounds S, Razzouk BI, Lacayo NJ, Cao X, Meshinchi S, Degar B, Airewele G, Raimondi SC, Onciu M, Coustan-Smith E, Downing JR, Leung W, Pui CH, Campana D: Minimal residual disease-directed therapy for childhood acute myeloid leukaemia: results of the AML02 multicentre trial. Lancet Oncol; 2010 Jun;11(6):543-52
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Minimal residual disease-directed therapy for childhood acute myeloid leukaemia: results of the AML02 multicentre trial.
  • BACKGROUND: We sought to improve outcome in patients with childhood acute myeloid leukaemia (AML) by applying risk-directed therapy that was based on genetic abnormalities of the leukaemic cells and measurements of minimal residual disease (MRD) done by flow cytometry during treatment.
  • METHODS: From Oct 13, 2002, to June 19, 2008, 232 patients with de-novo AML (n=206), therapy-related or myelodysplasia-related AML (n=12), or mixed-lineage leukaemia (n=14) were enrolled at eight centres.
  • 230 patients were assigned by block, non-blinded randomisation, stratified by cytogenetic or morphological subtype, to high-dose (18 g/m(2), n=113) or low-dose (2 g/m(2), n=117) cytarabine given with daunorubicin and etoposide (ADE; induction 1).
  • Other analyses were limited to the 216 patients with AML, excluding those with mixed-lineage leukaemia.
  • INTERPRETATION: Our findings suggest that the use of targeted chemotherapy and HSCT, in the context of a comprehensive risk-stratification strategy based on genetic features and MRD findings, can improve outcome in patients with childhood AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Adolescent. Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Cytarabine / administration & dosage. Cytogenetic Analysis. Daunorubicin / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Flow Cytometry. Humans. Infant. Infant, Newborn. Male. Neoplasm, Residual. Remission Induction. Survival Rate. Young Adult

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • [Cites] Blood. 2001 Jan 1;97(1):56-62 [11133742.001]
  • [Cites] J Clin Oncol. 2010 Feb 20;28(6):955-9 [20085940.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3727-32 [11389009.001]
  • [Cites] J Clin Oncol. 2002 May 1;20(9):2302-9 [11981001.001]
  • [Cites] Lancet. 2002 May 11;359(9318):1686-9 [12020548.001]
  • [Cites] Blood. 2003 May 1;101(9):3398-406 [12506020.001]
  • [Cites] Br J Haematol. 2003 Jun;121(6):823-38 [12786792.001]
  • [Cites] Br J Haematol. 2003 Oct;123(2):243-52 [14531905.001]
  • [Cites] Cancer. 2003 Dec 15;98(12):2715-22 [14669294.001]
  • [Cites] J Chronic Dis. 1974 Sep;27(7-8):365-75 [4612056.001]
  • [Cites] Br J Cancer. 1977 Jan;35(1):1-39 [831755.001]
  • [Cites] Biometrics. 1979 Sep;35(3):549-56 [497341.001]
  • [Cites] Blood. 1996 Mar 1;87(5):1710-7 [8634416.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4979-89 [8652810.001]
  • [Cites] Blood. 1996 Oct 15;88(8):2841-51 [8874180.001]
  • [Cites] Br J Haematol. 1998 Apr;101(1):130-40 [9576193.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2090-100 [16304571.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2130-8 [16304572.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1315-24 [16254147.001]
  • [Cites] Cancer. 2006 Jun 1;106(11):2495-502 [16639734.001]
  • [Cites] Blood. 2006 Jul 1;108(1):74-80 [16537811.001]
  • [Cites] Cancer. 2006 Jul 1;107(1):116-24 [16721819.001]
  • [Cites] J Clin Oncol. 2006 Aug 1;24(22):3686-92 [16877738.001]
  • [Cites] J Clin Oncol. 2006 Sep 20;24(27):4499-506 [16983120.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]
  • [Cites] Cancer. 2008 Jul 15;113(2):376-82 [18459178.001]
  • [Cites] J Clin Oncol. 2008 Oct 20;26(30):4944-51 [18606980.001]
  • [Cites] Blood. 2009 May 21;113(21):5083-9 [19131545.001]
  • [Cites] N Engl J Med. 2009 Jun 25;360(26):2730-41 [19553647.001]
  • [Cites] Blood. 2009 Jul 30;114(5):937-51 [19357394.001]
  • [Cites] Leukemia. 2009 Aug;23(8):1410-6 [19242495.001]
  • [Cites] J Clin Oncol. 2009 Aug 20;27(24):4007-13 [19620491.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2009;:385-95 [20008224.001]
  • [CommentIn] Lancet Oncol. 2010 Jun;11(6):502-3 [20522371.001]
  • (PMID = 20451454.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00136084
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA115422; United States / NCI NIH HHS / CA / R01 CA115422-02
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 93NS566KF7 / gemtuzumab; ZS7284E0ZP / Daunorubicin; DAV regimen
  • [Other-IDs] NLM/ NIHMS319127; NLM/ PMC3171799
  •  go-up   go-down


93. Marcucci G, Mrózek K, Bloomfield CD: Molecular heterogeneity and prognostic biomarkers in adults with acute myeloid leukemia and normal cytogenetics. Curr Opin Hematol; 2005 Jan;12(1):68-75
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular heterogeneity and prognostic biomarkers in adults with acute myeloid leukemia and normal cytogenetics.
  • PURPOSE OF REVIEW: Patients with acute myeloid leukemia (AML) and normal karyotype constitute the single largest cytogenetic group of AML, estimated to account for 45% of adults with de novo AML.
  • RECENT FINDINGS: Four prognostic biomarkers-the internal tandem duplication and point mutations in the FLT3 gene, partial tandem duplication of the MLL gene, mutations of the CEBPA gene, and overexpression of the BAALC gene-have been found to predict outcome in patients with AML and normal cytogenetics.
  • In addition, one study using gene expression profiling identified two subgroups of AML patients with a normal karyotype whose survival differs significantly.
  • SUMMARY: Considerable progress has been made in molecular characterization of AML patients with normal cytogenetics.
  • [MeSH-major] Biomarkers, Tumor / genetics. Chromosome Aberrations. Cytogenetic Analysis. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adult. CCAAT-Enhancer-Binding Protein-alpha / genetics. Gene Expression Profiling. Humans. Neoplasm Proteins / genetics. Prognosis. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics. fms-Like Tyrosine Kinase 3

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15604894.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / K08-CA90469; United States / NCI NIH HHS / CA / P30CA16058
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BAALC protein, human; 0 / Biomarkers, Tumor; 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 65
  •  go-up   go-down


94. Ma Y, Wang X, Xu X, Lin G: World Health Organization sub-types, initial treatment outcome and prognostic study of unselected adult patients with acute myeloid leukaemia in Shanghai: an analysis of 623 cases. J Int Med Res; 2009 Jul-Aug;37(4):1191-201
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] World Health Organization sub-types, initial treatment outcome and prognostic study of unselected adult patients with acute myeloid leukaemia in Shanghai: an analysis of 623 cases.
  • This study investigated the complete remission (CR) rate and survival of 623 newly diagnosed patients with acute myeloid leukaemia (AML) in Shanghai, China, classified according to World Health Organization and French-American-British criteria, and compared the differences in treatment effect with those reported in developed countries and those reported in Shanghai from 1984 to 1994.
  • Multilineage dysplasia in de novo AML was not an independent prognostic factor.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. China / epidemiology. Female. Hematopoietic Stem Cell Transplantation. Humans. Karyotyping. Male. Middle Aged. Prognosis. Remission Induction. Survival Rate. Treatment Outcome. World Health Organization. Young Adult

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19761704.001).
  • [ISSN] 0300-0605
  • [Journal-full-title] The Journal of international medical research
  • [ISO-abbreviation] J. Int. Med. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  •  go-up   go-down


95. Ostgård LS, Kjeldsen E, Holm MS, Brown Pde N, Pedersen BB, Bendix K, Johansen P, Kristensen JS, Nørgaard JM: Reasons for treating secondary AML as de novo AML. Eur J Haematol; 2010 Sep;85(3):217-26
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reasons for treating secondary AML as de novo AML.
  • In a Danish bi-regional registry-based study, we conducted an analysis of the incidence and clinical importance of secondary acute myeloid leukaemia (AML).
  • In a total of 630 cases of AML, we found 157 (25%) cases of secondary AML.
  • The secondary leukaemia arose from MDS (myelodysplastic syndrome) in 77 cases (49%), CMPD (chronic myeloproliferative disorder) in 43 cases (27%) and was therapy-related AML (t-AML) in 37 cases (24%).
  • Median age at diagnosis of AML was 69 yr in secondary cases when compared to 66 yr in de novo cases (P = 0.006).
  • In univariate analyses, secondary AML was associated with an inferior complete remission (CR) rate (P = 0.008) and poorer overall survival (OS, P = 0.003) whereas in complete remitters, disease-free survival (DFS) of secondary cases was equal to that of de novo cases.
  • Interestingly, in all further analyses of CR-rates, OS and DFS, when correcting for the influence of age, cytogenetic abnormalities, performance status and leucocyte count (WBC), presence of secondary AML completely lost prognostic significance.
  • We conclude that the presence of secondary AML does not per se convey an unfavourable prognosis and that patients with secondary AML should be offered the chance of benefiting from treatment according to current frontline AML protocols.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / complications
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cohort Studies. Cytogenetic Analysis. Disease-Free Survival. Female. Humans. Male. Middle Aged. Registries. Young Adult


96. Shali W, Hélias C, Fohrer C, Struski S, Gervais C, Falkenrodt A, Leymarie V, Lioure B, Raby P, Herbrecht R, Lessard M: Cytogenetic studies of a series of 43 consecutive secondary myelodysplastic syndromes/acute myeloid leukemias: conventional cytogenetics, FISH, and multiplex FISH. Cancer Genet Cytogenet; 2006 Jul 15;168(2):133-45
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic studies of a series of 43 consecutive secondary myelodysplastic syndromes/acute myeloid leukemias: conventional cytogenetics, FISH, and multiplex FISH.
  • We report a series of 43 consecutive therapy-related myelodysplastic syndromes (t-MDS) or acute myeloid leukemias (t-AML) observed for 6 years.
  • Conventional cytogenetic and fluorescent in situ hybridization (FISH)/ multiplex FISH (M-FISH) methods were used to analyze cytogenetic characteristics of secondary MDS/AML.
  • A considerable proportion of recurrent balanced translocations characterized t-AML secondary to therapy.
  • [MeSH-major] In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Female. Gene Amplification. Gene Deletion. Humans. Karyotyping. Male. Middle Aged. Translocation, Genetic


97. Hegenbart U, Niederwieser D, Sandmaier BM, Maris MB, Shizuru JA, Greinix H, Cordonnier C, Rio B, Gratwohl A, Lange T, Al-Ali H, Storer B, Maloney D, McSweeney P, Chauncey T, Agura E, Bruno B, Maziarz RT, Petersen F, Storb R: Treatment for acute myelogenous leukemia by low-dose, total-body, irradiation-based conditioning and hematopoietic cell transplantation from related and unrelated donors. J Clin Oncol; 2006 Jan 20;24(3):444-53
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment for acute myelogenous leukemia by low-dose, total-body, irradiation-based conditioning and hematopoietic cell transplantation from related and unrelated donors.
  • The study reported here assessed outcomes for patients with acute myeloid leukemia (AML) in different stages of their disease, who were not considered candidates for conventional hematopoietic cell transplantation (HCT) because of age and/or other known risk factors and were given minimal conditioning followed by HCT from related or unrelated donors.
  • PATIENTS AND METHODS: The present study included 122 patients with AML, who were conditioned with 2 Gy total-body irradiation (TBI) on day 0 with or without preceding fludarabine (30 mg/m2/d from days -4 to -2), and given postgrafting cyclosporine at 6.25 mg/kg twice daily from day -3 and mycophenolate mofetil at 15 mg/kg twice daily from day 0.
  • Cumulative incidences of acute graft-versus-host disease grades 2 to 4 at 6 months were 35% after related and 42% after unrelated HCT, respectively.
  • CONCLUSION: We conclude that HCT from related and unrelated donors after low-dose TBI is a promising treatment for elderly patients with AML.


98. Incedayi M, Turba UC, Arslan B, Sabri SS, Saad WE, Matsumoto AH, Angle JF: Endovascular therapy for patients with renal angiomyolipoma presenting with retroperitoneal haemorrhage. Eur J Vasc Endovasc Surg; 2010 Jun;39(6):739-44
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We report our experience treating four patients with acutely bleeding angiomyolipoma (AML) of sizes between 4 and 12 cm who were managed with endovascular embolisation with a mean follow-up of 10 months.
  • In our case series, we demonstrate that endovascular embolisation in the acute setting for bleeding AMLs is a viable treatment option.
  • AML should be in the differential diagnosis of acutely bleeding renal masses, even when there is no fat assessed by computed tomography (CT) imaging in the renal mass.
  • [MeSH-minor] Acute Disease. Adult. Angiography. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Male. Middle Aged. Nephrectomy. Retroperitoneal Space. Tomography, X-Ray Computed

  • MedlinePlus Health Information. consumer health - Bleeding.
  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2009 European Society for Vascular Surgery. Published by Elsevier Ltd. All rights reserved.
  • [CommentIn] Eur J Vasc Endovasc Surg. 2011 Jan;41(1):134; author reply 135 [20961776.001]
  • (PMID = 20096610.001).
  • [ISSN] 1532-2165
  • [Journal-full-title] European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery
  • [ISO-abbreviation] Eur J Vasc Endovasc Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  •  go-up   go-down


99. Silveira CC, Gorini MI: [Conceptions of the acute myeloid leukemia patient concerning fatigue]. Rev Gaucha Enferm; 2009 Mar;30(1):40-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Conceptions of the acute myeloid leukemia patient concerning fatigue].
  • The present work is a study with the objective of learning the conceptions of the patient bearer of acute myeloid leukemia (AML) concerning to fatigue symptoms and their repercussions in his/her daily life as well as the actions performed in order to minimize the fatigue.
  • Eight (8) adult subjects with diagnosis of AML were interviewed.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Fatigue.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19653554.001).
  • [ISSN] 0102-6933
  • [Journal-full-title] Revista gaucha de enfermagem
  • [ISO-abbreviation] Rev Gaucha Enferm
  • [Language] POR
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Brazil
  •  go-up   go-down


100. Virappane P, Gale R, Hills R, Kakkas I, Summers K, Stevens J, Allen C, Green C, Quentmeier H, Drexler H, Burnett A, Linch D, Bonnet D, Lister TA, Fitzgibbon J: Mutation of the Wilms' tumor 1 gene is a poor prognostic factor associated with chemotherapy resistance in normal karyotype acute myeloid leukemia: the United Kingdom Medical Research Council Adult Leukaemia Working Party. J Clin Oncol; 2008 Nov 20;26(33):5429-35
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutation of the Wilms' tumor 1 gene is a poor prognostic factor associated with chemotherapy resistance in normal karyotype acute myeloid leukemia: the United Kingdom Medical Research Council Adult Leukaemia Working Party.
  • PURPOSE: To determine the clinical relevance of Wilms' tumor 1 (WT1) gene mutations in acute myeloid leukemia (AML) with normal karyotype (NK).
  • PATIENTS AND METHODS: Exons 7 and 9 of WT1 were screened in samples from 470 young adult NK AMLs using a combination of direct sequencing and high-resolution capillary electrophoresis.
  • CONCLUSION: WT1 mutations are a negative prognostic indicator in NK AML and may be suitable for the development of targeted therapy.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Genes, Wilms Tumor. Leukemia, Myeloid, Acute / genetics. Mutation
  • [MeSH-minor] Adolescent. Adult. Disease-Free Survival. Exons / genetics. Female. Humans. Karyotyping. Male. Middle Aged. Prognosis. Survival Rate. Treatment Outcome. Young Adult






Advertisement