[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 12833
6. Palomino-Portilla EA, Valbuena JR, Quinones-Avila Mdel P, Medeiros LJ: Myeloid sarcoma of appendix mimicking acute appendicitis. Arch Pathol Lab Med; 2005 Aug;129(8):1027-31
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 of appendix mimicking acute appendicitis.
  • CONTEXT: Myeloid sarcoma is a neoplasm of immature myeloid cells involving an extramedullary anatomic site that is usually, although not always, associated with acute myeloid leukemia.
  • Any extramedullary site can be involved by myeloid sarcoma, but involvement of the cecal appendix is uncommon, and symptoms mimicking acute appendicitis as a result of appendiceal involvement are rare.
  • OBJECTIVE: To describe the clinicopathologic features of 2 patients with myeloid sarcoma involving the appendix who presented with right lower quadrant pain suggestive of acute appendicitis and prompting appendectomy.
  • Routine hematoxylin-eosin-stained slides, naphthol-ASD-chloroacetate stain, and immunohistochemical stains for myeloid, B-cell, and T-cell antigens were prepared.
  • RESULTS: Peripheral blood and bone marrow were infiltrated by coexistent acute myeloid leukemia in case 1 but were negative for leukemia in case 2.
  • In case 2, the patient had a history of acute myeloid leukemia that had been treated by an allogenic bone marrow transplant 7 months earlier.
  • Histologic examination of the appendix revealed poorly differentiated myeloid sarcoma in both cases.
  • CONCLUSIONS: Myeloid sarcoma involving the appendix can rarely cause pain or other symptoms mimicking acute appendicitis.
  • A high index of suspicion combined with the use of cytochemical and immunohistochemical studies are helpful in establishing the diagnosis.
  • [MeSH-major] Appendicitis / diagnosis. Appendix / pathology. Leukemia, Myeloid / diagnosis. Sarcoma, Myeloid / diagnosis
  • [MeSH-minor] Abdomen / ultrasonography. Adult. Biomarkers, Tumor / metabolism. Chemotherapy, Adjuvant. Child. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Palliative Care. Radiotherapy. Retrospective Studies. Treatment Outcome

  • Genetic Alliance. consumer health - Myeloid sarcoma.
  • MedlinePlus Health Information. consumer health - Appendicitis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16048393.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


7. DeAngelo DJ, Stone RM, Heaney ML, Nimer SD, Paquette RL, Klisovic RB, Caligiuri MA, Cooper MR, Lecerf JM, Karol MD, Sheng S, Holford N, Curtin PT, Druker BJ, Heinrich MC: Phase 1 clinical results with tandutinib (MLN518), a novel FLT3 antagonist, in patients with acute myelogenous leukemia or high-risk myelodysplastic syndrome: safety, pharmacokinetics, and pharmacodynamics. Blood; 2006 Dec 1;108(12):3674-81
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] Phase 1 clinical results with tandutinib (MLN518), a novel FLT3 antagonist, in patients with acute myelogenous leukemia or high-risk myelodysplastic syndrome: safety, pharmacokinetics, and pharmacodynamics.
  • Because of the correlation between FLT3 internal tandem duplication (ITD) mutations and poor prognosis in acute myelogenous leukemia (AML), we conducted a phase 1 trial of tandutinib in 40 patients with either AML or high-risk myelodysplastic syndrome (MDS).
  • Tandutinib at the MTD (525 mg twice daily) should be evaluated more extensively in patients with AML with FLT3-ITD mutations to better define its antileukemic activity.


8. Cerveira N, Santos J, Bizarro S, Costa V, Ribeiro FR, Lisboa S, Correia C, Torres L, Vieira J, Snijder S, Mariz JM, Norton L, Mellink CH, Buijs A, Teixeira MR: Both SEPT2 and MLL are down-regulated in MLL-SEPT2 therapy-related myeloid neoplasia. BMC Cancer; 2009;9:147
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] Both SEPT2 and MLL are down-regulated in MLL-SEPT2 therapy-related myeloid neoplasia.
  • BACKGROUND: A relevant role of septins in leukemogenesis has been uncovered by their involvement as fusion partners in MLL-related leukemia.
  • Recently, we have established the MLL-SEPT2 gene fusion as the molecular abnormality subjacent to the translocation t(2;11)(q37;q23) in therapy-related acute myeloid leukemia.
  • In this work we quantified MLL and SEPT2 gene expression in 58 acute myeloid leukemia patients selected to represent the major AML genetic subgroups, as well as in all three cases of MLL-SEPT2-associated myeloid neoplasms so far described in the literature.
  • METHODS: Cytogenetics, fluorescence in situ hybridization (FISH) and molecular studies (RT-PCR, qRT-PCR and qMSP) were used to characterize 58 acute myeloid leukemia patients (AML) at diagnosis selected to represent the major AML genetic subgroups: CBFB-MYH11 (n = 13), PML-RARA (n = 12); RUNX1-RUNX1T1 (n = 12), normal karyotype (n = 11), and MLL gene fusions other than MLL-SEPT2 (n = 10).
  • We also studied all three MLL-SEPT2 myeloid neoplasia cases reported in the literature, namely two AML patients and a t-MDS patient.
  • The down-regulation of SEPT2 in MLL-SEPT2 myeloid neoplasias was statistically significant when compared with all other leukemia genetic subgroups (including those with other MLL gene fusions).
  • In addition, MLL expression was also down-regulated in the group of MLL fusions other than MLL-SEPT2, when compared with the normal control group (p = 0.023) CONCLUSION: We found a significant down-regulation of both SEPT2 and MLL in MLL-SEPT2 myeloid neoplasias.
  • In addition, we also found that MLL is under-expressed in AML patients with MLL fusions other than MLL-SEPT2.
  • [MeSH-major] Down-Regulation. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasms, Second Primary / genetics. Phosphoric Monoester Hydrolases / genetics

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • 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
  • [Cites] Leukemia. 1999 Dec;13(12):1901-28 [10602411.001]
  • [Cites] Science. 2005 Mar 18;307(5716):1781-5 [15774761.001]
  • [Cites] Blood. 2000 Dec 1;96(12):3887-93 [11090074.001]
  • [Cites] Cancer Res. 2001 Apr 15;61(8):3410-8 [11309301.001]
  • [Cites] Cancer Res. 2002 Jan 15;62(2):333-7 [11809673.001]
  • [Cites] Blood. 2002 May 15;99(10):3780-5 [11986236.001]
  • [Cites] Leukemia. 2003 Feb;17(2):359-65 [12592336.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2474-86 [14562124.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2318-57 [14562125.001]
  • [Cites] In Silico Biol. 2003;3(3):235-40 [12954087.001]
  • [Cites] Leukemia. 2004 May;18(5):998-1005 [14999297.001]
  • [Cites] Oncogene. 2004 Jul 15;23(32):5468-75 [15122323.001]
  • [Cites] J Pathol. 2004 Nov;204(4):489-505 [15495264.001]
  • [Cites] Nucleic Acids Res. 1994 Aug 11;22(15):2990-7 [8065911.001]
  • [Cites] J Mol Biol. 1995 Jun 23;249(5):923-32 [7791218.001]
  • [Cites] Blood. 1995 Sep 15;86(6):2073-6 [7662954.001]
  • [Cites] Blood. 1996 Mar 15;87(6):2496-505 [8630416.001]
  • [Cites] Genes Dev. 1997 Jun 15;11(12):1535-47 [9203580.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 May 26;95(11):6413-8 [9600980.001]
  • [Cites] Leukemia. 1999 Feb;13(2):302-6 [10025907.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 May 25;96(11):6428-33 [10339604.001]
  • [Cites] Cancer Res. 1999 Sep 1;59(17):4261-5 [10485469.001]
  • [Cites] Leukemia. 1999 Oct;13(10):1525-33 [10516753.001]
  • [Cites] Blood. 2005 Jul 1;106(1):345-52 [15774615.001]
  • [Cites] Mol Biol Cell. 2005 Oct;16(10):4648-59 [16093351.001]
  • [Cites] Leukemia. 2006 Feb;20(2):218-23 [16341046.001]
  • [Cites] Leukemia. 2006 May;20(5):777-84 [16511515.001]
  • [Cites] Oncogene. 2006 Oct 5;25(45):6147-52 [16682951.001]
  • [Cites] Cancer Genet Cytogenet. 2007 Jul 1;176(1):72-5 [17574968.001]
  • [Cites] Cell. 2007 Sep 7;130(5):837-50 [17803907.001]
  • [Cites] Dev Cell. 2007 Nov;13(5):677-90 [17981136.001]
  • [Cites] EMBO Rep. 2007 Dec;8(12):1120-6 [17975554.001]
  • [Cites] Cancer Genet Cytogenet. 2008 Jan 15;180(2):149-52 [18206542.001]
  • [Cites] N Engl J Med. 2008 Mar 13;358(11):1148-59 [18337604.001]
  • [Cites] Nat Rev Mol Cell Biol. 2008 Jun;9(6):478-89 [18478031.001]
  • [Cites] Cancer Res. 2008 Jun 15;68(12):4494-9 [18559491.001]
  • [Cites] Cancer Genet Cytogenet. 2008 Aug;185(1):62-4 [18656699.001]
  • [Cites] Nucleic Acids Res. 2000 Apr 15;28(8):E32 [10734209.001]
  • (PMID = 19445675.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.1.3.- / Phosphoric Monoester Hydrolases
  • [Other-IDs] NLM/ PMC2689242
  •  go-up   go-down


9. Saito T, Ikezoe T, Daibata M, Takeuchi T, Ohtsuki Y, Taguchi H, Miyoshi I: Disseminated mucormycosis (zygomycosis) in acute myeloid leukemia. Intern Med; 2006;45(18):1073-4
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] Disseminated mucormycosis (zygomycosis) in acute myeloid leukemia.
  • [MeSH-major] Dexamethasone / adverse effects. Glucocorticoids / adverse effects. Immunocompromised Host. Leukemia, Promyelocytic, Acute / immunology. Mucormycosis / etiology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Zygomycosis.
  • MedlinePlus Health Information. consumer health - Steroids.
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17043382.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Glucocorticoids; 7S5I7G3JQL / Dexamethasone
  •  go-up   go-down


10. Nguyen LA, Pandolfi PP, Aikawa Y, Tagata Y, Ohki M, Kitabayashi I: Physical and functional link of the leukemia-associated factors AML1 and PML. Blood; 2005 Jan 1;105(1):292-300
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] Physical and functional link of the leukemia-associated factors AML1 and PML.
  • The AML1-CBFbeta transcription factor complex is the most frequent target of specific chromosome translocations in acute myeloid leukemia (AML).
  • The promyelocytic leukemia (PML) gene is also frequently involved in AML-associated translocation.
  • Overexpression of PML I stimulates myeloid cells to differentiate.
  • These results suggest that PML I could act as a mediator for AML1 and its coactivator p300/CBP to assemble into functional complexes and, consequently, activate AML1-dependent transcription and myeloid cell differentiation.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Leukemia / metabolism. Neoplasm Proteins / metabolism. Nuclear Proteins / metabolism. Proto-Oncogene Proteins / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Active Transport, Cell Nucleus. Amino Acid Sequence. Animals. Binding Sites. Cell Differentiation / drug effects. Cell Line, Tumor. Cell Nucleus / metabolism. Core Binding Factor Alpha 2 Subunit. E1A-Associated p300 Protein. Gene Expression Regulation, Neoplastic. Granulocyte Colony-Stimulating Factor / pharmacology. Humans. Mice. Molecular Sequence Data. Myeloid Cells / cytology. Myeloid Cells / drug effects. Protein Binding. Protein Isoforms / chemistry. Protein Isoforms / genetics. Protein Isoforms / metabolism. Protein Structure, Tertiary. Sequence Alignment. Signal Transduction. Trans-Activators / metabolism. Tumor Suppressor Proteins

  • MedlinePlus Health Information. consumer health - 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 = 15331439.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Ep300 protein, mouse; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Pml protein, mouse; 0 / Protein Isoforms; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Runx1 protein, mouse; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 143220-95-5 / PML protein, human; EC 2.3.1.48 / E1A-Associated p300 Protein
  •  go-up   go-down


11. Dik WA, Brahim W, Braun C, Asnafi V, Dastugue N, Bernard OA, van Dongen JJ, Langerak AW, Macintyre EA, Delabesse E: CALM-AF10+ T-ALL expression profiles are characterized by overexpression of HOXA and BMI1 oncogenes. Leukemia; 2005 Nov;19(11):1948-57
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.
  • The t(10;11)(p13;q14-21) is found in T-ALL and acute myeloid leukemia and fuses CALM (Clathrin-Assembly protein-like Lymphoid-Myeloid leukaemia gene) to AF10.
  • Microarray results were validated by quantitative RT-PCR on an independent group of T-ALL and compared to mixed lineage leukemia-translocated acute leukemias (MLL-t AL).
  • In addition, BMI1, located close to AF10 breakpoint, was overexpressed only in CALM-AF10+ T-ALL and not in MLL-t AL.
  • We propose to define a HOXA+ leukemia group composed of at least MLL-t, CALM-AF10 and HOXA-t AL, which may benefit from adapted management.
  • [MeSH-major] Homeodomain Proteins / biosynthesis. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Repressor Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Cell Proliferation. Cell Transformation, Neoplastic. Child. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Polycomb Repressive Complex 1. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Up-Regulation

  • 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 = 16107895.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 157907-48-7 / HoxA protein; EC 6.3.2.19 / Polycomb Repressive Complex 1
  •  go-up   go-down


12. von Falck C, Laenger F, Knapp WH, Galanski M: F-18 FDG PET/CT showing bilateral breast involvement in acute myeloid leukemia relapse. Clin Nucl Med; 2009 Oct;34(10):713-5
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] F-18 FDG PET/CT showing bilateral breast involvement in acute myeloid leukemia relapse.
  • Isolated extramedullary relapse with involvement of the breasts by acute myeloid leukemia (AML) after allogeneic stem cell transplantation is an uncommon event.
  • We here report the case of a 27-year-old female patient, who was diagnosed with high-risk AML (FAB M5, complex karyotype).
  • Ultrasound-guided biopsy was performed and histopathology revealed relapsing AML.
  • Isolated extramedullary disease recurrence was confirmed by bone marrow biopsy.
  • [MeSH-major] Breast / pathology. Breast / radionuclide imaging. Fluorodeoxyglucose F18. Leukemia, Myeloid, Acute / radiography. Leukemia, Myeloid, Acute / radionuclide imaging. Positron-Emission Tomography. Tomography, X-Ray Computed

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - CT Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19893411.001).
  • [ISSN] 1536-0229
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
  •  go-up   go-down


13. Takigawa N, Takeuchi M, Shibayama T, Yoshida I, Kawata N, Tada A, Ueoka H, Takahashi K: Successful treatment of a patient with synchronous advanced non-small cell lung cancer and acute myeloid leukemia by a combination of gefitinib, low-dose cytarabine and aclarubicin. Anticancer Res; 2005 May-Jun;25(3c):2579-82
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] Successful treatment of a patient with synchronous advanced non-small cell lung cancer and acute myeloid leukemia by a combination of gefitinib, low-dose cytarabine and aclarubicin.
  • There are few reports describing simultaneous occurrence of acute leukemia and lung cancer.
  • We describe here an 83-year-old woman who simultaneously developed advanced adenocarcinoma of the lung and acute myeloid leukemia.
  • She could not receive intensive chemotherapy due to poor performance status.
  • This combination could be safely administered in the elderly patient with poor performance status and was effective for both lung cancer and acute myeloid leukemia.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Frail Elderly. Leukemia, Myeloid / drug therapy. Lung Neoplasms / drug therapy. Neoplasms, Multiple Primary / drug therapy
  • [MeSH-minor] Aclarubicin / administration & dosage. Acute Disease. Aged. Aged, 80 and over. Cytarabine / administration & dosage. Dose-Response Relationship, Drug. Female. Humans. Quinazolines / administration & dosage


1
Advertisement
4. Glienke W, Chow KU, Bauer N, Bergmann L: Down-regulation of wt1 expression in leukemia cell lines as part of apoptotic effect in arsenic treatment using two compounds. Leuk Lymphoma; 2006 Aug;47(8):1629-38
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] Down-regulation of wt1 expression in leukemia cell lines as part of apoptotic effect in arsenic treatment using two compounds.
  • Arsenic trioxide (As2O3) induces remission in patients with acute promyelocytic leukemia (APL).
  • The Wilms' tumor gene (wt1) is up-regulated in acute myeloid leukemia (AML) and a variety of leukemia cell lines.
  • Low concentrations of 0.1 microM arsenic induced expression of the anti-apoptotic bcl-2 gene in both cell lines HL-60 and K562.
  • After arsenic treatment of the leukemia cell lines HL-60 and K562 the up-regulation of par-4 may contribute to the induction of apoptosis rather than down-regulation of bcl-2.
  • [MeSH-major] Apoptosis / drug effects. Arsenicals / pharmacology. Carrier Proteins / genetics. Leukemia / drug therapy. WT1 Proteins / genetics

  • MedlinePlus Health Information. consumer health - Leukemia.
  • Hazardous Substances Data Bank. ARSENIC TRIOXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16966277.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Arsenicals; 0 / Arsenites; 0 / Carrier Proteins; 0 / Oxides; 0 / Sodium Compounds; 0 / WT1 Proteins; 0 / WTIP protein, human; 48OVY2OC72 / sodium arsenite; S7V92P67HO / arsenic trioxide
  •  go-up   go-down


15. Ritter M, Kattmann D, Teichler S, Hartmann O, Samuelsson MK, Burchert A, Bach JP, Kim TD, Berwanger B, Thiede C, Jäger R, Ehninger G, Schäfer H, Ueki N, Hayman MJ, Eilers M, Neubauer A: Inhibition of retinoic acid receptor signaling by Ski in acute myeloid leukemia. Leukemia; 2006 Mar;20(3):437-43
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] Inhibition of retinoic acid receptor signaling by Ski in acute myeloid leukemia.
  • Acute myeloid leukemia (AML) is a heterogeneous disease with multiple different cytogenetic and molecular aberrations contributing to leukemic transformation.
  • We compared gene expression profiles of 4608 genes using cDNA-arrays from 20 AML patients (nine with -7/del7q and 11 with normal karyotype) with 23 CD34+ preparations from healthy bone marrow donors.
  • In a second set of 183 AML patients analyzed with real-time PCR, the highest expression level of SKI in AML with -7/del7q could be confirmed.
  • We wanted to investigate the interference of Ski with RARalpha signaling in AML.
  • We also found that overexpression of wild-type Ski inhibited the prodifferentiating effects of retinoic acid in U937 leukemia cells.
  • In conclusion, Ski seems to be involved in the blocking of differentiation in AML via inhibition of RARalpha signaling.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Leukemia, Myeloid / metabolism. Proto-Oncogene Proteins / metabolism. Receptors, Retinoic Acid / metabolism. Signal Transduction
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Chromosome Deletion. Chromosomes, Human, Pair 7. Enzyme Inhibitors / pharmacology. Female. Fluorescent Antibody Technique. Histone Deacetylase Inhibitors. Humans. Male. Middle Aged. Valproic Acid / pharmacology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. VALPROIC ACID .
  • 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 = 16424870.001).
  • [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 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Receptors, Retinoic Acid; 126648-96-2 / SKI protein, human; 614OI1Z5WI / Valproic Acid
  •  go-up   go-down


16. Moccia A, Ghielmini M: Monoclonal antibodies for the treatment of hematologic malignancies: schedule and maintenance therapy. Semin Hematol; 2008 Apr;45(2):75-84
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.
  • It is normally administered as single agent or in combination with chemotherapy to induce remission in B-cell neoplasias.
  • Alemtuzumab is administered with a schedule of 30 mg, three times per week, after an initial dose escalation in the first week, showing activity against chronic lymphocytic leukemia (B-CLL) and some T-cell neoplasias.
  • GO is administered at a dose of 9 mg/m(2) at 2-week intervals for two doses; it is the first monoclonal antibody approved for the treatment of relapsed or refractory CD33(+) acute myeloid leukemia (AML).

  • Hazardous Substances Data Bank. RITUXIMAB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18381101.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / gemtuzumab; 3A189DH42V / alemtuzumab; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 74
  •  go-up   go-down


17. Fröhling S, Schlenk RF, Kayser S, Morhardt M, Benner A, Döhner K, Döhner H, German-Austrian AML Study Group: Cytogenetics and age are major determinants of outcome in intensively treated acute myeloid leukemia patients older than 60 years: results from AMLSG trial AML HD98-B. Blood; 2006 Nov 15;108(10):3280-8
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] Cytogenetics and age are major determinants of outcome in intensively treated acute myeloid leukemia patients older than 60 years: results from AMLSG trial AML HD98-B.
  • To assess the prognostic impact of cytogenetics in elderly patients with acute myeloid leukemia (AML) receiving intensive induction and consolidation treatment according to a single protocol specifically designed for patients above age 60, pretreatment samples from 361 patients registered for the AML HD98-B trial of the German-Austrian AML Study Group were analyzed by chromosome banding and fluorescence in situ hybridization, and cytogenetic findings were correlated with outcome.
  • Thus, karyotype and age are major determinants of outcome in elderly patients with AML.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid / diagnosis
  • [MeSH-minor] Acute Disease. Age Factors. Aged. Aged, 80 and over. Cytogenetic Analysis / methods. Female. Humans. Male. Middle Aged. Prognosis. Proportional Hazards Models. Risk Assessment. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Myelocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16840728.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


18. Platzbecker U, Thiede C, Füssel M, Geissler G, Illmer T, Mohr B, Hänel M, Mahlberg R, Krümpelmann U, Weissinger F, Schaich M, Theuser C, Ehninger G, Bornhäuser M: Reduced intensity conditioning allows for up-front allogeneic hematopoietic stem cell transplantation after cytoreductive induction therapy in newly-diagnosed high-risk acute myeloid leukemia. Leukemia; 2006 Apr;20(4):707-14
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] Reduced intensity conditioning allows for up-front allogeneic hematopoietic stem cell transplantation after cytoreductive induction therapy in newly-diagnosed high-risk acute myeloid leukemia.
  • There is substantial need to improve the outcome of patients with high-risk acute myeloid leukemia (AML).
  • The clinical trial reported here investigated a new approach of up-front allogeneic hematopoietic stem cell transplantation (HSCT), provided a median of 40 days (range 22-74) after diagnosis, in twenty-six consecutive patients with newly-diagnosed high-risk AML characterized by poor-risk cytogenetics (n = 19) or inadequate blast clearance by induction chemotherapy (IC, n = 7).
  • Seventeen patients were not in remission before HSCT with a median marrow blast count of 34% (range 6-70).
  • All patients achieved rapid engraftment and went into remission with complete myeloid and lymphatic chimerism.
  • Grades II to IV acute GvHD occurred in 14 (56%) and extensive chronic GvHD was documented in 8 (35%) patients.
  • The probability of disease-free survival was 61% with only three patients relapsing 5, 6 and 7 months after transplantation, respectively.
  • Up-front allogeneic HSCT as part of primary induction therapy seems to be an effective strategy in high-risk AML patients and warrants further investigation.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chimerism. Female. Graft vs Host Disease / prevention & control. Graft vs Host Disease / therapy. Humans. Male. Middle Aged. Recurrence. Remission Induction. Risk Factors. Survival Rate. Transplantation, Homologous. Treatment Outcome

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16482208.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


19. Casanova I, Bosch R, Lasa A, Parreño M, Céspedes MV, Brunet S, Nomdedéu JF, Mangues MA, Sierra J, Mangues R: A celecoxib derivative inhibits focal adhesion signaling and induces caspase-8-dependent apoptosis in human acute myeloid leukemia cells. Int J Cancer; 2008 Jul 1;123(1):217-26
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] A celecoxib derivative inhibits focal adhesion signaling and induces caspase-8-dependent apoptosis in human acute myeloid leukemia cells.
  • Most acute myeloid leukemias (AMLs), including those with c-Kit or FLT3 mutations, show enhanced anchorage independent growth associated with constitutive activation of focal adhesion proteins.
  • Moreover, these alterations increase cell survival, inhibit apoptosis and are associated with poor prognosis and resistance to chemotherapy.
  • Therefore, the induction of apoptosis by selective inhibition of focal adhesion signaling may represent a novel anti-AML therapy.
  • Here, we have evaluated the antitumor effect and the mechanism of action of celecoxib and E7123, a non-Cox-2 inhibitor derivative, in a panel of human AML cell lines and bone marrow mononuclear cells from AML patients.
  • Both compounds induce cell death by inhibiting focal adhesion signaling through p130Cas, FAK and c-Src, leading to caspase-8 dependent apoptosis.
  • Therefore, both drugs could be developed as AML therapeutics; nevertheless, E7123 shows more activity than celecoxib against AML cells, and may not present its Cox-2 dependent cardiovascular toxicity.
  • Finally, our results support the evaluation of celecoxib in AML patients, and the preclinical evaluation of E7123, before its possible clinical testing.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Caspase 8 / metabolism. Leukemia, Myeloid, Acute / drug therapy. Pyrazoles / pharmacology. Sulfonamides / pharmacology
  • [MeSH-minor] Celecoxib. Cell Adhesion / drug effects. Cell Line, Tumor. Cyclooxygenase Inhibitors / pharmacology. Drug Design. Focal Adhesions / drug effects. Humans. Monocytes / drug effects. Signal Transduction / drug effects

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CELECOXIB .
  • 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
  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18398841.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-(5-(2,5-dimethylphenyl)-3-(trifluoromethyl)-4,5-dihydro-1H-pyrazol-1-yl)benzenesulfonamide; 0 / Antineoplastic Agents; 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; EC 3.4.22.- / Caspase 8; JCX84Q7J1L / Celecoxib
  •  go-up   go-down


20. Racanicchi S, Maccherani C, Liberatore C, Billi M, Gelmetti V, Panigada M, Rizzo G, Nervi C, Grignani F: Targeting fusion protein/corepressor contact restores differentiation response in leukemia cells. EMBO J; 2005 Mar 23;24(6):1232-42
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] Targeting fusion protein/corepressor contact restores differentiation response in leukemia cells.
  • The AML1/ETO and PML/RARalpha leukemia fusion proteins induce acute myeloid leukemia by acting as transcriptional repressors.
  • They interact with corepressors, such as N-CoR and SMRT, that recruit a multiprotein complex containing histone deacetylases on crucial myeloid differentiation genes.
  • We expressed in leukemia cells containing PML/RARalpha and AML1/ETO N-CoR protein fragments derived from fusion protein/corepressor interaction surfaces.
  • The N-CoR fragments are biologically effective also when directly transduced by virtue of a protein transduction domain.
  • Our data indicate that fusion protein activity is permanently required to maintain the leukemia phenotype and show the route to developing a novel therapeutic approach for leukemia, based on its molecular pathogenesis.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Leukemia, Myeloid / metabolism. Neoplasm Proteins / metabolism. Nuclear Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Repressor Proteins / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Acute Disease. Cell Differentiation / drug effects. Cell Line, Tumor. Cholecalciferol / pharmacology. Core Binding Factor Alpha 2 Subunit. Gene Expression Regulation, Neoplastic / drug effects. Humans. Nuclear Receptor Co-Repressor 1. Nuclear Receptor Co-Repressor 2. Peptides / genetics. Peptides / physiology. Protein Structure, Tertiary / genetics. Protein Structure, Tertiary / physiology. Tretinoin / pharmacology

  • 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. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. CHOLECALCIFEROL .
  • 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
  • [Cites] Blood. 1999 May 15;93(10):3167-215 [10233871.001]
  • [Cites] Blood. 1993 Oct 1;82(7):1949-53 [8400247.001]
  • [Cites] Nat Med. 2004 Dec;10(12):1329-35 [15531890.001]
  • [Cites] Genes Dev. 2000 Jan 15;14(2):121-41 [10652267.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1541-50 [10688806.001]
  • [Cites] Trends Cell Biol. 2000 Jul;10(7):290-5 [10856932.001]
  • [Cites] Mol Cell. 2000 May;5(5):811-20 [10882117.001]
  • [Cites] Mol Cell. 2000 May;5(5):821-30 [10882118.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1531-7 [10942402.001]
  • [Cites] Science. 1999 Sep 3;285(5433):1569-72 [10477521.001]
  • [Cites] Nature. 1999 Nov 4;402(6757):93-6 [10573424.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14807-12 [10611294.001]
  • [Cites] Genes Dev. 1999 Dec 15;13(24):3198-208 [10617569.001]
  • [Cites] Genes Dev. 1999 Dec 15;13(24):3209-16 [10617570.001]
  • [Cites] J Biol Chem. 2000 Jan 7;275(1):651-6 [10617663.001]
  • [Cites] Br J Haematol. 1995 Apr;89(4):805-11 [7772516.001]
  • [Cites] Cancer Res. 1996 Jul 1;56(13):2945-8 [8674046.001]
  • [Cites] Blood. 1996 Oct 15;88(8):2826-32 [8874178.001]
  • [Cites] EMBO J. 1996 Sep 16;15(18):4949-58 [8890168.001]
  • [Cites] Blood. 1997 Jun 15;89(12):4282-9 [9192750.001]
  • [Cites] Science. 1997 Nov 7;278(5340):1059-64 [9353180.001]
  • [Cites] Cancer Res. 1998 Jan 1;58(1):14-9 [9426049.001]
  • [Cites] Nat Genet. 1998 Feb;18(2):126-35 [9462740.001]
  • [Cites] Nature. 1998 Feb 19;391(6669):811-4 [9486654.001]
  • [Cites] Nature. 1998 Feb 19;391(6669):815-8 [9486655.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10860-5 [9724795.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2244-51 [9746761.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):7176-84 [9819404.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):7185-91 [9819405.001]
  • [Cites] Cancer Res. 2001 Jan 1;61(1):2-7 [11196162.001]
  • [Cites] J Biol Chem. 2001 Jan 12;276(2):1317-25 [11038364.001]
  • [Cites] Methods Enzymol. 2001;332:36-49 [11305111.001]
  • [Cites] Mol Cell Biol. 2001 Nov;21(21):7172-82 [11585900.001]
  • [Cites] Oncogene. 2001 Oct 29;20(49):7257-65 [11704854.001]
  • [Cites] Science. 2002 Feb 8;295(5557):1079-82 [11834837.001]
  • [Cites] Oncogene. 2002 May 13;21(21):3445-58 [12032781.001]
  • [Cites] Nat Med. 2002 Jul;8(7):743-50 [12091906.001]
  • [Cites] Science. 2002 Jul 5;297(5578):63-4 [12098689.001]
  • [Cites] Science. 2002 Jul 5;297(5578):102-4 [12098700.001]
  • [Cites] Semin Cancer Biol. 2002 Oct;12(5):331-7 [12191632.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2989-95 [12351412.001]
  • [Cites] J Exp Med. 2002 Nov 4;196(9):1227-40 [12417632.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Dec 24;99(26):17107-12 [12475933.001]
  • [Cites] Nat Rev Cancer. 2003 Feb;3(2):89-101 [12563308.001]
  • [Cites] Nat Med. 2003 Apr;9(4):383-6 [12669051.001]
  • [Cites] Stroke. 2003 May;34(5):1304-10 [12677018.001]
  • [Cites] Nat Rev Mol Cell Biol. 2003 Sep;4(9):690-9 [14506472.001]
  • [Cites] Cell. 2003 Oct 31;115(3):305-18 [14636558.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1751-61 [14660751.001]
  • [Cites] Mol Cell Biol. 2004 Feb;24(3):1033-43 [14729951.001]
  • [Cites] Cell. 2004 Feb 20;116(4):511-26 [14980219.001]
  • [Cites] J Exp Med. 2004 Apr 19;199(8):1163-74 [15096541.001]
  • [Cites] Blood. 1991 Mar 1;77(5):1080-6 [1995093.001]
  • [Cites] EMBO J. 1992 Feb;11(2):629-42 [1311253.001]
  • [Cites] Cancer Res. 1992 Jul 1;52(13):3687-92 [1319828.001]
  • [Cites] Blood. 1992 Jul 15;80(2):492-7 [1320955.001]
  • [Cites] Cell. 1993 Aug 13;74(3):423-31 [8394219.001]
  • [ErratumIn] EMBO J. 2005 May 18;24(10):1899
  • (PMID = 15729358.001).
  • [ISSN] 0261-4189
  • [Journal-full-title] The EMBO journal
  • [ISO-abbreviation] EMBO J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / NCOR1 protein, human; 0 / NCOR2 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Nuclear Receptor Co-Repressor 1; 0 / Nuclear Receptor Co-Repressor 2; 0 / Oncogene Proteins, Fusion; 0 / Peptides; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 1C6V77QF41 / Cholecalciferol; 5688UTC01R / Tretinoin
  • [Other-IDs] NLM/ PMC556397
  •  go-up   go-down


21. Choschzick M, Bacher U, Ayuk F, Lebeau A: Immunohistochemistry and molecular analyses in myeloid sarcoma of the breast in a patient with relapse of NPM1-mutated and FLT3-mutated AML after allogeneic stem cell transplantation. J Clin Pathol; 2010 Jun;63(6):558-61
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] Immunohistochemistry and molecular analyses in myeloid sarcoma of the breast in a patient with relapse of NPM1-mutated and FLT3-mutated AML after allogeneic stem cell transplantation.
  • Myeloid sarcoma of the breast is a rare manifestation of acute myeloid leukaemia (AML).
  • This report describes a patient who was diagnosed with AML FAB M2.
  • Molecular analysis showed evidence of an NPM1 mutation (subtype A) and internal tandem duplications of the FLT3 gene (FLT3-ITD).
  • Eight months after allogeneic stem cell transplantation, the patient developed a palpable mass in the left breast initially suspected as breast carcinoma.
  • Core needle biopsy of the lesion resulted in diagnosis of myeloid sarcoma.
  • The myeloid sarcoma showed complete transient resolution following treatment with the kinase inhibitor sorafenib.
  • However, the patient developed bone marrow relapse and died in fatal cerebral haemorrhage 1 year after initial diagnosis of AML.
  • In summary, combined molecular and immunohistochemical examination of NPM1 and FLT3 is helpful in the diagnosis of extramedullary manifestations of AML in core needle biopsies.
  • [MeSH-major] Breast Neoplasms / genetics. Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics. Sarcoma, Myeloid / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Female. Humans. Mutation. Stem Cell Transplantation


22. Qin T, Youssef EM, Jelinek J, Chen R, Yang AS, Garcia-Manero G, Issa JP: Effect of cytarabine and decitabine in combination in human leukemic cell lines. Clin Cancer Res; 2007 Jul 15;13(14):4225-32
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] Effect of cytarabine and decitabine in combination in human leukemic cell lines.
  • PURPOSE: 1-beta-D-Arabinofuranosylcytosine (cytarabine; ara-C) is the most active agent in myeloid leukemia.
  • 5-Aza-2'-deoxycytidine (DAC) is a cytosine analogue that inhibits DNA methylation and also has activity in myeloid leukemia.
  • Therefore, we investigated combining these two drugs in human leukemia cell lines in vitro.
  • EXPERIMENTAL DESIGN: We initially examined the effects of ara-C and DAC on human leukemia cell lines HL60, ML-1, RAji, and Jurkat.
  • We measured IC(50) of DAC and ara-C in these cell lines and calculated a combination index of these two drugs given either simultaneously or sequentially.
  • RESULTS: The combination of DAC and ara-C showed additive induction of cell death in ML-1 and synergistic induction in HL60, Raji, and Jurkat.
  • Sequentially, DAC followed by ara-C was a synergistic combination in all cell lines.
  • CONCLUSION: The combination of DAC and ara-C showed additive or synergistic effects on cell death in four human leukemia cell lines in vitro, but antagonism in terms of epigenetic effects.
  • One possible explanation for these paradoxical observations is that hypomethylated cells are sensitized to cell killing by ara-C.
  • These data suggest that DAC used in combination with ara-C has clinical potential in the treatment of acute myeloid leukemia.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. AZACITIDINE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17634552.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 100632; United States / NCI NIH HHS / CA / CA 108631
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antimetabolites, Antineoplastic; 0 / DNA, Neoplasm; 04079A1RDZ / Cytarabine; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
  •  go-up   go-down


23. Miyake F, Yoshikawa T, Fujita A, Usui C, Akimoto S, Tanaka T, Saito Y, Asano Y: Pneumonia with marked pleural effusion caused by Aspergillus infection. Pediatr Infect Dis J; 2006 Feb;25(2):186-7
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.
  • The patient was previously diagnosed with acute myeloid leukemia, developing the pneumonia during induction treatment.
  • [MeSH-major] Aspergillosis / complications. Lung Diseases, Fungal / complications. Pleural Effusion / etiology. Pneumonia / complications

  • MedlinePlus Health Information. consumer health - Aspergillosis.
  • MedlinePlus Health Information. consumer health - Pneumonia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16462306.001).
  • [ISSN] 0891-3668
  • [Journal-full-title] The Pediatric infectious disease journal
  • [ISO-abbreviation] Pediatr. Infect. Dis. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Fungal
  •  go-up   go-down


24. Haferlach T, Bacher U, Kern W, Schnittger S, Haferlach C: Diagnostic pathways in acute leukemias: a proposal for a multimodal approach. Ann Hematol; 2007 May;86(5):311-27
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] Diagnostic pathways in acute leukemias: a proposal for a multimodal approach.
  • Acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) each represent a heterogeneous complex of disorders, which result from diverse mechanisms of leukemogenesis.
  • Modern therapeutic concepts are based on individual risk stratification at diagnosis and during follow-up.
  • For some leukemia subtypes such as AML M3/M3v with t(15;17)/PML-RARA or Philadelphia-positive ALL targeted therapy options are available.
  • Thus, optimal therapeutic conditions are based on exact classification of the acute leukemia subtype at diagnosis and are guided by exact and sensitive quantification of minimal residual disease during complete hematologic remission.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Leukocytes / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Acute Disease. Algorithms. Chromosome Aberrations / classification. Flow Cytometry. Humans. Immunohistochemistry. Molecular Diagnostic Techniques

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17375301.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 157
  •  go-up   go-down


25. Lee J, Kern WF, Cain JB, Mulvihill JJ, Li S: A variant t(8;10;21) in a patient with pathological features mimicking atypical chronic myeloid leukemia. Cancer Genet Cytogenet; 2005 May;159(1):79-83
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] A variant t(8;10;21) in a patient with pathological features mimicking atypical chronic myeloid leukemia.
  • We report the case of an 11-year-old girl who was initially diagnosed with a chronic myeloproliferative disorder, possibly chronic myelogenous leukemia (CML), based on laboratory and blood and marrow morphological findings.
  • The patient's high leukocyte count did not respond to hydroxyurea, a standard initial therapy for CML.
  • Chromosomal analysis revealed that the patient did not have t(9;22), but a complex t(8;10;21)(q22;q24;q22), a variant of t(8;21).
  • The treatment regime was switched to an acute myeloid leukemia (AML) protocol; the patient responded well and is now in remission.
  • This case demonstrates again that routine clinical cytogenetic analysis plays an important role in the clinical diagnosis, guidance of treatment, and prognostication in hematological disorders.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Genetic Variation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Translocation, Genetic


26. Linabery AM, Blair CK, Gamis AS, Olshan AF, Heerema NA, Ross JA: Congenital abnormalities and acute leukemia among children with Down syndrome: a Children's Oncology Group study. Cancer Epidemiol Biomarkers Prev; 2008 Oct;17(10):2572-7
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] Congenital abnormalities and acute leukemia among children with Down syndrome: a Children's Oncology Group study.
  • Children with Down syndrome, due to their heightened risk of leukemia and increased prevalence of congenital abnormalities, comprise a valuable population in which to study etiology.
  • A Children's Oncology Group study investigated the causes of childhood leukemia in children with Down syndrome diagnosed at ages 0 to 19 years during the period 1997-2002.
  • Telephone interviews were completed with mothers of 158 cases [n=97 acute lymphoblastic leukemia (ALL) and n=61 acute myeloid leukemia (AML)] and 173 controls.
  • Odds ratios (OR) and 95% confidence intervals (95% CI) were computed via unconditional logistic regression to evaluate the association between congenital abnormalities and acute leukemia overall, and ALL and AML analyzed separately.
  • The results do not provide evidence for an association among the index children (OR(Combined), 0.74; 95% CI, 0.45-1.23; OR(ALL), 0.67; 95% CI, 0.38-1.20; OR(AML),1.03; 95% CI, 0.49-2.16) or their siblings (OR(Combined), 1.23; 95% CI, 0.71-2.13; OR(ALL), 1.12; 95% CI, 0.60-2.09; OR(AML), 1.60; 95% CI, 0.66-3.86), suggesting congenital malformations do not confer additional risk of leukemia beyond the risk attributable to trisomy 21 in this population.

  • Genetic Alliance. consumer health - Down Syndrome.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Birth Defects.
  • MedlinePlus Health Information. consumer health - Down Syndrome.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pediatr Hematol Oncol. 1987;4(3):211-30 [2978961.001]
  • [Cites] Am J Hum Genet. 1990 Mar;46(3):478-85 [2309699.001]
  • [Cites] J Pediatr Hematol Oncol. 2001 Mar-Apr;23(3):175-8 [11305722.001]
  • [Cites] Int J Epidemiol. 2001 Apr;30(2):350-2 [11369741.001]
  • [Cites] Int J Pediatr Otorhinolaryngol. 2001 Dec 1;61(3):199-205 [11700189.001]
  • [Cites] Cancer. 2003 Mar 1;97(5):1339-45 [12599243.001]
  • [Cites] Toxicol Appl Pharmacol. 2004 Sep 1;199(2):162-74 [15313588.001]
  • [Cites] Cancer Res. 1991 Jul 15;51(14):3696-701 [2065325.001]
  • [Cites] Leukemia. 1992;6 Suppl 1:5-7 [1532221.001]
  • [Cites] Am J Epidemiol. 1993 Mar 15;137(6):629-38 [8470664.001]
  • [Cites] Br J Cancer. 1993 Aug;68(2):357-63 [8347491.001]
  • [Cites] Cancer. 1996 Jan 1;77(1):201-7 [8630931.001]
  • [Cites] Am J Hum Genet. 1997 Mar;60(3):474-85 [9042906.001]
  • [Cites] Am J Med Genet. 1998 Jan 6;75(1):22-7 [9450852.001]
  • [Cites] Am J Med Genet. 1998 Jun 5;77(5):431-8 [9632176.001]
  • [Cites] Br J Cancer. 1998 Nov;78(9):1244-9 [9820188.001]
  • [Cites] J Pediatr. 1998 Nov;133(5):617-23 [9821417.001]
  • [Cites] Arch Dis Child. 1999 Jan;80(1):1-3 [10325750.001]
  • [Cites] Pediatr Blood Cancer. 2005 Jan;44(1):8-12 [15390275.001]
  • [Cites] Cancer. 2005 May 1;103(9):1939-48 [15770693.001]
  • [Cites] Cancer. 2005 Jul 15;104(2):405-10 [15952191.001]
  • [Cites] J Pediatr Health Care. 2006 Jan-Feb;20(1):47-54 [16399479.001]
  • [Cites] Nature. 2006 Jun 1;441(7093):595-600 [16554754.001]
  • [Cites] Pediatrics. 2006 Nov;118(5):e1499-508 [17030598.001]
  • [Cites] Curr Opin Pediatr. 2007 Feb;19(1):9-14 [17224656.001]
  • [Cites] JAMA. 2008 Jan 2;299(1):61-9 [18167407.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Mar;17(3):500-6 [18296646.001]
  • [Cites] Lancet. 1981 Nov 7;2(8254):1020-2 [6118480.001]
  • [Cites] Dev Med Child Neurol. 1982 Dec;24(6):817-29 [6218002.001]
  • [Cites] Lancet. 2000 Jan 15;355(9199):165-9 [10675114.001]
  • (PMID = 18829445.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA016086-259036; United States / NIEHS NIH HHS / ES / P30 ES10126; United States / NCI NIH HHS / CA / T32 CA099936-01A1; United States / NIEHS NIH HHS / ES / P30 ES010126; United States / NCI NIH HHS / CA / R01 CA075169-03; United States / NCI NIH HHS / CA / P30 CA016086; United States / NCI NIH HHS / CA / R01 CA075169; United States / NCI NIH HHS / CA / R01 CA75169; United States / NCI NIH HHS / CA / CA075169-03; United States / NCI NIH HHS / CA / T32 CA099936; United States / NCI NIH HHS / CA / P30 CA016086-259036; United States / NCI NIH HHS / CA / CA099936-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS78459; NLM/ PMC2610427
  •  go-up   go-down


27. Ishikawa Y, Kiyoi H, Tsujimura A, Miyawaki S, Miyazaki Y, Kuriyama K, Tomonaga M, Naoe T: Comprehensive analysis of cooperative gene mutations between class I and class II in de novo acute myeloid leukemia. Eur J Haematol; 2009 Aug;83(2):90-8
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] Comprehensive analysis of cooperative gene mutations between class I and class II in de novo acute myeloid leukemia.
  • Acute myeloid leukemia (AML) has been thought to be the consequence of two broad complementation classes of mutations: class I and class II.
  • However, overlap-mutations between them or within the same class and the position of TP53 mutation are not fully analyzed.
  • We comprehensively analyzed the FLT3, cKIT, N-RAS, C/EBPA, AML1, MLL, NPM1, and TP53 mutations in 144 newly diagnosed de novo AML.
  • However, mutated genes overlapped with the same class were limited in N-RAS, TP53, MLL-PTD, and NPM1, suggesting the possibility that these irregular overlap-mutations might cooperatively participate in the development of AML.
  • Notably, TP53 mutation was overlapped with both class I and class II mutations, and associated with morphologic multilineage dysplasia and complex karyotype.
  • The genotype consisting of complex karyotype and TP53 mutation was an unfavorable prognostic factor in entire AML patients, indicating this genotype generates a disease entity in de novo AML.
  • [MeSH-major] Cytogenetic Analysis. Leukemia, Myeloid, Acute / genetics. Mutation
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. CCAAT-Enhancer-Binding Proteins / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Female. Genotype. Humans. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Oncogene Protein p21(ras) / genetics. Prognosis. Proto-Oncogene Proteins c-kit / genetics. Risk Factors. Tumor Suppressor Protein p53 / genetics. fms-Like Tyrosine Kinase 3 / genetics

  • 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 = 19309322.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Nuclear Proteins; 0 / RUNX1 protein, human; 0 / Tumor Suppressor Protein p53; 117896-08-9 / nucleophosmin; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.5.2 / Oncogene Protein p21(ras)
  •  go-up   go-down


28. Sun Y, Boyd K, Xu W, Ma J, Jackson CW, Fu A, Shillingford JM, Robinson GW, Hennighausen L, Hitzler JK, Ma Z, Morris SW: Acute myeloid leukemia-associated Mkl1 (Mrtf-a) is a key regulator of mammary gland function. Mol Cell Biol; 2006 Aug;26(15):5809-26
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] Acute myeloid leukemia-associated Mkl1 (Mrtf-a) is a key regulator of mammary gland function.
  • Extracellular signals regulate Srf in part via a pathway involving megakaryoblastic leukemia 1 (Mkl1, also known as myocardin-related transcription factor A [Mrtf-a]), which coactivates Srf-responsive genes downstream of Rho GTPases.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Oxytocin .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • SciCrunch. Marmoset Gene list: Data: Gene Annotation .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 1992 Mar 15;267(8):5021-4 [1371993.001]
  • [Cites] Nat Genet. 2000 May;25(1):25-9 [10802651.001]
  • [Cites] Adv Exp Med Biol. 2000;480:129-38 [10959419.001]
  • [Cites] J Biol Chem. 2000 Sep 15;275(37):29123-31 [10867011.001]
  • [Cites] Oncogene. 2000 Dec 14;19(54):6386-91 [11175354.001]
  • [Cites] Curr Top Dev Biol. 2001;51:69-89 [11236716.001]
  • [Cites] J Clin Invest. 2001 Apr;107(7):823-34 [11285301.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 May 8;98(10):5776-9 [11344311.001]
  • [Cites] J Biol Chem. 2001 May 25;276(21):18313-20 [11359793.001]
  • [Cites] Pflugers Arch. 2001 Apr;442(1):57-63 [11374069.001]
  • [Cites] Biochem J. 2001 Jul 1;357(Pt 1):33-8 [11415433.001]
  • [Cites] Nat Genet. 2001 Jul;28(3):220-1 [11431691.001]
  • [Cites] J Biol Chem. 2001 Jul 6;276(27):24531-9 [11342553.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9440-5 [12883005.001]
  • [Cites] Circ Res. 2003 Aug 22;93(4):292-301 [12933700.001]
  • [Cites] Mol Cell Biol. 2003 Sep;23(18):6597-608 [12944485.001]
  • [Cites] Bioinformatics. 2003 Oct 12;19(15):1945-51 [14555628.001]
  • [Cites] J Biol Chem. 2003 Oct 24;278(43):41977-87 [14565952.001]
  • [Cites] Cells Tissues Organs. 2003;175(2):72-83 [14605486.001]
  • [Cites] Nucleic Acids Res. 2004;32(4):1372-81 [14988425.001]
  • [Cites] J Biol Chem. 2004 Mar 5;279(10):9557-64 [14662765.001]
  • [Cites] J Biol Chem. 2004 Apr 23;279(17):17578-86 [14970199.001]
  • [Cites] Dev Cell. 2004 Jul;7(1):85-93 [15239956.001]
  • [Cites] BMC Mol Biol. 2004 Aug 25;5:13 [15329155.001]
  • [Cites] Curr Opin Genet Dev. 2004 Oct;14(5):558-66 [15380248.001]
  • [Cites] Genome Biol. 2004;5(10):R80 [15461798.001]
  • [Cites] Endocrinology. 1966 Mar;78(3):522-6 [4286621.001]
  • [Cites] J Cell Biol. 1973 Mar;56(3):797-818 [4569313.001]
  • [Cites] Cell Tissue Res. 1980;209(1):1-10 [7191782.001]
  • [Cites] Biochem J. 1985 Jan 15;225(2):463-72 [3977840.001]
  • [Cites] J Natl Cancer Inst. 1986 Aug;77(2):343-9 [2426509.001]
  • [Cites] Cell. 2001 Jun 29;105(7):851-62 [11439182.001]
  • [Cites] Nat Rev Mol Cell Biol. 2001 Aug;2(8):589-98 [11483992.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Jan;33(1):22-8 [11746984.001]
  • [Cites] J Clin Invest. 2001 Dec;108(12):1735-40 [11748254.001]
  • [Cites] J Biol Chem. 2002 Aug 9;277(32):28853-60 [12019265.001]
  • [Cites] Endocrinology. 2002 Sep;143(9):3641-50 [12193580.001]
  • [Cites] Development. 2002 Oct;129(19):4547-57 [12223411.001]
  • [Cites] J Mol Cell Cardiol. 2002 Oct;34(10):1345-56 [12392995.001]
  • [Cites] Mol Biol Cell. 2002 Nov;13(11):4088-99 [12429848.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):14855-60 [12397177.001]
  • [Cites] Nucleic Acids Res. 2003 Jan 1;31(1):374-8 [12520026.001]
  • [Cites] Mol Cell Biol. 2003 Apr;23(7):2425-37 [12640126.001]
  • [Cites] J Histochem Cytochem. 2003 May;51(5):555-65 [12704203.001]
  • [Cites] J Cell Sci. 1991 Nov;100 ( Pt 3):459-71 [1808200.001]
  • [Cites] Curr Opin Genet Dev. 1994 Feb;4(1):96-101 [8193547.001]
  • [Cites] J Cell Sci. 1994 Oct;107 ( Pt 10):2931-9 [7876358.001]
  • [Cites] J Biol Chem. 1995 Mar 31;270(13):7365-74 [7706280.001]
  • [Cites] Eur J Biochem. 1995 Apr 1;229(1):1-13 [7744019.001]
  • [Cites] Cell. 1995 Jun 30;81(7):1159-70 [7600583.001]
  • [Cites] Biochim Biophys Acta. 1995 Jul 28;1242(1):1-10 [7626651.001]
  • [Cites] Biochim Biophys Acta. 1996 Jul 18;1275(1-2):127-32 [8688445.001]
  • [Cites] Hum Mol Genet. 1996 Jun;5(6):711-25 [8776585.001]
  • [Cites] Eur J Cell Biol. 1997 Jun;73(2):158-65 [9208229.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Oct 20;239(2):598-605 [9344877.001]
  • [Cites] Mol Cell Biol. 1998 Apr;18(4):2108-17 [9528783.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jun 8;96(12):6964-9 [10359822.001]
  • [Cites] Cell. 1999 Jul 23;98(2):159-69 [10428028.001]
  • [Cites] Genes Dev. 1999 Oct 1;13(19):2604-16 [10521404.001]
  • [Cites] J Physiol. 1955 Nov 28;130(2):257-67 [13278901.001]
  • [Cites] Breast Cancer Res. 2004;6(2):R75-91 [14979920.001]
  • [Cites] Breast Cancer Res. 2004;6(2):R92-109 [14979921.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 25;102(4):1082-7 [15647354.001]
  • [Cites] Nature. 2005 Mar 31;434(7033):652-8 [15800626.001]
  • [Cites] Nature. 2005 Mar 31;434(7033):658-62 [15800627.001]
  • [Cites] Nat Cell Biol. 2005 Apr;7(4):392-8 [15793565.001]
  • [Cites] J Biol Chem. 2005 May 13;280(19):19115-26 [15699019.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Jun;6(6):505-10 [15928714.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 21;102(25):8916-21 [15951419.001]
  • [Cites] Oncogene. 2005 Sep 15;24(41):6314-22 [16007201.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 18;102(42):15122-7 [16204380.001]
  • [Cites] Mol Cell Biol. 2006 Aug;26(15):5797-808 [16847332.001]
  • [Cites] Circ Res. 2003 May 2;92(8):856-64 [12663482.001]
  • [Cites] Cell. 2003 May 2;113(3):329-42 [12732141.001]
  • [Cites] J Mol Cell Cardiol. 2003 Jun;35(6):577-93 [12788374.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jun 10;100(12):7129-34 [12756293.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 2002;67:97-105 [12858529.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9366-70 [12867591.001]
  • [Cites] Cell. 1988 Dec 23;55(6):989-1003 [3203386.001]
  • [Cites] J Histochem Cytochem. 1989 Jul;37(7):1087-100 [2471725.001]
  • [Cites] J Cell Sci. 1989 Nov;94 ( Pt 3):545-52 [2534395.001]
  • [Cites] Differentiation. 1991 Apr;46(3):209-21 [1833254.001]
  • (PMID = 16847333.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA087064; United States / PHS HHS / / 21765; United States / NCI NIH HHS / CA / CA 87064; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MKL1 protein, mouse; 0 / STAT3 Transcription Factor; 0 / Serum Response Factor; 0 / Stat3 protein, mouse; 0 / Trans-Activators; 50-56-6 / Oxytocin; 9002-62-4 / Prolactin
  • [Other-IDs] NLM/ PMC1592762
  •  go-up   go-down


29. Ziegler S, Sperr WR, Knöbl P, Lehr S, Weltermann A, Jäger U, Valent P, Lechner K: Symptomatic venous thromboembolism in acute leukemia. Incidence, risk factors, and impact on prognosis. Thromb Res; 2005;115(1-2):59-64
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] Symptomatic venous thromboembolism in acute leukemia. Incidence, risk factors, and impact on prognosis.
  • No systematic study on the incidence and prognostic impact of venous thromboembolism in acute leukemia has been performed as yet.
  • We retrospectively evaluated the incidence of symptomatic venous thromboembolism before chemotherapy in 719 patients (371 males and 348 females, median age of 57.4 years), diagnosed with acute leukemia [534 with acute myelogenous leukemia, 185 with acute lymphoblastic leukemia].
  • Fifteen patients (2.09%) had venous thromboembolism (objectively confirmed in 13 patients) in close temporal relationship to the onset of acute leukemia.
  • The incidence of venous thromboembolism was the same in acute myelogenous and lymphoblastic leukemia.
  • Venous thromboembolism occurred in all subtypes of acute leukemia, but was most common in promyelocytic leukemia.
  • Overall, survival, disease-free survival, and remission duration did not differ between the patient groups with and without venous thromboembolism.
  • In contrast to solid tumors, venous thromboembolism before or at diagnosis of acute leukemia is not associated with poor prognosis.
  • [MeSH-major] Leukemia / complications. Thromboembolism / etiology. Venous Thrombosis / etiology
  • [MeSH-minor] Acute Disease. Anticoagulants / therapeutic use. Antineoplastic Agents / therapeutic use. Female. Humans. Incidence. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / etiology. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Prognosis. Remission Induction. Retrospective Studies. Risk Factors. Survival Analysis

  • MedlinePlus Health Information. consumer health - Deep Vein Thrombosis.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15567454.001).
  • [ISSN] 0049-3848
  • [Journal-full-title] Thrombosis research
  • [ISO-abbreviation] Thromb. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Antineoplastic Agents
  •  go-up   go-down


30. Krishnan B, Morgan GJ: Non-Hodgkin lymphoma secondary to cancer chemotherapy. Cancer Epidemiol Biomarkers Prev; 2007 Mar;16(3):377-80
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] Non-Hodgkin lymphoma secondary to cancer chemotherapy.
  • Therapy-related acute myeloid leukemia has been frequently documented in these patient cohorts, and its biology well studied.
  • Recognition of secondary non-Hodgkin lymphoma as a cause of significant morbidity and mortality in these patients is equally important.
  • The patterns of incidence and latency of secondary lymphomas is distinct from that of myeloid malignancies and other solid cancers.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Lymphoma, Non-Hodgkin / chemically induced. Neoplasms / drug therapy. Neoplasms, Second Primary / chemically induced

  • Genetic Alliance. consumer health - Hodgkin lymphoma.
  • Genetic Alliance. consumer health - Non-Hodgkin Lymphoma.
  • 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
  • (PMID = 17372233.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 24
  •  go-up   go-down


31. Capria S, Gentile G, Capobianchi A, Cardarelli L, Gianfelici V, Trisolini SM, Foà R, Martino P, Meloni G: Prospective cytomegalovirus monitoring during first-line chemotherapy in patients with acute myeloid leukemia. J Med Virol; 2010 Jul;82(7):1201-7
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] Prospective cytomegalovirus monitoring during first-line chemotherapy in patients with acute myeloid leukemia.
  • Little is known about the incidence and clinical impact of cytomegalovirus (CMV) infection in patients with acute myeloid leukemia at the time of diagnosis and during chemotherapy.
  • The aims of the present study were to assess prospectively the incidence of active CMV infection in 69 consecutive patients with acute myeloid leukemia and to describe the outcomes of treatment. pp65 antigenemia was monitored at diagnosis, post-induction and post-consolidation chemotherapy, and whenever CMV reactivation was suspected.
  • Five patients received no anti-CMV treatment and did not develop CMV disease.
  • In conclusion, patients with acute myeloid leukemia receiving chemotherapy should be monitored for active CMV infection.
  • Controlled studies are needed to assess the relevance of pre-emptive anti-CMV therapy in patients with acute myeloid leukemia receiving chemotherapy.
  • [MeSH-major] Antiviral Agents / therapeutic use. Cytarabine / therapeutic use. Cytomegalovirus / isolation & purification. Cytomegalovirus Infections / drug therapy. Cytomegalovirus Infections / epidemiology. Leukemia, Myeloid, Acute / virology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Cytomegalovirus Infections.
  • Hazardous Substances Data Bank. HYDROXYUREA .
  • 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
  • [Copyright] (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20513085.001).
  • [ISSN] 1096-9071
  • [Journal-full-title] Journal of medical virology
  • [ISO-abbreviation] J. Med. Virol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Viral; 0 / Antigens, Viral; 0 / Antineoplastic Agents; 0 / Antiviral Agents; 0 / Phosphoproteins; 0 / Viral Matrix Proteins; 0 / cytomegalovirus matrix protein 65kDa; 04079A1RDZ / Cytarabine; X6Q56QN5QC / Hydroxyurea; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


32. Peterson LF, Yan M, Zhang DE: The p21Waf1 pathway is involved in blocking leukemogenesis by the t(8;21) fusion protein AML1-ETO. Blood; 2007 May 15;109(10):4392-8
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] The p21Waf1 pathway is involved in blocking leukemogenesis by the t(8;21) fusion protein AML1-ETO.
  • The 8;21 translocation is a major contributor to acute myeloid leukemia (AML) of the M2 classification occurring in approximately 40% of these cases.
  • Here, we show that the negative cell cycle regulator p21(WAF1) gene is up-regulated by AML1-ETO at the protein, RNA, and promoter levels.
  • Retroviral transduction and hematopoietic cell transplantation experiments with p21(WAF1)-deficient cells show that AML1-ETO is able to promote leukemogenesis in the absence of p21(WAF1).
  • Thus, loss of p21(WAF1) facilitates AML1-ETO-induced leukemogenesis, suggesting that mutagenic events in the p21(WAF1) pathway to bypass the growth inhibitory effect from AML1-ETO-induced p21(WAF1) expression can be a significant factor in AML1-ETO-associated acute myeloid leukemia.

  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • Addgene Non-profit plasmid repository. clones/clone libraries - Get Article's Plasmids - Addgene (subscription/membership/fee required).
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Science. 1997 Sep 26;277(5334):1996-2000 [9302295.001]
  • [Cites] Leukemia. 1997 Oct;11(10):1696-9 [9324291.001]
  • [Cites] Blood. 1997 Nov 1;90(9):3707-13 [9345056.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1812-7 [9465099.001]
  • [Cites] Blood. 1998 May 1;91(9):3134-43 [9558367.001]
  • [Cites] Blood. 1998 Jun 1;91(11):4028-37 [9596646.001]
  • [Cites] Leukemia. 1998 Jun;12(6):893-8 [9639417.001]
  • [Cites] Gene. 1998 May 28;212(1):103-9 [9661669.001]
  • [Cites] EMBO J. 1999 Mar 1;18(5):1223-34 [10064589.001]
  • [Cites] Blood. 1999 Mar 15;93(6):2067-74 [10068680.001]
  • [Cites] Cancer Res. 1999 Mar 15;59(6):1259-67 [10096557.001]
  • [Cites] Genes Dev. 1999 Jun 15;13(12):1501-12 [10385618.001]
  • [Cites] Oncogene. 1999 Jul 15;18(28):4055-62 [10435586.001]
  • [Cites] Oncogene. 1999 Sep 23;18(39):5381-92 [10498892.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):166-75 [10508512.001]
  • [Cites] Mol Cell Biol. 2004 Apr;24(7):2890-904 [15024077.001]
  • [Cites] Mol Cell Biol. 1996 Jun;16(6):2987-97 [8649410.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 7;101(49):17186-91 [15569932.001]
  • [Cites] Mol Cell Biol. 2005 Mar;25(6):2419-30 [15743834.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4523-6 [15705784.001]
  • [Cites] J Clin Invest. 2005 Aug;115(8):2159-68 [16025155.001]
  • [Cites] Leuk Res. 2005 Nov;29(11):1357-60 [15936816.001]
  • [Cites] Gene Ther. 2005 Oct;12(19):1444-52 [15877047.001]
  • [Cites] Cell Cycle. 2005 Aug;4(8):1113-9 [16082198.001]
  • [Cites] Mol Cell Biol. 2005 Dec;25(23):10205-19 [16287839.001]
  • [Cites] Am J Hematol. 2005 Dec;80(4):282-7 [16315255.001]
  • [Cites] Leukemia. 2006 Feb;20(2):224-9 [16357831.001]
  • [Cites] J Cell Physiol. 2006 Jun;207(3):582-93 [16250015.001]
  • [Cites] Blood. 2006 Apr 15;107(8):3303-12 [16380455.001]
  • [Cites] Cancer Cell. 2006 Apr;9(4):249-60 [16616331.001]
  • [Cites] J Cell Physiol. 2006 Sep;208(3):594-601 [16741927.001]
  • [Cites] J Biol Chem. 1996 Jun 28;271(26):15782-6 [8663132.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4255-62 [15156181.001]
  • [Cites] Cancer Res. 2004 Jul 1;64(13):4547-54 [15231665.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 19;101(42):15184-9 [15477599.001]
  • [Cites] Blood. 1984 Jul;64(1):318-20 [6329379.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Dec 1;88(23):10431-4 [1720541.001]
  • [Cites] Mol Cell Biol. 1993 Oct;13(10):6336-45 [8413232.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):4004-8 [8171026.001]
  • [Cites] Nature. 1994 Jun 16;369(6481):574-8 [7911228.001]
  • [Cites] Nature. 1994 Oct 6;371(6497):534-7 [7935768.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 May 23;92(11):4917-21 [7761424.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jun 6;92(12):5545-9 [7777546.001]
  • [Cites] Cell. 1995 Aug 25;82(4):675-84 [7664346.001]
  • [Cites] Oncogene. 1995 Nov 2;11(9):1761-9 [7478604.001]
  • [Cites] Cell. 1996 Jan 26;84(2):321-30 [8565077.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3444-9 [8622955.001]
  • [Cites] Proc Assoc Am Physicians. 1995 Jul;107(2):175-80 [8624850.001]
  • [Cites] J Biol Chem. 2000 Jan 7;275(1):651-6 [10617663.001]
  • [Cites] Science. 2000 Mar 10;287(5459):1804-8 [10710306.001]
  • [Cites] Mol Cell Biol. 2000 Apr;20(8):2676-86 [10733570.001]
  • [Cites] Oncogene. 2000 May 15;19(21):2511-22 [10851050.001]
  • [Cites] J Biol Chem. 2000 Jun 23;275(25):18794-800 [10764767.001]
  • [Cites] Blood. 2000 Jul 15;96(2):655-63 [10887131.001]
  • [Cites] Blood. 2000 Sep 15;96(6):2108-15 [10979955.001]
  • [Cites] Mol Cell Biol. 2001 Aug;21(16):5577-90 [11463839.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10398-403 [11526243.001]
  • [Cites] Oncogene. 2001 Sep 10;20(40):5660-79 [11607817.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1364-72 [11830488.001]
  • [Cites] Leukemia. 2002 May;16(5):874-85 [11986950.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):63-74 [12086889.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(15):5506-17 [12101243.001]
  • [Cites] J Exp Med. 2002 Nov 4;196(9):1227-40 [12417632.001]
  • [Cites] J Biol Chem. 2002 Dec 6;277(49):47338-47 [12354776.001]
  • [Cites] Cell Cycle. 2002 Sep-Oct;1(5):343-50 [12461297.001]
  • [Cites] Gene. 2003 Jan 16;303:1-10 [12559562.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3157-63 [12480707.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1665-6 [12886257.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9506-11 [12881486.001]
  • [Cites] Oncogene. 2003 Aug 28;22(36):5646-57 [12944913.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1751-61 [14660751.001]
  • [Cites] Blood. 2004 Jan 15;103(2):743-6 [14702288.001]
  • [Cites] J Biol Chem. 2004 Jan 9;279(2):825-30 [14561740.001]
  • [Cites] Mol Pharmacol. 2004 Mar;65(3):571-81 [14978235.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Mar 26;316(1):85-92 [15003515.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):14059-64 [8943060.001]
  • [Cites] J Immunol. 1997 Mar 1;158(5):2251-8 [9036972.001]
  • [Cites] Nat Genet. 1997 Mar;15(3):303-6 [9054947.001]
  • [Cites] Leuk Lymphoma. 1997 Jun;26(1-2):35-41 [9250785.001]
  • (PMID = 17284535.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096735; United States / NCI NIH HHS / CA / CA96735
  • [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 / AML1-ETO fusion protein, human; 0 / CDKN1A protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Oncogene Proteins, Fusion
  • [Other-IDs] NLM/ PMC1885483
  •  go-up   go-down


33. Kuendgen A, Lübbert M: Current status of epigenetic treatment in myelodysplastic syndromes. Ann Hematol; 2008 Aug;87(8):601-11
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.
  • The great interest in epigenetics in hematology and oncology results from the fact that epigenetic, in contrast to genetic, alterations are, in principle, amenable to pharmacological reversal.
  • The largest experience in MDS and acute myeloid leukemia exists with the anticonvulsant valproic acid.


34. Grimwade D, Hills RK: Independent prognostic factors for AML outcome. Hematology Am Soc Hematol Educ Program; 2009;:385-95
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] Independent prognostic factors for AML outcome.
  • Over the last three decades there have been dramatic advances in deciphering the cytogenetic and molecular lesions underlying the pathogenesis of acute myeloid leukemia (AML).
  • These have not only afforded greater insights into disease biology, but also provided useful information predicting the likelihood of any given patient achieving and maintaining remission following conventional chemotherapy, leading to the development of risk-stratified treatment approaches.
  • However, it is becoming increasingly apparent that AML is highly heterogeneous at the molecular level.
  • Defining the individual genetic abnormalities or combinations of markers that provide significant independent prognostic information and establishing their respective relationships to other pre-treatment characteristics that impact on outcome, such as age and presenting white blood cell count, presents a major ongoing challenge.
  • Moreover, there is increasing evidence that risk of relapse and overall survival can be predicted by assessment of kinetics and depth of response following front-line therapy and monitoring of the leukemic burden using molecular or immunological approaches to minimal residual disease (MRD) detection.
  • These advances present the exciting prospect that panels of pre-treatment parameters affording independent prognostic information can be integrated with precise measurement of treatment response using MRD technologies to provide greater refinement in risk-adapted management of AML.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20008224.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Number-of-references] 44
  •  go-up   go-down


35. Wang YZ, Liu YR, Zhu HH, Wu HH, Cao H, Chan Y, Hao L, Jiang B, Huang XJ: [Prognostic significance of minimal residual disease detected by multiparameter flow cytometry in acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Jun;17(3):551-6
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] [Prognostic significance of minimal residual disease detected by multiparameter flow cytometry in acute myeloid leukemia].
  • This study was aimed to explore prognostic significance of minimal residual disease (MRD) detection in patients with acute myeloid leukemia (AML) by multiparameter flow cytometry (MCF).
  • Leukemia-associated immunophenotype (LAIP) of newly diagnosed AML patients were determined by 4-color 5 antibody panels and patients with sensitive LAIP were chosen for MRD detection.
  • Patients with MRD positive had a median relapse-free survival time of 11 months, 11.5 months and 11 months at 1 - 2, 3 - 4 and 5 - 6 months respectively, while all patients with MRD negative were not observed to reach median release-free survival time (p < 0.05).
  • It is concluded that MRD detection by multi-parameter flow cytometry can predict outcome of AML patients, which should be continuously monitored after treatment.

  • 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 = 19549362.001).
  • [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; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  •  go-up   go-down


36. Bradbury CA, Khanim FL, Hayden R, Bunce CM, White DA, Drayson MT, Craddock C, Turner BM: Histone deacetylases in acute myeloid leukaemia show a distinctive pattern of expression that changes selectively in response to deacetylase inhibitors. Leukemia; 2005 Oct;19(10):1751-9
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] Histone deacetylases in acute myeloid leukaemia show a distinctive pattern of expression that changes selectively in response to deacetylase inhibitors.
  • To explore mechanisms of disease-specific HDI activity in acute myeloid leukaemia (AML), we have characterised expression of all 18 members of the histone deacetylase family in primary AML blasts and in four control cell types, namely CD34+ progenitors from umbilical cord, either quiescent or cycling (post-culture), cycling CD34+ progenitors from GCSF-stimulated adult donors and peripheral blood mononuclear cells.
  • Only SIRT1 was consistently overexpressed (>2 fold) in AML samples compared with all controls, while HDAC6 was overexpressed relative to adult, but not neo-natal cells.
  • AML blasts and cell lines, exposed to HDIs in culture, showed both histone hyperacetylation and, unexpectedly, specific hypermethylation of H3 lysine 4.
  • Such treatment also modulated the pattern of HDAC expression, with strong induction of HDAC11 in all myeloid cells tested and with all inhibitors (valproate, butyrate, TSA, SAHA), and lesser, more selective, induction of HDAC9 and SIRT4.
  • The distinct pattern of HDAC expression in AML and its response to HDIs is of relevance to the development of HDI-based therapeutic strategies and may contribute to observed patterns of clinical response and development of drug resistance.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Histone Deacetylases / metabolism. Histones / metabolism. Leukemia, Myeloid / enzymology
  • [MeSH-minor] Acetylation. Acute Disease. Adult. Antigens, CD34 / metabolism. Butyrates / pharmacology. DNA Methylation. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Hydroxamic Acids / pharmacology. Myeloid Cells. Tumor Cells, Cultured. Valproic Acid / pharmacology

  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. Vorinostat .
  • Hazardous Substances Data Bank. VALPROIC ACID .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16121216.001).
  • [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 / Antigens, CD34; 0 / Butyrates; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Hydroxamic Acids; 3X2S926L3Z / trichostatin A; 58IFB293JI / vorinostat; 614OI1Z5WI / Valproic Acid; EC 3.5.1.98 / Histone Deacetylases
  •  go-up   go-down


37. Hildebrandt A, Hunfeld KP, Baier M, Krumbholz A, Sachse S, Lorenzen T, Kiehntopf M, Fricke HJ, Straube E: First confirmed autochthonous case of human Babesia microti infection in Europe. Eur J Clin Microbiol Infect Dis; 2007 Aug;26(8):595-601
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.
  • A 42-year-old female patient with acute myeloid leukemia presented with fever and heavy chest pain after her first cycle of specific chemotherapy.
  • Acute myocardial infarction was excluded, but surprisingly, parasitic inclusions in erythrocytes became obvious in Pappenheim and Giemsa-stained peripheral blood smears.
  • The patient did not remember a tick bite but acknowledged having received several blood transfusions in her recent medical history.
  • Suspicion of malaria was ruled out by use of a dip-stick test.
  • The diagnosis of Babesia microti infection was finally established by specific polymerase chain reaction (PCR).
  • [MeSH-major] Babesia microti / pathogenicity. Babesiosis / diagnosis. Blood Transfusion / adverse effects. Zoonoses / transmission
  • [MeSH-minor] Acute Disease. Adult. Animals. Blood Donors. Female. Furans. Germany. Humans. Leukemia, Myeloid. Thiophenes

  • MedlinePlus Health Information. consumer health - Animal Diseases and Your Health.
  • MedlinePlus Health Information. consumer health - Blood Transfusion and Donation.
  • COS Scholar Universe. author profiles.
  • SILVA. SILVA SSU Database .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Microbiol. 2000 Jan;38(1):362-8 [10618117.001]
  • [Cites] Med Microbiol Immunol. 2004 Nov;193(4):219-26 [13680214.001]
  • [Cites] Tropenmed Parasitol. 1981 Dec;32(4):228-30 [7345687.001]
  • [Cites] J Clin Microbiol. 2002 Jul;40(7):2431-6 [12089258.001]
  • [Cites] Emerg Infect Dis. 2002 Jul;8(7):722-6 [12095442.001]
  • [Cites] Int J Parasitol. 2006 Jun;36(7):779-89 [16725142.001]
  • [Cites] Clin Microbiol Rev. 2000 Jul;13(3):451-69 [10885987.001]
  • [Cites] Transfusion. 1991 May;31(4):296-8 [2020992.001]
  • [Cites] Emerg Infect Dis. 2003 Aug;9(8):942-8 [12967491.001]
  • [Cites] J Clin Microbiol. 2000 Dec;38(12):4511-6 [11101588.001]
  • [Cites] Int J Med Microbiol. 2006 May;296 Suppl 40:131-6 [16524772.001]
  • [Cites] Int J Parasitol. 1986 Aug;16(4):381-5 [3744675.001]
  • [Cites] Curr Opin Hematol. 2003 Nov;10(6):405-11 [14564169.001]
  • [Cites] Doc Med Geogr Trop. 1957 Mar;9(1):11-6 [13427667.001]
  • [Cites] Curr Microbiol. 2004 Jun;48(6):435-7 [15170239.001]
  • [Cites] Clin Microbiol Rev. 2003 Oct;16(4):622-36 [14557289.001]
  • [Cites] Parasitology. 2003 Oct;127(Pt 4):301-9 [14636016.001]
  • [Cites] Ann Trop Med Parasitol. 1998 Jun;92(4):489-501 [9683900.001]
  • [Cites] Int J Med Microbiol. 2004 Apr;293 Suppl 37:86-92 [15146989.001]
  • [Cites] N Engl J Med. 1998 Jul 16;339(3):160-5 [9664092.001]
  • [Cites] Pharmacogenomics J. 2001;1(3):167-70 [11908751.001]
  • [Cites] Int J Med Microbiol. 2004 Apr;293 Suppl 37:93-103 [15146990.001]
  • (PMID = 17587072.001).
  • [ISSN] 0934-9723
  • [Journal-full-title] European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology
  • [ISO-abbreviation] Eur. J. Clin. Microbiol. Infect. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 3,4-bis-(2,4,5-trimethyl-thiophen-3-yl)furan-2,5-dione; 0 / Furans; 0 / Thiophenes
  •  go-up   go-down


38. Natelson EA: Benzene exposure and refractory sideroblastic erythropoiesis: is there an association? Am J Med Sci; 2007 Nov;334(5):356-60
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.
  • The myelodysplastic syndromes (MDS) consist of a group of diverse hematological disorders that carry an increased risk of transforming into acute myeloid leukemia.
  • They may appear de novo and without obvious cause (primary or de novo MDS) or be induced by certain mutagenic environmental or therapeutic toxins (secondary MDS).
  • Excessive exposures to benzene are generally considered to be a potential environmental risk factor for both MDS and acute myeloid leukemia.
  • However, such risk is unproven for each disease component within the MDS classification.
  • A critical review of the refractory sideroblastic disorders strongly suggests that benzene exposure is not a potential cause of this distinct and still-evolving subset of MDS.
  • The widely disparate nature of MDS suggests that epidemiologic studies can only provide meaningful data on associations and potential causation of its component syndromes by a disease-specific analysis, as is currently advocated for other hematological malignancies.
  • [MeSH-minor] Erythropoiesis / physiology. Humans. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / physiopathology. Risk Factors

  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • Hazardous Substances Data Bank. BENZENE .
  • 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 = 18004090.001).
  • [ISSN] 0002-9629
  • [Journal-full-title] The American journal of the medical sciences
  • [ISO-abbreviation] Am. J. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Environmental Pollutants; J64922108F / Benzene
  • [Number-of-references] 59
  •  go-up   go-down


39. McGrath P, Paton MA, Huff N: Beginning treatment for pediatric acute myeloid leukemia: the family connection. Issues Compr Pediatr Nurs; 2005 Apr-Jun;28(2):97-114
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] Beginning treatment for pediatric acute myeloid leukemia: the family connection.
  • There is a loud silence on psycho-oncology research in relation to pediatric Acute Myeloid Leukemia (AML).
  • This article is part of a series that begins to address the psycho-social hiatus.
  • The present article documents the less obvious, often hidden, aspect of beginning treatment for pediatric AML--the "behind the scenes" experience of the home and family connection.
  • The findings are from the first stage of a five year longitudinal study that examines through qualitative research the experience of childhood leukemia from the perspective of the child, siblings and parents.
  • Open-ended interviews, audio-recorded and transcribed verbatim, were thematically analyzed with the assistance of the Non-numerical Unstructured Data by processes of Indexing Searching and Theory-building (NUD*IST) computer program.
  • The findings emphasise the need for support for families coping with childhood AML.
  • [MeSH-major] Adaptation, Psychological. Attitude to Health. Child, Hospitalized / psychology. Family / psychology. Leukemia, Myeloid / psychology
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Family Health. Health Services Needs and Demand. Holistic Health. Hospitals, Pediatric. Humans. Infant. Longitudinal Studies. Models, Psychological. Nursing Methodology Research. Parent-Child Relations. Qualitative Research. Queensland. Sibling Relations. Social Support. Surveys and Questionnaires

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Children's Health.
  • MedlinePlus Health Information. consumer health - Family Issues.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16006383.001).
  • [ISSN] 0146-0862
  • [Journal-full-title] Issues in comprehensive pediatric nursing
  • [ISO-abbreviation] Issues Compr Pediatr Nurs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


40. Lee SS, Lee JH, Lee JH, Kim DY, Kim SH, Lim SN, Lee YS, Seol M, Ryu SG, Kang YA, Jang S, Park CJ, Chi HS, Yun SC, Lee KH: Single-dose mitoxantrone in combination with continuous infusion intermediate-dose cytarabine plus etoposide for treatment of refractory or early relapsed acute myeloid leukemia. Leuk Res; 2009 Apr;33(4):511-7
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] Single-dose mitoxantrone in combination with continuous infusion intermediate-dose cytarabine plus etoposide for treatment of refractory or early relapsed acute myeloid leukemia.
  • This prospective phase II clinical trial evaluated the effects of single-dose mitoxantrone (36 mg/m2 on day 1) in combination with continuous infusion intermediate-dose cytarabine plus etoposide in 25 patients with refractory or early relapsed acute myeloid leukemia (AML).
  • We compared the results of our current study with those of a previous phase II trial, which had the same eligibility criteria and chemotherapy schedule except that a conventional divided dose of mitoxantrone (12 mg/m2 on days 1-3) was used.
  • CR duration and overall survival were not significantly different between the two regimens.
  • In conclusion, single-dose mitoxantrone was inferior to conventional divided-dose mitoxantrone for treatment of refractory or early relapsed AML in terms of CR rate.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Neoplasm Recurrence, Local / drug therapy. Salvage Therapy / methods

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18819710.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone
  •  go-up   go-down


41. Jeddi R, Ghédira H, Menif S, Ben Neji H, Ben Amor R, Kacem K, Aissaoui L, Bouteraâ W, Abdennebi Y, Raihane BL, Gouider E, Raouf H, Hèla BA, Saad A, Zaher B, Meddeb B: Treatment of acute promyelocytic leukemia with PETHEMA LPA 99 protocol: a Tunisian single center experience. Hematology; 2010 Aug;15(4):204-9
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] Treatment of acute promyelocytic leukemia with PETHEMA LPA 99 protocol: a Tunisian single center experience.
  • Acute promyelocytic leukemia (APL) has now become the most curable of all subtypes of acute myeloid leukemia.
  • In Tunisia, the ATRA era began in 1998 with the use, consecutively, of two regimens of a combination of ATRA with anthracycline and cytarabine (APL93), and without cytarabine (LPA99).
  • Baseline blood cell count (WBC) >10 x 10(9)/l (P=0.26) and creatinine >1.4 mg/dl (P=0.42) were not predictive of mortality.
  • Event free survival from diagnosis was 80% and overall survival was 82%.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20670478.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin; AYI8EX34EU / Creatinine; ZRP63D75JW / Idarubicin; AIDA protocol
  •  go-up   go-down


42. Russo V, Scott IU, Querques G, Stella A, Barone A, Delle Noci N: Orbital and ocular manifestations of acute childhood leukemia: clinical and statistical analysis of 180 patients. Eur J Ophthalmol; 2008 Jul-Aug;18(4):619-23
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] Orbital and ocular manifestations of acute childhood leukemia: clinical and statistical analysis of 180 patients.
  • PURPOSE: To investigate the association between presence of orbital or ocular lesions and type and stage of leukemia and to investigate whether orbital and ocular lesions are significant in predicting leukemia prognosis.
  • METHODS: The authors evaluated 180 patients with acute childhood leukemia.
  • Lesions associated with leukemia may be classified as specific (due to leukemic infiltration of various ocular tissues), nonspecific (due to one of the secondary complications), or iatrogenic manifestations caused by chemotherapy.
  • Risk-based treatment assignment is based on clinical and laboratory features at diagnosis.
  • Children with presenting white blood cell count below 50,000 mm3 are considered at standard risk for treatment failure, while all others are considered at high risk for treatment failure.
  • RESULTS: Specific lesions were noted in 66% of patients with acute myeloid leukemia (AML) and 11.5% patients with acute lymphocytic leukemia (ALL) (p<0.05), and were more severe in patients with high risk leukemia than in patients with standard risk leukemia.
  • Orbital or ocular lesions were noted more commonly in patients with AML (66.6%) compared to patients with ALL (15.1%).
  • In both the AML and ALL groups, there was a higher frequency of leukemic relapses in the bone marrow and/or central nervous system in patients with specific lesions (63.1%) compared to patients with nonspecific lesions (42%), and in patients without orbital or ocular lesions (29.2%) (p<0.05).
  • CONCLUSIONS: In both the AML and ALL groups, the presence of specific orbital or ocular lesions was associated with a higher frequency of bone marrow relapses and CNS involvement (p<0.05), leading to a lower survival rate.
  • [MeSH-major] Eye Neoplasms / pathology. Leukemia, Myeloid, Acute / pathology. Leukemic Infiltration / pathology. Orbital Neoplasms / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Eye Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18609485.001).
  • [ISSN] 1120-6721
  • [Journal-full-title] European journal of ophthalmology
  • [ISO-abbreviation] Eur J Ophthalmol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


43. Sucić M, Batinić D, Zadro R, Mrsić S, Labar B: [Cytomorphology of acute mixed leukemia]. Acta Med Croatica; 2008 Oct;62(4):379-85
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] [Cytomorphology of acute mixed leukemia].
  • Biphenotypic acute leukemias (AL) with blasts expressing both myeloid and lymphoid antigens are grouped with undifferentiated AL and bilineal AL in the group of AL of ambiguous lineage.
  • Not all AL with myeloid and lymphoid antigens (ALMy+Ly) are true biphenotypic AL.
  • According to EGIL scoring system, true biphenotypic ALMy+Ly are those with a sum of antigens 2 or more points for both myeloid and lymphoid lineage or for B and T lineage.
  • RESULTS AND DISCUSSION: In the group of 169 adult AL patients, 116 were cytomorphologically classified as acute myeloblastic leukemias (AML), 35 as acute lymphoblastic leukemias (ALL) and 18 as acute undifferentiated leukemias (ANLM).
  • In 6 (3.4%) of 169 AL patients, blasts expressed both myeloid and lymphoid antigens.
  • In 64 patients cytomorphologically classified into AML subgroup out of 102 AL patients, there were 15 (14.7%/102; 23.4%/64) AML with lymphoid antigens (AMLLy+).
  • In 35 patients cytomorphologically diagnosed as ALL and 3 as ANLM out of 102 AL, there were 4 (3.9%/102; 10.5%/38) ALL with myeloid antigens (ALLMy+).
  • CONCLUSION: In both groups of 169 and 102 AL patients, the majority of AL cases were cytomorphologically classified as AML.
  • In one ANLM,My+ out of 169 AL and also one ANLM,My+ out of 102 AL, blasts were cytomorphologically undifferentiated; in 3 ALLMy+ of 102 AL blasts expressed lymphoid morphology.
  • According to EGIL scoring system, among 15 AMLLy+ of 102 AL there were 4 true biphenotypic ALMy+Ly (1 M1, 2 M3, 1 M4), and in 4 ALMy+Ly with undifferentiated and lymphoid morphology there were 2 true biphenotypic AL (1 L2; 1 ANLM).
  • These observations are consistent with other studies and WHO determinations indicating that the majority of true biphenotypic leukemias are associated with immature monoblastic or myeloid cytomorphology or with lymphoid or undifferentiated characteristics, but may also express any AML cytomorphology type.
  • Thus, there is no direct correlation of leukemic cell cytomorphology and biphenotypic AL immunophenotype.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / pathology
  • [MeSH-minor] Acute Disease. Humans. Immunophenotyping. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19205415.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Croatia
  •  go-up   go-down


44. Ratei R, Karawajew L, Lacombe F, Jagoda K, Del Poeta G, Kraan J, De Santiago M, Kappelmayer J, Björklund E, Ludwig WD, Gratama JW, Orfao A, European Working Group of Clinical Cell Analysis: Discriminant function analysis as decision support system for the diagnosis of acute leukemia with a minimal four color screening panel and multiparameter flow cytometry immunophenotyping. Leukemia; 2007 Jun;21(6):1204-11
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] Discriminant function analysis as decision support system for the diagnosis of acute leukemia with a minimal four color screening panel and multiparameter flow cytometry immunophenotyping.
  • Despite several recommendations for standardization of multiparameter flow cytometry (MFC) the number, specificity and combinations of reagents used by diagnostic laboratories for the diagnosis and classification of acute leukemias (AL) are still very diverse.
  • We determined the potential value of a minimal four-color combination panel of 13 monoclonal antibodies (mAbs) with a CD45/sideward light scatter-gating strategy for a standardized MFC immunophenotyping of the clinically most relevant subgroups of AL.
  • Bone marrow samples from 155 patients with acute myeloid leukemia (AML, n=79), B-cell precursor acute lymphoblastic leukemia (BCP-ALL, n=29), T-cell precursor acute lymphoblastic leukemia (T-ALL, n=12) and normal bone marrow donors (NBMD, n=35) were analyzed.
  • A knowledge-based learning algorithm was generated by comparing the results of the minimal panel with the actual diagnosis, using discriminative function analysis.
  • Correct classification of the test sample according to lineage, that is, BCP-ALL, T-ALL, AML and differentiation of NBMD was achieved in 97.2% of all cases with only six of the originally applied 13 mAbs of the panel.
  • [MeSH-major] Diagnosis, Computer-Assisted / methods. Flow Cytometry / methods. Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Algorithms. Antibodies, Monoclonal. Bone Marrow / pathology. Cell Lineage. Color. Humans. Immunophenotyping. Reference Standards

  • MedlinePlus Health Information. consumer health - 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 = 17410192.001).
  • [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 / Antibodies, Monoclonal
  •  go-up   go-down


45. McLaughlin J, Markovtsov V, Li H, Wong S, Gelman M, Zhu Y, Franci C, Lang D, Pali E, Lasaga J, Low C, Zhao F, Chang B, Gururaja TL, Xu W, Baluom M, Sweeny D, Carroll D, Sran A, Thota S, Parmer M, Romane A, Clemens G, Grossbard E, Qu K, Jenkins Y, Kinoshita T, Taylor V, Holland SJ, Argade A, Singh R, Pine P, Payan DG, Hitoshi Y: Preclinical characterization of Aurora kinase inhibitor R763/AS703569 identified through an image-based phenotypic screen. J Cancer Res Clin Oncol; 2010 Jan;136(1):99-113
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: Cell-based screening methods have an advantage over biochemical approaches because hits can be optimized to inhibit targets in the proper intracellular context.
  • The anti-proliferative effect was examined in a panel of tumor cell lines and primary cells.
  • RESULTS: R763/AS703569 inhibits Aurora kinases, along with a limited number of other kinases including FMS-related tyrosine kinase 3 (FLT3), and has potent anti-proliferative activity against many cell types accompanying unique phenotypic changes such as enlarged cell size, endoreduplication and apoptosis.
  • Oral administration of R763/AS703569 demonstrated marked inhibition of tumor growth in xenograft models of pancreatic, breast, colon, ovarian, and lung tumors and leukemia.
  • An acute myeloid leukemia cell line MV4-11, which carries a FLT3 internal tandem duplication mutation, is particularly sensitive to R763/AS703569 in vivo.
  • [MeSH-major] Apoptosis / drug effects. Cell Proliferation / drug effects. Microscopy, Fluorescence / methods. Norbornanes / pharmacology. Protein Kinase Inhibitors / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Pyrimidines / pharmacology
  • [MeSH-minor] Animals. Aurora Kinases. Cell Cycle / drug effects. Cell Line, Tumor. Cells, Cultured. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical. Female. Flow Cytometry. HL-60 Cells. HeLa Cells. Humans. Mice. Mice, Inbred NOD. Mice, Inbred Strains. Mice, Nude. Mice, SCID. Survival Analysis. Xenograft Model Antitumor Assays

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4106-11 [17360485.001]
  • [Cites] Clin Cancer Res. 2007 Jun 15;13(12):3682-8 [17575233.001]
  • [Cites] Mol Cancer Ther. 2004 Apr;3(4):451-7 [15078988.001]
  • [Cites] Mol Cell Biol. 2007 Jun;27(12):4513-25 [17438137.001]
  • [Cites] Oncogene. 1997 May 8;14(18):2195-200 [9174055.001]
  • [Cites] Assay Drug Dev Technol. 2006 Apr;4(2):153-63 [16712419.001]
  • [Cites] J Surg Oncol. 2005 Sep 1;91(3):173-80 [16118771.001]
  • [Cites] Clin Cancer Res. 2005 Mar 1;11(5):1827-34 [15756006.001]
  • [Cites] Cancer Res. 2005 Oct 1;65(19):9038-46 [16204078.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5697-702 [14522886.001]
  • [Cites] Lancet. 2007 Dec 15;370(9604):2011-9 [18083403.001]
  • [Cites] N Engl J Med. 2004 Jun 3;350(23 ):2335-42 [15175435.001]
  • [Cites] Bioorg Med Chem Lett. 2006 Mar 1;16(5):1320-3 [16337122.001]
  • [Cites] Int J Cancer. 2001 May 1;92(3):370-3 [11291073.001]
  • [Cites] Cancer Res. 2006 May 15;66(10):4996-5002 [16707419.001]
  • [Cites] Clin Cancer Res. 2000 May;6(5):1833-9 [10815905.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Feb;90(2):928-35 [15562011.001]
  • [Cites] Cancer Res. 1999 May 1;59(9):2041-4 [10232583.001]
  • [Cites] J Cell Biol. 2002 Aug 19;158(4):617-23 [12177045.001]
  • [Cites] Nat Med. 2004 Mar;10(3):262-7 [14981513.001]
  • [Cites] Curr Biol. 2001 Jun 5;11(11):886-90 [11516652.001]
  • [Cites] Mol Cell. 2005 Apr 29;18(3):379-91 [15866179.001]
  • [Cites] Mol Cell. 2003 Oct;12(4):851-62 [14580337.001]
  • [Cites] Cell. 2003 Sep 5;114(5):585-98 [13678582.001]
  • [Cites] J Natl Cancer Inst. 2002 Sep 4;94(17):1320-9 [12208897.001]
  • [Cites] J Cell Biol. 2003 Apr 28;161(2):267-80 [12719470.001]
  • [Cites] Clin Cancer Res. 2003 Apr;9(4):1420-6 [12684414.001]
  • [Cites] J Med Chem. 2005 Apr 21;48(8):3080-4 [15828847.001]
  • [Cites] J Med Chem. 2006 Feb 9;49(3):955-70 [16451062.001]
  • [Cites] J Clin Oncol. 2005 Jun 1;23 (16):3697-705 [15738537.001]
  • [Cites] EMBO J. 1998 Feb 2;17(3):667-76 [9450992.001]
  • [Cites] Br J Cancer. 2001 Mar 23;84(6):824-31 [11259099.001]
  • [Cites] Cancer Res. 1998 Nov 1;58(21):4811-6 [9809983.001]
  • [Cites] Chem Biol. 2008 Jun;15(6):525-6 [18559262.001]
  • [Cites] J Endocrinol. 2004 May;181(2):263-70 [15128274.001]
  • [Cites] Mol Cancer Ther. 2007 Dec;6(12 Pt 1):3158-68 [18089710.001]
  • [Cites] Nat Rev Mol Cell Biol. 2003 Nov;4(11):842-54 [14625535.001]
  • [Cites] Cancer. 2004 Jan 1;100(1):12-9 [14692019.001]
  • [Cites] Curr Biol. 2000 Oct 5;10(19):1172-81 [11050385.001]
  • [Cites] Hum Pathol. 2005 Dec;36(12):1281-8 [16311121.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15):7668-77 [16885368.001]
  • [Cites] Mol Cancer Ther. 2006 Jul;5(7):1764-73 [16891462.001]
  • [Cites] Br J Cancer. 2005 Sep 19;93(6):719-29 [16222316.001]
  • [Cites] Clin Cancer Res. 2006 Jul 1;12(13):4080-9 [16818708.001]
  • [Cites] Prostate. 2006 Feb 15;66(3):326-33 [16267859.001]
  • [Cites] FEBS Lett. 2005 Jun 20;579(16):3385-91 [15922328.001]
  • [Cites] Mol Cancer Ther. 2007 Dec;6(12 Pt 1):3147-57 [18089709.001]
  • [Cites] N Engl J Med. 2003 Jul 31;349(5):427-34 [12890841.001]
  • [Cites] Nat Genet. 1998 Oct;20(2):189-93 [9771714.001]
  • [Cites] Chem Biol. 2008 Jun;15(6):552-62 [18559266.001]
  • [Cites] Cancer Res. 2004 May 1;64(9):3103-11 [15126347.001]
  • [Cites] Clin Cancer Res. 2004 Mar 15;10(6):2065-71 [15041727.001]
  • [Cites] Leuk Lymphoma. 2004 Sep;45(9):1741-6 [15223631.001]
  • [Cites] J Clin Oncol. 2005 Jun 1;23(16):3706-12 [15867200.001]
  • [Cites] Jpn J Cancer Res. 2000 Oct;91(10):1007-14 [11050471.001]
  • [Cites] Curr Med Chem Anticancer Agents. 2005 Jan;5(1):65-71 [15720262.001]
  • [Cites] Curr Biol. 2000 Sep 7;10(17):1075-8 [10996078.001]
  • [Cites] Prostate. 2005 Sep 1;64(4):341-6 [15754349.001]
  • [Cites] J Cell Biol. 2003 Apr 28;161(2):281-94 [12707311.001]
  • [Cites] Science. 1977 Jul 29;197(4302):461-3 [560061.001]
  • [Cites] J Clin Oncol. 2006 Jan 1;24(1):16-24 [16330672.001]
  • [Cites] EMBO J. 1998 Jun 1;17(11):3052-65 [9606188.001]
  • [Cites] Cancer Res. 2005 Apr 1;65(7):2899-905 [15805292.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 Dec;12(12):1518-22 [14693746.001]
  • [Cites] Jpn J Cancer Res. 2002 Oct;93(10):1114-22 [12417041.001]
  • [Cites] J Neurooncol. 2004 Mar-Apr;67(1-2):53-64 [15072448.001]
  • [Cites] N Engl J Med. 2006 Dec 14;355(24):2542-50 [17167137.001]
  • [Cites] Nat Rev Cancer. 2005 Jan;5(1):42-50 [15630414.001]
  • [Cites] J Biol Chem. 2003 Dec 19;278(51):51786-95 [14523000.001]
  • (PMID = 19609559.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / MSC1992371A; 0 / Norbornanes; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  •  go-up   go-down


51. Christ O, Feuring-Buske M, Hiddemann W, Buske C: [Pathobiology of acute myeloid leukemia]. Med Klin (Munich); 2007 Apr 15;102(4):290-5
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] [Pathobiology of acute myeloid leukemia].
  • Acute myeloid leukemia (AML) arises from the clonal expansion of primitive myeloid precursor cells.
  • Over the last several years, a number of clinical and basic research studies have elucidated important pathogenetic mechanisms leading to the initiation of AML.
  • The identification of numerous chromosomal aberrations and mutations specific for AML has deepened our insights into the biology of AML and has allowed to improve our diagnostic tools, the definition of prognostic subgroups and therapeutic concepts.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Biomarkers, Tumor / genetics. Bone Marrow / pathology. Cell Differentiation / genetics. Cell Division / genetics. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Chromosome Aberrations. Hematopoiesis / genetics. Humans. Mutation / genetics. Myeloid Progenitor Cells / pathology. Prognosis

  • 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 = 17426932.001).
  • [ISSN] 0723-5003
  • [Journal-full-title] Medizinische Klinik (Munich, Germany : 1983)
  • [ISO-abbreviation] Med. Klin. (Munich)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 63
  •  go-up   go-down


52. Tabori U, Revach G, Nathan PC, Strahm B, Rachlis A, Shago M, Grant R, Doyle J, Malkin D: Toxicity and outcome of children with treatment related acute myeloid leukemia. Pediatr Blood Cancer; 2008 Jan;50(1):17-23
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] Toxicity and outcome of children with treatment related acute myeloid leukemia.
  • BACKGROUND: The aim of this study was to evaluate the clinical course and outcome of children with treatment related acute myeloid leukemia (tAML) and compare them to children with primary AML (pAML).
  • All survivors were treated with allogeneic hematopoietic stem cell transplantation (HSCT).
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Neoplasms, Second Primary / therapy
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Child. Disease Progression. Female. Hematopoietic Stem Cell Transplantation / adverse effects. Humans. Male. Survival Analysis. Survival Rate


53. Benesch M, Sovinz P, Lackner H, Schwinger W, Dornbusch HJ, Urban C: Five-month marrow aplasia in a child with refractory acute myeloid leukemia: successful management with continuous granulocyte support and reduced-intensity conditioning followed by matched unrelated bone marrow transplantation. J Pediatr Hematol Oncol; 2005 Apr;27(4):236-8
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] Five-month marrow aplasia in a child with refractory acute myeloid leukemia: successful management with continuous granulocyte support and reduced-intensity conditioning followed by matched unrelated bone marrow transplantation.
  • A 10-year-old girl diagnosed with acute myeloid leukemia FAB M4 failed to achieve remission following several courses of induction chemotherapy.
  • Graft-versus-host disease did not occur.
  • [MeSH-major] Anemia, Aplastic / etiology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Transplantation. Graft vs Host Disease / prevention & control. Leukemia, Myelomonocytic, Acute / therapy. Neoplasm Recurrence, Local / therapy. Transplantation Conditioning. Vidarabine / analogs & derivatives

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Aplastic Anemia.
  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • Hazardous Substances Data Bank. MELPHALAN .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15838401.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
  •  go-up   go-down


54. Steidl U, Steidl C, Ebralidze A, Chapuy B, Han HJ, Will B, Rosenbauer F, Becker A, Wagner K, Koschmieder S, Kobayashi S, Costa DB, Schulz T, O'Brien KB, Verhaak RG, Delwel R, Haase D, Trümper L, Krauter J, Kohwi-Shigematsu T, Griesinger F, Tenen DG: A distal single nucleotide polymorphism alters long-range regulation of the PU.1 gene in acute myeloid leukemia. J Clin Invest; 2007 Sep;117(9):2611-20
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] A distal single nucleotide polymorphism alters long-range regulation of the PU.1 gene in acute myeloid leukemia.
  • Targeted disruption of a highly conserved distal enhancer reduces expression of the PU.1 transcription factor by 80% and leads to acute myeloid leukemia (AML) with frequent cytogenetic aberrations in mice.
  • Here we identify a SNP within this element in humans that is more frequent in AML with a complex karyotype, leads to decreased enhancer activity, and reduces PU.1 expression in myeloid progenitors in a development-dependent manner.
  • Interestingly, disruption of SATB1 in mice led to a selective decrease of PU.1 RNA in specific progenitor types (granulocyte-macrophage and megakaryocyte-erythrocyte progenitors) and a similar effect was observed in AML samples harboring this SNP.
  • Thus we have identified a SNP within a distal enhancer that is associated with a subtype of leukemia and exerts a deleterious effect through remote transcriptional dysregulation in specific progenitor subtypes.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • 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
  • [Cites] Nat Genet. 2002 Dec;32(4):666-9 [12402038.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1519-24 [15914558.001]
  • [Cites] Nat Rev Cancer. 2003 Feb;3(2):89-101 [12563308.001]
  • [Cites] Nat Genet. 2003 May;34(1):42-51 [12692553.001]
  • [Cites] Nat Genet. 2003 Dec;35(4):341-8 [14608356.001]
  • [Cites] Nat Genet. 2004 Jun;36(6):624-30 [15146183.001]
  • [Cites] Blood. 2004 Jul 1;104(1):81-8 [15016651.001]
  • [Cites] Nat Genet. 2004 Jul;36(7):725-31 [15184899.001]
  • [Cites] N Engl J Med. 2004 Aug 12;351(7):657-67 [15306667.001]
  • [Cites] Cell. 2004 Oct 29;119(3):431-43 [15507213.001]
  • [Cites] Cell. 1992 Aug 21;70(4):631-45 [1505028.001]
  • [Cites] Science. 1994 Sep 9;265(5178):1573-7 [8079170.001]
  • [Cites] EMBO J. 1996 Oct 15;15(20):5647-58 [8896458.001]
  • [Cites] Blood. 1997 Jul 15;90(2):489-519 [9226149.001]
  • [Cites] Mol Cell Biol. 1997 Sep;17(9):5275-87 [9271405.001]
  • [Cites] Biochemistry. 1997 Oct 7;36(40):12005-10 [9340009.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3437-44 [15304397.001]
  • [Cites] Cancer Cell. 2004 Dec;6(6):587-96 [15607963.001]
  • [Cites] J Exp Med. 2005 Jan 17;201(2):221-31 [15657291.001]
  • [Cites] J Immunol. 2005 Feb 1;174(3):1525-31 [15661912.001]
  • [Cites] N Engl J Med. 2005 Feb 24;352(8):786-92 [15728811.001]
  • [Cites] J Biol Chem. 2002 Sep 13;277(37):33968-77 [12121983.001]
  • [Cites] Blood. 2005 Apr 15;105(8):3330-9 [15618465.001]
  • [Cites] J Hum Genet. 2005;50(3):133-8 [15744455.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 30;102(35):12513-8 [16113082.001]
  • [Cites] Trends Cell Biol. 2005 Sep;15(9):494-501 [16084092.001]
  • [Cites] Gene. 2005 Oct 10;359:44-52 [16102917.001]
  • [Cites] Nat Genet. 2006 Jan;38(1):27-37 [16311598.001]
  • [Cites] Blood. 2006 Apr 15;107(8):3330-8 [16352814.001]
  • [Cites] Science. 2006 May 26;312(5777):1215-7 [16728641.001]
  • [Cites] Nat Genet. 2006 Nov;38(11):1269-77 [17041602.001]
  • [Cites] Nat Genet. 2006 Nov;38(11):1278-88 [17057718.001]
  • [Cites] Genes Dev. 2000 Mar 1;14(5):521-35 [10716941.001]
  • [Cites] Nature. 2000 Mar 9;404(6774):193-7 [10724173.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4075-83 [11110676.001]
  • [Cites] Br J Haematol. 2001 Jan;112(1):118-26 [11167792.001]
  • [Cites] Blood. 2001 Nov 15;98(10):2958-65 [11698277.001]
  • [Cites] Blood. 2002 Mar 15;99(6):2037-44 [11877277.001]
  • [Cites] Blood. 2002 Aug 1;100(3):998-1007 [12130514.001]
  • [Cites] J Pathol. 2002 Sep;198(1):115-20 [12210071.001]
  • [Cites] Nature. 2002 Oct 10;419(6907):641-5 [12374985.001]
  • [Cites] Mol Cell Biol. 2005 Apr;25(7):2832-45 [15767686.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Sep 3;99(18):11872-7 [12193648.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] J Exp Med. 2005 May 2;201(9):1487-502 [15867096.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Jul;43(3):227-38 [15846790.001]
  • [Cites] Hum Genet. 2005 Jun;117(1):16-26 [15806396.001]
  • [Cites] Oncogene. 2005 May 19;24(22):3678-83 [15750630.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1590-600 [15914556.001]
  • [Cites] Blood. 2003 Jan 1;101(1):270-7 [12393465.001]
  • (PMID = 17694175.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA041456; United States / NCI NIH HHS / CA / CA41456
  • [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 / Cell Adhesion Molecules, Neuronal; 0 / Proto-Oncogene Proteins; 0 / Receptors, Lymphocyte Homing; 0 / STAB1 protein, human; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1
  • [Other-IDs] NLM/ PMC1937499
  •  go-up   go-down


55. Park SH, Chi HS, Park SJ, Jang S, Park CJ: [Clinical importance of morphological multilineage dysplasia in acute myeloid leukemia with myelodysplasia related changes]. Korean J Lab Med; 2010 Jun;30(3):231-8
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] [Clinical importance of morphological multilineage dysplasia in acute myeloid leukemia with myelodysplasia related changes].
  • BACKGROUND: AML with myelodysplasia related changes (AML MRC) is known to show a poor prognosis compared with de novo AML, but controversies exist about the prognostic impact of multilineage dysplasia (MLD) among MRC.
  • We investigated the prognostic impact of MLD in AML MRC.
  • METHODS: A total of 357 patients newly diagnosed as AML at Asan Medical Center from January 2001 to December 2005 were analyzed.
  • They were diagnosed and classified as AML with recurrent genetic abnormalities, AML MRC, and AML not otherwise specified (AML NOS).
  • RESULTS: AML MRC patients showed a lower complete remission (CR) rate (44.7% vs. 64.9%, P=0.002) and shorter OS (297 vs. 561 days, P=0.004) and EFS (229 vs. 374 days, P=0.004) than AML NOS patients.
  • Patients with MLD among AML MRC also showed a lower CR rate (37.7%, P=0.001) and shorter OS (351 days, P=0.036) and EFS (242 days, P=0.076) than AML NOS patients.
  • However, among AML MRC patients, there were no differences in OS, EFS and CR between patients with and without MLD.
  • CONCLUSIONS: AML MRC patients showed a lower CR rate and shorter OS and EFS than AML NOS patients.
  • AML MRC patients with MLD showed similar results and their prognosis was not different from those without MLD.
  • MLD findings among AML MRC could be an independent poor prognostic factor in de novo AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Myelodysplastic Syndromes / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Lineage. Child. Child, Preschool. Data Interpretation, Statistical. Disease-Free Survival. Female. Humans. Infant. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis


56. Whitworth KW, Symanski E, Coker AL: Childhood lymphohematopoietic cancer incidence and hazardous air pollutants in southeast Texas, 1995-2004. Environ Health Perspect; 2008 Nov;116(11):1576-80
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.
  • RESULTS: Census tracts with the highest benzene levels had elevated rates of all leukemia [rate ratio (RR) = 1.37; 95% confidence interval (CI), 1.05, 1.78].
  • This association was higher for acute myeloid leukemia (AML) (RR = 2.02; 95% CI, 1.03-3.96) than for acute lymphocytic leukemia (ALL) (RR = 1.24; 95% CI, 0.92-1.66).
  • Among census tracts with the highest 1,3-butadiene levels, we observed RRs of 1.40 (95% CI, 1.07-1.81), 1.68 (95% CI, 0.84-3.35), and 1.32 (95% CI, 0.98-1.77) for all leukemia, AML, and ALL, respectively.
  • CONCLUSIONS: Our ecologic analysis suggests an association between childhood leukemia and hazardous air pollution; further research using more sophisticated methodology is warranted.

  • Genetic Alliance. consumer health - Childhood Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Air Waste Manag Assoc. 2000 Feb;50(2):175-80 [10680346.001]
  • [Cites] Occup Environ Med. 1999 Nov;56(11):774-80 [10658564.001]
  • [Cites] J Am Stat Assoc. 1995 Mar;90(429):64-71 [12155398.001]
  • [Cites] Cancer Causes Control. 2002 Sep;13(7):665-73 [12296514.001]
  • [Cites] Environ Health Perspect. 2003 Apr;111(4):663-8 [12676632.001]
  • [Cites] Epidemiology. 2003 Jul;14(4):386-91 [12843760.001]
  • [Cites] Int J Cancer. 2004 Feb 10;108(4):596-9 [14696126.001]
  • [Cites] Environ Health Perspect. 2004 Feb;112(2):257-65 [14754581.001]
  • [Cites] Occup Environ Med. 2004 Sep;61(9):773-8 [15317919.001]
  • [Cites] Environ Health Perspect. 2004 Oct;112(14):1386-92 [15471730.001]
  • [Cites] IARC Monogr Eval Carcinog Risk Chem Hum. 1982 May;29:1-398 [6957379.001]
  • [Cites] IARC Monogr Eval Carcinog Risks Hum Suppl. 1987;7:1-440 [3482203.001]
  • [Cites] Environ Health Perspect. 1995 Sep;103 Suppl 6:105-10 [8549455.001]
  • [Cites] J Epidemiol Community Health. 1995 Dec;49 Suppl 2:S20-7 [8594128.001]
  • [Cites] Milbank Q. 1996;74(2):215-38 [8632735.001]
  • [Cites] Int Arch Occup Environ Health. 1997;70(1):57-60 [9258708.001]
  • [Cites] IARC Monogr Eval Carcinog Risks Hum. 1999;71 Pt 1:1-315 [10507919.001]
  • [Cites] Science. 2004 Dec 3;306(5702):1774-6 [15576619.001]
  • [Cites] J Epidemiol Community Health. 2005 Feb;59(2):101-5 [15650139.001]
  • [Cites] Cancer Invest. 2005;23(1):60-75 [15779869.001]
  • [Cites] J Epidemiol Community Health. 2005 Sep;59(9):755-60 [16100313.001]
  • [Cites] Mutat Res. 2006 Jan;612(1):14-39 [16027031.001]
  • [Cites] J Epidemiol Community Health. 2006 Feb;60(2):136-41 [16415262.001]
  • [Cites] Int J Cancer. 2006 Jun 15;118(12):2920-9 [16425269.001]
  • [Cites] J Expo Sci Environ Epidemiol. 2006 Nov;16(6):538-43 [16736057.001]
  • [Cites] Environ Health Perspect. 2007 Jan;115(1):138-45 [17366834.001]
  • [Cites] Environ Health Perspect. 2007 Oct;115(10):1388-93 [17938725.001]
  • [Cites] J Expo Sci Environ Epidemiol. 2008 Jan;18(1):45-58 [17878926.001]
  • [Cites] Cancer. 2008 Jan 15;112(2):416-32 [18074355.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Environ Health Perspect. 1995 Sep;103 Suppl 6:13-8 [8549460.001]
  • [Cites] Am J Epidemiol. 2001 Mar 1;153(5):433-43 [11226975.001]
  • (PMID = 19057714.001).
  • [ISSN] 0091-6765
  • [Journal-full-title] Environmental health perspectives
  • [ISO-abbreviation] Environ. Health Perspect.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R03 CA128106; United States / NCI NIH HHS / CA / 1 R03 CA128106-01A1
  • [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 / Air Pollutants
  • [Other-IDs] NLM/ PMC2592281
  • [Keywords] NOTNLM ; 1,3-butadiene / air toxics / benzene / childhood cancer / epidemiology / hazardous air pollution
  •  go-up   go-down


57. Ammatuna E, Noguera NI, Zangrilli D, Curzi P, Panetta P, Bencivenga P, Amadori S, Federici G, Lo-Coco F: Rapid detection of nucleophosmin (NPM1) mutations in acute myeloid leukemia by denaturing HPLC. Clin Chem; 2005 Nov;51(11):2165-7
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] Rapid detection of nucleophosmin (NPM1) mutations in acute myeloid leukemia by denaturing HPLC.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics

  • 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 = 16244291.001).
  • [ISSN] 0009-9147
  • [Journal-full-title] Clinical chemistry
  • [ISO-abbreviation] Clin. Chem.
  • [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
  •  go-up   go-down


58. Zhang SJ, Shi JY, Li JY: GATA-2 L359 V mutation is exclusively associated with CML progression but not other hematological malignancies and GATA-2 P250A is a novel single nucleotide polymorphism. Leuk Res; 2009 Aug;33(8):1141-3
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] GATA-2 L359 V mutation is exclusively associated with CML progression but not other hematological malignancies and GATA-2 P250A is a novel single nucleotide polymorphism.
  • Chronic myeloid leukemia (CML) progression is characterized by occurrence of new cytogenetic and molecular abnormalities.
  • Finally, no GATA-2 L359 V mutation was found in 270 acute myeloid leukemia, 30 myelodysplastic syndrome, 50 acute lymphoblastic leukemia, 12 chronic lymphocytic leukemia, 40 CML chronic phase and 286 BCR/ABL negative myeloproliferative disorders except CML blast crisis.
  • A new variation of GATA-2 resulted in P250A change was identified, which was not found to have statistical difference between patients with hematological malignancies and healthy control.
  • Hence, we concluded GATA-2 L359 V is exclusively associated with CML progression but not other hematological malignancies and P250A is a new single nucleotide polymorphism.
  • [MeSH-major] Amino Acid Substitution. Blast Crisis / genetics. GATA2 Transcription Factor / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mutation, Missense. Polymorphism, Single Nucleotide
  • [MeSH-minor] DNA Mutational Analysis. Disease Progression. Female. Hematologic Neoplasms / genetics. Hematologic Neoplasms / metabolism. Humans. Male

  • MedlinePlus Health Information. consumer health - Chronic 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 = 19304323.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GATA2 Transcription Factor; 0 / GATA2 protein, human
  •  go-up   go-down


59. Maurillo L, Buccisano F, Spagnoli A, Del Poeta G, Panetta P, Neri B, Del Principe MI, Mazzone C, Consalvo MI, Tamburini A, Ottaviani L, Fraboni D, Sarlo C, De Fabritiis P, Amadori S, Venditti A: Monitoring of minimal residual disease in adult acute myeloid leukemia using peripheral blood as an alternative source to bone marrow. Haematologica; 2007 May;92(5):605-11
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] Monitoring of minimal residual disease in adult acute myeloid leukemia using peripheral blood as an alternative source to bone marrow.
  • BACKGROUND AND OBJECTIVES: To date, bone marrow (BM) is the most common source of cells to use in order to assess minimal residual disease (MRD) in acute myeloid leukemia (AML).
  • In the present study, we investigated whether peripheral blood (PB) could be an alternative source of cells for monitoring MRD in AML.
  • DESIGN AND METHODS: Fifty patients with AML were monitored for MRD after the achievement of complete remission.
  • Thirty-three of 43 (77%) patients with >1.5x10 (-4)residual leukemic cells in PB after induction had a relapse, whereas the seven patients with lower levels did not (p=0.0002).
  • INTERPRETATION AND CONCLUSIONS: These preliminary results indicate that: (i) PB evaluation can integrate BM assessment for MRD detection in patients with AML;.
  • [MeSH-major] Blood Cells / chemistry. Bone Marrow Examination. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Flow Cytometry. Humans. Idarubicin / administration & dosage. Kaplan-Meier Estimate. Male. Middle Aged. Mitoxantrone / administration & dosage. Neoplasm, Residual. Organ Specificity. Randomized Controlled Trials as Topic / statistics & numerical data. Remission Induction. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17488683.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; ZRP63D75JW / Idarubicin; ZS7284E0ZP / Daunorubicin; EORTC GIMEMA AML-10 protocol; EORTC GIMEMA AML-13 protocol
  •  go-up   go-down


60. Gery S, Park DJ, Vuong PT, Virk RK, Muller CI, Hofmann WK, Koeffler HP: RTP801 is a novel retinoic acid-responsive gene associated with myeloid differentiation. Exp Hematol; 2007 Apr;35(4):572-8
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] RTP801 is a novel retinoic acid-responsive gene associated with myeloid differentiation.
  • OBJECTIVE: Retinoids are crucial in the regulation of fundamental cellular processes including terminal differentiation of both normal and malignant myeloid progenitors.
  • METHODS AND RESULTS: RTP801 is a recently cloned stress response gene that acts as a negative regulator of the mTOR pathway.
  • Here we identified RTP801 as a novel early RA target gene in myeloid cells.
  • RTP801 mRNA levels are induced in acute myeloid leukemia (AML) cell lines during RA-dependent differentiation and are differentially expressed during maturation of normal CD34(+) cells.
  • The myeloid-specific, differentiation-related transcription factor C/EBPepsilon also induces RTP801 expression.
  • CONCLUSION: Taken together, our data suggest that RTP801 is an important RA-regulated gene involved in myeloid differentiation, which could represent a therapeutic target in leukemia.
  • [MeSH-major] Cell Differentiation / genetics. Leukemia, Myeloid / pathology. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Apoptosis. Cell Division. Granulocytes / cytology. Humans. Phosphorylation. Protein Kinases / metabolism. RNA, Messenger / genetics. TOR Serine-Threonine Kinases. U937 Cells

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochem J. 2005 Nov 15;392(Pt 1):93-102 [16008523.001]
  • [Cites] J Biol Chem. 2003 Jul 18;278(29):27053-8 [12736248.001]
  • [Cites] Mol Cell Biol. 2005 Jul;25(14):5834-45 [15988001.001]
  • [Cites] J Biol Chem. 2005 Mar 18;280(11):9769-72 [15632201.001]
  • [Cites] Blood. 2005 Mar 15;105(6):2527-34 [15550488.001]
  • [Cites] Oncogene. 2005 Feb 10;24(7):1138-49 [15592522.001]
  • [Cites] Nat Genet. 2005 Jan;37(1):19-24 [15624019.001]
  • [Cites] Blood. 2004 Dec 15;104(13):3911-7 [15308577.001]
  • [Cites] Genes Dev. 2004 Dec 1;18(23):2879-92 [15545626.001]
  • [Cites] Genes Dev. 2004 Dec 1;18(23):2893-904 [15545625.001]
  • [Cites] J Clin Invest. 1999 May 15;103(10):1399-408 [10330422.001]
  • [Cites] Blood. 1992 May 15;79(10):2733-40 [1586720.001]
  • [Cites] Genes Dev. 2004 Aug 15;18(16):1926-45 [15314020.001]
  • [Cites] Annu Rev Nutr. 2004;24:201-21 [15189119.001]
  • [Cites] Curr Cancer Drug Targets. 2004 May;4(3):285-98 [15134535.001]
  • [Cites] Onkologie. 2004 Feb;27(1):83-90 [15007254.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(1):58-70 [14673143.001]
  • [Cites] Cell. 2003 Oct 31;115(3):305-18 [14636558.001]
  • [Cites] Oncogene. 2003 Oct 20;22(47):7305-15 [14576840.001]
  • [Cites] Cancer Biol Ther. 2003 Jul-Aug;2(4 Suppl 1):S150-6 [14508093.001]
  • [Cites] Curr Treat Options Oncol. 2006 Jul;7(4):285-94 [16916489.001]
  • [Cites] Blood. 2006 Jan 15;107(2):698-707 [16166593.001]
  • [Cites] Nat Cell Biol. 2000 Aug;2(8):515-20 [10934472.001]
  • [Cites] Cancer Res. 2001 Jan 15;61(2):700-5 [11212271.001]
  • [Cites] Mol Cell Biol. 2002 Apr;22(7):2283-93 [11884613.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3553-60 [12411319.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):995-1005 [12453409.001]
  • [Cites] J Biol Regul Homeost Agents. 2003 Jan-Mar;17(1):46-65 [12757021.001]
  • [Cites] Clin Cancer Res. 2005 Oct 15;11(20):7243-54 [16243794.001]
  • (PMID = 17379067.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA026038
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DDIT4 protein, human; 0 / RNA, Messenger; 0 / Transcription Factors; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases
  • [Other-IDs] NLM/ NIHMS20594; NLM/ PMC1922386
  •  go-up   go-down


61. Whitson BA, Maddaus MA, Andrade RS: Thoracoscopic lingulectomy for invasive pulmonary aspergillosis. Am Surg; 2007 Mar;73(3):279-80
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.
  • Large or deep-seated lesions may require an anatomic resection such as segmentectomy, lobectomy, or pneumonectomy.
  • Thoracoscopic lobectomy has been described as a treatment of localized IPA; however, thoracoscopic anatomic segmentectomy has not been reported until now.
  • Herein, we describe a case of thoracoscopic lingulectomy for localized IPA in an immunocompromised patient: this operation minimized the delay in resuming therapy for the patient's underlying acute myeloid leukemia.
  • [MeSH-major] Aspergillosis / surgery. Lung Diseases, Fungal / surgery. Pneumonectomy / methods. Thoracic Surgery, Video-Assisted

  • Genetic Alliance. consumer health - Aspergillosis.
  • MedlinePlus Health Information. consumer health - Aspergillosis.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17375787.001).
  • [ISSN] 0003-1348
  • [Journal-full-title] The American surgeon
  • [ISO-abbreviation] Am Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


62. Qian Z, Lin J, Qian J, Yao DM, Wang YL, Han LX, Zhu ZH, Xiao GF: [Quantification of GRAF gene expression in patients with acute myeloid leukemia using EvaGreen real time quantitative PCR]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2010 Jun;27(3):290-3
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] [Quantification of GRAF gene expression in patients with acute myeloid leukemia using EvaGreen real time quantitative PCR].
  • OBJECTIVE: To quantify the expression level of GRAF gene in acute myeloid leukemia (AML) and analyze its clinical significance.
  • METHODS: The EvaGreen real-time quantitative polymerase chain reaction (RQ-PCR) assay was established and performed to measure the GRAF gene transcripts in 71 cases with AML and 21 with nonmalignant hematological diseases.
  • The GRAF expression level was significantly lower in AML (0.01%-169.75%, median 3.82%) than that in controls (14.49%-126.85%, median 56.04%) (P<0.05).
  • CONCLUSION: The GRAF gene was down-regulated in AML, which might play a role in the leukemogenesis.
  • [MeSH-major] GTPase-Activating Proteins / genetics. Leukemia, Myeloid, Acute / genetics. 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
  • (PMID = 20533268.001).
  • [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 / ARHGAP26 protein, human; 0 / GTPase-Activating Proteins
  •  go-up   go-down


63. Gray TL, Ooi CY, Tran D, Traubici J, Gerstle JT, Sung L: Gastrointestinal complications in children with acute myeloid leukemia. Leuk Lymphoma; 2010 May;51(5):768-77
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] Gastrointestinal complications in children with acute myeloid leukemia.
  • Gastrointestinal complications in pediatric acute myeloid leukemia (AML) have not been systematically described in the literature.
  • Our objective was to describe complications related to the small and large bowel in children with AML.
  • We included any study design that described gastrointestinal complications in children and/or adults with AML.
  • Both leukemia infiltration and intensive chemotherapy likely play a role in the etiology of these conditions.
  • Gastrointestinal complications are relatively common in children with AML.
  • Randomized trials are required to develop evidence-based guidelines for the management of gastrointestinal complications in pediatric AML.
  • [MeSH-major] Gastrointestinal Diseases / etiology. Leukemia, Myeloid, Acute / complications

  • 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 = 20350277.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 73
  •  go-up   go-down


64. Wetzler M, Brady MT, Tracy E, Li ZR, Donohue KA, O'Loughlin KL, Cheng Y, Mortazavi A, McDonald AA, Kunapuli P, Wallace PK, Baer MR, Cowell JK, Baumann H: Arsenic trioxide affects signal transducer and activator of transcription proteins through alteration of protein tyrosine kinase phosphorylation. Clin Cancer Res; 2006 Nov 15;12(22):6817-25
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.
  • PURPOSE: Arsenic trioxide decreases proliferation of acute myeloid leukemia (AML) cells, but its precise mechanism of action is unknown.
  • EXPERIMENTAL DESIGN: We studied the effect of arsenic trioxide on patient samples and the AML cell line HEL, which, like leukemic blasts from 50% of AML cases, has constitutively activated signal transducer and activator of transcription (STAT) proteins.
  • RESULTS: Arsenic trioxide induced mitotic arrest starting at 24 hours and significant cell death at 48 hours.
  • CONCLUSIONS: These results suggest a selective activity of arsenic trioxide on PTKs and will assist in developing clinical trials in AML.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ARSENIC TRIOXIDE .
  • 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 .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncogene. 2003 May 29;22(22):3417-23 [12776193.001]
  • [Cites] J Biol Chem. 2003 May 16;278(20):17800-9 [12624089.001]
  • [Cites] Cancer Res. 2003 Nov 15;63(22):7950-8 [14633726.001]
  • [Cites] Leuk Res. 2004 Sep;28(9):909-19 [15234567.001]
  • [Cites] Science. 1990 Feb 16;247(4944):824-30 [2406902.001]
  • [Cites] Mol Cell Biol. 1991 Apr;11(4):2057-65 [1848670.001]
  • [Cites] Mol Biol Med. 1991 Apr;8(2):267-85 [1725449.001]
  • [Cites] Science. 1993 Sep 24;261(5129):1739-44 [8397445.001]
  • [Cites] J Biol Chem. 1994 Aug 26;269(34):21411-4 [8063772.001]
  • [Cites] J Biol Chem. 1995 Apr 7;270(14):8298-310 [7713938.001]
  • [Cites] Blood. 1996 Jan 15;87(2):439-46 [8555464.001]
  • [Cites] Blood. 1996 Feb 1;87(3):882-6 [8562957.001]
  • [Cites] J Exp Med. 1996 Mar 1;183(3):811-20 [8642285.001]
  • [Cites] Blood. 1997 May 1;89(9):3354-60 [9129042.001]
  • [Cites] Acta Haematol. 1997;98(1):14-21 [9210908.001]
  • [Cites] J Biol Chem. 1997 Sep 26;272(39):24542-9 [9305919.001]
  • [Cites] J Immunol. 1997 Nov 15;159(10):4720-8 [9366395.001]
  • [Cites] EMBO J. 1998 Jan 2;17(1):61-70 [9427741.001]
  • [Cites] Mol Cell Biol. 1998 May;18(5):2545-52 [9566874.001]
  • [Cites] Mol Cell Biol. 1998 May;18(5):2553-8 [9566875.001]
  • [Cites] Cancer Res. 1998 Jul 15;58(14):3173-80 [9679986.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1456-8 [9694738.001]
  • [Cites] Leuk Lymphoma. 1998 Aug;30(5-6):433-42 [9711905.001]
  • [Cites] Mol Cell. 1998 Aug;2(2):233-9 [9734360.001]
  • [Cites] Hepatology. 1999 Sep;30(3):682-97 [10462375.001]
  • [Cites] J Pharmacokinet Biopharm. 1998 Dec;26(6):717-33 [10485082.001]
  • [Cites] J Biol Chem. 2005 Feb 18;280(7):5361-9 [15574429.001]
  • [Cites] Clin Cancer Res. 2005 Jul 15;11(14):5281-91 [16033847.001]
  • [Cites] Leukemia. 1990 Nov;4(11):745-50 [2232885.001]
  • [Cites] Leukemia. 2006 Jun;20(6):971-8 [16598306.001]
  • [Cites] Oncogene. 2000 Feb 3;19(5):624-31 [10698507.001]
  • [Cites] Blood. 2000 Jun 15;95(12):3765-70 [10845908.001]
  • [Cites] J Immunol. 2000 Oct 15;165(8):4290-7 [11035063.001]
  • [Cites] Br J Haematol. 2001 Mar;112(3):783-6 [11260084.001]
  • [Cites] J Exp Med. 2001 Jun 18;193(12):1361-71 [11413191.001]
  • [Cites] Eur J Haematol. 2001 Jun;66(6):357-64 [11488934.001]
  • [Cites] Mol Cell Biol. 2001 Nov;21(21):7172-82 [11585900.001]
  • [Cites] Blood. 2001 Dec 15;98(13):3778-83 [11739186.001]
  • [Cites] Blood. 2002 Jan 1;99(1):252-7 [11756179.001]
  • [Cites] Blood. 2002 Jan 15;99(2):664-71 [11781252.001]
  • [Cites] Blood. 2002 Jun 1;99(11):3885-91 [12010785.001]
  • [Cites] Cancer Res. 2002 Jul 15;62(14):3893-903 [12124315.001]
  • [Cites] Mol Pharmacol. 2002 Sep;62(3):529-38 [12181429.001]
  • [Cites] Cell Cycle. 2002 May-Jun;1(3):201-9 [12429934.001]
  • [Cites] Mol Cancer Ther. 2002 Aug;1(10):851-60 [12492118.001]
  • [Cites] Blood. 2003 Apr 15;101(8):2940-54 [12480704.001]
  • [Cites] J Biol Chem. 2003 May 2;278(18):16198-208 [12594223.001]
  • [Cites] Clin Cancer Res. 2003 Jun;9(6):2140-50 [12796379.001]
  • (PMID = 17121903.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA099238-01A1; United States / NCI NIH HHS / CA / R21 CA099238-02; United States / NCI NIH HHS / CA / P30 CA016056; United States / NCI NIH HHS / CA / CA16056; United States / NCI NIH HHS / CA / CA099238-02; United States / NCI NIH HHS / CA / CA85580; None / None / / R21 CA099238-01A1; United States / NCI NIH HHS / CA / CA76167; United States / NCI NIH HHS / CA / CA99238; United States / NCI NIH HHS / CA / R01 CA085580; United States / NCI NIH HHS / CA / R01 CA076167; United States / NCI NIH HHS / CA / R21 CA099238
  • [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 / Antineoplastic Agents; 0 / Arsenicals; 0 / Carrier Proteins; 0 / DNA-Binding Proteins; 0 / FGFR1OP protein, human; 0 / Oxides; 0 / Proto-Oncogene Proteins; 0 / STAT Transcription Factors; 0 / STAT3 Transcription Factor; 0 / Transcription Factors; 0 / ZMYM2 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; S7V92P67HO / arsenic trioxide
  • [Other-IDs] NLM/ NIHMS82726; NLM/ PMC2649745
  •  go-up   go-down


65. Fujita K, Sanada M, Harada H, Mori H, Niikura H, Omine M, Inazawa J, Imoto I: Molecular cloning of t(2;7)(p24.3;p14.2), a novel chromosomal translocation in myelodysplastic syndrome-derived acute myeloid leukemia. J Hum Genet; 2009 Jun;54(6):355-9
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] Molecular cloning of t(2;7)(p24.3;p14.2), a novel chromosomal translocation in myelodysplastic syndrome-derived acute myeloid leukemia.
  • In this study, we report the molecular structure of the breakpoint region in a new chromosomal translocation, t(2;7)(p24.3;p14.2), in a case of acute myeloid leukemia transformed from myelodysplastic syndrome (MDS).
  • Interestingly, this transcript encoded a truncated molecular form of 3'ELMO1 as the result of a frameshift caused by the chromosomal translocation.
  • Although this study does not provide direct evidence that a defect in NAG-ELMO1 plays a role in the pathogenesis or the leukemic change in MDS, it does suggest that defects in NAG-ELMO1 potentially contributed to the leukemic progression in this case.
  • [MeSH-major] Chromosomes, Human, Pair 2 / genetics. Chromosomes, Human, Pair 7 / genetics. Leukemia, Myelomonocytic, Acute / genetics. Myelodysplastic Syndromes / genetics. Translocation, Genetic


66. Wildenhain S, Ruckert C, Röttgers S, Harbott J, Ludwig WD, Schuster FR, Beldjord K, Binder V, Slany R, Hauer J, Borkhardt A: Expression of cell-cell interacting genes distinguishes HLXB9/TEL from MLL-positive childhood acute myeloid leukemia. Leukemia; 2010 Sep;24(9):1657-60
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.
  • [Title] Expression of cell-cell interacting genes distinguishes HLXB9/TEL from MLL-positive childhood acute myeloid leukemia.
  • [MeSH-major] Homeodomain Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Transcription Factors / genetics

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • 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 = 20596032.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / MNX1 protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


67. Shahin D, Aly R, Ebrahim MA: Prognostic significance of FLT3 internal tandem duplication in egyptian patients with acute myeloid leukemia with normal or favorable risk cytogenetics. Egypt J Immunol; 2010;17(2):23-32
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] Prognostic significance of FLT3 internal tandem duplication in egyptian patients with acute myeloid leukemia with normal or favorable risk cytogenetics.
  • Internal tandem duplication (ITD) of the FLT3 gene (FLT3/ITD) has been linked to poor outcome in acute myeloid leukemia (AML).
  • The aim of this study was to evaluate the prognostic significance of FLT3/ITD in patients with de novo AML and normal or favorable risk cytogenetics (NFC-AML).
  • Blood samples from 39 patients with AML were subjected to PCR of exons 14 and 15 of the FLT3 gene.
  • Patients were M1 3/13, M2 2/12, M3 1/9, M4 0/4 and M5 0/1.
  • The patients were followed up for a mean of 34.5 +/- 2.3 months.
  • Interestingly, disease free survival (DFS) at 3 years was significantly different in studied patients: DFS was 5% in patients with FLT3/ITD+ vs 30% of patients with FLT3/ITD- (P = 0.001).

  • 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 = 23082484.001).
  • [ISSN] 1110-4902
  • [Journal-full-title] The Egyptian journal of immunology
  • [ISO-abbreviation] Egypt J Immunol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  •  go-up   go-down


68. Blum W: Post-remission therapy in acute myeloid leukemia: what should I do now? Haematologica; 2008 Jun;93(6):801-5
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] Post-remission therapy in acute myeloid leukemia: what should I do now?
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy. Medical Oncology / methods

  • 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
  • [CommentOn] Haematologica. 2008 Jun;93(6):834-41 [18469352.001]
  • [CommentOn] Haematologica. 2008 Jun;93(6):826-33 [18469349.001]
  • (PMID = 18515876.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] Italy
  •  go-up   go-down


69. Zou Y, Wang H, Chen XJ, Wang SC, Zhang L, Chen YM, Zhu XF: [Study of clinical outcome and analysis of prognosis related factor in children with acute myeloid leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2006 Sep;27(9):621-5
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] [Study of clinical outcome and analysis of prognosis related factor in children with acute myeloid leukemia].
  • OBJECTIVE: To analyse the clinical outcome and the prognostic factor of childhood acute myeloid leukemia (AML).
  • METHODS: Disease-free survival (DFS), event-free survival (EFS) and overall survival (OS) rates were estimated by Kaplan-Meier method and prognostic factors were evaluated by Cox regression with SPSS in 141 childhood AML in our hospital from August 1995 to July 2004.
  • The patients were divided into 2 groups: acute promyelocytic leukemia (APL) as group A and AML other than APL as group B.
  • The cumulative 5 year DFS and OS rate for group B patients were (28.4 +/- 9.0)% and (35.5 +/- 6.3)%, the 51 group A patients were (94.3 +/- 4.0)% and (81.4 +/- 5.7)%, and for total 141 AML patients were (56.9 +/- 6.3)% and (53.3 +/- 4.8)% respectively.
  • Multivariate analysis demonstrated that higher bone marrow blast cell percentage at diagnosis, CR after more than one course of chemotherapy and less than six courses of consolidation chemotherapy were risk prognostic factors in childhood AML other than APL (P < 0.05).
  • CONCLUSION: The prognosis of childhood APL is better, while of childhood t(8;21) AML is no better than other FAB subtypes.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Bone Marrow Cells / cytology. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Prognosis. Regression Analysis. Retrospective Studies. 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 = 17278430.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] Controlled Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
  •  go-up   go-down


70. Abdul-Nabi AM, Yassin ER, Varghese N, Deshmukh H, Yaseen NR: In vitro transformation of primary human CD34+ cells by AML fusion oncogenes: early gene expression profiling reveals possible drug target in AML. PLoS One; 2010 Aug 27;5(8):e12464
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] In vitro transformation of primary human CD34+ cells by AML fusion oncogenes: early gene expression profiling reveals possible drug target in AML.
  • Different fusion oncogenes in acute myeloid leukemia (AML) have distinct clinical and laboratory features suggesting different modes of malignant transformation.
  • Here we compare the in vitro effects of representatives of 4 major groups of AML fusion oncogenes on primary human CD34+ cells.
  • They both caused erythroid hyperplasia and a clear block in erythroid and myeloid maturation.
  • On the other hand, AML1-ETO and PML-RARA had only modest effects on myeloid and erythroid differentiation.
  • Nutlin-3, an inhibitor of the interaction between MDM2 and p53, specifically inhibited the proliferation and self-renewal of primary human CD34+ cells transduced with AML1-ETO, suggesting that MDM2 upregulation plays a role in cell transformation by AML1-ETO.
  • These data show that differences among AML fusion oncogenes can be recapitulated in vitro using primary human CD34+ cells and that early gene expression profiling in these cells can reveal potential drug targets in AML.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • SciCrunch. ArrayExpress: Data: Microarray .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2002 Jan 1;99(1):15-23 [11756147.001]
  • [Cites] Cancer Res. 2009 Feb 1;69(3):1109-16 [19155294.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Apr;33(4):331-45 [11921269.001]
  • [Cites] Oncogene. 2002 May 13;21(21):3475-95 [12032783.001]
  • [Cites] Nat Med. 2002 Jul;8(7):743-50 [12091906.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):10008-13 [12105272.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Jun;37(2):149-58 [12696063.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1857-65 [12750176.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2395-402 [12805060.001]
  • [Cites] Mol Cancer Res. 2003 Dec;1(14):1001-8 [14707283.001]
  • [Cites] Science. 2004 Feb 6;303(5659):844-8 [14704432.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1605-16 [15084693.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1617-28 [15084694.001]
  • [Cites] Leukemia. 2004 Jul;18(7):1238-45 [15152269.001]
  • [Cites] Nat Genet. 2004 Oct;36(10):1084-9 [15361874.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 May;87(9):3584-8 [2333304.001]
  • [Cites] Science. 1997 Nov 7;278(5340):1059-64 [9353180.001]
  • [Cites] Cell. 1998 Mar 20;92(6):713-23 [9529248.001]
  • [Cites] Cell. 1998 Mar 20;92(6):725-34 [9529249.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 15;102(11):4016-21 [15731354.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1189-98 [15878973.001]
  • [Cites] Oncogene. 2005 Aug 29;24(37):5693-700 [16123802.001]
  • [Cites] Trends Cell Biol. 2005 Sep;15(9):494-501 [16084092.001]
  • [Cites] Blood. 2005 Nov 1;106(9):3150-9 [16014563.001]
  • [Cites] Leukemia. 2006 Feb;20(2):218-23 [16341046.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 24;103(4):1030-5 [16418266.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Feb;7(2):131-42 [16493418.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):2990-6 [16540647.001]
  • [Cites] Leukemia. 2006 Apr;20(4):696-706 [16467868.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6628-37 [16818636.001]
  • [Cites] Blood. 2006 Jul 15;108(2):685-96 [16597596.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1690-7 [16670269.001]
  • [Cites] Cancer Res. 2006 Dec 15;66(24):11781-91 [17178874.001]
  • [Cites] Curr Opin Hematol. 2007 Mar;14(2):85-9 [17255784.001]
  • [Cites] Science. 2007 Apr 27;316(5824):600-4 [17463288.001]
  • [Cites] Cancer Lett. 2007 Jun 28;251(2):179-86 [17125917.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1531-7 [10942402.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] Leukemia. 2001 Nov;15(11):1689-95 [11681408.001]
  • [Cites] Clin Cancer Res. 1998 Dec;4(12):3051-62 [9865920.001]
  • [Cites] Int J Biochem Cell Biol. 2007;39(6):1063-70 [17468032.001]
  • [Cites] Leukemia. 2007 Aug;21(8):1638-47 [17554387.001]
  • [Cites] J Interferon Cytokine Res. 2007 Jul;27(7):543-52 [17651015.001]
  • [Cites] Blood. 2008 Feb 15;111(4):2190-9 [17975013.001]
  • [Cites] Semin Cell Dev Biol. 2008 Jun;19(3):294-308 [18343170.001]
  • [Cites] Blood. 2008 May 1;111(9):4668-80 [18299449.001]
  • [Cites] Cancer Cell. 2008 Jun;13(6):483-95 [18538732.001]
  • [Cites] Oncogene. 2008 Jun 19;27(27):3765-79 [18264136.001]
  • [Cites] Arch Pathol Lab Med. 2008 Nov;132(11):1835-7 [18976025.001]
  • [Cites] Methods Mol Biol. 2009;538:263-85 [19277588.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2009;49:223-41 [18834305.001]
  • [Cites] Cell. 2009 May 15;137(4):609-22 [19450511.001]
  • [Cites] Haematologica. 2009 Jul;94(7):984-93 [19535349.001]
  • [Cites] Leukemia. 2009 Jul;23(7):1303-10 [19225539.001]
  • [Cites] Blood. 2010 Jul 8;116(1):71-80 [20404136.001]
  • [Cites] Leukemia. 2002 Feb;16(2):186-95 [11840284.001]
  • (PMID = 20805992.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL082549; United States / NCI NIH HHS / CA / T32CA009547; United States / NCI NIH HHS / CA / T32 CA009547; United States / NHLBI NIH HHS / HL / K02 HL084179; United States / NCI NIH HHS / CA / P30 CA091842; United States / NCI NIH HHS / CA / P30CA91842; United States / NHLBI NIH HHS / HL / R01HL082549; United States / NHLBI NIH HHS / HL / K02HL084179
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Other-IDs] NLM/ PMC2929205
  •  go-up   go-down


71. Agirre X, Román-Gómez J, Vázquez I, Jiménez-Velasco A, Garate L, Montiel-Duarte C, Artieda P, Cordeu L, Lahortiga I, Calasanz MJ, Heiniger A, Torres A, Minna JD, Prósper F: Abnormal methylation of the common PARK2 and PACRG promoter is associated with downregulation of gene expression in acute lymphoblastic leukemia and chronic myeloid leukemia. Int J Cancer; 2006 Apr 15;118(8):1945-53
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] Abnormal methylation of the common PARK2 and PACRG promoter is associated with downregulation of gene expression in acute lymphoblastic leukemia and chronic myeloid leukemia.
  • We have studied the role of promoter hypermethylation in the regulation of PARK2 and PACRG expression in different tumor cell lines and primary patient samples.
  • Abnormal methylation of the common promoter of PARK2 and PACRG was observed in 26% of patients with acute lymphoblastic leukemia and 20% of patients with chronic myelogenous leukemia (CML) in lymphoid blast crisis, but not in ovarian, breast, lung, neuroblastoma, astrocytoma or colon cancer cells.
  • By FISH, we demonstrated that a lack of PARK2 and PACRG expression was due to biallelic hypermethylation and not to deletion of either PARK2 or PACRG in ALL.
  • In conclusion, our results demonstrate for the first time that the candidate tumor suppressor genes PARK2 and PACRG are epigenetically regulated in human leukemia, suggesting that abnormal methylation and regulation of PARK2 and PACRG may play a role in the pathogenesis and development of this hematological neoplasm.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proteins / physiology. Ubiquitin-Protein Ligases / biosynthesis

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16287063.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50CA70907; United States / NCI NIH HHS / CA / U01CA7629303
  • [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 / Molecular Chaperones; 0 / PACRG protein, human; 0 / Proteins; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / parkin protein
  •  go-up   go-down


72. Qin YZ, Ruan GR, Li JL, Fu JY, Chang Y, Wang H, Li LD, Liu YR, Chen SS: [Significance of quantification of WT1 mRNA for monitoring minimal residual disease in acute myeloid leukemia patients]. Zhonghua Xue Ye Xue Za Zhi; 2005 Nov;26(11):649-52
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] [Significance of quantification of WT1 mRNA for monitoring minimal residual disease in acute myeloid leukemia patients].
  • OBJECTIVE: To evaluate the significance of quantification of WT1 mRNA for monitoring minimal residual disease (MRD) in patients with acute myeloid leukemia (AML).
  • METHODS: WT1 mRNA level was detected with real-time quantitative RT-PCR (RQ-PCR) technique in bone marrow samples from 15 normal subjects (NBM) and 123 AML patients.
  • Sixty-two AML samples were also detected AML1-ETO mRNA expression by RQ-PCR.
  • Simultaneously follow-up of WT1 and AML1-ETO levels were carried out in 50 samples from 8 AML patients.
  • Higher levels of WT1 expression were found in 61 of 67 (91%) newly diagnosed AML patients compared with NBMs and 37 of the 67 (55.2%) showed 100-fold higher WT1 levels than that in NBMs.
  • CONCLUSIONS: Quantification of WT1 expression level by RQ-PCR may be used to monitor MRD for most AML patients, but it is less sensitive than fusion gene.
  • [MeSH-major] Leukemia, Myeloid, Acute / metabolism. Neoplasm, Residual / metabolism. WT1 Proteins / metabolism

  • 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 = 16620548.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / WT1 Proteins
  •  go-up   go-down


73. Al-Mawali A, Gillis D, Lewis I: The use of receiver operating characteristic analysis for detection of minimal residual disease using five-color multiparameter flow cytometry in acute myeloid leukemia identifies patients with high risk of relapse. Cytometry B Clin Cytom; 2009 Mar;76(2):91-101
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] The use of receiver operating characteristic analysis for detection of minimal residual disease using five-color multiparameter flow cytometry in acute myeloid leukemia identifies patients with high risk of relapse.
  • BACKGROUND: Multiparameter flow cytometry (MFC) has been shown to be a useful approach for detection of minimal residual disease (MRD).
  • This study analyzed 54 acute myeloid leukemia (AML) patients.
  • MRD was evaluated in the bone marrow (BM) in morphologic complete remission from 25 and 22 patients after induction and consolidation, respectively.
  • MRD level postinduction not only influenced relapse-free survival (RFS) (P = 0.004) but also overall survival (OS) (P = 0.003).
  • CONCLUSIONS: Using the ROC analysis, the threshold of 0.15% was defined as the optimal value in discriminating risk categories in AML, and postinduction MRD assessment is able to better predict disease outcome than consolidation.
  • [MeSH-major] Flow Cytometry / methods. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / diagnosis
  • [MeSH-minor] Adult. Aged. Antineoplastic Protocols. Bone Marrow Cells / cytology. Bone Marrow Cells / pathology. Cell Count / methods. Female. Humans. Male. Middle Aged. Predictive Value of Tests. Prognosis. Risk Factors. Secondary Prevention. Signal Processing, Computer-Assisted. Survival Rate. 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
  • [Copyright] 2008 Clinical Cytometry Society.
  • (PMID = 18727068.001).
  • [ISSN] 1552-4957
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


74. Benjamin R, Khwaja A, Singh N, McIntosh J, Meager A, Wadhwa M, Streck C, Ng C, Davidoff AM, Nathwani AC: Continuous delivery of human type I interferons (alpha/beta) has significant activity against acute myeloid leukemia cells in vitro and in a xenograft model. Blood; 2007 Feb 1;109(3):1244-7
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] Continuous delivery of human type I interferons (alpha/beta) has significant activity against acute myeloid leukemia cells in vitro and in a xenograft model.
  • In this study, we focused primarily on the antileukemic activity of interferon-beta (IFN-beta) in a murine xenograft model of acute myeloid leukemia (AML).
  • Bolus administration of recombinant IFN-beta via the subcutaneous or intravenous route failed to show efficacy in mice injected with AML cells despite achieving peak plasma IFN-beta levels of more than 200 IU/mL.
  • In contrast, stable expression of IFN-beta following adeno-associated virus (AAV) vector-mediated gene transfer resulted in significant antileukemic activity against primary AML cells derived from patients with poor prognostic markers.
  • An almost linear relationship was observed with stable plasma levels of IFN-beta and antileukemic activity in mice.
  • Therefore, approaches capable of maintaining stable plasma levels of IFN-beta merit further clinical evaluation in patients with AML.
  • [MeSH-major] Interferon-beta / administration & dosage. Interferon-beta / pharmacology. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adenoviridae / genetics. Animals. Dose-Response Relationship, Drug. Drug Administration Routes. Drug Evaluation, Preclinical. Genetic Therapy / methods. Humans. Interferon Type I / administration & dosage. Interferon Type I / pharmacology. Interferon-alpha / administration & dosage. Interferon-alpha / pharmacology. Mice. Transfection. Transplantation, Heterologous. Tumor Burden / drug effects

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17047156.001).
  • [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 / Interferon Type I; 0 / Interferon-alpha; 77238-31-4 / Interferon-beta
  •  go-up   go-down


75. Licht JD, Sternberg DW: The molecular pathology of acute myeloid leukemia. Hematology Am Soc Hematol Educ Program; 2005;:137-42
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] The molecular pathology of acute myeloid leukemia.
  • The pathogenesis of acute myelogenous leukemia (AML) involves an array of molecular alterations that disrupt almost every facet of cell transformation.
  • These processes include the regulation of cell proliferation, differentiation, self-renewal, survival, cell cycle checkpoint control, DNA repair and chromatin stability, and cell dissemination.
  • This overview describes some of the critical molecular alterations and implicates the rogue leukemogenic proteins in the onset and progression of AML.

  • 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 = 16304371.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA82261; United States / NCI NIH HHS / CA / R01 CA59936
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Transcription Factors
  • [Number-of-references] 40
  •  go-up   go-down


76. Marzac C, Teyssandier I, Calendini O, Perrot JY, Faussat AM, Tang R, Casadevall N, Marie JP, Legrand O: Flt3 internal tandem duplication and P-glycoprotein functionality in 171 patients with acute myeloid leukemia. Clin Cancer Res; 2006 Dec 1;12(23):7018-24
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] Flt3 internal tandem duplication and P-glycoprotein functionality in 171 patients with acute myeloid leukemia.
  • PURPOSE: Patients with adult acute myeloid leukemia (AML) with intermediate cytogenetics remain a heterogeneous group with highly variable individual prognoses.
  • We did a multivariate analysis on 171 patients with adult AML treated in the European Organization for Research and Treatment of Cancer protocols.
  • In the Pgp-ITD- group (41 of 95), CR rates were 70% versus 44% for others (P = 0.012), OS achieved 48% versus 16% (P < 0.0001) and disease-free survival was 56% versus 27% (P = 0.024), respectively.
  • Furthermore, the OS curves of the intermediate cytogenetics-Pgp-ITD- group were not significantly different from the favorable cytogenetic group.
  • CONCLUSION: Flt3/ITD and Pgp activity are independent and additive prognostic factors which provide a powerful risk classification that can be routinely used to stratify the treatment of patients with intermediate cytogenetic AML.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid / genetics. Leukemia, Myeloid / metabolism. P-Glycoproteins / metabolism. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Cytogenetic Analysis. Follow-Up Studies. Humans. Middle Aged. Multivariate Analysis. Prognosis. Remission Induction. Risk Factors. Survival Rate. Tandem Repeat Sequences. Treatment Outcome

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17145823.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / P-Glycoproteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  •  go-up   go-down


77. Xia Q, Wang HX, Wang J, Zhang JY, Liu BY, Li AL, Lv M, Hu MR, Yu M, Feng JN, Yang SC, Zhang XM, Shen BF: Proteomic analysis of interleukin 6-induced differentiation in mouse myeloid leukemia cells. Int J Biochem Cell Biol; 2005 Jun;37(6):1197-207
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] Proteomic analysis of interleukin 6-induced differentiation in mouse myeloid leukemia cells.
  • Cytokine-induced differentiation of myeloid leukemia cells has important therapeutic implications, but the mechanism remains to be clarified.
  • M1 cell, a mouse acute myeloid leukemia cell line, which underwent growth inhibition, terminal differentiation and apoptosis in response to IL-6, was selected as an experimental model to study on the molecular mechanisms of myeloid cell differentiation on a proteome-wide scale.
  • Cell differentiation was evaluated by cell morphology and CD11b expression.
  • The identified proteins were known to be involved in different cellular functions, including protein synthesis, transcription, signal transduction, cell cycle control, cell rescue and defense, cellular organization, and metabolism.
  • Notably, seven proteins were not described before to be involved in differentiation.
  • Our data provide novel information for a better understanding of the mechanisms by which terminal differentiation of acute myeloid leukemia cells induced by IL-6.
  • [MeSH-major] Cell Differentiation / drug effects. Interleukin-6 / pharmacology. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. Proteomics
  • [MeSH-minor] Animals. Antigens, CD11b / biosynthesis. Apoptosis / drug effects. Cell Line, Tumor. Cystatin B. Cystatins / biosynthesis. Electrophoresis, Gel, Two-Dimensional. Fructose-Bisphosphate Aldolase / biosynthesis. Membrane Proteins / biosynthesis. Mice. Peroxidases / biosynthesis. Peroxiredoxins. Recombinant Proteins / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Spectrometry, Mass, Electrospray Ionization. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • 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 = 15778084.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Cstb protein, mouse; 0 / Cystatins; 0 / Interleukin-6; 0 / Membrane Proteins; 0 / Recombinant Proteins; 88844-95-5 / Cystatin B; EC 1.11.1.- / Peroxidases; EC 1.11.1.15 / Peroxiredoxins; EC 4.1.2.13 / Fructose-Bisphosphate Aldolase
  •  go-up   go-down


78. Omidvar N, Pearn L, Burnett AK, Darley RL: Ral is both necessary and sufficient for the inhibition of myeloid differentiation mediated by Ras. Mol Cell Biol; 2006 May;26(10):3966-75
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] Ral is both necessary and sufficient for the inhibition of myeloid differentiation mediated by Ras.
  • Hyperactivation of Ras is one of the most common abnormalities in acute myeloid leukemia.
  • In experimental models, Ras inhibits myeloid differentiation, which is characteristic of leukemia; however, the mechanism through which it disrupts hematopoiesis is poorly understood.
  • Cells expressing Ras mutants selectively activating Raf (Ras*T35S) or phosphatidylinositol 3-kinase (Ras*Y40C) did not significantly affect differentiation or proliferative capacity, whereas Ras*E37G (which selectively activates RalGEFs) perpetuated proliferation and blocked neutrophil development in a manner similar to that of Ras.
  • [MeSH-major] Cell Differentiation. Genes, ras. Leukemia, Myeloid / physiopathology. ral Guanine Nucleotide Exchange Factor / physiology. ras Proteins / physiology
  • [MeSH-minor] Animals. Blotting, Western. Cell Culture Techniques. Cell Line, Tumor. Cell Proliferation. Clone Cells. Dose-Response Relationship, Drug. Enzyme Activation. Gene Expression Regulation, Leukemic. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Mice. Mutation. Neutrophils / cytology. Neutrophils / metabolism. Retroviridae / genetics

  • 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
  • [Cites] Blood. 1994 Nov 15;84(10):3435-9 [7949098.001]
  • [Cites] Cell. 1995 Feb 24;80(4):533-41 [7867061.001]
  • [Cites] J Exp Med. 1995 Jun 1;181(6):2189-99 [7539043.001]
  • [Cites] Mol Cell Biol. 1995 Aug;15(8):4578-84 [7623849.001]
  • [Cites] J Biol Chem. 1995 Sep 22;270(38):22473-7 [7673236.001]
  • [Cites] Nature. 1995 Nov 23;378(6555):409-12 [7477381.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):137-43 [8563750.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):144-8 [8563751.001]
  • [Cites] EMBO J. 1996 Feb 15;15(4):810-6 [8631302.001]
  • [Cites] J Biol Chem. 1996 Mar 29;271(13):7587-92 [8631792.001]
  • [Cites] J Biol Chem. 1996 Jul 12;271(28):16439-42 [8663585.001]
  • [Cites] Oncogene. 1996 Jul 18;13(2):353-62 [8710374.001]
  • [Cites] Curr Opin Cell Biol. 1996 Apr;8(2):197-204 [8791426.001]
  • [Cites] Trends Biochem Sci. 1996 Nov;21(11):438-41 [8987400.001]
  • [Cites] J Biol Chem. 1997 Jan 17;272(3):1990-6 [8999891.001]
  • [Cites] Blood. 1997 May 15;89(10):3534-43 [9160658.001]
  • [Cites] J Neurosci. 1997 Aug 15;17(16):6256-63 [9236236.001]
  • [Cites] Curr Biol. 1997 Oct 1;7(10):794-7 [9368762.001]
  • [Cites] Blood. 1998 Mar 15;91(6):1924-33 [9490675.001]
  • [Cites] Mol Cell Biol. 1998 May;18(5):2486-91 [9566869.001]
  • [Cites] Leukemia. 1998 Jun;12(6):887-92 [9639416.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Mar;85(5):1629-33 [3278322.001]
  • [Cites] Cancer Res. 1989 Sep 1;49(17):4682-9 [2547513.001]
  • [Cites] Blood. 1991 Mar 1;77(5):925-9 [1704804.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3314-8 [1826565.001]
  • [Cites] J Biol Chem. 1991 Sep 15;266(26):17700-6 [1894650.001]
  • [Cites] Int Rev Immunol. 1998;16(5-6):651-82 [9646181.001]
  • [Cites] Oncogene. 1998 Nov 26;17(21):2701-9 [9840934.001]
  • [Cites] Mol Cell Biol. 1999 Mar;19(3):1731-41 [10022860.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Feb 16;255(2):502-7 [10049738.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 2;96(5):2122-8 [10051605.001]
  • [Cites] Leukemia. 1999 Apr;13(4):585-9 [10214865.001]
  • [Cites] Blood. 1999 May 1;93(9):3074-80 [10216104.001]
  • [Cites] J Biol Chem. 1999 Jun 25;274(26):18141-4 [10373409.001]
  • [Cites] N Engl J Med. 1999 Jul 15;341(3):164-72 [10403855.001]
  • [Cites] J Biol Chem. 1999 Jul 30;274(31):21847-52 [10419502.001]
  • [Cites] J Biol Chem. 1999 Aug 13;274(33):23633-41 [10438546.001]
  • [Cites] Curr Biol. 1999 Sep 23;9(18):991-8 [10508610.001]
  • [Cites] EMBO J. 2005 Jan 12;24(1):54-62 [15592429.001]
  • [Cites] Cancer Cell. 2005 Mar;7(3):219-26 [15766660.001]
  • [Cites] Cancer Cell. 2005 Jun;7(6):533-45 [15950903.001]
  • [Cites] J Cell Biol. 2005 Dec 5;171(5):857-69 [16330713.001]
  • [Cites] Cell Mol Life Sci. 2000 Dec;57(13-14):1950-63 [11215520.001]
  • [Cites] EMBO J. 2001 Feb 15;20(4):743-54 [11179219.001]
  • [Cites] EMBO J. 2001 Feb 15;20(4):755-66 [11179220.001]
  • [Cites] J Biol Chem. 2001 May 4;276(18):15298-305 [11278419.001]
  • [Cites] Curr Biol. 2001 May 1;11(9):R342-4 [11369243.001]
  • [Cites] Exp Hematol. 1999 Nov;27(11):1599-608 [10560907.001]
  • [Cites] Leuk Res. 2000 Jan;24(1):47-54 [10634645.001]
  • [Cites] EMBO J. 2000 Feb 15;19(4):623-30 [10675331.001]
  • [Cites] Br J Haematol. 2000 Feb;108(2):322-30 [10691863.001]
  • [Cites] Development. 2000 Jun;127(12):2629-42 [10821761.001]
  • [Cites] Blood. 2000 Dec 1;96(12):3907-14 [11090077.001]
  • [Cites] J Biol Chem. 2001 Jan 26;276(4):2752-7 [11022048.001]
  • [Cites] J Neurosci. 2001 Jun 1;21(11):3839-48 [11356872.001]
  • [Cites] J Biol Chem. 2001 Oct 5;276(40):37307-16 [11489882.001]
  • [Cites] Nat Cell Biol. 2002 Jan;4(1):66-72 [11740492.001]
  • [Cites] Br J Haematol. 2002 Mar;116(3):511-8 [11849206.001]
  • [Cites] EMBO J. 2002 Mar 15;21(6):1327-38 [11889038.001]
  • [Cites] Mol Biol Cell. 2002 Mar;13(3):947-64 [11907274.001]
  • [Cites] Genes Dev. 2002 Aug 15;16(16):2045-57 [12183360.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2607-16 [12239175.001]
  • [Cites] Blood. 2002 Dec 1;100(12):4185-92 [12393454.001]
  • [Cites] Cancer Cell. 2002 Dec;2(6):507-14 [12498719.001]
  • [Cites] Mol Cell Biol. 2003 Feb;23(3):1112-24 [12529414.001]
  • [Cites] Cell. 2003 Apr 18;113(2):147-58 [12705864.001]
  • [Cites] Leukemia. 2003 Jun;17(6):1058-67 [12764369.001]
  • [Cites] Trends Cell Biol. 2003 Aug;13(8):419-25 [12888294.001]
  • [Cites] EMBO Rep. 2003 Aug;4(8):800-6 [12856001.001]
  • [Cites] Development. 2003 Nov;130(22):5543-52 [14530299.001]
  • [Cites] J Biol Chem. 2003 Oct 17;278(42):41347-54 [12902328.001]
  • [Cites] J Biol Chem. 2003 Dec 19;278(51):51743-8 [14525976.001]
  • [Cites] Blood. 2004 Jan 1;103(1):267-74 [12969963.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jan 13;101(2):597-602 [14699048.001]
  • [Cites] Exp Hematol. 2004 Jan;32(1):36-44 [14725899.001]
  • [Cites] J Clin Invest. 2004 Feb;113(4):528-38 [14966562.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 May 18;101(20):7618-23 [15128949.001]
  • [Cites] Mol Cell Biol. 2004 Jul;24(13):5746-56 [15199131.001]
  • [Cites] Mol Cell Biol. 2004 Aug;24(16):6993-7002 [15282300.001]
  • [Cites] Cancer Cell. 2004 Aug;6(2):171-83 [15324700.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1679-87 [15166036.001]
  • [Cites] Oncogene. 2004 Sep 20;23(43):7188-98 [15378079.001]
  • [Cites] Differentiation. 1986;31(2):111-8 [3091439.001]
  • [Cites] Semin Hematol. 1986 Oct;23(4):300-14 [3535084.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Dec;84(24):9228-32 [3122217.001]
  • [Cites] EMBO J. 1993 Jan;12(1):339-47 [8094051.001]
  • [Cites] Mol Cell Biol. 1993 Oct;13(10):6572-85 [7692230.001]
  • [Cites] Nature. 1993 Dec 16;366(6456):643-54 [8259209.001]
  • [Cites] Biotechnol Prog. 1993 Nov-Dec;9(6):671-4 [7764357.001]
  • [Cites] Blood. 1994 Apr 15;83(8):2248-54 [8161790.001]
  • (PMID = 16648489.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ral Guanine Nucleotide Exchange Factor; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ PMC1489015
  •  go-up   go-down


79. El-Shemy HA, Aboul-Soud MA, Nassr-Allah AA, Aboul-Enein KM, Kabash A, Yagi A: Antitumor properties and modulation of antioxidant enzymes' activity by Aloe vera leaf active principles isolated via supercritical carbon dioxide extraction. Curr Med Chem; 2010;17(2):129-38
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 vivo, active principles exhibited significant prolongation of the life span of tumor-transplanted animals in the following order: barbaloin> octapeptide> aloesin > aloe-emodin. A. vera active principles exhibited significant inhibition on Ehrlich ascite carcinoma cell (EACC) number, when compared to positive control group, in the following order: barbaloin> aloe-emodin > octapeptide > aloesin.
  • Moreover, in trypan blue cell viability assay, active principles showed a significant concentration-dependent cytotoxicity against acute myeloid leukemia (AML) and acute lymphocytes leukemia (ALL) cancerous cells.
  • Furthermore, in MTT cell viability test, aloe-emodin was found to be active against two human colon cancer cell lines (i.e.
  • Treatments of human AML leukemic cells with active principles (100 microg ml(-1)) resulted in varying intensities of internucleosomal DNA fragmentation, hallmark of cells undergoing apoptosis, in the following order: aloe-emodin> aloesin> barbaloin> octapeptide.
  • These findings are discussed in the light of the potential of A. vera plant extracts for developing efficient, specific and non-toxic anticancer drugs that are affordable for developing countries.

  • MedlinePlus Health Information. consumer health - Antioxidants.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. Carbon dioxide .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19941474.001).
  • [ISSN] 1875-533X
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Antioxidants; 0 / Enzymes; 0 / Plant Extracts; 142M471B3J / Carbon Dioxide
  • [Number-of-references] 49
  •  go-up   go-down


80. Corm S, Berthon C, Imbenotte M, Biggio V, Lhermitte M, Dupont C, Briche I, Quesnel B: Indoleamine 2,3-dioxygenase activity of acute myeloid leukemia cells can be measured from patients' sera by HPLC and is inducible by IFN-gamma. Leuk Res; 2009 Mar;33(3):490-4
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] Indoleamine 2,3-dioxygenase activity of acute myeloid leukemia cells can be measured from patients' sera by HPLC and is inducible by IFN-gamma.
  • The enzyme indoleamine 2,3-dioxygenase (IDO) converts tryptophan to kynurenine, blocking T-cell activation and inducing immunosuppression.
  • In patients with acute myeloid leukemia (AML), the serum kynurenine/tryptophan ratio (Kyn/Trp) was raised, suggesting a higher IDO activity than in healthy people.
  • IDO activity was also detected in AML cells after exposure to IFN-gammain vitro, suggesting that the higher Kyn/Trp ratio in serum of AML patients might have resulted from stimulated leukemic blast cells.
  • Thus, in AML, the activity of IDO can be easily monitored, providing a tool for future clinical testing of IDO-blocking drugs.
  • [MeSH-major] Indoleamine-Pyrrole 2,3,-Dioxygenase / metabolism. Interferon-gamma / pharmacology. Leukemia, Myeloid, Acute / enzymology. Transcriptional Activation / drug effects
  • [MeSH-minor] Blast Crisis / pathology. Chromatography, High Pressure Liquid / methods. Humans. Kynurenine / blood. Lymphocyte Activation. Survival Rate. Tryptophan / blood. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. (L)-Tryptophan .
  • 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 = 18639339.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Indoleamine-Pyrrole 2,3,-Dioxygenase; 343-65-7 / Kynurenine; 82115-62-6 / Interferon-gamma; 8DUH1N11BX / Tryptophan
  •  go-up   go-down


81. Eleni LD, Nicholas ZC, Alexandros S: Challenges in treating older patients with acute myeloid leukemia. J Oncol; 2010;2010:943823
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] Challenges in treating older patients with acute myeloid leukemia.
  • Whereas in younger patients diagnosed with acute myeloid leukemia (AML) treatment is straightforward and the goal is cure, the optimal treatment decision for older adults remains highly controversial.
  • This requires understanding of the biology and risk profile of the AML, clinical judgment in evaluating the functional status of the patient, communication skills in understanding the patient's wishes and social background, and medical expertise in available therapies.
  • The physician has to accurately inform the patient about (a) the unique biological considerations of his leukemia and his prognosis;.
  • Last but not least, he has to recommend a treatment.

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2004 Jan 15;103(2):725-31 [12947008.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4496-504 [14673036.001]
  • [Cites] Haematologica. 2004 Mar;89(3):296-302 [15020267.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1616-23 [15059843.001]
  • [Cites] Blood. 2004 Aug 1;104(3):857-64 [15073038.001]
  • [Cites] Blood. 2004 Aug 15;104(4):961-8 [15113759.001]
  • [Cites] Leukemia. 2005 Jan;19(1):7-12 [15526016.001]
  • [Cites] Blood. 2005 Jul 1;106(1):27-34 [15761020.001]
  • [Cites] Ann Hematol. 2006 Apr;85(4):250-6 [16416114.001]
  • [Cites] Blood. 2006 May 1;107(9):3481-5 [16455952.001]
  • [Cites] Blood. 2006 Jun 15;107(12):4614-22 [16484584.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3280-8 [16840728.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1395-400 [17038533.001]
  • [Cites] Cancer. 2007 Mar 15;109(6):1114-24 [17315155.001]
  • [Cites] Br J Haematol. 2007 Jul;138(2):186-95 [17593025.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2007;:420-8 [18024660.001]
  • [Cites] Blood. 2008 Jul 15;112(2):415-25 [18451310.001]
  • [Cites] Rev Recent Clin Trials. 2007 Jan;2(1):33-41 [18473986.001]
  • [Cites] Leukemia. 2009 Jan;23(1):194-6 [18580956.001]
  • [Cites] J Clin Oncol. 2008 Nov 10;26(32):5183-91 [18768435.001]
  • [Cites] Blood. 2009 Jan 1;113(1):28-36 [18827183.001]
  • [Cites] Haematologica. 2009 Jan;94(1):102-12 [19001282.001]
  • [Cites] Leuk Lymphoma. 2008 Nov;49(11):2141-7 [19021057.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6206-14 [19050309.001]
  • [Cites] Haematologica. 2009 Jan;94(1):54-60 [19059939.001]
  • [Cites] Lancet Oncol. 2009 Mar;10(3):223-32 [19230772.001]
  • [Cites] Curr Opin Oncol. 2009 Jun;21 Suppl 1:S7-9 [19561415.001]
  • [Cites] J Clin Oncol. 2009 Oct 1;27(28):4747-53 [19720919.001]
  • [Cites] N Engl J Med. 2009 Sep 24;361(13):1235-48 [19776405.001]
  • [Cites] Haematologica. 2009 Jan;94(1):10-6 [19118375.001]
  • [Cites] Cancer. 2009 May 1;115(9):1899-905 [19235255.001]
  • [Cites] Cancer. 2005 May 15;103(10):2082-90 [15830348.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1154-63 [15870183.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5675-87 [16110027.001]
  • [Cites] Cancer. 2005 Oct 1;104(7):1442-52 [16116598.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):444-53 [16344316.001]
  • [Cites] Oncologist. 2009 Mar;14(3):222-32 [19282349.001]
  • [Cites] Br J Haematol. 2009 May;145(3):318-32 [19291085.001]
  • [Cites] Blood. 2009 Aug 6;114(6):1166-73 [19470696.001]
  • [Cites] Br J Haematol. 2009 Jun;146(1):54-63 [19438472.001]
  • [Cites] Biol Blood Marrow Transplant. 2009 Jul;15(7):890-1; author reply 891 [19539224.001]
  • [Cites] J Clin Oncol. 2009 Sep 20;27(27):4570-7 [19652066.001]
  • [Cites] Cancer. 2009 Dec 15;115(24):5746-51 [19795507.001]
  • [Cites] J Clin Oncol. 1989 Sep;7(9):1268-74 [2475589.001]
  • [Cites] J Clin Oncol. 1986 Dec;4(12):1857-64 [3537219.001]
  • [Cites] N Engl J Med. 1987 Aug 20;317(8):468-73 [3614291.001]
  • [Cites] Leukemia. 1996 Mar;10(3):389-95 [8642852.001]
  • [Cites] Blood. 1996 Oct 15;88(8):2841-51 [8874180.001]
  • [Cites] Blood. 1997 Apr 1;89(7):2578-85 [9116305.001]
  • [Cites] Leuk Lymphoma. 1997 Mar;25(1-2):111-9 [9130619.001]
  • [Cites] Bone Marrow Transplant. 1998 May;21(10):1043-7 [9632279.001]
  • [Cites] Blood. 2000 Feb 15;95(4):1188-94 [10666189.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1312-20 [11520776.001]
  • [Cites] Rev Clin Exp Hematol. 2002 Mar;6(1):46-59; discussion 86-7 [12060483.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2957-64 [12351408.001]
  • [Cites] J Clin Oncol. 2003 Apr 15;21(8):1480-4 [12697870.001]
  • [Cites] Ann Hematol. 2003 Jul;82(7):381-9 [12756497.001]
  • [Cites] Eur J Haematol. 1991 Apr;46(4):240-7 [2015877.001]
  • [Cites] Blood. 1989 Apr;73(5):1272-8 [2784697.001]
  • [Cites] N Engl J Med. 1995 Jun 22;332(25):1678-83 [7539109.001]
  • [Cites] Br J Haematol. 1996 Jul;94(1):89-98 [8757514.001]
  • [Cites] Blood. 1997 May 1;89(9):3323-9 [9129038.001]
  • [Cites] Blood. 1998 Feb 1;91(3):756-63 [9446633.001]
  • [Cites] J Clin Oncol. 1999 Nov;17(11):3569-76 [10550156.001]
  • [Cites] Blood. 2001 Dec 1;98(12):3212-20 [11719356.001]
  • [Cites] Arch Intern Med. 2002 Jul 22;162(14):1597-603 [12123403.001]
  • [Cites] Ann Hematol. 2003 Jun;82(6):336-42 [12728337.001]
  • [Cites] Blood. 2003 Sep 15;102(6):2021-30 [12791654.001]
  • [Cites] Blood. 2003 Oct 15;102(8):3052-9 [12842990.001]
  • [Cites] Leukemia. 2004 Apr;18(4):809-16 [14762444.001]
  • [Cites] J Clin Oncol. 2004 Mar 15;22(6):1078-86 [15020609.001]
  • [Cites] Blood. 2004 Aug 1;104(3):865-72 [15090449.001]
  • [Cites] Haematologica. 2004 Aug;89(8):950-6 [15339678.001]
  • [Cites] Bone Marrow Transplant. 2005 Feb;35(3):277-82 [15558037.001]
  • [Cites] Blood. 2005 May 15;105(10):4147-8 [15867422.001]
  • [Cites] Clin Cancer Res. 2005 May 15;11(10):3604-8 [15897554.001]
  • [Cites] Leukemia. 2006 Feb;20(2):322-8 [16307018.001]
  • [Cites] J Natl Compr Canc Netw. 2006 Jan;4(1):16-36 [16403402.001]
  • [Cites] Cancer. 2006 Mar 1;106(5):1090-8 [16435386.001]
  • [Cites] Blood. 2006 Jul 15;108(2):685-96 [16597596.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3262-70 [16857985.001]
  • [Cites] Leukemia. 2007 Jul;21(7):1357-62 [17508002.001]
  • [Cites] Ann Oncol. 2008 Jan;19(1):128-34 [17906298.001]
  • [Cites] Br J Haematol. 2008 May;141(5):744-5 [18373704.001]
  • [Cites] Blood. 2008 Sep 1;112(5):1638-45 [18565853.001]
  • [Cites] J Clin Oncol. 2008 Oct 10;26(29):4791-7 [18695255.001]
  • [Cites] Haematologica. 2008 Dec;93(12):1806-13 [18838471.001]
  • [Cites] Blood. 2009 Apr 30;113(18):4179-87 [19008455.001]
  • [Cites] J Clin Oncol. 2009 Jan 1;27(1):61-9 [19047294.001]
  • [Cites] Bone Marrow Transplant. 2003 Jun;31(12):1089-95 [12796788.001]
  • (PMID = 20628485.001).
  • [ISSN] 1687-8469
  • [Journal-full-title] Journal of oncology
  • [ISO-abbreviation] J Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2902223
  •  go-up   go-down


82. Park TS, Song J, Lee KA, Min YH, Lee SG, Park Y, Kim J, Lee EY, Choi JR: Paracentric inversion-associated t(8;21) variant in de novo acute myelogenous leukemia: characteristic patterns of conventional cytogenetics, FISH, and multicolor banding analysis. Cancer Genet Cytogenet; 2008 May;183(1):72-6
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] Paracentric inversion-associated t(8;21) variant in de novo acute myelogenous leukemia: characteristic patterns of conventional cytogenetics, FISH, and multicolor banding analysis.
  • Acute myelogenous leukemia (AML) with t(8;21)(q22;q22) demonstrates unique clinico-pathologic disease entity in patients with hematologic malignancies.
  • The t(8;21), which results in fusion of the AML1 gene on 21q22 and the ETO gene on 8q22 on a molecular level, is one of the most common nonrandom chromosomal changes, and it is found in about 5-12% of patients with AML.
  • Here, we describe a rare case report of reciprocal paracentric inversion-associated t(8;21) variant in a 28-year old male patient with de novo AML.
  • This report emphasizes the value of "conventional" cytogenetics, as well as "newly developed" molecular cytogenetic methods in the diagnosis of rare complex t(8;21) variant in patients with AML.
  • [MeSH-major] Centromere / genetics. Chromosome Inversion. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Cytogenetic Analysis / methods. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2008 Elsevier Inc.
  • (PMID = 18474302.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


83. Sada E, Henzan H, Ohtani R, Takase K, Miyamoto T, Fukuda T, Nagafuji K, Yamauchi K, Takamatsu Y, Inaba S, Harada M: Conditioning with targeted busulfan for autologous peripheral blood stem cells transplantation for acute myelogenous leukemia in an XYY male. Am J Hematol; 2005 Jan;78(1):55-8
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] Conditioning with targeted busulfan for autologous peripheral blood stem cells transplantation for acute myelogenous leukemia in an XYY male.
  • We report herein a 19-year-old Japanese male with XYY syndrome who developed acute myelogenous leukemia.
  • The patient was treated with granulocyte colony-stimulating factor combined with etoposide, cytarabine, and busulfan (the latter adjusted to a targeting dose) followed by autologous peripheral blood stem cell transplantation.
  • He had no severe regimen-related toxicities and is now free of leukemia.
  • [MeSH-major] Busulfan / administration & dosage. Immunosuppressive Agents / administration & dosage. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / surgery. Peripheral Blood Stem Cell Transplantation. Transplantation Conditioning. XYY Karyotype


84. Kajiguchi T, Chung EJ, Lee S, Stine A, Kiyoi H, Naoe T, Levis MJ, Neckers L, Trepel JB: FLT3 regulates beta-catenin tyrosine phosphorylation, nuclear localization, and transcriptional activity in acute myeloid leukemia cells. Leukemia; 2007 Dec;21(12):2476-84
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] FLT3 regulates beta-catenin tyrosine phosphorylation, nuclear localization, and transcriptional activity in acute myeloid leukemia cells.
  • Recently, acute myeloid leukemia (AML) cells with activating mutations of FMS-like tyrosine kinase-3 (FLT3) were reported to display elevated beta-catenin-dependent nuclear signaling.
  • Finally, FLT3 inhibitor decreased tyrosine phosphorylation of beta-catenin in leukemia cells obtained from FLT3-ITD-positive AML patients.
  • These data demonstrate that FLT3 activation induces beta-catenin tyrosine phosphorylation and nuclear localization, and thus suggest a mechanism for the association of FLT3 activation and beta-catenin oncogeneic signaling in AML.
  • [MeSH-major] Active Transport, Cell Nucleus / physiology. Gene Expression Regulation, Leukemic. Leukemia, Myeloid / metabolism. Neoplasm Proteins / physiology. Protein Processing, Post-Translational / physiology. Transcription, Genetic / physiology. beta Catenin / metabolism. fms-Like Tyrosine Kinase 3 / physiology
  • [MeSH-minor] Acute Disease. Animals. Cell Line, Tumor. Glycogen Synthase Kinase 3 / antagonists & inhibitors. Glycogen Synthase Kinase 3 / physiology. Humans. Interleukin-3 / pharmacology. Membrane Proteins / pharmacology. Mice. Phosphorylation. Phosphotyrosine / metabolism. RNA, Small Interfering / pharmacology. Recombinant Proteins / metabolism. Staurosporine / analogs & derivatives. Staurosporine / pharmacology. Tyrphostins / pharmacology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • 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 = 17851558.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-3; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / RNA, Small Interfering; 0 / Recombinant Proteins; 0 / Tyrphostins; 0 / beta Catenin; 0 / flt3 ligand protein; 120685-11-2 / 4'-N-benzoylstaurosporine; 146535-11-7 / 6,7-dimethoxy-3-phenylquinoxaline; 21820-51-9 / Phosphotyrosine; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; H88EPA0A3N / Staurosporine
  •  go-up   go-down


85. Narimatsu H, Emi N, Kohno A, Iwai M, Yanada M, Yokozawa T, Saito S, Shimada K, Kiyoi H, Naoe T, Yamamoto K, Morishita Y: High incidence of secondary failure of platelet recovery after autologous and syngeneic peripheral blood stem cell transplantation in acute promyelocytic leukemia. Bone Marrow Transplant; 2007 Oct;40(8):773-8
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] High incidence of secondary failure of platelet recovery after autologous and syngeneic peripheral blood stem cell transplantation in acute promyelocytic leukemia.
  • However, its clinical characteristics have not been well described in autologous SCT for acute myeloid leukemia.
  • We reviewed 11 consecutive patients who had received autologous or syngeneic SCT for acute promyelocytic leukemia.
  • SFPR was not associated with relapse of underlying diseases, graft failure or other fatal morbidities.
  • The unexpectedly high prevalence and the characteristics of SFPR may provide additional information on management following autologous SCT for acute myeloid leukemia.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / surgery. Peripheral Blood Stem Cell Transplantation / adverse effects. Thrombocytopenia / etiology

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17700597.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


86. Wang H, Ni W, Chen Z, Lou J, Xu H, Yu Y, Qian W, Jin J: [Clinical and cytogenetic features of hematologic malignancies associated with acquired trisomy 21]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2008 Oct;25(5):576-8
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.
  • RESULTS: Thirteen patients (1.5%) with acute myeloid leukemia (AML) including 6 cases of M5b, 8 (2.2%) with acute lymphoblastic leukemia (ALL) and 4 cases with other hematologic malignancies had acquired trisomy 21, and in 13 patients it occurred as the sole cytogenetic abnormality.
  • CONCLUSION: M5b was the major type in AML with sole acquired trisomy 21.Trisomy 21 as the sole abnormality appeared to have a poor prognosis.
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Follow-Up Studies. Humans. Karyotyping. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Male. Middle Aged. Phenotype. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Survival Rate

  • MedlinePlus Health Information. consumer health - Down Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18841576.001).
  • [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
  •  go-up   go-down


87. Gupta A, Singh M, Singh H, Kumar L, Sharma A, Bakhshi S, Raina V, Thulkar S: Infections in acute myeloid leukemia: an analysis of 382 febrile episodes. Med Oncol; 2010 Dec;27(4):1037-45
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] Infections in acute myeloid leukemia: an analysis of 382 febrile episodes.
  • Neutropenic fever is an important cause of morbidity and mortality during therapy of acute myeloid leukemia (AML).
  • Between May, 2001 and December, 2006, 95 patients with de novo non-M3 AML received remission induction chemotherapy followed by consolidation in those who achieved complete remission.
  • Febrile neutropenia was defined as per international guidelines.
  • A total of 382 febrile episodes were recorded; neutropenic 347 (induction phase 172, consolidation phase 175) and non-neutropenic 35 (induction 16, consolidation 19).
  • Careful selection of antibiotics and early institution of antifungal therapy besides considering alternative diagnosis peculiar to the region (e.g. tuberculosis, malaria) may help in reducing morbidity and mortality during AML therapy.
  • [MeSH-major] Fever / etiology. Infection / etiology. Leukemia, Myeloid, Acute / complications. Neutropenia / etiology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Fever.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Bone Marrow Transplant. 2000 Jan;25(2):147-52 [10673672.001]
  • [Cites] Clin Infect Dis. 2002 Mar 15;34(6):730-51 [11850858.001]
  • [Cites] Blood. 1998 Apr 15;91(8):2722-30 [9531581.001]
  • [Cites] Jpn J Antibiot. 1994 Sep;47(9):1196-201 [7990260.001]
  • [Cites] Ann Intern Med. 1984 Mar;100(3):345-51 [6696356.001]
  • [Cites] Jpn J Antibiot. 1992 Aug;45(8):1003-8 [1433888.001]
  • [Cites] Drugs. 1997 May;53(5):789-804 [9129866.001]
  • [Cites] J Clin Oncol. 1996 Jul;14(7):2150-9 [8683249.001]
  • [Cites] Blood. 1998 May 15;91(10):3607-15 [9572995.001]
  • [Cites] Eur J Haematol. 2008 Nov;81(5):354-63 [18637030.001]
  • [Cites] Blood. 1997 Dec 15;90(12):4710-8 [9389686.001]
  • [Cites] J Clin Oncol. 2008 Dec 10;26(35):5684-8 [18955453.001]
  • [Cites] Support Care Cancer. 2008 Sep;16(9):1085-8 [18274787.001]
  • [Cites] Ann Oncol. 2003 May;14(5):795-801 [12702536.001]
  • [Cites] J Infect. 2006 Oct;53(4):266-73 [16388852.001]
  • [Cites] Hematol J. 2003;4(6):420-6 [14671614.001]
  • [Cites] Int J Antimicrob Agents. 2007 Nov;30 Suppl 1:S51-9 [17689933.001]
  • [Cites] Leukemia. 2004 Jan;18(1):72-7 [14586478.001]
  • [Cites] Jpn J Antibiot. 1993 Mar;46(3):251-8 [8510322.001]
  • [Cites] Haematologica. 2006 Aug;91(8):1068-75 [16885047.001]
  • [Cites] Clin Infect Dis. 1996 Oct;23(4):795-805 [8909847.001]
  • [Cites] J Infect. 2007 Jun;54(6):567-71 [17188750.001]
  • [Cites] Infect Control Hosp Epidemiol. 1994 Feb;15(2):101-4 [8201230.001]
  • [Cites] Clin Infect Dis. 2002 Jan 1;34(1):7-14 [11731939.001]
  • [Cites] Isr Med Assoc J. 2007 Jun;9(6):424-9 [17642387.001]
  • [Cites] Jpn J Antibiot. 1993 Oct;46(10):912-7 [8254893.001]
  • [Cites] Clin Infect Dis. 2001 Dec 1;33(11):1816-23 [11668430.001]
  • [Cites] Jpn J Antibiot. 1991 Sep;44(9):979-86 [1960859.001]
  • [Cites] Cancer. 2004 Aug 1;101(3):567-77 [15274070.001]
  • [Cites] Med Oncol. 2000 May;17(2):111-6 [10871816.001]
  • [Cites] Eur J Haematol. 2007 Sep;79(3):226-33 [17655696.001]
  • [Cites] J Med Assoc Thai. 2005 Nov;88 Suppl 8:S124-34 [16858853.001]
  • [Cites] Pediatr Infect Dis J. 2008 Nov;27(11):974-80 [18833026.001]
  • [Cites] J Clin Oncol. 1998 Mar;16(3):1179-87 [9508206.001]
  • [Cites] Clin Infect Dis. 2003 May 1;36(9):1103-10 [12715303.001]
  • [Cites] J Hosp Infect. 2002 Aug;51(4):288-96 [12183144.001]
  • [Cites] J Assoc Physicians India. 1992 Jan;40(1):18-20 [1634456.001]
  • [Cites] Hematology. 2006 Oct;11(5):335-40 [17607583.001]
  • [Cites] Cancer. 2004 Jan 15;100(2):228-37 [14716755.001]
  • (PMID = 19830601.001).
  • [ISSN] 1559-131X
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents
  •  go-up   go-down


88. Fu L, Katsube K, Tohda S: Transition of cleaved Notch1 and gene expression changes in myeloblastic leukemia cells stimulated with notch ligands. Anticancer Res; 2009 Oct;29(10):3967-70
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] Transition of cleaved Notch1 and gene expression changes in myeloblastic leukemia cells stimulated with notch ligands.
  • BACKGROUND: Notch activation by ligand stimulation regulates the growth of acute myeloid leukemia (AML) cells.
  • However, the molecular mechanisms underlying this have not been fully elucidated.
  • MATERIALS AND METHODS: Two AML cell lines, THP-1 and TMD7, and three Notch ligands, Jagged1, Dll1 and Dll4, were used.
  • The effects of the ligands on cell growth, cleavage of Notch1, and the expression of various genes were examined by cell culture, immunoblotting, and quantitative RT-PCR, respectively.
  • Ligand stimulation changed the expression levels of various genes related to cell proliferation.
  • Some genes changed in opposite directions in the two cell lines.
  • [MeSH-major] Calcium-Binding Proteins / pharmacology. Intercellular Signaling Peptides and Proteins / pharmacology. Leukemia, Myeloid, Acute / metabolism. Membrane Proteins / pharmacology. Receptor, Notch1 / metabolism
  • [MeSH-minor] Animals. CHO Cells. Cell Growth Processes / drug effects. Cell Line, Tumor. Cricetinae. Cricetulus. Gene Expression / drug effects. Humans. Immunoblotting. Intracellular Signaling Peptides and Proteins. Ligands. Recombinant Proteins / pharmacology. Reverse Transcriptase Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19846937.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Dlk1 protein, mouse; 0 / Intercellular Signaling Peptides and Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Ligands; 0 / Membrane Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Recombinant Proteins; 0 / delta protein; 134324-36-0 / Serrate proteins
  •  go-up   go-down


89. Buchert M, Darido C, Lagerqvist E, Sedello A, Cazevieille C, Buchholz F, Bourgaux JF, Pannequin J, Joubert D, Hollande F: The symplekin/ZONAB complex inhibits intestinal cell differentiation by the repression of AML1/Runx1. Gastroenterology; 2009 Jul;137(1):156-64, 164.e1-3
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] The symplekin/ZONAB complex inhibits intestinal cell differentiation by the repression of AML1/Runx1.
  • Mobility shift and chromatin immunoprecipitation were used to detect AML1 and ZONAB/DbpA binding to promoter regions of the Krüppel-like factor 4 (KLF4) and acute myeloid leukemia-1 (AML1) genes, respectively.
  • Down-regulation of symplekin or ZONAB/Dbpa induced de novo expression of the transcription factor AML1/Runx1, thereby increasing the expression of KLF4 and promoting goblet cell differentiation.
  • Furthermore, increased AML1 expression was required for the induction of goblet cell differentiation after symplekin down-regulation.
  • KLF4 expression and goblet cell numbers were reduced in the intestines of AML1(Delta/Delta) mice, confirming the role of AML1 as a promoter of intestinal differentiation in vivo.
  • CONCLUSIONS: Symplekin cooperates with ZONAB to negatively regulate intestinal goblet cell differentiation, acting by repression of AML1 and KLF4.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / metabolism. Cell Differentiation. Core Binding Factor Alpha 2 Subunit / metabolism. Goblet Cells / metabolism. Heat-Shock Proteins / metabolism. Intestines / metabolism. Nuclear Proteins / metabolism
  • [MeSH-minor] Animals. Cell Proliferation. Glyceraldehyde-3-Phosphate Dehydrogenases / metabolism. HT29 Cells. Humans. Kruppel-Like Transcription Factors / metabolism. Mice. Mice, Transgenic. Mucin-2 / metabolism. RNA Interference. Transfection

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19328795.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CSDA protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / GKLF protein; 0 / Heat-Shock Proteins; 0 / Kruppel-Like Transcription Factors; 0 / Muc2 protein, mouse; 0 / Mucin-2; 0 / Nuclear Proteins; 0 / RUNX1 protein, human; 0 / Runx1 protein, mouse; 0 / SYMPK protein, human; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases
  •  go-up   go-down


90. Liu J, Mi Y, Fu M, Yu W, Wang Y, Lin D, Bian S, Wang J: Intensive induction chemotherapy with regimen containing intermediate dose cytarabine in the treatment of de novo acute myeloid leukemia. Am J Hematol; 2009 Jul;84(7):422-7
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] Intensive induction chemotherapy with regimen containing intermediate dose cytarabine in the treatment of de novo acute myeloid leukemia.
  • To improve long-term outcome of de novo acute myeloid leukemia (AML) patients by intermediate dose of cytarabine integrated in induction therapy and to explore the impact of cytogenetic abnormalities on the prognosis.
  • Eighty-seven AML patients were treated with HAD regimen containing intermediate dose cytarabine (IDAra-C) as induction therapy, 83 from which with karyotype results were divided into three cytogenetic groups according to SWOG criteria.
  • Complete remission (CR) rate, disease-free survival (DFS), and overall survival (OS) among different groups were evaluated.
  • Median DFS and OS have not reached (NR).
  • HAD regimen containing IDAra-C as induction chemotherapy regimen is effective in de novo AML of adult patients and can achieve higher CR rate and longer survival than standard dose of cytarabine (SDAra-C) regimen.
  • [MeSH-minor] Adolescent. Adult. Chromosome Aberrations. Dose-Response Relationship, Drug. Female. Humans. Kaplan-Meier Estimate. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / physiopathology. Male. Middle Aged. Prognosis. Remission Induction. Young Adult

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • 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 = 19484734.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / HAD protocol; 0 / Harringtonines; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


91. Caramazza D, Hussein K, Siragusa S, Pardanani A, Knudson RA, Ketterling RP, Tefferi A: Chromosome 1 abnormalities in myeloid malignancies: a literature survey and karyotype-phenotype associations. Eur J Haematol; 2010 Mar;84(3):191-200
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] Chromosome 1 abnormalities in myeloid malignancies: a literature survey and karyotype-phenotype associations.
  • It is, therefore, not surprising that recurrent chromosome 1 abnormalities are regularly encountered in both neoplastic and non-neoplastic medical conditions.
  • The current review is focused on myeloid malignancies where we summarize the relevant published literature and discuss specific karyotype-phenotype associations.
  • Although occasionally seen in chronic phase MPN, unbalanced 1;7 translocations, e.g. der(1;7)(q10;p10), are usually seen in acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), and post-MPN AML/MDS.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 1. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics


92. Wang N, Kim HG, Cotta CV, Wan M, Tang Y, Klug CA, Cao X: TGFbeta/BMP inhibits the bone marrow transformation capability of Hoxa9 by repressing its DNA-binding ability. EMBO J; 2006 Apr 5;25(7):1469-80
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.
  • Homeobox (Hox) gene mutations and their altered expressions are frequently linked to human leukemia.
  • Here, we report that transforming growth factor beta (TGFbeta)/bone morphogenetic protein (BMP) inhibits the bone marrow transformation capability of Hoxa9 and Nup98-Hoxa9, the chimeric fusion form of Hoxa9 identified in human acute myeloid leukemia (AML), through Smad4, the common Smad (Co-Smad) in the TGFbeta/BMP signaling pathway.
  • These studies establish a novel mechanism by which TGFbeta/BMP regulates hematopoiesis and suggest that modification of Hox DNA-binding activity may serve as a novel therapeutic intervention for those leukemias that involve deregulation of Hox.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell Biol. 2000 May;20(9):3274-85 [10757811.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 May 27;94(11):5877-81 [9159168.001]
  • [Cites] Eur J Biochem. 2000 Dec;267(24):6954-67 [11106403.001]
  • [Cites] J Biol Chem. 2001 Jan 5;276(1):850-5 [11042172.001]
  • [Cites] EMBO J. 2001 Feb 1;20(3):350-61 [11157742.001]
  • [Cites] Exp Cell Res. 2001 Mar 10;264(1):111-6 [11237527.001]
  • [Cites] Oncogene. 2001 Jan 4;20(1):88-96 [11244507.001]
  • [Cites] Development. 2002 Mar;129(6):1455-66 [11880354.001]
  • [Cites] Science. 2002 May 31;296(5573):1646-7 [12040180.001]
  • [Cites] Blood Cells Mol Dis. 2002 Mar-Apr;28(2):221-33 [12064918.001]
  • [Cites] Oncogene. 2002 Jun 20;21(27):4247-56 [12082612.001]
  • [Cites] Br J Haematol. 1997 Jun;97(3):612-20 [9207409.001]
  • [Cites] Genes Dev. 1998 Jan 15;12(2):186-97 [9436979.001]
  • [Cites] EMBO J. 1998 Jul 1;17(13):3714-25 [9649441.001]
  • [Cites] Nature. 1998 Jul 2;394(6688):92-6 [9665135.001]
  • [Cites] Mol Cell Biol. 1999 Jan;19(1):764-76 [9858599.001]
  • [Cites] J Biol Chem. 1999 Jan 15;274(3):1415-22 [9880515.001]
  • [Cites] Mol Cell Biol. 1999 Apr;19(4):3051-61 [10082572.001]
  • [Cites] J Exp Med. 1999 Apr 5;189(7):1139-48 [10190905.001]
  • [Cites] Cell. 1999 Apr 2;97(1):29-39 [10199400.001]
  • [Cites] Leukemia. 1999 Apr;13(4):535-41 [10214859.001]
  • [Cites] J Biol Chem. 1999 May 7;274(19):13711-7 [10224145.001]
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Exp Hematol. 2005 Jul;33(7):719-37 [15963848.001]
  • [Cites] Exp Cell Res. 2006 Apr 1;312(6):854-64 [16405960.001]
  • [Cites] J Biol Chem. 2000 Jan 14;275(2):1065-72 [10625647.001]
  • [Cites] J Biol Chem. 2000 Mar 24;275(12):8267-70 [10722652.001]
  • [Cites] Leuk Res. 2002 Dec;26(12):1105-11 [12443883.001]
  • [Cites] Blood. 2003 Jan 1;101(1):124-33 [12393578.001]
  • [Cites] Leukemia. 2003 Sep;17(9):1731-7 [12970772.001]
  • [Cites] Nature. 2003 Oct 9;425(6958):577-84 [14534577.001]
  • [Cites] EMBO J. 2003 Nov 17;22(22):6057-67 [14609952.001]
  • [Cites] J Biol Chem. 2003 Dec 5;278(49):48805-14 [14551209.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15577-82 [14671321.001]
  • [Cites] J Biol Chem. 2004 Jan 9;279(2):866-75 [14561764.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1676-84 [14604967.001]
  • [Cites] J Biol Chem. 2004 Apr 9;279(15):14484-7 [14988407.001]
  • [Cites] Mol Cell Biol. 2004 May;24(9):3827-37 [15082777.001]
  • [Cites] Blood. 1988 Jul;72(1):159-64 [3291977.001]
  • [Cites] Blood. 1988 Nov;72(5):1504-11 [2460153.001]
  • [Cites] Blood. 1992 Nov 15;80(10):2445-53 [1358259.001]
  • [Cites] Stem Cells. 1993 Jul;11(4):336-47 [7691312.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Dec 6;91(25):12223-7 [7527557.001]
  • [Cites] Genes Dev. 1995 Mar 15;9(6):663-74 [7729685.001]
  • [Cites] Mol Cell Biol. 1995 Oct;15(10):5434-43 [7565694.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):154-8 [8563753.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):159-67 [8563754.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Aug 6;93(16):8508-11 [8710900.001]
  • [Cites] Blood. 1996 Dec 15;88(12):4534-46 [8977245.001]
  • [Cites] Blood. 1997 Mar 15;89(6):1922-30 [9058712.001]
  • [Cites] Trends Genet. 1997 Apr;13(4):145-51 [9097725.001]
  • [Cites] Genes Dev. 1997 Apr 1;11(7):900-13 [9106661.001]
  • [Cites] Blood. 2000 Sep 15;96(6):2022-36 [10979943.001]
  • (PMID = 16525506.001).
  • [ISSN] 0261-4189
  • [Journal-full-title] The EMBO journal
  • [ISO-abbreviation] EMBO J.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK060913; United States / NIDDK NIH HHS / DK / DK60913
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bone Morphogenetic Proteins; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / Smad4 Protein; 0 / Smad4 protein, mouse; 0 / Transforming Growth Factor beta; 0 / homeobox protein HOXA9; 0 / nuclear pore complex protein 98
  • [Other-IDs] NLM/ PMC1440313
  •  go-up   go-down


93. Reindl C, Quentmeier H, Petropoulos K, Greif PA, Benthaus T, Argiropoulos B, Mellert G, Vempati S, Duyster J, Buske C, Bohlander SK, Humphries KR, Hiddemann W, Spiekermann K: CBL exon 8/9 mutants activate the FLT3 pathway and cluster in core binding factor/11q deletion acute myeloid leukemia/myelodysplastic syndrome subtypes. Clin Cancer Res; 2009 Apr 1;15(7):2238-47
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] CBL exon 8/9 mutants activate the FLT3 pathway and cluster in core binding factor/11q deletion acute myeloid leukemia/myelodysplastic syndrome subtypes.
  • In this study, we determined the frequency of CBL mutations in acute leukemias and evaluated the oncogenic potential of mutant CBL.
  • EXPERIMENTAL DESIGN: The cDNA of 300 acute myeloid leukemia (AML)/myelodysplastic syndrome (MDS) and acute lymphoblastic leukemia (ALL) patients and 82 human leukemic cell lines was screened for aberrations in the linker and RING finger domain of CBL.
  • RESULTS: We identified 3 of 279 AML/MDS patients expressing CBL exon 8/9 deletion mutants.
  • Three of four cases at diagnosis expressed deleted transcripts missing exon 8 or exon 8/9.
  • One of 116 sequenced AML/MDS cases carried a R420G missense mutation.
  • All AML/MDS patients with identified CBL mutants belonged to the core binding factor and 11q deletion AML subtypes.
  • CONCLUSION: CBL exon8/9 mutants occur in genetically defined AML/MDS subtypes and transform hematopoietic cells by constitutively activating the FLT3 pathway.
  • This phenotype resembles the one of mutated RTKs and suggests that CBL mutant AML patients might benefit from treatment with FLT3 PTK inhibitors.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins c-cbl / genetics. fms-Like Tyrosine Kinase 3 / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Transformation, Neoplastic. Chromosome Deletion. Chromosomes, Human, Pair 11. Core Binding Factors / genetics. Exons. Humans. Sequence Deletion. Signal Transduction


94. Plesa C, Chelghoum Y, Plesa A, Elhamri M, Tigaud I, Michallet M, Dumontet C, Thomas X: Prognostic value of immunophenotyping in elderly patients with acute myeloid leukemia: a single-institution experience. Cancer; 2008 Feb 1;112(3):572-80
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 value of immunophenotyping in elderly patients with acute myeloid leukemia: a single-institution experience.
  • BACKGROUND: The poor prognosis for elderly patients with acute myeloid leukemia (AML) raises questions regarding the benefit of treating them with intensive chemotherapy.
  • METHODS: The authors investigated expression of the membrane antigens CD13, CD15, CD33, and CD34 by flow cytometry in elderly patients with newly diagnosed AML and analyzed whether these parameters had clinical or prognostic relevance to help physicians in their choice of therapy.
  • Three risk groups were defined based on CD34 and CD33 antigen expression: The poor-risk group included patients with CD34-positive/CD33-positive or CD34-negative/CD33-negative disease, the intermediate-risk group included patients with CD34-positive/CD33-negative disease, and the favorable-risk group included patients with CD34-negative/CD33-positive disease.
  • CONCLUSIONS: Immunophenotypic characteristics appeared to be a major prognostic factor in this population of elderly patients with AML.
  • By using 2 simple parameters assessed at the time of diagnosis, the authors devised a prognostic system of immediate clinical utility for prognostic stratification and risk-adapted therapeutic choices.
  • [MeSH-major] Antigens, CD / metabolism. Antigens, CD13 / metabolism. Antigens, CD15 / metabolism. Antigens, CD34 / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Immunophenotyping / methods. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18085638.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD15; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
  •  go-up   go-down


95. Doepfner KT, Spertini O, Arcaro A: Autocrine insulin-like growth factor-I signaling promotes growth and survival of human acute myeloid leukemia cells via the phosphoinositide 3-kinase/Akt pathway. Leukemia; 2007 Sep;21(9):1921-30
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] Autocrine insulin-like growth factor-I signaling promotes growth and survival of human acute myeloid leukemia cells via the phosphoinositide 3-kinase/Akt pathway.
  • Therefore, the role of insulin-like growth factor I (IGF-I) signaling in growth and survival of acute myeloid leukemia (AML) cells was investigated.
  • Expression of the IGF-I receptor (IGF-IR) and its ligand IGF-I were detected in a panel of human AML blasts and cell lines.
  • IGF-I and insulin promoted the growth of human AML blasts in vitro and activated the phosphoinositide 3-kinase (PI3K)/Akt and the extracellular signal-regulated kinase (Erk) pathways.
  • IGF-I-stimulated growth of AML blasts was blocked by an inhibitor of the PI3K/Akt pathway.
  • Moreover, downregulation of the class Ia PI3K isoforms p110beta and p110delta by RNA interference impaired IGF-I-stimulated Akt activation, cell growth and survival in AML cells.
  • Proliferation of a panel of AML cell lines and blasts isolated from patients with AML was inhibited by the IGF-IR kinase inhibitor NVP-AEW541 or by an IGF-IR neutralizing antibody.
  • In addition to its antiproliferative effects, NVP-AEW541 sensitized primary AML blasts and cell lines to etoposide-induced apoptosis.
  • Together, our data describe a novel role for autocrine IGF-I signaling in the growth and survival of primary AML cells.
  • IGF-IR inhibitors in combination with chemotherapeutic agents may represent a novel approach to target human AML.
  • [MeSH-major] Insulin-Like Growth Factor I / metabolism. Leukemia, Myeloid / pathology. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Acute Disease. Antibodies / pharmacology. Antimetabolites, Antineoplastic / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Apoptosis / physiology. Autocrine Communication. Cell Division / physiology. Cell Line, Tumor. Cytarabine / pharmacology. Down-Regulation. Etoposide / pharmacology. Humans. Receptor, IGF Type 1 / immunology. Receptor, IGF Type 1 / metabolism

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • 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 = 17581609.001).
  • [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 / Antibodies; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 04079A1RDZ / Cytarabine; 67763-96-6 / Insulin-Like Growth Factor I; 6PLQ3CP4P3 / Etoposide; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  •  go-up   go-down


96. Schroeder T, Hildebrandt B, Mayatepek E, Germing U, Haas R: A patient with glycogen storage disease type Ib presenting with acute myeloid leukemia (AML) bearing monosomy 7 and translocation t(3;8)(q26;q24) after 14 years of treatment with granulocyte colony-stimulating factor (G-CSF): a case report. J Med Case Rep; 2008;2:319
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] A patient with glycogen storage disease type Ib presenting with acute myeloid leukemia (AML) bearing monosomy 7 and translocation t(3;8)(q26;q24) after 14 years of treatment with granulocyte colony-stimulating factor (G-CSF): a case report.
  • INTRODUCTION: Glycogen storage disease type Ib is an autosomal recessive transmitted disorder of glycogen metabolism caused by mutations in the glucose-6-phosphate translocase gene on chromosome 11q23 and leads to disturbed glycogenolysis as well as gluconeogenesis.
  • In order to attenuate these complications, long-term treatment with granulocyte colony-stimulating factor is common but this is associated with an increased risk for acute myeloid leukemia or myelodysplastic syndromes in patients with inherited bone marrow failures such as severe congenital neutropenia.
  • Onset of these myeloid malignancies is linked to cytogenetic aberrations involving chromosome 7.
  • To our knowledge, we report for the first time a case report of a patient with glycogen storage disease type Ib, who developed acute myeloid leukemia with a classical monosomy 7 and acute myeloid leukemia-associated translocation t(3;8)(q26;q24) after 14 years of continuous treatment with granulocyte colony-stimulating factor.
  • CASE PRESENTATION: A 28-year-old Turkish man with glycogen storage disease type Ib was admitted to our department because of dyspnea and increasing fatigue.
  • A bone marrow biopsy was taken which showed a hypercellular marrow with dysplastic features of all three cell lines, while blast count was 20%.
  • Based on these findings, the diagnosis of acute myeloid leukemia was made.
  • CONCLUSION: Our observations suggest that bone marrow examinations including cytogenetic analysis should be carried out on a regular basis in patients with glycogen storage disease type Ib who are on long-term treatment with granulocyte colony-stimulating factor for severe neutropenia, since this treatment might also contribute to an increased risk for acute myeloid leukemia or myelodysplastic syndromes.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Hematology Am Soc Hematol Educ Program. 2007;:29-39 [18024606.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5704-11 [18420828.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1937-44 [17611569.001]
  • [Cites] Cancer Genet Cytogenet. 2007 Aug;177(1):37-42 [17693189.001]
  • [Cites] Bone Marrow Transplant. 2007 Aug;40(3):185-92 [17563736.001]
  • [Cites] World J Gastroenterol. 2007 May 14;13(18):2541-53 [17552001.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Sep 26;103(39):14483-8 [16980411.001]
  • [Cites] Blood. 2006 Jun 15;107(12):4628-35 [16497969.001]
  • [Cites] Haematologica. 2005 Jan;90(1):45-53 [15642668.001]
  • [Cites] J Pediatr. 1984 Sep;105(3):428-31 [6590826.001]
  • [Cites] J Pediatr Hematol Oncol. 2002 Dec;24(9):756-8 [12468919.001]
  • (PMID = 18826620.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2566578
  •  go-up   go-down


97. Bogason A, Bhuiyan H, Masquelier M, Paul C, Gruber A, Vitols S: Uptake of anthracyclines in vitro and in vivo in acute myeloid leukemia cells in relation to apoptosis and clinical response. Eur J Clin Pharmacol; 2009 Dec;65(12):1179-86
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] Uptake of anthracyclines in vitro and in vivo in acute myeloid leukemia cells in relation to apoptosis and clinical response.
  • AIMS: To study anthracycline-induced apoptosis in leukemic cells isolated from patients with acute myelogenous leukemia (AML) in vitro and to compare intracellular anthracycline concentrations causing apoptosis in vitro with those obtained in vivo during anthracycline treatment.
  • METHODS: Mononuclear blood cells from AML patients were isolated before (n = 20) and after anthracycline infusion (n = 24).
  • [MeSH-major] Anthracyclines / pharmacokinetics. Anthracyclines / pharmacology. Apoptosis / drug effects. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leuk Res. 1989;13(2):191-6 [2927175.001]
  • [Cites] Adv Exp Med Biol. 1999;457:437-44 [10500820.001]
  • [Cites] Cancer Chemother Pharmacol. 1984;13(3):230-4 [6488444.001]
  • [Cites] Br J Cancer. 1994 Aug;70(2):324-9 [7914424.001]
  • [Cites] Leukemia. 2001 Jun;15(6):898-902 [11417474.001]
  • [Cites] Scand J Clin Lab Invest Suppl. 1968;97:77-89 [4179068.001]
  • [Cites] Pharmacol Ther. 1993 Nov;60(2):185-214 [8022857.001]
  • [Cites] Mol Pharmacol. 1994 Nov;46(5):901-8 [7969078.001]
  • [Cites] Ther Drug Monit. 1989;11(2):140-8 [2718219.001]
  • [Cites] Leuk Res. 1999 Jun;23(6):539-48 [10374847.001]
  • [Cites] Br J Haematol. 1976 Aug;33(4):451-8 [188440.001]
  • [Cites] Br J Cancer. 1992 Aug;66(2):266-72 [1380280.001]
  • [Cites] Oncology (Williston Park). 1991 Sep;5(9):93-103; disc. 104, 111-4, 117-8 [1835882.001]
  • [Cites] Acta Biochim Pol. 2002;49(1):99-107 [12136962.001]
  • [Cites] Leukemia. 1988 Aug;2(8):511-7 [3166077.001]
  • [Cites] Klin Padiatr. 2007 May-Jun;219(3):134-8 [17525906.001]
  • [Cites] Bull Exp Biol Med. 2004 Aug;138(2):114-8 [15662449.001]
  • [Cites] Cancer Chemother Pharmacol. 1987;20(4):311-5 [3690804.001]
  • [Cites] Curr Drug Metab. 2001 Dec;2(4):355-66 [11766987.001]
  • [Cites] J Clin Oncol. 1988 May;6(5):802-12 [3163363.001]
  • [Cites] Leukemia. 2000 Jul;14(7):1266-75 [10914552.001]
  • [Cites] Eur J Haematol. 2001 Mar;66(3):160-7 [11350484.001]
  • [Cites] J Immunol Methods. 1991 Jun 3;139(2):271-9 [1710634.001]
  • [Cites] Acta Oncol. 2001;40(2-3):231-52 [11441935.001]
  • [Cites] Biochem Pharmacol. 2004 Mar 15;67(6):1047-56 [15006541.001]
  • [Cites] Br J Cancer. 1989 Aug;60(2):206-10 [2765367.001]
  • [Cites] Br J Haematol. 1992 Jul;81(3):455-6 [1390226.001]
  • [Cites] Eur J Haematol. 1992 May;48(5):254-8 [1353726.001]
  • [Cites] Cancer Lett. 2002 Apr 25;178(2):141-9 [11867198.001]
  • [Cites] Cancer Chemother Pharmacol. 1984;12(2):125-30 [6697426.001]
  • [Cites] Leukemia. 1996 Jun;10(6):937-42 [8667648.001]
  • [Cites] Cancer Lett. 1984 Oct;24(3):305-9 [6594191.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1154-63 [15870183.001]
  • [Cites] Blood. 1995 Apr 15;85(8):2147-53 [7536492.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Jan 26;280(3):951-9 [11162617.001]
  • (PMID = 19820921.001).
  • [ISSN] 1432-1041
  • [Journal-full-title] European journal of clinical pharmacology
  • [ISO-abbreviation] Eur. J. Clin. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anthracyclines; ZRP63D75JW / Idarubicin; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


98. Gondek LP, Tiu R, O'Keefe CL, Sekeres MA, Theil KS, Maciejewski JP: Chromosomal lesions and uniparental disomy detected by SNP arrays in MDS, MDS/MPD, and MDS-derived AML. Blood; 2008 Feb 1;111(3):1534-42
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] Chromosomal lesions and uniparental disomy detected by SNP arrays in MDS, MDS/MPD, and MDS-derived AML.
  • We hypothesized that with new precise methods more cryptic karyotypic lesions can be uncovered that may show important clinical implications.
  • We have applied 250K single nucleotide polymorphisms (SNP) arrays (SNP-A) to study chromosomal lesions in samples from 174 patients (94 MDS, 33 secondary acute myeloid leukemia [sAML], and 47 myelodysplastic/myeloproliferative disease [MDS/MPD]) and 76 controls.
  • Previously unrecognized lesions were detected in patients with normal MC and in those with known lesions.
  • Moreover, segmental uniparental disomy (UPD) was found in 20% of MDS, 23% of sAML, and 35% of MDS/MPD patients, a lesion resulting in copy-neutral loss of heterozygosity undetectable by MC.
  • The potential clinical significance of abnormalities detected by SNP-A, but not seen on MC, was demonstrated by their impact on overall survival.