[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 284
1. Skärby TV, Anderson H, Heldrup J, Kanerva JA, Seidel H, Schmiegelow K, Nordic Society of Paediatric Haematology and Oncology (NOPHO): High leucovorin doses during high-dose methotrexate treatment may reduce the cure rate in childhood acute lymphoblastic leukemia. Leukemia; 2006 Nov;20(11):1955-62
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 leucovorin doses during high-dose methotrexate treatment may reduce the cure rate in childhood acute lymphoblastic leukemia.
  • We explored the relationship between time to relapse and different exposure variables (serum methotrexate (S-MTX) 23, 36 and 42 h after start of administration, MTX elimination time and leucovorin (LV) dose) during high-dose MTX (HDM) treatment of 445 children with acute lymphoblastic leukemia.
  • MTX was infused at 5 g/m2 (non-high risk) or 8 g/m2 (high risk) over 24 h, 2-9 times per patient.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Leucovorin / adverse effects. Methotrexate / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vitamin B Complex / adverse effects
  • [MeSH-minor] Case-Control Studies. Child. Child, Preschool. Disease-Free Survival. Drug Interactions. Female. Humans. Male. Registries. Risk Factors. Secondary Prevention


2. Büchner T, Berdel WE, Schoch C, Haferlach T, Serve HL, Kienast J, Schnittger S, Kern W, Tchinda J, Reichle A, Lengfelder E, Staib P, Ludwig WD, Aul C, Eimermacher H, Balleisen L, Sauerland MC, Heinecke A, Wörmann B, Hiddemann W: Double induction containing either two courses or one course of high-dose cytarabine plus mitoxantrone and postremission therapy by either autologous stem-cell transplantation or by prolonged maintenance for acute myeloid leukemia. J Clin Oncol; 2006 Jun 1;24(16):2480-9
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] Double induction containing either two courses or one course of high-dose cytarabine plus mitoxantrone and postremission therapy by either autologous stem-cell transplantation or by prolonged maintenance for acute myeloid leukemia.
  • PURPOSE: Intensification by high-dose cytarabine in postremission or induction therapy and prolonged maintenance are established strategies to improve the outcome in patients with acute myeloid leukemia (AML).
  • PATIENTS AND METHODS: A total of 1,770 patients (age 16 to 85 years) with de novo or secondary AML or high-risk myelodysplastic syndrome (MDS) were randomly assigned upfront for induction therapy containing one course with standard dose and one course with high-dose cytarabine, or two courses with high-dose cytarabine, and in the same step received postremission prolonged maintenance or busulfan/cyclophosphamide chemotherapy with autologous stem-cell transplantation.
  • There was no significant difference in any prognostic subgroup according to secondary AML/MDS, cytogenetics, WBC, lactate dehydrogenase, and early blast clearance.
  • CONCLUSION: The regimen of one course with standard-dose cytarabine and one course with high-dose cytarabine for induction, and prolonged maintenance for postremission chemotherapy in patients with AML is not improved by additional escalation in cytotoxic treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / surgery. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / surgery
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Cytarabine / administration & dosage. Drug Administration Schedule. Female. Humans. L-Lactate Dehydrogenase / blood. Leukocyte Count. Male. Middle Aged. Mitoxantrone / administration & dosage. Multivariate Analysis. Prognosis. Prospective Studies. Remission Induction. Risk Factors. Transplantation, Autologous. Treatment Outcome

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Clin Oncol. 2006 Dec 1;24(34):5471-2; author reply 5472-3 [17135654.001]
  • [ErratumIn] J Clin Oncol. 2011 Jul 1;29(19):2739
  • (PMID = 16735702.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; EC 1.1.1.27 / L-Lactate Dehydrogenase
  •  go-up   go-down


3. Barresi V, Palumbo GA, Musso N, Consoli C, Capizzi C, Meli CR, Romano A, Di Raimondo F, Condorelli DF: Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML. Leuk Res; 2010 Nov;34(11):1539-42
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] Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML.
  • By conventional metaphase and SNP array cytogenetics we serially studied a patient affected by high-risk myelodysplastic syndrome (MDS), documenting the conversion from partial trisomy 8q to trisomy 8 and partial tetrasomy 8q during progression to acute myeloid leukemia (AML).
  • Moreover, the serial application of high resolution genomic array analysis at different disease stages allowed the description of cryptic abnormalities and the demonstration of their enrichment in the AML phase.
  • In particular the detection and quantification of a copy-neutral loss of heterozygosity region located in chromosome 11q guided the search for point mutations in the CBL gene, thus allowing the escription of the novel missense mutation K382E and the demonstration of its selection during progression to secondary AML.
  • [MeSH-major] Chromosomes, Human, Pair 11. Leukemia, Myeloid, Acute / genetics. Loss of Heterozygosity. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins c-cbl / genetics

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • 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
  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20674974.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  •  go-up   go-down


Advertisement
4. Szotkowski T, Rohon P, Zapletalova L, Sicova K, Hubacek J, Indrak K: Secondary acute myeloid leukemia - a single center experience. Neoplasma; 2010;57(2):170-8
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] Secondary acute myeloid leukemia - a single center experience.
  • Secondary acute myeloid leukemia (sAML) may arise from the previous clonal disorder of hematopoiesis, usually from myelodysplastic syndrome (MDS) or from chronic myeloproliferative neoplasia (cMPN) or after exposure to a leukemogenic agent (previous chemotherapy or radiotherapy, some immunosuppressive drugs or environmental leukemogenic agents).
  • Secondary origin of AML is associated with unfavorable prognosis and it is not considered to be conventionally curable (with the exception of secondary acute promyelocytic leukemia).
  • Over that period of time, a total 574 patients with AML were diagnosed.
  • Of those, 430 patients were diagnosed as having primary AML; in 86 patients, sAML transformed from myelodysplastic syndrome and 58 patients were followed or treated for various malignancies or were treated with potentially leukemogenic agents because of non-malignant disorders.
  • Patients with secondary AML are older and less commonly treated with curative intention than those with primary AML.
  • With the exception of secondary acute promyelocytic leukemia, the prognosis of which does not differ from very good prognosis of the primary forms, secondary AML is not considered a conventionally curable disease.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / complications. Myeloproliferative Disorders / complications. Neoplasm Recurrence, Local / etiology. Neoplasms, Second Primary / etiology


5. Perl AE, Kasner MT, Tsai DE, Vogl DT, Loren AW, Schuster SJ, Porter DL, Stadtmauer EA, Goldstein SC, Frey NV, Nasta SD, Hexner EO, Dierov JK, Swider CR, Bagg A, Gewirtz AM, Carroll M, Luger SM: A phase I study of the mammalian target of rapamycin inhibitor sirolimus and MEC chemotherapy in relapsed and refractory acute myelogenous leukemia. Clin Cancer Res; 2009 Nov 1;15(21):6732-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I study of the mammalian target of rapamycin inhibitor sirolimus and MEC chemotherapy in relapsed and refractory acute myelogenous leukemia.
  • PURPOSE: Inhibiting mammalian target of rapamycin (mTOR) signaling in acute myelogenous leukemia (AML) blasts and leukemic stem cells may enhance their sensitivity to cytotoxic agents.
  • We sought to determine the safety and describe the toxicity of this approach by adding the mTOR inhibitor, sirolimus (rapamycin), to intensive AML induction chemotherapy.
  • EXPERIMENTAL DESIGN: We performed a phase I dose escalation study of sirolimus with the chemotherapy regimen MEC (mitoxantrone, etoposide, and cytarabine) in patients with relapsed, refractory, or untreated secondary AML.
  • Future studies are planned with different schedules to clarify the clinical and biochemical effects of sirolimus in AML and to determine whether target inhibition predicts chemotherapy response.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Sirolimus / administration & dosage


6. Makishima H, Cazzolli H, Szpurka H, Dunbar A, Tiu R, Huh J, Muramatsu H, O'Keefe C, Hsi E, Paquette RL, Kojima S, List AF, Sekeres MA, McDevitt MA, Maciejewski JP: Mutations of e3 ubiquitin ligase cbl family members constitute a novel common pathogenic lesion in myeloid malignancies. J Clin Oncol; 2009 Dec 20;27(36):6109-16
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] Mutations of e3 ubiquitin ligase cbl family members constitute a novel common pathogenic lesion in myeloid malignancies.
  • PURPOSE: Acquired somatic uniparental disomy (UPD) is commonly observed in myelodysplastic syndromes (MDS), myelodysplastic/myeloproliferative neoplasms (MDS/MPN), or secondary acute myelogenous leukemia (sAML) and may point toward genes harboring mutations.
  • METHODS: We applied high-density SNP-A karyotyping to identify loss of heterozygosity of 11q in 442 patients with MDS, MDS/MPN, MPN, sAML evolved from these conditions, and primary AML.
  • RESULTS: We identified c-Cbl mutations in 5% and 9% of patients with chronic myelomonocytic leukemia (CMML) and sAML, and also in CML blast crisis and juvenile myelomonocytic leukemia (JMML).
  • CONCLUSION: Mutations in the Cbl family RING finger domain or linker sequence constitute important pathogenic lesions associated with not only preleukemic CMML, JMML, and other MPN, but also progression to AML, suggesting that impairment of degradation of activated tyrosine kinases constitutes an important cancer mechanism.

  • COS Scholar Universe. author profiles.
  • 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).
  • 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. 2009 Mar;23(3):610-4 [18818701.001]
  • [Cites] Haematologica. 2008 Oct;93(10):1595-7 [18698078.001]
  • [Cites] Nat Genet. 2004 Sep;36(9):949-51 [15286789.001]
  • [Cites] Oncogene. 1991 Apr;6(4):653-7 [2030914.001]
  • [Cites] Mol Cell Biol. 1998 Aug;18(8):4872-82 [9671496.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Dec;6(12):907-18 [16227975.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1242-3 [16434499.001]
  • [Cites] PLoS Genet. 2005 Dec;1(6):e49 [16444292.001]
  • [Cites] Blood. 2006 Mar 1;107(5):1791-9 [16254134.001]
  • [Cites] J Cell Physiol. 2006 Oct;209(1):21-43 [16741904.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2173-81 [16741247.001]
  • [Cites] PLoS Med. 2006 Jul;3(7):e270 [16834459.001]
  • [Cites] Am J Surg Pathol. 2007 Feb;31(2):233-9 [17255768.001]
  • [Cites] Blood. 2007 Aug 1;110(3):1004-12 [17446348.001]
  • [Cites] Blood. 2007 Aug 1;110(3):1022-4 [17475912.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2058-61 [17525728.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3365-73 [17634407.001]
  • [Cites] PLoS One. 2007;2(11):e1225 [18030353.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1534-42 [17954704.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]
  • [Cites] Blood. 2008 Aug 15;112(4):965-74 [18505780.001]
  • [Cites] Semin Oncol. 2008 Aug;35(4):365-77 [18692687.001]
  • [Cites] Leukemia. 2008 Aug;22(8):1539-41 [18528419.001]
  • [Cites] Cancer Res. 2008 Dec 15;68(24):10349-57 [19074904.001]
  • [Cites] Blood. 2008 Sep 1;112(5):2017-9 [18566322.001]
  • [Cites] Curr Opin Hematol. 2001 Jul;8(4):189-91 [11561153.001]
  • (PMID = 19901108.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K24 HL077522; United States / NHLBI NIH HHS / HL / R01 HL082983; United States / NCRR NIH HHS / RR / U54 RR019391; United States / NHLBI NIH HHS / HL / K24 HL-077522; United States / NHLBI NIH HHS / HL / R01HL-082983; United States / NCRR NIH HHS / RR / S10 RR019391
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Other-IDs] NLM/ PMC3040009
  •  go-up   go-down


7. Manvelyan M, Kempf P, Weise A, Mrasek K, Heller A, Lier A, Höffken K, Fricke HJ, Sayer HG, Liehr T, Mkrtchyan H: Preferred co-localization of chromosome 8 and 21 in myeloid bone marrow cells detected by three dimensional molecular cytogenetics. Int J Mol Med; 2009 Sep;24(3):335-41
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] Preferred co-localization of chromosome 8 and 21 in myeloid bone marrow cells detected by three dimensional molecular cytogenetics.
  • In this study, BM of three secondary acute myelogenous leukemia (AML) cases with trisomy 8 and otherwise normal karyotype were evaluated.
  • Bone marrow cells of one AML and one ALL (acute lymphoblastic leukemia) case, peripheral blood lymphocytes and human sperm, all of them with normal karyotype, served as controls.
  • Interestingly, in myeloid bone marrow cells chromosomes 8 (di- and trisomic) and 21 tended to co-localize with their homologue chromosome(s), rather than to be separated.
  • Thus, the co-localization of chromosomes 8 and 21 might promote a translocation providing a selective advantage of t(8;21) cells in AML-M2.
  • [MeSH-major] Bone Marrow Cells / metabolism. Chromosomes, Human, Pair 21 / metabolism. Chromosomes, Human, Pair 8 / metabolism. Cytogenetic Analysis / methods. Myeloid Cells / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19639225.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  •  go-up   go-down


8. Peter A, Heiden T, Taube T, Körner G, Seeger K: Interphase FISH on TEL/AML1 positive acute lymphoblastic leukemia relapses--analysis of clinical relevance of additional TEL and AML1 copy number changes. Eur J Haematol; 2009 Nov;83(5):420-32
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] Interphase FISH on TEL/AML1 positive acute lymphoblastic leukemia relapses--analysis of clinical relevance of additional TEL and AML1 copy number changes.
  • OBJECTIVES: TEL/AML1 (ETV6/RUNX1) fusion resulting from the translocation t(12;21)(p13;q22) constitutes the most common chimeric fusion gene in initial childhood B-cell precursor (BCP) acute lymphoblastic leukemia (ALL) (19-27%) and has been associated with good prognosis.
  • Three secondary aberrations in TEL/AML1 positive ALL have been suspected to negatively influence outcome: deletion of the second TEL allele (T), gain of the second AML1 allele (A) and duplication of the derivative chromosome 21 (der(21), TA).
  • They also show that it is important to consider combined mutations in the analysis of this leukemia entity.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Dosage. In Situ Hybridization, Fluorescence. Interphase. Mutation. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19594616.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
  •  go-up   go-down


9. Kröger N, Shimoni A, Zabelina T, Schieder H, Panse J, Ayuk F, Wolschke C, Renges H, Dahlke J, Atanackovic D, Nagler A, Zander A: Reduced-toxicity conditioning with treosulfan, fludarabine and ATG as preparative regimen for allogeneic stem cell transplantation (alloSCT) in elderly patients with secondary acute myeloid leukemia (sAML) or myelodysplastic syndrome (MDS). Bone Marrow Transplant; 2006 Feb;37(4):339-44
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-toxicity conditioning with treosulfan, fludarabine and ATG as preparative regimen for allogeneic stem cell transplantation (alloSCT) in elderly patients with secondary acute myeloid leukemia (sAML) or myelodysplastic syndrome (MDS).
  • We investigated a dose-reduced conditioning regimen consisting of treosulfan and fludarabine followed by allogeneic stem cell transplantation (SCT) in 26 patients with secondary AML or MDS.
  • Acute graft-versus-host disease (GvHD) grade II-IV was seen in 23% and severe grade III GvHD in 12% of the patients.
  • No patients experienced grade IV acute GvHD.
  • [MeSH-major] Antilymphocyte Serum / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Busulfan / analogs & derivatives. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adult. Aged. Disease-Free Survival. Female. Graft vs Host Disease / drug therapy. Graft vs Host Disease / prevention & control. HLA Antigens / analysis. Humans. Male. Middle Aged. Prospective Studies. Recurrence. Siblings. Survival Rate. Transplantation, Homologous. Treatment Outcome


10. Szotkowski T, Muzik J, Voglova J, Koza V, Maaloufova J, Kozak T, Jarosova M, Michalova K, Zak P, Steinerova K, Vydra J, Lanska M, Katrincsakova B, Sicova K, Pavlik T, Dusek L, Indrak K: Prognostic factors and treatment outcome in 1,516 adult patients with de novo and secondary acute myeloid leukemia in 1999-2009 in 5 hematology intensive care centers in the Czech Republic. Neoplasma; 2010;57(6):578-89
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 factors and treatment outcome in 1,516 adult patients with de novo and secondary acute myeloid leukemia in 1999-2009 in 5 hematology intensive care centers in the Czech Republic.
  • Acute myeloid leukemia (AML) is a severe condition with a high mortality.
  • The study represents a detailed analysis of the role of these factors and treatment outcomes based on a long-term follow-up of patients treated in 5 hematology intensive care centers in the Czech Republic.The studied group comprised 1,188 patients with de novo AML and 328 patients with secondary AML.
  • Curatively treated patients achieved fewer complete remissions and relapsed more often than those with de novo AML.
  • Patients with secondary AML had lower rates of allogeneic transplantation as part of consolidation therapy and a significantly shorter median overall survival.
  • However, the treatment outcome of de novo AML patients is not satisfactory, the only exception being those with acute promyelocytic leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Neoplasms, Second Primary / mortality


11. Ikawa Y, Sugimoto N, Koizumi S, Yachie A, Saikawa Y: Dense methylation of types 1 and 2 regulatory regions of the CD10 gene promoter in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene. J Pediatr Hematol Oncol; 2010 Jan;32(1):4-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dense methylation of types 1 and 2 regulatory regions of the CD10 gene promoter in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene.
  • SUMMARY: Infant acute lymphoblastic leukemia (ALL) displays distinct biologic and clinical features with a poor prognosis.
  • The CD10-negative immunophenotype of infant ALL is a hallmark and provides a predictable signature of mixed-lineage leukemia (MLL) rearrangement.
  • Discordance between immunophenotype and genotype of infant ALL suggests an aberrant process in immunophenotypic steps of differentiation or a secondary down-regulation of CD10 expression.
  • In this study, CD10-negative infant ALL with MLL/AF4, CD10-positive infant ALL with germline MLL, CD10-positive pre-B ALL cell line, infant acute myeloid leukemia (AML;.
  • M5) with MLL/AF9 and pediatric AML (M2) with AML1/ETO were analyzed for VDJH status and methylation of CD10 gene promoters.
  • [MeSH-major] DNA Methylation. Myeloid-Lymphoid Leukemia Protein. Neprilysin / genetics. Oncogene Proteins, Fusion. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Regulatory Sequences, Nucleic Acid / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • National BioResource Project. culture/stock collections - NBRP resources .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20051780.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Sp1 Transcription Factor; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.4.24.11 / Neprilysin
  •  go-up   go-down


12. Girod A, Breton P: [Two cases of malignant tumors of the face after hematopoietic stem cell transplantation]. Rev Stomatol Chir Maxillofac; 2005 Apr;106(2):107-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBSERVATION: Two patients underwent HSCT for acute leukemia.
  • DISCUSSION: Several factors are involved in the development of secondary malignant tumors after HSCT.
  • Squamous cell carcinoma of the oral cavity after HSCT presents the same clinical, histological and prognostic features as in the non-grafted patient.
  • [MeSH-major] Carcinoma, Mucoepidermoid / etiology. Carcinoma, Squamous Cell / etiology. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid, Acute / therapy. Parotid Neoplasms / etiology. Tongue Neoplasms / etiology
  • [MeSH-minor] Adult. Female. Graft vs Host Disease / etiology. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15924098.001).
  • [ISSN] 0035-1768
  • [Journal-full-title] Revue de stomatologie et de chirurgie maxillo-faciale
  • [ISO-abbreviation] Rev Stomatol Chir Maxillofac
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down


13. Nevill TJ, Shepherd JD, Sutherland HJ, Abou Mourad YR, Lavoie JC, Barnett MJ, Nantel SH, Toze CL, Hogge DE, Forrest DL, Song KW, Power MM, Nitta JY, Dai Y, Smith CA: IPSS poor-risk karyotype as a predictor of outcome for patients with myelodysplastic syndrome following myeloablative stem cell transplantation. Biol Blood Marrow Transplant; 2009 Feb;15(2):205-13
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.
  • A retrospective review was performed of 156 patients who underwent SCT (114 BM, 42 BSC) for MDS or secondary acute myelogenous leukemia (sAML) at our institution.
  • Multivariate analysis showed IPSS poor-risk cytogenetics (P< .001), time from diagnosis to SCT (P< .001), FAB subgroup (P= .001), recipients not in complete remission (CR1) at SCT (P= .005), and the development of acute graft-versus-host disease (aGVHD) (P= .04) were all predictive of an inferior EFS.
  • The FAB subgroup (P= .002), poor-risk karyotype (P= .004), and non-CR1 status also correlated with ROR in multivariate analysis.


14. Chau M, Christensen JL, Ajami AM, Capizzi RL: Amonafide, a topoisomerase II inhibitor, is unaffected by P-glycoprotein-mediated efflux. Leuk Res; 2008 Mar;32(3):465-73
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.
  • Over-expression of P-glycoprotein (Pgp+) has been related to resistance to classical Topo II inhibitors used in the treatment of AML and is common in patients with poor-prognosis, such as those with secondary AML (sAML).
  • Since clinical trials with amonafide, a unique ATP-independent Topo II inhibitor, in combination with cytarabine, have shown significant efficacy for remission induction in patients with sAML, we compared the cytotoxic effect of amonafide (amonafide l-malate, Xanafide) to the classical Topo II inhibitors (daunorubicin, doxorubicin, idarubicin, etoposide, and mitoxantrone) in K562 leukemia cells and in the MDR subline, K562/DOX.
  • Pgp expression was found to be approximately 6.5-fold greater in K562/DOX and causes the rapid efflux of these drugs from the leukemia cell.
  • A similar result was also observed in murine P388 and P388/ADR leukemia cells.
  • These observations suggest that amonafide is a promising therapeutic candidate directed toward bypassing this common mechanism of drug resistance encountered in the treatment of patients with AML, and possibly in other resistant hematological malignancies as well.

  • 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 = 17826829.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Imides; 0 / Isoquinolines; 0 / Naphthalimides; 0 / P-Glycoprotein; 0 / Topoisomerase II Inhibitors; 1Q8D39N37L / amonafide
  •  go-up   go-down


15. Tavil B, Cetin M, Tuncer M: CD34/CD117 positivity in assessment of prognosis in children with myelodysplastic syndrome. Leuk Res; 2006 Feb;30(2):222-4
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.
  • Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal stem cell disorders that are characterized by morphology identifying dysplastic changes in one or more cell lineages, peripheral blood cytopenias and a propensity to evolve into secondary acute myeloid leukemia (AML).
  • CD34 is commonly expressed in all types of childhood leukemias, whereas CD117 is a reliable and specific marker to detect leukemia cells committed to myeloid lineage.
  • Co-expression of CD34/CD117 may strongly suggest the diagnosis of AML (Rytting ME.
  • May; Uçkan D, Hiçsönmez G, Yetgin S, Gürgey A, Cetin M, Karaağaoğlu E, et al. CD34/CD117 co-expression in childhood acute leukemia.
  • Leukemia Res 2000;24:201-6.).
  • We describe the case of a 22 month-old-girl with MDS and Down syndrome who was presented with severe anemia and thrombocytosis at diagnosis, transformed into AML-M7.
  • As the disease progressed, CD34/117 co-existence was increased and MDS transformed into AML.
  • [MeSH-minor] Bone Marrow Examination. Female. Humans. Infant. Leukemia, Myeloid, Acute / etiology. Prognosis


16. Verma D, O'Brien S, Thomas D, Faderl S, Koller C, Pierce S, Kebriaei P, Garcia-Manero G, Cortes J, Kantarjian H, Ravandi F: Therapy-related acute myelogenous leukemia and myelodysplastic syndrome in patients with acute lymphoblastic leukemia treated with the hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone regimens. Cancer; 2009 Jan 1;115(1):101-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related acute myelogenous leukemia and myelodysplastic syndrome in patients with acute lymphoblastic leukemia treated with the hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone regimens.
  • BACKGROUND: Secondary malignancies including myeloid neoplasms occur infrequently in acute lymphoblastic leukemia (ALL) and to the authors' knowledge have not been as well documented in adults as in children.
  • RESULTS: Sixteen patients (2.49%) developed secondary acute myelogenous leukemia (AML) (6 patients) or myelodysplastic syndrome (MDS) (10 patients).
  • Karyotype at time of AML/MDS diagnosis was -5, -7 in 9 patients, normal in 1 patient, complex in 1 patient, inv(11) in 1 patient, t(4;11) in 1 patient, del(20) in 1 patient, and unavailable in 2 patients.
  • Secondary AML/MDS developed at a median of 32 months after ALL diagnosis.
  • Cytarabine plus anthracycline-based treatment was given to 12 patients with AML and high-risk MDS.
  • Eight patients (1 with AML and 7 with MDS) underwent allogeneic stem cell transplantation, and all but 2 died at a median of 3 months (range, 0.5-11 months) after transplantation.
  • The median overall survival after a diagnosis of secondary AML and MDS was 9.25 months (range, 1+ to 26+ months).
  • CONCLUSIONS: Secondary AML and MDS occur infrequently in adult patients with de novo ALL treated with the hyper-CVAD regimens, and response to therapy is poor.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


17. Winter SS, Holdsworth MT, Devidas M, Raisch DW, Chauvenet A, Ravindranath Y, Ducore JM, Amylon MD: Antimetabolite-based therapy in childhood T-cell acute lymphoblastic leukemia: a report of POG study 9296. Pediatr Blood Cancer; 2006 Feb;46(2):179-86
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] Antimetabolite-based therapy in childhood T-cell acute lymphoblastic leukemia: a report of POG study 9296.
  • PURPOSE: A previous Pediatric Oncology Group (POG) study showed high incidence of secondary acute myelogenous leukemia (AML) in children treated for T-cell acute lymphoblastic leukemia (T-ALL) or higher-stage lymphoblastic lymphoma.
  • To prevent secondary neoplasms, induce prolonged asparagine depletion, and maintain high event-free survival (EFS) in children with newly diagnosed T-ALL or higher-stage non-Hodgkins lymphoma (NHL), we designed this pilot study to determine feasibility and safety of substituting methotrexate/mercaptopurine for teniposide/cytarabine and PEG-asparaginase for native asparaginase.
  • No patients treated entirely on this study developed secondary neoplasms.
  • One patient taken off study for asparaginase toxicity was treated with multiagent therapy that contained teniposide, and died from secondary myelodysplasia (sMDS)/AML.
  • EFS was not compromised and secondary neoplasms were decreased.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Anthracyclines / administration & dosage. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Agents, Alkylating / administration & dosage. Asparaginase / administration & dosage. Asparaginase / adverse effects. Child. Child, Preschool. Disease-Free Survival. Drug Hypersensitivity / etiology. Female. Follow-Up Studies. Humans. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / mortality. Male. Pilot Projects. Remission Induction. Sepsis / etiology. Sepsis / mortality

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16007607.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5 U10 CA5312; United States / NCI NIH HHS / CA / CA29139
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Alkylating; EC 3.5.1.1 / Asparaginase
  •  go-up   go-down


18. Spiegler BJ, Kennedy K, Maze R, Greenberg ML, Weitzman S, Hitzler JK, Nathan PC: Comparison of long-term neurocognitive outcomes in young children with acute lymphoblastic leukemia treated with cranial radiation or high-dose or very high-dose intravenous methotrexate. J Clin Oncol; 2006 Aug 20;24(24):3858-64
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] Comparison of long-term neurocognitive outcomes in young children with acute lymphoblastic leukemia treated with cranial radiation or high-dose or very high-dose intravenous methotrexate.
  • PURPOSE: Cranial radiation therapy (CRT) is associated with neurocognitive morbidity in survivors of childhood acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Cognition / drug effects. Cognition / radiation effects. Cranial Irradiation / adverse effects. Methotrexate / administration & dosage. Methotrexate / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy
  • [MeSH-minor] Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Attention / drug effects. Attention / radiation effects. Brain Neoplasms / prevention & control. Brain Neoplasms / secondary. Child, Preschool. Cohort Studies. Dose Fractionation. Educational Status. Female. Humans. Infant. Infusions, Intravenous. Intelligence Tests. Male. Memory / drug effects. Memory / radiation effects. Retrospective Studies

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. METHOTREXATE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Clin Oncol. 2007 Feb 20;25(6):734-5; author reply 735 [17308283.001]
  • [ErratumIn] J Clin Oncol. 2006 Nov 10;24(32):5181
  • (PMID = 16921038.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


19. Giles F, Rizzieri D, Karp J, Vey N, Ravandi F, Faderl S, Khan KD, Verhoef G, Wijermans P, Advani A, Roboz G, Kantarjian H, Bilgrami SF, Ferrant A, Daenen SM, Karsten V, Cahill A, Albitar M, Mufti G, O'Brien S: Cloretazine (VNP40101M), a novel sulfonylhydrazine alkylating agent, in patients age 60 years or older with previously untreated acute myeloid leukemia. J Clin Oncol; 2007 Jan 1;25(1):25-31
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] Cloretazine (VNP40101M), a novel sulfonylhydrazine alkylating agent, in patients age 60 years or older with previously untreated acute myeloid leukemia.
  • A multicenter phase II study of cloretazine was conducted in patients 60 years of age or older with previously untreated acute myeloid leukemia (AML) or high-risk myelodysplastic syndrome (MDS).
  • Patients were stratified by age, performance score, cytogenetic risk category, type of AML, and comorbidity.
  • Response rates in 44 de novo AML patients, 45 secondary AML patients, and 15 high-risk MDS patients were 50%, 11%, and 40%, respectively.
  • CONCLUSION: Cloretazine has significant activity and modest extramedullary toxicity in elderly patients with AML or high-risk MDS.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Hydrazines / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Sulfonamides / therapeutic use


20. Stifter G, Heiss S, Gastl G, Tzankov A, Stauder R: Over-expression of tumor necrosis factor-alpha in bone marrow biopsies from patients with myelodysplastic syndromes: relationship to anemia and prognosis. Eur J Haematol; 2005 Dec;75(6):485-91
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Enhanced bone marrow (BM) angiogenesis is regarded as an essential cofactor in the progression of MDS to acute myelogenous leukemia (AML) and microvessel formation may be induced by TNF-alpha as well.
  • METHODS: TNF-alpha expression and BM vessels were immunohistochemically analyzed on 89 paraffin-embedded BM biopsies from patients with MDS and secondary AML, including 12 control samples.
  • MVD was increased in MDS and secondary AML and correlated with marrow cellularity and expression of TNF-alpha, but was not of prognostic significance.
  • CONCLUSIONS: TNF-alpha expression and MVD are elevated in MDS and secondary AML.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Erythroid Precursor Cells / metabolism. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism. Tumor Necrosis Factor-alpha / biosynthesis


21. Récher C, Beyne-Rauzy O, Demur C, Chicanne G, Dos Santos C, Mas VM, Benzaquen D, Laurent G, Huguet F, Payrastre B: Antileukemic activity of rapamycin in acute myeloid leukemia. Blood; 2005 Mar 15;105(6):2527-34
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] Antileukemic activity of rapamycin in acute myeloid leukemia.
  • In this study, we show that mTOR inhibition by rapamycin strongly inhibits the growth of the most immature acute myeloid leukemia (AML) cell lines through blockade in G0/G1 phase of the cell cycle.
  • Accordingly, 2 downstream effectors of mTOR, 4E-BP1 and p70S6K, are phosphorylated in a rapamycin-sensitive manner in a series of 23 AML cases.
  • Interestingly, the mTOR inhibitor markedly impairs the clonogenic properties of fresh AML cells while sparing normal hematopoietic progenitors.
  • Moreover, rapamycin induces significant clinical responses in 4 of 9 patients with either refractory/relapsed de novo AML or secondary AML.
  • Overall, our data strongly suggest that mTOR is aberrantly regulated in most AML cells and that rapamycin and analogs, by targeting the clonogenic compartment of the leukemic clone, may be used as new compounds in AML therapy.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. G0 Phase / drug effects. G1 Phase / drug effects. Leukemia, Myeloid, Acute / metabolism. Protein Kinases / metabolism. Sirolimus / pharmacology


22. Sun XF, Han B, Feng J, Zhou DB, Wang SJ, Xu Y, Chen JL, Jiao L, Zhang W, Li J, Duan MH, Zhu TN, Zou N, Hua BL, Cai HC, Zhao YQ: [Clinical features of invasive pulmonary fungal infection secondary to malignant blood diseases]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao; 2009 Oct;31(5):575-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical features of invasive pulmonary fungal infection secondary to malignant blood diseases].
  • OBJECTIVE: To summarize the clinical features of invasive pulmonary fungal infection (IPFI) secondary to malignant blood diseases (MBD).
  • METHODS: We retrospectively analyzed the clinical data of 52 patients with IPFI secondary to MBD admitted to Peking Union Medical College Hospital from January 1995 to December 2008.
  • RESULTS: The incidences of IPFI secondary to acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), non-Hodgkin's lymphoma (NHL), and aplastic anemia (AA) were 4.6%, 3.2%, 2.8%, and 2.5%, respectively.
  • In patients with IPFI secondary to AML, 88.5% (23/26) of the patients suffered from the infections during the non-remission (NR) period (including relapse), and 11.5% (3/26) in the complete-remission (CR) period.
  • In all the patients with IPFI secondary to malignant blood diseases, 86.5% (45/52) of MBD were neutropenic or agranulocytic, and 67.3% (35/52) had been treated with broad-spectrum antibiotics for more than 96 hours before anti-fungal therapy.
  • CONCLUSIONS: IPFI secondary to MBD is most common in AML patients.
  • Patients with NR of AML, neutropenia or agranulocytosis, and long-term broad-spectrum antibiotics usage are susceptible to IPFI.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19968074.001).
  • [ISSN] 1000-503X
  • [Journal-full-title] Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae
  • [ISO-abbreviation] Zhongguo Yi Xue Ke Xue Yuan Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  •  go-up   go-down


23. Boehm A, Sperr WR, Leitner G, Worel N, Oehler L, Jaeger E, Mitterbauer M, Haas OA, Valent P, Kalhs P, Rabitsch W: Comorbidity predicts survival in myelodysplastic syndromes or secondary acute myeloid leukaemia after allogeneic stem cell transplantation. Eur J Clin Invest; 2008 Dec;38(12):945-52
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] Comorbidity predicts survival in myelodysplastic syndromes or secondary acute myeloid leukaemia after allogeneic stem cell transplantation.
  • PATIENTS AND METHODS: We examined the overall survival (OS) and underlying risk factors in 45 adult patients with MDS (n = 38), chronic myelomonocytic leukaemia (n = 1), or secondary acute myeloid leukaemia (AML) arising from MDS (n = 6), who underwent allogeneic SCT at our Institution.
  • CONCLUSIONS: Based on these data and similar published data we recommend selecting patients with MDS or secondary AML for SCT according to the presence of comorbidities.
  • [MeSH-major] Disease-Free Survival. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / mortality. Leukemia, Myelomonocytic, Chronic / mortality. Neoplasms, Second Primary / mortality


24. Faraci M, Cappelli B, Morreale G, Lanino E, Moroni C, Bandettini R, Terranova MP, Di Martino D, Coccia C, Castagnola E: Nitazoxanide or CD3+/CD4+ lymphocytes for recovery from severe Cryptosporidium infection after allogeneic bone marrow transplant? Pediatr Transplant; 2007 Feb;11(1):113-6
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.
  • We describe a case of Cryptosporidium infection occurring in a child after allogeneic SCT for acute non-lymphoblastic leukemia.
  • The increase in CD3+/CD4+ cells secondary to the reduction of steroid therapy associated with the improvement of aGvHD and the use of antiparasitic treatments (especially nitazoxanide) improved the infection-related symptoms and led to a complete clearance of the Cryptosporidium.
  • [MeSH-major] Antiparasitic Agents / therapeutic use. Cryptosporidiosis / therapy. Leukemia, Myeloid, Acute / therapy. Lymphocyte Transfusion. Stem Cell Transplantation. Thiazoles / therapeutic use

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Cryptosporidiosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17239134.001).
  • [ISSN] 1397-3142
  • [Journal-full-title] Pediatric transplantation
  • [ISO-abbreviation] Pediatr Transplant
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD3; 0 / Antiparasitic Agents; 0 / Thiazoles; 55981-09-4 / nitazoxanide
  •  go-up   go-down


25. Ariffin H, Muthukkumaran T, Stanslas J, Sabariah AR, Veerasekaran N, Lin HP: Secondary B-cell acute lymphoblastic leukemia following Wilms' tumor: clinical and in vitro chemosensitivity studies. Leuk Lymphoma; 2005 Aug;46(8):1233-7
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] Secondary B-cell acute lymphoblastic leukemia following Wilms' tumor: clinical and in vitro chemosensitivity studies.
  • We report the clinical features and in vitro chemosensitivity assay findings of a 13-year-old girl who developed secondary B-cell acute lymphoblastic leukemia (ALL) 7 years after a diagnosis of Wilms' tumor.


26. Schmid C, Schleuning M, Hentrich M, Markl GE, Gerbitz A, Tischer J, Ledderose G, Oruzio D, Hiddemann W, Kolb HJ: High antileukemic efficacy of an intermediate intensity conditioning regimen for allogeneic stem cell transplantation in patients with high-risk acute myeloid leukemia in first complete remission. Bone Marrow Transplant; 2008 Apr;41(8):721-7
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] High antileukemic efficacy of an intermediate intensity conditioning regimen for allogeneic stem cell transplantation in patients with high-risk acute myeloid leukemia in first complete remission.
  • The goal of this analysis was to define the role of the moderate-intensity fludarabin Ara-C amsacrin (FLAMSA)-reduced intensity conditioning (RIC) regimen for patients with high-risk AML undergoing allogeneic SCT (alloSCT) in first CR1.
  • High-risk was defined by (1) AML secondary to MDS or radio/chemotherapy, (2) unfavorable cytogenetics or (3) delayed response to induction chemotherapy.
  • A total of 23 of 44 AML patients referred to the University of Munich for alloSCT in CR1 between 1999 and 2006 fulfilled these criteria and received FLAMSA chemotherapy, followed by RIC (4 Gy TBI/cyclophosphamide/ATG) for alloSCT.
  • Four-year overall and leukemia-free survival was 72.7% (median follow-up among survivors: 35 months).
  • The results of this high-risk cohort were compared to the outcome of 21 consecutive standard-risk patients <55 years, who had received standard, myeloablative sibling SCT in CR1 AML within the same center and time period.
  • In conclusion, the FLAMSA-RIC regimen produces long-term remission in a high proportion of patients with high-risk AML transplanted in CR1.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Transplantation Conditioning / methods


27. Ferrara F, D'Arco AM, De Simone M, Mele G, Califano C, Pocali B, Danise P, Palmieri S: Fludarabine and cytarabine as continuous sequential infusion for elderly patients with acute myeloid leukemia. Haematologica; 2005 Jun;90(6):776-84
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] Fludarabine and cytarabine as continuous sequential infusion for elderly patients with acute myeloid leukemia.
  • BACKGROUND AND OBJECTIVES: A phase II study was conducted to investigate the effects of a therapeutic program based on the combination of fludarabine and cytarabine (ARA-C) administered as a sequential continuous infusion in untreated elderly patients with acute myeloid leukemia (AML).
  • DESIGN AND METHODS: Sixty-three patients with non-M3 AML, median age 69 years (range 61-81), were accrued.
  • Twenty-four patients (38%) had AML secondary to myelodysplastic syndrome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Vidarabine / analogs & derivatives

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15951290.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD34; 04079A1RDZ / Cytarabine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  •  go-up   go-down


28. Ozbek U, Kandilci A, van Baal S, Bonten J, Boyd K, Franken P, Fodde R, Grosveld GC: SET-CAN, the product of the t(9;9) in acute undifferentiated leukemia, causes expansion of early hematopoietic progenitors and hyperproliferation of stomach mucosa in transgenic mice. Am J Pathol; 2007 Aug;171(2):654-66
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] SET-CAN, the product of the t(9;9) in acute undifferentiated leukemia, causes expansion of early hematopoietic progenitors and hyperproliferation of stomach mucosa in transgenic mice.
  • Leukemia-specific chromosome translocations involving the nucleoporin CAN/NUP214 lead to expression of different fusion genes including DEK-CAN, CAN-ABL, and SET-CAN.
  • DEK-CAN and CAN-ABL1 are associated with acute myeloid leukemia and T-cell acute lymphoblastic leukemia, respectively, whereas SET-CAN was identified in a patient with acute undifferentiated leukemia.
  • Although SET-CAN mice showed expansion of an early progenitor cell pool and partial depletion of lymphocytes, the animals were not leukemia-prone and did not show shortening of disease latency after retroviral tagging.
  • This suggests that SET-CAN expression in acute undifferentiated leukemia might determine the primitive phenotype of the disease, whereas secondary genetic lesions are necessary for disease development.

  • MedlinePlus Health Information. consumer health - Leukemia.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • 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 CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • SciCrunch. Marmoset Gene list: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Genet. 2004 Oct;36(10):1084-9 [15361874.001]
  • [Cites] Cancer Treat Rev. 2004 Aug;30(5):451-9 [15245777.001]
  • [Cites] Immunogenetics. 1984;20(1):47-56 [6746027.001]
  • [Cites] J Clin Pathol. 1986 Jun;39(6):590-3 [3013945.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Jun;86(12):4634-8 [2660142.001]
  • [Cites] Mol Cell Biol. 1990 Aug;10(8):4016-26 [2370860.001]
  • [Cites] Cell. 1991 May 31;65(5):737-52 [1904008.001]
  • [Cites] Anat Rec. 1992 Feb;232(2):231-46 [1546802.001]
  • [Cites] Blood. 1992 Jun 1;79(11):2990-7 [1586743.001]
  • [Cites] Mol Cell Biol. 1992 Aug;12(8):3346-55 [1630450.001]
  • [Cites] Anat Rec. 1993 Jun;236(2):259-79 [8338232.001]
  • [Cites] J Biol Chem. 1994 Jan 21;269(3):2258-62 [8294483.001]
  • [Cites] Nature. 1994 Nov 10;372(6502):143-9 [7969446.001]
  • [Cites] Oncogene. 1995 May 4;10(9):1739-48 [7753551.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 May 9;92(10):4279-83 [7753797.001]
  • [Cites] J Exp Med. 1996 Apr 1;183(4):1797-806 [8666936.001]
  • [Cites] Oncogene. 1996 Oct 17;13(8):1801-8 [8895527.001]
  • [Cites] EMBO J. 1996 Oct 15;15(20):5574-83 [8896451.001]
  • [Cites] Curr Biol. 1996 Dec 1;6(12):1664-8 [8994831.001]
  • [Cites] Development. 1997 Jan;124(2):537-47 [9053329.001]
  • [Cites] Cell. 1997 Sep 19;90(6):1051-60 [9323133.001]
  • [Cites] J Biol Chem. 1997 Nov 7;272(45):28407-14 [9353299.001]
  • [Cites] Mol Cell Biol. 1998 Mar;18(3):1236-47 [9488438.001]
  • [Cites] Mol Cell Biol. 1999 Sep;19(9):6276-85 [10454574.001]
  • [Cites] FEBS Lett. 2005 Jan 31;579(3):757-62 [15670842.001]
  • [Cites] Mol Cell Biol. 2005 Mar;25(6):2395-405 [15743832.001]
  • [Cites] Haematologica. 2007 Feb;92(2):232-5 [17296573.001]
  • [Cites] Mol Endocrinol. 2000 Jun;14(6):875-88 [10847589.001]
  • [Cites] J Cell Biol. 2000 Oct 2;151(1):1-14 [11018049.001]
  • [Cites] Cell. 2001 Jan 12;104(1):119-30 [11163245.001]
  • [Cites] J Biol Chem. 2001 Nov 16;276(46):43285-93 [11555662.001]
  • [Cites] J Biol Chem. 2002 May 17;277(20):17901-5 [11834740.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):63-74 [12086889.001]
  • [Cites] J Biol Chem. 2002 Jul 12;277(28):25026-31 [11978794.001]
  • [Cites] EMBO Rep. 2002 Sep;3(9):834-9 [12223464.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6395-9 [12438222.001]
  • [Cites] J Biol Chem. 2003 Jan 10;278(2):1158-64 [12407107.001]
  • [Cites] Cell. 2003 Mar 7;112(5):659-72 [12628186.001]
  • [Cites] J Virol. 2003 Apr;77(8):4965-71 [12663802.001]
  • [Cites] Blood. 2003 Jul 1;102(1):94-101 [12623852.001]
  • [Cites] Leukemia. 2004 Feb;18(2):337-40 [14671643.001]
  • [Cites] J Biol Chem. 2004 Feb 13;279(7):5263-7 [14630927.001]
  • [Cites] Science. 2004 Mar 5;303(5663):1483-7 [15001769.001]
  • [Cites] Int J Cancer. 2004 Sep 10;111(4):539-42 [15239131.001]
  • [Cites] Blood. 1976 May;47(5):705-21 [1260131.001]
  • (PMID = 17569777.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-76480
  • [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 / Chromosomal Proteins, Non-Histone; 0 / Ki-67 Antigen; 0 / Nuclear Pore Complex Proteins; 0 / Nup214 protein, mouse; 0 / Oncogene Proteins, Fusion
  • [Other-IDs] NLM/ PMC1934515
  •  go-up   go-down


29. Rizzieri DA, O'Brien JA, Broadwater G, Decastro CM, Dev P, Diehl L, Beaven A, Lagoo A, Gockerman JP, Chao NJ, Moore JO: Outcomes of patients who undergo aggressive induction therapy for secondary acute myeloid leukemia. Cancer; 2009 Jul 1;115(13):2922-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcomes of patients who undergo aggressive induction therapy for secondary acute myeloid leukemia.
  • BACKGROUND: Response and survival in 96 patients with secondary acute myeloid leukemia (sAML) who received aggressive induction chemotherapy was reviewed.
  • Patients with AML after previous chemotherapy or radiation therapy had a higher morphologic remission rate compared with those arising from myelodysplastic syndrome or myeloproliferative disease (82% vs 62%; P = .027).
  • In this population of patients who received aggressive chemotherapy, Charlson comorbidity index or a higher number of factors recognized as high risk in leukemia patients did not affect the chance of OS, DFS, and EFS, although having more recognized leukemia risk factors was related to a lower chance of surviving 1 year.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Neoplasms, Second Primary / drug therapy

  • 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 = 19452542.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


30. Fianchi L, Pagano L, Leoni F, Storti S, Voso MT, Valentini CG, Rutella S, Scardocci A, Caira M, Gianfaldoni G, Leone G: Gemtuzumab ozogamicin, cytosine arabinoside, G-CSF combination (G-AraMy) in the treatment of elderly patients with poor-prognosis acute myeloid leukemia. Ann Oncol; 2008 Jan;19(1):128-34
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] Gemtuzumab ozogamicin, cytosine arabinoside, G-CSF combination (G-AraMy) in the treatment of elderly patients with poor-prognosis acute myeloid leukemia.
  • BACKGROUND: Gemtuzumab ozogamicin (GO) is effective as single agent in the treatment of acute myeloid leukemia (AML).
  • We evaluated efficacy and safety of a chemotherapy including growth factors, cytarabine, and GO (G-AraMy) in the treatment of poor-prognosis AML in elderly patients.
  • PATIENTS AND METHODS: In three Italian hematology departments from September 2003 to September 2006, 53 elderly patients [median age 69 years (range 65-77)] with untreated or primary refractory/relapsed AML were enrolled on the combination G-AraMy administered according to two consecutive schedules (G-AraMy1 and G-AraMy2), with intensified consolidation in the second.
  • Twenty-three of 53 patients had a secondary acute myeloid leukemia (sAML).
  • No differences for response rate and toxicity profile were observed between untreated and primary resistant/relapsed patients, de novo AML and sAML, and in the two treatment trials.
  • CONCLUSIONS: G-AraMy therapy may be considered an useful treatment approach for poor-risk elderly AML patients, with a complete remission rate comparable to literature data with reduced side-effects, also in a poor-prognosis population.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17906298.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / gemtuzumab; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor
  •  go-up   go-down


31. Sandlund JT, Pui CH, Zhou Y, Behm FG, Onciu M, Razzouk BI, Hijiya N, Campana D, Hudson MM, Ribeiro RC: Effective treatment of advanced-stage childhood lymphoblastic lymphoma without prophylactic cranial irradiation: results of St Jude NHL13 study. Leukemia; 2009 Jun;23(6):1127-30
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] Effective treatment of advanced-stage childhood lymphoblastic lymphoma without prophylactic cranial irradiation: results of St Jude NHL13 study.
  • There has been a steady improvement in cure rates for children with advanced-stage lymphoblastic non-Hodgkin's lymphoma.
  • To further improve cure rates whereas minimizing long-term toxicity, we designed a protocol (NHL13) based on a regimen for childhood T-cell acute lymphoblastic leukemia, which features intensive intrathecal chemotherapy for central -nervous system-directed therapy and excludes prophylactic cranial irradiation.
  • From 1992 to 2002, 41 patients with advanced-stage lymphoblastic lymphoma were enrolled on the protocol.
  • Adverse events included two induction failures, one death from typhlitis during remission, three relapses and one secondary acute myeloid leukemia.
  • The treatment described here produces high cure rates in children with lymphoblastic lymphoma without the use of prophylactic cranial irradiation.

  • Genetic Alliance. consumer health - Lymphoblastic lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. MERCAPTOPURINE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1340-6 [12663724.001]
  • [Cites] Rev Clin Exp Hematol. 2002 Jun;6(2):161-80; discussion 200-2 [12196214.001]
  • [Cites] Blood. 2002 Jul 1;100(1):52-8 [12070008.001]
  • [Cites] Blood. 2002 Jul 1;100(1):43-7 [12070006.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2286-94 [11187920.001]
  • [Cites] Blood. 2000 Jan 15;95(2):416-21 [10627444.001]
  • [Cites] J Clin Oncol. 2003 Oct 1;21(19):3616-22 [14512392.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):491-9 [16421426.001]
  • [Cites] Leukemia. 1999 Mar;13(3):335-42 [10086723.001]
  • [Cites] Lancet. 1998 Feb 21;351(9102):550-4 [9492773.001]
  • [Cites] Cancer. 1997 Nov 1;80(9):1717-26 [9351539.001]
  • [Cites] N Engl J Med. 1996 May 9;334(19):1238-48 [8606720.001]
  • [Cites] J Clin Oncol. 1995 Jun;13(6):1368-76 [7751881.001]
  • [Cites] J Clin Oncol. 1993 Jun;11(6):1024-32 [8501488.001]
  • [Cites] Med Pediatr Oncol. 1992;20(2):105-13 [1734214.001]
  • [Cites] Med Pediatr Oncol. 1990;18(4):273-9 [2355886.001]
  • [Cites] Blood. 1985 Nov;66(5):1110-4 [3840395.001]
  • [Cites] J Clin Oncol. 1983 Sep;1(9):537-41 [6689428.001]
  • [Cites] Cancer. 1982 May 15;49(10):2112-35 [6896167.001]
  • [Cites] Semin Oncol. 1980 Sep;7(3):332-9 [7414342.001]
  • [Cites] Cancer. 1980 Feb 15;45(4):630-7 [6986967.001]
  • (PMID = 19194463.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-31; United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / P30 CA021765-31
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS161582; NLM/ PMC2843413
  •  go-up   go-down


32. Varet B, Ifrah N: [Criteria for suspecting a myelodysplastic syndrome]. Rev Prat; 2010 Dec 20;60(10):1404-7
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 myelodysplastic syndromes are a group of heterogeneous acquired and clonal disorders that are characterized by the intramedullar, abnormal death of myeloid progenitors leading to peripheral variable cytopenias.
  • It is predictive for the risk of transformation in secondary acute myeloid leukemia.

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21425539.001).
  • [ISSN] 0035-2640
  • [Journal-full-title] La Revue du praticien
  • [ISO-abbreviation] Rev Prat
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down


33. Anwar Iqbal M, Al-Omar HM, Owaidah T, Al-Humaidan H, Bhuiyan ZA, Sahovic E: del(6)(p23) in two cases of de novo AML--a new recurrent primary chromosome abnormality. Eur J Haematol; 2006 Sep;77(3):245-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] del(6)(p23) in two cases of de novo AML--a new recurrent primary chromosome abnormality.
  • OBJECTIVE: Previously, deletion 6p23 was generally reported in therapy-related secondary acute myeloid leukemia (AML) as part of complex karyotypes.
  • In this report, we present two young adult patients with de novo AML-M2 and a terminal deletion 6p23 as a sole primary abnormality, confirmed by chromosome 6 specific subtelomeric probes.
  • RESULTS: A diagnosis of AML-M2 was confirmed in both patients by morphological and immunophenotyping studies.
  • The common morphological, immunophenotypic, and cytogenetic features in our two patients strongly support a separate new entity of de novo AML with deletion 6p23.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 6 / genetics. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adult. Chromosomal Proteins, Non-Histone / genetics. Cytogenetics. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Oncogene Proteins / genetics. Oncogenes. Recurrence

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16856925.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Dek protein, human; 0 / Oncogene Proteins
  •  go-up   go-down


34. Ruutu T, Corradini P, Gratwohl A, Holler E, Apperley J, Dini G, Rocha V, Schmitz N, Socié G, Niederwieser D: Use of intrathecal prophylaxis in allogeneic haematopoietic stem cell transplantation for malignant blood diseases: a survey of the European Group for Blood and Marrow Transplantation (EBMT). Bone Marrow Transplant; 2005 Jan;35(2):121-4
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.
  • The main indications were acute lymphoblastic leukaemia (ALL), acute myeloid leukaemia (AML), and lymphoma (53, 33, and 23% of all centres, respectively).
  • Prophylaxis was usually given to all patients with ALL, but often restricted to high-risk patients in AML and lymphoma.
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Data Collection. Humans. Injections, Spinal. Leukemia / pathology. Leukemia / therapy. Lymphoma / pathology. Lymphoma / therapy. Secondary Prevention. Transplantation, Homologous

  • 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 = 15543201.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


35. Tam CS, Seymour JF, Prince HM, Kenealy M, Wolf M, Januszewicz EH, Westerman D: Treatment-related myelodysplasia following fludarabine combination chemotherapy. Haematologica; 2006 Nov;91(11):1546-50
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.
  • Although myelodysplasia (MDS) and secondary acute myeloid leukemia (sAML) are rare following fludarabine monotherapy, the risk of these diseases may potentially be increased when fludarabine is combined with cyclophosphamide or mitoxantrone due to synergistic effects on the inhibition of DNA repair.


36. Römermann D, Hasemeier B, Metzig K, Schlegelberger B, Länger F, Kreipe H, Lehmann U: [Methylation status of LINE-1 sequences in patients with MDS or secondary AML]. Verh Dtsch Ges Pathol; 2007;91:338-42
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] [Methylation status of LINE-1 sequences in patients with MDS or secondary AML].
  • [Transliterated title] Methylierungszustand von LINE-1-Sequenzen bei Patienten mit MDS oder sekundärer AML.
  • [MeSH-minor] Humans. Leukemia, Myeloid, Acute / genetics

  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • 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 = 18314632.001).
  • [ISSN] 0070-4113
  • [Journal-full-title] Verhandlungen der Deutschen Gesellschaft für Pathologie
  • [ISO-abbreviation] Verh Dtsch Ges Pathol
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


37. Schwarz J, Pytlík R, Doubek M, Brychtová Y, Dulícek P, Campr V, Kren L, Penka M: Analysis of risk factors: the rationale of the guidelines of the Czech Hematological Society for diagnosis and treatment of chronic myeloproliferative disorders with thrombocythemia. Semin Thromb Hemost; 2006 Apr;32(3):231-45
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.
  • The histopathology-based nosological distinction provided by these classifications yields valuable information on prognosis (including the risks of transition into secondary acute myeloid leukemia and myelofibrosis).

  • Genetic Alliance. consumer health - Chronic Myeloproliferative Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16673277.001).
  • [ISSN] 0094-6176
  • [Journal-full-title] Seminars in thrombosis and hemostasis
  • [ISO-abbreviation] Semin. Thromb. Hemost.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


38. Creutzig U, Diekamp S, Zimmermann M, Reinhardt D: Longitudinal evaluation of early and late anthracycline cardiotoxicity in children with AML. Pediatr Blood Cancer; 2007 Jun 15;48(7):651-62
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] Longitudinal evaluation of early and late anthracycline cardiotoxicity in children with AML.
  • BACKGROUND: Anthracyclines are effective antineoplastic drugs in acute myelogenous leukemia (AML).
  • PROCEDURE: To evaluate anthracycline-associated cardiomyopathy in pediatric AML-patients, the incidence of early and late (>1 year after intensive AML chemotherapy) clinical and subclinical cardiotoxicity was analyzed out of a total of 1,207 patients <18 years treated between 1993 and 2003 in trials AML-BFM93/98: 1,010 protocol patients with de novo AML, 121 with Down syndrome (DS)-AML, and 76 with secondary AML.
  • RESULTS: Thirty-eight patients (4.3%), including 3 DS-AML and 1 secondary AML, suffered from early cardiomyopathy.
  • After 5 years, four patients showed temporarily or persistently a reduced shortening fraction, which led to death in one DS-AML patient.
  • Late clinical cardiomyopathy mainly affected patients with a second anthracycline therapy (secondary malignancy) and those with early cardiotoxicity.
  • CONCLUSION: In spite of a highly intensive and effective treatment, the frequency of anthracycline-associated cardiomyopathy was low in the AML-BFM studies.
  • [MeSH-major] Anthracyclines / adverse effects. Heart / drug effects. Heart Diseases / chemically induced. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Dose-Response Relationship, Drug. Drug-Related Side Effects and Adverse Reactions. Echocardiography / methods. Female. Follow-Up Studies. Humans. Infant. Longitudinal Studies. Male. Pilot Projects. Risk Factors. Survivors. Time. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Heart Disease in Women.
  • MedlinePlus Health Information. consumer health - Heart Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • [CommentIn] Pediatr Blood Cancer. 2007 Jun 15;48(7):649-50 [17318875.001]
  • (PMID = 17183582.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines
  •  go-up   go-down


39. Tretiak NM, Vakul'chuk OM, Kalinina SIu: [Induced acute non-lymphoblastic leukemia and prognostic significance of cytogenetic abnormalities: trisomy in chromosome 8, inv(16)(p13q22), and t(8;21)(q22;q22)]. Lik Sprava; 2008 Jan-Feb;(1-2):89-96
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] [Induced acute non-lymphoblastic leukemia and prognostic significance of cytogenetic abnormalities: trisomy in chromosome 8, inv(16)(p13q22), and t(8;21)(q22;q22)].
  • 3 patients with secondary acute non-lymphoblastic leucosis have been observed.


40. Rubin J, Frost BM, Arvidson J, Wide K, Gustafsson-Jernberg A, Gustafsson B: Intrathecal chemoprophylaxis after HSCT in children. Pediatr Transplant; 2008 Dec;12(8):889-95
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.
  • We compared 74 patients (56 ALL/18 AML), who received i.t. therapy post-HSCT with 46 patients (36 ALL/10 AML) who did not receive post-HSCT i.t. therapy.
  • Secondary end-points were other types of relapse, death, and neurological complications.
  • Our study did not demonstrate a protective effect of i.t. therapy indicating that post-HSCT i.t. therapy may only be of limited use in the treatment of acute childhood leukemia.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Stem Cell Transplantation / methods

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18822104.001).
  • [ISSN] 1399-3046
  • [Journal-full-title] Pediatric transplantation
  • [ISO-abbreviation] Pediatr Transplant
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  •  go-up   go-down


41. Then Bergh F, Niklas A, Strauss A, von Ahsen N, Niederwieser D, Schwarz J, Wagner A, Al-Ali HK: Rapid progression of Myelodysplastic syndrome to acute myeloid leukemia on sequential azathioprine, IFN-beta and copolymer-1 in a patient with multiple sclerosis. Acta Haematol; 2006;116(3):207-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rapid progression of Myelodysplastic syndrome to acute myeloid leukemia on sequential azathioprine, IFN-beta and copolymer-1 in a patient with multiple sclerosis.
  • Within several months, unusually rapid for this subtype, MDS progressed to secondary acute myeloid leukemia.
  • [MeSH-major] Azathioprine / adverse effects. Interferon-beta / adverse effects. Leukemia, Myeloid / chemically induced. Multiple Sclerosis / complications. Multiple Sclerosis / drug therapy. Myelodysplastic Syndromes / complications. Peptides / adverse effects
  • [MeSH-minor] Acute Disease. Disease Progression. Fatal Outcome. Female. Glatiramer Acetate. Humans. Middle Aged


42. 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 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.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • 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] Cancer Res. 2005 Oct 1;65(19):8597-603 [16204023.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9152-4 [16230371.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3553-8 [16030187.001]
  • [Cites] Clin Cancer Res. 2006 Jan 1;12(1):5-10 [16397017.001]
  • [Cites] Cancer Res. 2006 Apr 1;66(7):3471-9 [16585170.001]
  • [Cites] Leukemia. 2006 May;20(5):904-5 [16511509.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1733-43 [16705090.001]
  • [Cites] Leukemia. 2006 Sep;20(9):1610-7 [16826223.001]
  • [Cites] N Engl J Med. 2006 Oct 5;355(14):1456-65 [17021321.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Nov;171(1):9-16 [17074585.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3280-8 [16840728.001]
  • [Cites] Nature. 2006 Nov 23;444(7118):444-54 [17122850.001]
  • [Cites] J Clin Pathol. 2007 Jan;60(1):1-7 [16790693.001]
  • [Cites] Blood. 2007 Feb 1;109(3):1202-10 [17053054.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2058-61 [17525728.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3365-73 [17634407.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3835-49 [10577857.001]
  • [Cites] Br J Haematol. 2000 Feb;108(2):346-56 [10691865.001]
  • [Cites] Am J Pathol. 2001 Apr;158(4):1253-62 [11290543.001]
  • [Cites] J Med Genet. 2001 Aug;38(8):497-507 [11483637.001]
  • [Cites] Int J Hematol. 2001 Jun;73(4):429-37 [11503956.001]
  • [Cites] Exp Hematol. 2002 Mar;30(3):229-36 [11882360.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3586-90 [11891338.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2263-8 [15238427.001]
  • [Cites] Leukemia. 1993 Sep;7(9):1315-23 [8371581.001]
  • [Cites] Br J Haematol. 1996 Mar;92(3):574-81 [8616020.001]
  • [Cites] Blood. 1997 Mar 15;89(6):2079-88 [9058730.001]
  • [Cites] N Engl J Med. 1999 May 27;340(21):1649-60 [10341278.001]
  • [Cites] Br J Haematol. 1999 Aug;106(2):455-63 [10460606.001]
  • [Cites] N Engl J Med. 2005 Feb 10;352(6):549-57 [15703420.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3053-8 [15833833.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6071-9 [16024607.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):334-7 [16015648.001]
  • [Cites] Haematologica. 2005 Sep;90(9):1168-78 [16154839.001]
  • (PMID = 17954704.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K24 HL077522; United States / NHLBI NIH HHS / HL / R01 HL082983; United States / NCRR NIH HHS / RR / S10 RR019391; United States / NCRR NIH HHS / RR / U54 RR019391
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2214746
  •  go-up   go-down


43. Junghanss C, Waak M, Knopp A, Kleine HD, Kundt G, Leithäuser M, Hilgendorf I, Wolff D, Casper J, Freund M: Multivariate analyses of prognostic factors in acute myeloid leukemia: relevance of cytogenetic abnormalities and CD34 expression. Neoplasma; 2005;52(5):402-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multivariate analyses of prognostic factors in acute myeloid leukemia: relevance of cytogenetic abnormalities and CD34 expression.
  • Identification of additional prognostic factors besides karyotype is important for the improvement of the risk adapted treatment strategies in acute myeloid leukemia (AML).
  • The aim of this study was to investigate whether other factors besides karyotype could be used as a prognostic tool in newly diagnosed AML.
  • Biological and disease related established and potential prognostic factors were retrospectively analysed in 124 consecutive AML patients treated between 1993 and 2002 at the University hospital Rostock (Germany).
  • In patients that received potential curative therapies LDH >or=2000 U/l, WBC >50 GPT/l, CD34 surface expression on the AML blasts, secondary AML, unfavorable karyotype and no allogeneic HSCT at some point of treatment course were associated with unfavorable prognosis.
  • However, in the multivariate risk factor analyses only unfavorable karyotype (p=0.012), CD34 positivity of AML blasts (p=0.046), no allogeneic HSCT (p=0.008) and first diagnosis after 1997 (p=0.025) were independent unfavourable prognostic factors.
  • In conclusion, karyotype and CD34 expression are independent prognostic markers in newly diagnosed AML.
  • Furthermore, receiving an allogeneic HSCT at some point of the treatment course seems to be of benefit for AML patients.
  • [MeSH-major] Antigens, CD34 / metabolism. Biomarkers, Tumor / analysis. Chromosome Aberrations. Leukemia, Myeloid / genetics. Leukemia, Myeloid / mortality
  • [MeSH-minor] Acute Disease / therapy. Adult. Age Factors. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Flow Cytometry. Hematopoietic Stem Cell Transplantation. Humans. Karyotyping. Middle Aged. Multivariate Analysis. Palliative Care. Prognosis. Remission Induction. Retrospective Studies. Risk Factors. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16151585.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers, Tumor
  •  go-up   go-down


44. Moorman AV, Raimondi SC, Pui CH, Baruchel A, Biondi A, Carroll AJ, Forestier E, Gaynon PS, Harbott J, Harms DO, Heerema N, Pieters R, Schrappe M, Silverman LB, Vilmer E, Harrison CJ, Ponte di Legno Working Group: No prognostic effect of additional chromosomal abnormalities in children with acute lymphoblastic leukemia and 11q23 abnormalities. Leukemia; 2005 Apr;19(4):557-63
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] No prognostic effect of additional chromosomal abnormalities in children with acute lymphoblastic leukemia and 11q23 abnormalities.
  • This study characterized the additional chromosomal abnormalities (ACA) associated with 11q23 rearrangements in 450 infants and children with acute lymphoblastic leukemia (ALL) and examined the impact of these ACA on survival.
  • Del(11)(q23) abnormalities were heterogeneous and occasionally secondary to t(9;22)(q34;q11.2).
  • This study has conclusively demonstrated that there is no prognostic effect of secondary chromosomal changes in association with 11q23 abnormalities in childhood ALL.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15744345.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA36401; United States / NCI NIH HHS / CA / CA51001; United States / NCI NIH HHS / CA / CA60419; United States / NCI NIH HHS / CA / CA78224; United States / NIGMS NIH HHS / GM / GM61393
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  •  go-up   go-down


45. Dale DC: Advances in the treatment of neutropenia. Curr Opin Support Palliat Care; 2009 Sep;3(3):207-12
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Current guidelines recommend the prophylactic use of the myeloid growth factors for the first cycle of chemotherapy for patients with more than a 20% risk of febrile neutropenia.
  • Meta analysis from randomized trials shows that granulocyte colony-stimulating factor prophylaxis is associated with patients receiving more intensive chemotherapy, having better survival, but also having a higher risk of secondary acute myeloid leukemia.
  • SUMMARY: The myeloid growth factor granulocyte colony-stimulating factor has radically changed our approach to the prevention of febrile neutropenia.

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Crit Rev Oncol Hematol. 2008 Jun;66(3):237-47 [18243010.001]
  • [Cites] Niger J Med. 2008 Jan-Mar;17(1):57-60 [18390135.001]
  • [Cites] Ann Oncol. 2008 May;19 Suppl 2:ii116-8 [18456747.001]
  • [Cites] J Support Oncol. 2008 May-Jun;6(5):199-208 [18551855.001]
  • [Cites] Infection. 2008 Jun;36(3):250-5 [18458815.001]
  • [Cites] Am J Med. 2008 Aug;121(8):709-14 [18691485.001]
  • [Cites] Scand J Infect Dis. 2008;40(4):301-7 [17918015.001]
  • [Cites] Drugs. 2008;68(14):1941-62 [18778118.001]
  • [Cites] Clin Infect Dis. 2008 Nov 1;47(9):1176-84 [18808352.001]
  • [Cites] J Clin Pharm Ther. 2008 Oct;33(5):459-64 [18834359.001]
  • [Cites] Eur J Clin Microbiol Infect Dis. 2008 Oct;27(10):969-76 [18449581.001]
  • [Cites] Cochrane Database Syst Rev. 2008;(4):CD003189 [18843642.001]
  • [Cites] Am J Clin Oncol. 2008 Aug;31(4):369-74 [18845996.001]
  • [Cites] Pediatr Blood Cancer. 2008 Dec;51(6):778-83 [18726920.001]
  • [Cites] Br J Haematol. 2008 Oct;143(2):222-9 [18713253.001]
  • [Cites] Int J Antimicrob Agents. 2008 Nov;32 Suppl 2:S119-23 [19013335.001]
  • [Cites] Blood. 2008 Dec 1;112(12):4445-51 [18799726.001]
  • [Cites] Bone Marrow Transplant. 2008 Nov;42(10):679-84 [18695660.001]
  • [Cites] Lancet Oncol. 2008 Dec;9(12):1157-65 [19038762.001]
  • [Cites] Curr Opin Hematol. 2009 Jan;16(1):1-2 [19057197.001]
  • [Cites] N Engl J Med. 2009 Jan 1;360(1):3-5 [19118300.001]
  • [Cites] J Natl Compr Canc Netw. 2009 Jan;7(1):92-8 [19176209.001]
  • [Cites] J Natl Compr Canc Netw. 2009 Jan;7(1):99-108 [19176210.001]
  • [Cites] Br J Haematol. 2009 Feb;144(4):459-67 [19120359.001]
  • [Cites] Br J Haematol. 2009 Mar;144(5):677-85 [19055662.001]
  • [Cites] Support Care Cancer. 2009 Jun;17(6):735-44 [19096882.001]
  • [Cites] Am J Hematol. 2009 Jul;84(7):414-7 [19415727.001]
  • [Cites] Value Health. 2009 Mar-Apr;12(2):217-25 [18673353.001]
  • [Cites] Blood. 1996 Jul 1;88(1):335-40 [8704192.001]
  • [Cites] Am J Hematol. 1998 Jan;57(1):7-15 [9423810.001]
  • [Cites] J Clin Oncol. 2006 Jul 1;24(19):3187-205 [16682719.001]
  • [Cites] J Natl Compr Canc Netw. 2007 Feb;5(2):188-202 [17335688.001]
  • [Cites] Pharmacoeconomics. 2007;25(4):343-51 [17402806.001]
  • [Cites] Ann Intern Med. 2007 May 1;146(9):657-65 [17470834.001]
  • [Cites] Curr Opin Hematol. 2008 Jan;15(1):15-21 [18043241.001]
  • [Cites] Support Care Cancer. 2008 Jan;16(1):47-56 [17619911.001]
  • [Cites] Vox Sang. 2007 Nov;93(4):363-9 [18070282.001]
  • [Cites] Ann Hematol. 2008 Feb;87(2):139-45 [17938926.001]
  • [Cites] Br J Haematol. 2008 Jan;140(2):210-3 [18028488.001]
  • [Cites] Eur J Cancer Care (Engl). 2008 Jan;17(1):19-25 [18181887.001]
  • [Cites] J Clin Oncol. 2008 Jan 10;26(2):290-6 [18182670.001]
  • [Cites] Support Care Cancer. 2008 Feb;16(2):181-91 [17943327.001]
  • [Cites] J Natl Compr Canc Netw. 2008 Feb;6(2):109-18 [18319047.001]
  • [Cites] Value Health. 2008 Mar-Apr;11(2):172-9 [18380630.001]
  • [Cites] Eur J Oncol Nurs. 2008 Feb;12(1):14-25 [18291720.001]
  • (PMID = 19550332.001).
  • [ISSN] 1751-4266
  • [Journal-full-title] Current opinion in supportive and palliative care
  • [ISO-abbreviation] Curr Opin Support Palliat Care
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R24 AI049393; United States / NIAID NIH HHS / AI / R24 AI049393-09
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor
  • [Number-of-references] 48
  • [Other-IDs] NLM/ NIHMS202938; NLM/ PMC3390973
  •  go-up   go-down


46. Willems L, Suarez F, Messas E, Baubion N, Decaudin D, Fourquet A, Ghez D, Delarue R, Hermine O, Buzyn A, Varet B, Rubio MT: [High risk of cardiac dysfunction after treatment of secondary acute myeloid leukemia following chemotherapy and radiotherapy for breast cancer]. Bull Cancer; 2010 Feb;97(2):245-54
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [High risk of cardiac dysfunction after treatment of secondary acute myeloid leukemia following chemotherapy and radiotherapy for breast cancer].
  • Secondary acute myeloid leukaemia (AML) occurring after breast cancer is a rare long-term complication of the chemo- and/or radiation therapy required to treat breast cancer.
  • The usually recognized curative option of these secondary AML includes courses of anthracycline-based chemotherapy followed by haematopoietic stem cell transplantation (HSCT).
  • Cardiac dysfunction during AML treatment of these patients previously treated with anthracyclines for breast cancer has not been reported to date.
  • We evaluated the evolution of cardiac function in seven patients treated with anthracyclines and/or autologous or allogeneic bone marrow transplantation for secondary AML occurring after breast cancer.
  • All of the patients who received a cumulative anthracycline dose above the cardiac toxicity threshold developed cardiac symptoms during AML chemotherapy courses.
  • Thus, the risk of severe cardiac dysfunction after treatment of secondary AML following breast cancer must be taken in account as part of the therapeutic strategy of those patients.
  • As discussed here, an accurate evaluation of risk factors, the use of sensitive detection tests and of cardioprotective drugs as well as that of non-cardiotoxic chemotherapy might decrease the occurrence and severity of this life-threatening complication.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Breast Neoplasms. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid / therapy. Neoplasms, Second Primary / therapy
  • [MeSH-minor] Acute Disease. Adult. Chemotherapy, Adjuvant / adverse effects. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Epirubicin / administration & dosage. Epirubicin / adverse effects. Female. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Heart Diseases / chemically induced. Heart Diseases / drug therapy. Heart Diseases / physiopathology. Humans. Middle Aged. Remission Induction. Stroke Volume / drug effects. Stroke Volume / physiology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • Hazardous Substances Data Bank. EPIRUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19819776.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; U3P01618RT / Fluorouracil; ZS7284E0ZP / Daunorubicin; FEC protocol
  •  go-up   go-down


47. Paulsson K, Forestier E, Lilljebjörn H, Heldrup J, Behrendtz M, Young BD, Johansson B: Genetic landscape of high hyperdiploid childhood acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2010 Dec 14;107(50):21719-24
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] Genetic landscape of high hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploid acute lymphoblastic leukemia (ALL) is one of the most common malignancies in children.
  • Here we provide a comprehensive characterization of the genetic landscape of high hyperdiploid childhood ALL, including the heterogeneous pattern of secondary genetic events.
  • [MeSH-major] Chromosome Aberrations. Diploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


48. Li Y, Qiu L, Zou D, Zhao Y, Mi Y, Wang J: Additional chromosomal abnormalities and their prognostic significance in adult Philadelphia-positive acute lymphoblastic leukemia: with or without imatinib in chemotherapy. Ann Hematol; 2009 Nov;88(11):1069-77
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] Additional chromosomal abnormalities and their prognostic significance in adult Philadelphia-positive acute lymphoblastic leukemia: with or without imatinib in chemotherapy.
  • The study analyzed the characteristics and prognostic significance of additional chromosomal abnormalities in 110 Chinese adults with Philadelphia chromosome-positive (Ph-positive) acute lymphoblastic leukemia (ALL).
  • Secondary aberrations were present in 60.9% of the cases.
  • All chromosomes were involved in secondary aberrations, and chromosomes 9, 7, 21, 18, and 14 were most frequently abnormal.
  • Patients with loss of chromosomes 7, 7p, 9, and 9p had inferior outcome compared to patients with other secondary aberrations and those without secondary aberrations, in both CT and ICT group.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Pyrimidines / therapeutic use. Salvage Therapy

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. MERCAPTOPURINE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINDESINE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19277658.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8A1O1M485B / Imatinib Mesylate; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; E7WED276I5 / 6-Mercaptopurine; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.5.1.1 / Asparaginase; RSA8KO39WH / Vindesine; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


49. Ferrara F, Mele G, Palmieri S, Pedata M, Copia C, Riccardi C, Izzo T, Criscuolo C, Musto P: Continuous infusion idarubicin and intravenous busulphan as conditioning regimen to autologous stem cell transplantation for patients with acute myeloid leukaemia. Hematol Oncol; 2009 Dec;27(4):198-202
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] Continuous infusion idarubicin and intravenous busulphan as conditioning regimen to autologous stem cell transplantation for patients with acute myeloid leukaemia.
  • The current study aimed to evaluate the efficacy and toxicity of a combination of intravenous (iv) busulfan (Bu) and continuous infusion Idarubicin (IDA) as a conditioning regimen to autologous haematopoietic stem cell transplantation (ASCT) in patients with acute myeloid leukaemia (AML).
  • In order to perform a comparison in terms of haematological and non haematological toxicity, a group of 30 patients, who were previously autografted after conditioning with IDA and oral Bu was considered.
  • Selection of factors for a matched pair analysis included median age, percentage of subjects aged over 60 years, median CD34+ cell received, cytogenetic and molecular findings and per cent of secondary AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation / methods. Transplantation Conditioning / methods

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. BUSULFAN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2009 John Wiley & Sons, Ltd.
  • (PMID = 19475701.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] G1LN9045DK / Busulfan; ZRP63D75JW / Idarubicin
  •  go-up   go-down


50. Bastianutto C, Mian A, Symes J, Mocanu J, Alajez N, Sleep G, Shi W, Keating A, Crump M, Gospodarowicz M, Medin J, Minden M, Liu FF: Local radiotherapy induces homing of hematopoietic stem cells to the irradiated bone marrow. Cancer Res; 2007 Nov 1;67(21):10112-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Local breast radiation therapy (RT) is associated with a 3-fold increased risk of secondary acute myeloid leukemia.
  • Our data also suggest some opportunities for leukemia prevention in breast cancer patients undergoing RT.
  • [MeSH-major] Bone Marrow Cells / radiation effects. Hematopoietic Stem Cells / radiation effects. Leukemia, Myeloid, Acute / etiology. Leukemia, Radiation-Induced / etiology. Radiotherapy / adverse effects

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Radiation Therapy.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17974951.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokine CXCL12; 0 / Cxcl12 protein, mouse; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


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

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

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


52. Yanada M, Takeuchi J, Sugiura I, Akiyama H, Usui N, Yagasaki F, Nishii K, Ueda Y, Takeuchi M, Miyawaki S, Maruta A, Narimatsu H, Miyazaki Y, Ohtake S, Jinnai I, Matsuo K, Naoe T, Ohno R, Japan Adult Leukemia Study Group: Karyotype at diagnosis is the major prognostic factor predicting relapse-free survival for patients with Philadelphia chromosome-positive acute lymphoblastic leukemia treated with imatinib-combined chemotherapy. Haematologica; 2008 Feb;93(2):287-90
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] Karyotype at diagnosis is the major prognostic factor predicting relapse-free survival for patients with Philadelphia chromosome-positive acute lymphoblastic leukemia treated with imatinib-combined chemotherapy.
  • To identify factors associated with relapse-free survival (RFS), 80 patients with newly diagnosed Philadelphia chromosome-positive acute lymphoblastic leukemia, enrolled in a phase II study of imatinib-combined chemotherapy, were analyzed.
  • Multivariate analysis revealed that the presence of secondary chromosome aberrations in addition to t(9;22) at diagnosis constitute an independent predictive value for RFS (p=0.027), and increase the risk of treatment failure by 2.8-fold.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Philadelphia Chromosome. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Pyrimidines / administration & dosage

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18223280.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  •  go-up   go-down


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

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

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


54. Ayash LJ, Ratanatharathorn V, Braun T, Silver SM, Reynolds CM, Uberti JP: Unrelated donor bone marrow transplantation using a chemotherapy-only preparative regimen for adults with high-risk acute myelogenous leukemia. Am J Hematol; 2007 Jan;82(1):6-14
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] Unrelated donor bone marrow transplantation using a chemotherapy-only preparative regimen for adults with high-risk acute myelogenous leukemia.
  • Limited data are available for adults undergoing unrelated donor (URD) BMT for AML using chemotherapy-only preparative regimens.
  • Previous studies incorporated irradiation, included adults and children, and excluded secondary leukemia.
  • Herein we report long-term outcomes for adults with poor-prognostic AML receiving a novel regimen of busulfan (16 mg/kg), cytarabine (8,000 mg/m(2)), and cyclophosphamide (120 mg/kg) (BAC), followed by URD BMT.
  • Adverse features included unfavorable cytogenetics (49%), secondary AML (47%), leukemia at transplant (42%), and extramedullary disease (16%).
  • At time of BMT, 23 were in remission (12 CR1) while 22 had leukemia.
  • Acute and chronic GVHD rates were 44 and 67%, respectively.
  • Seventeen (38%) were disease-free 52 months post-BMT; 13 were leukemia-free (eight CR1) at transplant.
  • Secondary leukemia, cytogenetics, cell dose, and GVHD did not influence outcome.
  • In poor-risk AML, BAC provided cytoreduction comparable to reported TBI-containing regimens, when administered for URD BMT.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Bone Marrow Transplantation. Leukemia, Myeloid, Acute / therapy. Tissue Donors. Transplantation Conditioning
  • [MeSH-minor] Acute Disease. Adult. Chronic Disease. Disease-Free Survival. Doxorubicin / administration & dosage. Doxorubicin / adverse effects. Factor XIII / administration & dosage. Factor XIII / adverse effects. Female. Fibrinogen / administration & dosage. Fibrinogen / adverse effects. Follow-Up Studies. Graft vs Host Disease / etiology. Graft vs Host Disease / mortality. Humans. Male. Middle Aged. Recurrence. Remission Induction. Retrospective Studies. Thrombin / administration & dosage. Thrombin / adverse effects. Transplantation, Homologous


55. Mansour MR, Duke V, Foroni L, Patel B, Allen CG, Ancliff PJ, Gale RE, Linch DC: Notch-1 mutations are secondary events in some patients with T-cell acute lymphoblastic leukemia. Clin Cancer Res; 2007 Dec 01;13(23):6964-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Notch-1 mutations are secondary events in some patients with T-cell acute lymphoblastic leukemia.
  • PURPOSE: Activating Notch-1 mutations are frequent in T-cell acute lymphoblastic leukemia (T-ALL), occurring in >50% of patients.
  • In murine models of T-ALL, Notch-1 activation can both directly initiate leukemia and cooperate secondarily to other primary events.
  • Whether acquisition of Notch-1 mutations is an early initiating event or a secondary event in the pathogenesis of human T-ALL is unclear.
  • Seven of these were low-level mutations (quantified at < or =10%), despite high blast counts, suggesting that they were acquired as a secondary event in a subclone.
  • One relapsed with a secondary T-cell leukemia and different Notch mutation.
  • CONCLUSIONS: These results suggest that Notch-1 mutations can sometimes be acquired as secondary events in leukemogenesis and must be used cautiously as solitary minimal residual disease markers.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation. Receptor, Notch1 / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18056171.001).
  • [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 Kingdom / Medical Research Council / / G0500389
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
  •  go-up   go-down


56. Sovinz P, Urban C, Hausegger K: Life-threatening hemangiomatosis of the liver in an infant: multimodal therapy including cyclophosphamide and secondary acute myeloid leukemia. Pediatr Blood Cancer; 2006 Dec;47(7):972-3
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] Life-threatening hemangiomatosis of the liver in an infant: multimodal therapy including cyclophosphamide and secondary acute myeloid leukemia.
  • [MeSH-major] Cyclophosphamide / adverse effects. Hemangioma / therapy. Leukemia, Myeloid, Acute / etiology. Liver Neoplasms / therapy. Neoplasms, Second Primary / etiology


57. Harousseau JL, Martinelli G, Jedrzejczak WW, Brandwein JM, Bordessoule D, Masszi T, Ossenkoppele GJ, Alexeeva JA, Beutel G, Maertens J, Vidriales MB, Dombret H, Thomas X, Burnett AK, Robak T, Khuageva NK, Golenkov AK, Tothova E, Mollgard L, Park YC, Bessems A, De Porre P, Howes AJ, FIGHT-AML-301 Investigators: A randomized phase 3 study of tipifarnib compared with best supportive care, including hydroxyurea, in the treatment of newly diagnosed acute myeloid leukemia in patients 70 years or older. Blood; 2009 Aug 6;114(6):1166-73
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 randomized phase 3 study of tipifarnib compared with best supportive care, including hydroxyurea, in the treatment of newly diagnosed acute myeloid leukemia in patients 70 years or older.
  • This phase 3, multicenter, open-label study evaluated the efficacy and safety of tipifarnib compared with best supportive care (BSC), including hydroxyurea, as first-line therapy in elderly patients (>or=70 years) with newly diagnosed, de novo, or secondary acute myeloid leukemia.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Hydroxyurea / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / mortality. Quinolones / administration & dosage

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. HYDROXYUREA .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19470696.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00093990
  • [Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinolones; 192185-72-1 / tipifarnib; X6Q56QN5QC / Hydroxyurea
  • [Investigator] Bezares R; Calahonra R; Fernandez I; Bosly J; Bries G; Bron D; Demuynck H; Ferrant A; Maertens J; Noens L; Selleslag D; Zachee P; Del Giglio; Figueiras R; Hungria V; Brandwein J; Kassis J; Sheridan D; Van der Jagt R; Mayer J; Dufva I; Juul Nielsen O; Friis L; Scholer Kristensen J; Bordessoule D; Dombret H; Fenaux P; Harousseau JL; Huguet F; Ifrah N; Pigneaux A; Quesnel B; Randriamalala E; Rossi JF; Thomas X; Vey N; Ganser A; Germing U; Hänel M; Moritz T; Niederwieser; Noppeney R; Borbényi Z; Losonczy H; Masszi T; Radványi G; Udvardy M; Conneally E; O'Dwyer M; Alimena G; Baccarani M; De Fabritiis P; Fanin R; Martinelli G; Kim I; Lee KH; Min YH; Garcés O; Plasencia A; Sobrevilla P; Vela J; Dmoszynska A; Jedrzejczak W; Kloczko J; Kuliczkowski K; Robak T; Skotnicki A; Sulek K; Alexeeva JA; Abdulkadyrov KM; Domnikova N; Dunaev YA; Gaisarova G; Gavrilenko A; Golenkov AK; Khuageva NK; Khlevnaya N; Loginov AB; Patrin VF; Pristupa A; Rossiev VA; Samoilova OS; Shneider TV; Suvorov A; Yablokova VV; Demeckova E; Tothova E; Wild A; Brunet S; Esteve J; Garcia J; Laraña; San Miguel J; Björkholm M; Mollgard L; Tidefelt U; Chou WC; Hsiao LT; Kuo CY; Lin TL; Löwenberg B; Van Marwijk Kooy M; Muus P; Ossenkoppele GJ; Schipperus MR; Schouten HC; Wittebol S; Gülbas Z; Burnett AK; Carr R; El-Agnaf M; Mufti GJ; Rudin C; Kaplan PE; Kryachok IA; Lysa I; Masliak ZV; Pylypenko HV; Stulginskaya MA; Manges RF
  •  go-up   go-down


58. Sekeres MA, Elson P, Kalaycio ME, Advani AS, Copelan EA, Faderl S, Kantarjian HM, Estey E: Time from diagnosis to treatment initiation predicts survival in younger, but not older, acute myeloid leukemia patients. Blood; 2009 Jan 1;113(1):28-36
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] Time from diagnosis to treatment initiation predicts survival in younger, but not older, acute myeloid leukemia patients.
  • Acute myeloid leukemia (AML) is considered an oncologic emergency.
  • We examined the effect of time from AML diagnosis to treatment (TDT) on complete remission (CR) and overall survival (OS), using patient characteristics available at diagnosis.
  • Regression models were applied to older (> or = 60 years) and younger (< 60 years) adults, controlling for age, baseline white blood cell count, secondary AML (sAML), and performance status.
  • AML therapy should be initiated immediately in younger patients.


59. Rubio S, Martins C, Lacerda JF, Carmo JA, Lourenço F, Lacerda JM: Allogeneic stem cell transplantation in patients with myelodysplastic syndrome: outcome analysis according to the International Prognostic Scoring System. Acta Med Port; 2006 Sep-Oct;19(5):343-7
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.
  • We determined the outcome of patients with myelodysplastic syndrome (MDS) and secondary acute myeloid leukemia (sAML) after allogeneic stem cell transplantation according to their international prognostic scoring system (IPSS) risk categories at diagnosis.
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Female. Humans. Leukemia, Myeloid / surgery. Male. Middle Aged. Prognosis. Recurrence. Risk Assessment. Treatment Outcome


60. Amare Kadam PS, Raje GC, Pais AP, Banavali S: Coexistence of ETV6/RUNX1 and MLL aberrations in B-cell precursor acute lymphoblastic leukemia discloses a small subclass of BCP-ALL. Cancer Genet Cytogenet; 2008 Apr 1;182(1):27-32
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] Coexistence of ETV6/RUNX1 and MLL aberrations in B-cell precursor acute lymphoblastic leukemia discloses a small subclass of BCP-ALL.
  • Out of 76 pediatric cases of B-cell precursor acute lymphoblastic leukemia (BCP-ALL) positive for ETV6/RUNX1 (previously TEL/AML1) resulting from t(12;21), 7 cases revealed coexistence of ETV6/RUNX1 and MLL aberrations.
  • ETV6/RUNX1 and MLL aberration clone size in these cases was suggestive of ETV6/RUNX1 as an early primary event, originating in the embryonic or infant stage and developing into leukemia by later acquisition of MLL aberration, ETV6 loss, and ETV6/RUNX1 duplication as secondary events.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18328947.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


61. Tefferi A: Novel mutations and their functional and clinical relevance in myeloproliferative neoplasms: JAK2, MPL, TET2, ASXL1, CBL, IDH and IKZF1. Leukemia; 2010 Jun;24(6):1128-38
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Beginning in early 2005, a number of novel mutations involving Janus kinase 2 (JAK2), Myeloproliferative Leukemia Virus (MPL), TET oncogene family member 2 (TET2), Additional Sex Combs-Like 1 (ASXL1), Casitas B-lineage lymphoma proto-oncogene (CBL), Isocitrate dehydrogenase (IDH) and IKAROS family zinc finger 1 (IKZF1) have been described in BCR-ABL1-negative MPNs.
  • The incidence of TET2, ASXL1, CBL, IDH or IKZF1 mutations in these disorders ranges from 0 to 17%; these latter mutations are more common in chronic (TET2, ASXL1, CBL) or juvenile (CBL) myelomonocytic leukemias, mastocytosis (TET2), myelodysplastic syndromes (TET2, ASXL1) and secondary acute myeloid leukemia, including blast-phase MPN (IDH, ASXL1, IKZF1).

  • 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
  • [Cites] Haematologica. 2007 Dec;92(12):1717-8 [18056003.001]
  • [Cites] Haematologica. 2008 Jan;93(1):34-40 [18166783.001]
  • [Cites] Leukemia. 2008 Jan;22(1):216 [17851549.001]
  • [Cites] N Engl J Med. 1976 Oct 21;295(17):913-6 [967201.001]
  • [Cites] Blood. 1981 Nov;58(5):916-9 [7296002.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1411-5 [15920487.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1207-9 [15860661.001]
  • [Cites] N Engl J Med. 2005 Sep 29;353(13):1416-7; author reply 1416-7 [16192494.001]
  • [Cites] Br J Haematol. 2005 Oct;131(2):166-71 [16197445.001]
  • [Cites] Br J Haematol. 2005 Nov;131(3):320-8 [16225651.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3377-9 [16081687.001]
  • [Cites] Lancet. 2005 Dec 3;366(9501):1945-53 [16325696.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):18962-7 [16365288.001]
  • [Cites] Cancer. 2006 Feb 1;106(3):631-5 [16369984.001]
  • [Cites] Blood. 2006 Mar 1;107(5):2098-100 [16293597.001]
  • [Cites] Leukemia. 2006 Jan;20(1):157-8 [16331280.001]
  • [Cites] Leukemia. 2006 Jun;20(6):971-8 [16598306.001]
  • [Cites] Gastroenterology. 2006 Jun;130(7):2031-8 [16762626.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1377-80 [16675710.001]
  • [Cites] J Cell Physiol. 2006 Oct;209(1):21-43 [16741904.001]
  • [Cites] Leukemia. 2006 Nov;20(11):2067-70 [16990759.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3472-6 [16868251.001]
  • [Cites] PLoS Med. 2006 Jul;3(7):e270 [16834459.001]
  • [Cites] Br J Haematol. 2006 Dec;135(5):683-7 [17107350.001]
  • [Cites] N Engl J Med. 2007 Feb 1;356(5):459-68 [17267906.001]
  • [Cites] Br J Haematol. 2007 Feb;136(4):678-9 [17223913.001]
  • [Cites] J Immunol. 2007 Mar 1;178(5):2623-9 [17312100.001]
  • [Cites] Br J Haematol. 2007 May;137(3):244-7 [17408465.001]
  • [Cites] Cancer. 2007 Jun 1;109(11):2279-84 [17440984.001]
  • [Cites] Blood. 2007 Jul 1;110(1):375-9 [17363731.001]
  • [Cites] Leukemia. 2007 Aug;21(8):1658-68 [17541402.001]
  • [Cites] Blood. 2007 Aug 1;110(3):840-6 [17379742.001]
  • [Cites] Blood. 2007 Aug 1;110(3):1004-12 [17446348.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1092-7 [17488875.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2074-5 [17476276.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1960-3 [17597810.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1952-9 [17625606.001]
  • [Cites] Stem Cells. 2007 Sep;25(9):2358-62 [17540852.001]
  • [Cites] Leukemia. 2007 Oct;21(10):2206-7 [17507998.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3735-43 [17709604.001]
  • [Cites] Blood. 2007 Dec 1;110(12):4030-6 [17712047.001]
  • [Cites] Leukemia. 2008 Jan;22(1):14-22 [17882280.001]
  • [Cites] Leukemia. 2008 Jan;22(1):23-30 [17882282.001]
  • [Cites] Leukemia. 2008 Jan;22(1):3-13 [17882283.001]
  • [Cites] Leukemia. 2008 Jan;22(1):87-95 [18033315.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1686-9 [17984312.001]
  • [Cites] Leukemia. 2008 Feb;22(2):450-1 [17851561.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2785-9 [18006699.001]
  • [Cites] Blood. 2008 Apr 15;111(8):3931-40 [18160670.001]
  • [Cites] Leukemia. 2008 Apr;22(4):870-3 [17914411.001]
  • [Cites] Leukemia. 2008 Sep;22(9):1790-2 [18354492.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1807-12 [18772396.001]
  • [Cites] Haematologica. 2008 Oct;93(10):1595-7 [18698078.001]
  • [Cites] Leukemia. 2008 Oct;22(10):1813-7 [18754026.001]
  • [Cites] Leukemia. 2008 Oct;22(10):1841-8 [18754034.001]
  • [Cites] Leukemia. 2008 Oct;22(10):1828-40 [18769448.001]
  • [Cites] Trends Cell Biol. 2008 Nov;18(11):545-51 [18848449.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Nov 4;105(44):17050-4 [18957548.001]
  • [Cites] Acta Neuropathol. 2008 Dec;116(6):597-602 [18985363.001]
  • [Cites] Leukemia. 2009 Jan;23(1):144-52 [18843287.001]
  • [Cites] Hum Mutat. 2009 Jan;30(1):7-11 [19117336.001]
  • [Cites] N Engl J Med. 2009 Feb 19;360(8):765-73 [19228619.001]
  • [Cites] Leuk Lymphoma. 2009 Feb;50(2):247-53 [19235016.001]
  • [Cites] Blood. 2009 Feb 26;113(9):2022-7 [19047681.001]
  • [Cites] Br J Haematol. 2009 Mar;144(6):904-8 [19170680.001]
  • [Cites] Leukemia. 2009 Mar;23(3):610-4 [18818701.001]
  • [Cites] J Cell Mol Med. 2009 Feb;13(2):215-37 [19175693.001]
  • [Cites] Immunol Rev. 2009 Mar;228(1):273-87 [19290934.001]
  • [Cites] Blood. 2009 Mar 26;113(13):2895-901 [18988864.001]
  • [Cites] Nat Genet. 2009 Apr;41(4):446-9 [19287382.001]
  • [Cites] Nat Genet. 2009 Apr;41(4):450-4 [19287385.001]
  • [Cites] Blood. 1978 Feb;51(2):189-94 [620081.001]
  • [Cites] Clin Cancer Res. 2009 Apr 1;15(7):2238-47 [19276253.001]
  • [Cites] Science. 2009 Apr 10;324(5924):261-5 [19359588.001]
  • [Cites] Eur J Haematol. 2009 May;82(5):329-38 [19141119.001]
  • [Cites] Leukemia. 2009 May;23(5):1008-9 [19151782.001]
  • [Cites] Leukemia. 2009 May;23(5):852-5 [19194467.001]
  • [Cites] Leukemia. 2009 May;23(5):900-4 [19262599.001]
  • [Cites] Leukemia. 2009 May;23(5):905-11 [19262601.001]
  • [Cites] Leukemia. 2009 May;23(5):834-44 [19295544.001]
  • [Cites] Science. 2009 May 15;324(5929):930-5 [19372391.001]
  • [Cites] N Engl J Med. 2009 May 28;360(22):2289-301 [19474426.001]
  • [Cites] Int J Cancer. 2009 Jul 15;125(2):353-5 [19378339.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6182-92 [19387008.001]
  • [Cites] Blood. 2009 Jun 18;113(25):6403-10 [19372255.001]
  • [Cites] Nat Genet. 2009 Jul;41(7):838-42 [19483684.001]
  • [Cites] Blood. 2009 Jul 2;114(1):144-7 [19420352.001]
  • [Cites] Leukemia. 2009 Jul;23(7):1343-5 [19295549.001]
  • [Cites] Br J Haematol. 2009 Jun;145(6):788-800 [19388938.001]
  • [Cites] Blood. 2009 Jul 30;114(5):937-51 [19357394.001]
  • [Cites] Leukemia. 2009 Aug;23(8):1441-5 [19295546.001]
  • [Cites] Nature. 2009 Aug 13;460(7257):904-8 [19620960.001]
  • [Cites] J Clin Oncol. 2009 Aug 20;27(24):4002-6 [19528370.001]
  • [Cites] Blood. 2009 Aug 20;114(8):1477-83 [19549988.001]
  • [Cites] Blood. 2009 Aug 27;114(9):1859-63 [19571318.001]
  • [Cites] J Clin Oncol. 2009 Sep 1;27(25):4150-4 [19636000.001]
  • [Cites] Acta Neuropathol. 2009 Oct;118(4):469-74 [19554337.001]
  • [Cites] N Engl J Med. 2009 Sep 10;361(11):1058-66 [19657110.001]
  • [Cites] N Engl J Med. 2009 Sep 10;361(11):1117; author reply 1117-8 [19741235.001]
  • [Cites] Leukemia. 2003 Mar;17(3):637-41 [12646957.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Jun;37(2):214-9 [12696071.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 3;101(31):11444-7 [15269348.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] J Clin Oncol. 2009 Dec 20;27(36):6109-16 [19901108.001]
  • [Cites] Am J Hematol. 2010 Jan;85(1):81-3 [19957346.001]
  • [Cites] J Biol Chem. 2010 Jan 1;285(1):18-29 [19880879.001]
  • [Cites] Blood. 2010 Jan 7;115(1):38-46 [19861679.001]
  • [Cites] Haematologica. 2010 Jan;95(1):65-70 [19713221.001]
  • [Cites] Leukemia. 2010 Jan;24(1):201-3 [19710701.001]
  • [Cites] Leukemia. 2010 Jan;24(1):110-4 [19847198.001]
  • [Cites] Leukemia. 2010 Jan;24(1):105-9 [19847199.001]
  • [Cites] Cancer Res. 2010 Jan 15;70(2):447-52 [20068184.001]
  • [Cites] N Engl J Med. 2010 Jan 28;362(4):369-70 [20107228.001]
  • [Cites] Blood. 2010 Jan 28;115(4):778-82 [19965680.001]
  • [Cites] Blood. 2010 Feb 4;115(5):1037-48 [19996410.001]
  • [Cites] Leukemia. 2010 Feb;24(2):469-73 [19865112.001]
  • [Cites] Blood. 2010 Feb 11;115(6):1254-63 [19880496.001]
  • [Cites] J Biol Chem. 2010 Feb 19;285(8):5296-307 [20028972.001]
  • [Cites] J Exp Med. 2010 Feb 15;207(2):339-44 [20142433.001]
  • [Cites] Hum Mutat. 2010 Mar;31(3):E1186-99 [20077503.001]
  • [Cites] J Clin Endocrinol Metab. 2010 Mar;95(3):1274-8 [19915015.001]
  • [Cites] Haematologica. 2010 Mar;95(3):518-9 [19903679.001]
  • [Cites] Blood. 2010 Mar 11;115(10):1969-75 [20008299.001]
  • [Cites] Blood. 2010 Mar 11;115(10):2003-7 [20061559.001]
  • [Cites] Cancer Cell. 2010 Mar 16;17(3):225-34 [20171147.001]
  • [Cites] Acta Neuropathol. 2010 Apr;119(4):487-94 [20127344.001]
  • [Cites] Hum Mol Genet. 2010 Apr 15;19(8):1507-14 [20093295.001]
  • [Cites] Blood. 2010 Apr 8;115(14):2891-900 [20008300.001]
  • [Cites] Leukemia. 2010 Apr;24(4):859-60 [20111067.001]
  • [Cites] Blood. 2010 Apr 29;115(17):3589-97 [20197548.001]
  • [Cites] Leukemia. 2010 May;24(5):1069-73 [20182460.001]
  • [Cites] Leukemia. 2010 Jun;24(6):1146-51 [20410924.001]
  • [Cites] Leukemia. 2008 Apr;22(4):740-7 [18079739.001]
  • [Cites] Leukemia. 2008 Apr;22(4):756-61 [18216871.001]
  • [Cites] Nature. 2008 May 1;453(7191):110-4 [18408710.001]
  • [Cites] Leuk Lymphoma. 2008 May;49(5):847-9 [18464105.001]
  • [Cites] Leukemia. 2008 May;22(5):1059-62 [17972958.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1295-8 [18059483.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1289 [18079740.001]
  • [Cites] Blood. 2008 Jul 1;112(1):141-9 [18451306.001]
  • [Cites] Leukemia. 2008 Jul;22(7):1472-4 [18239619.001]
  • [Cites] Leukemia. 2008 Jul;22(7):1299-307 [18496562.001]
  • [Cites] Blood. 2008 Aug 1;112(3):844-7 [18519816.001]
  • [Cites] Blood. 2008 Aug 15;112(4):1402-12 [18515659.001]
  • [Cites] Leukemia. 2008 Aug;22(8):1557-66 [18528423.001]
  • [Cites] Blood. 2008 Sep 15;112(6):2199-204 [18451307.001]
  • [Cites] Blood. 2008 Sep 15;112(6):2429-38 [18612101.001]
  • [Cites] Int J Cancer. 2009 Nov 15;125(10):2485-6 [19530255.001]
  • [Cites] Blood. 2009 Oct 1;114(14):3018-23 [19541820.001]
  • [Cites] Clin Cancer Res. 2009 Oct 1;15(19):6002-7 [19755387.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Sep 29;106(39):16616-21 [19805346.001]
  • [Cites] Nature. 2009 Oct 8;461(7265):819-22 [19783980.001]
  • [Cites] Blood. 2009 Oct 8;114(15):3285-91 [19666869.001]
  • [Cites] Leukemia. 2009 Oct;23(10):1924-6 [19440215.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2009 Nov;297(5):H1545-56 [19717737.001]
  • [Cites] N Engl J Med. 2009 Nov 5;361(19):1872-85 [19890130.001]
  • [Cites] Blood. 2009 Nov 5;114(19):4197-208 [19734451.001]
  • [Cites] Leukemia. 2009 Nov;23(11):2183-6 [19609284.001]
  • [Cites] J Clin Oncol. 2009 Dec 1;27(34):5743-50 [19805672.001]
  • [Cites] Haematologica. 2009 Dec;94(12):1676-81 [19797729.001]
  • [Cites] J Clin Oncol. 2009 Dec 10;27(35):5874-80 [19901110.001]
  • [Cites] Nature. 2009 Dec 10;462(7274):739-44 [19935646.001]
  • (PMID = 20428194.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ASXL1 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / IKZF1 protein, human; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Thrombopoietin; 0 / Repressor Proteins; 0 / TET2 protein, human; 143641-95-6 / MPL protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Number-of-references] 171
  • [Other-IDs] NLM/ PMC3035972
  •  go-up   go-down


62. Stanulla M, Dynybil C, Bartels DB, Dördelmann M, Löning L, Claviez A, Schrappe M, ALL-BFM study group: The NQO1 C609T polymorphism is associated with risk of secondary malignant neoplasms after treatment for childhood acute lymphoblastic leukemia: a matched-pair analysis from the ALL-BFM study group. Haematologica; 2007 Nov;92(11):1581-2
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 NQO1 C609T polymorphism is associated with risk of secondary malignant neoplasms after treatment for childhood acute lymphoblastic leukemia: a matched-pair analysis from the ALL-BFM study group.
  • In a matched-pair study, we analyzed the association of a phenotypically relevant NQO1 polymorphism (C609T) with risk of secondary malignant neoplasms (SMN) after treatment for childhood acute lymphoblastic leukemia.
  • [MeSH-major] NAD(P)H Dehydrogenase (Quinone) / genetics. Neoplasms, Second Primary / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18024413.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; PVDA protocol
  •  go-up   go-down


63. Hatzistilianou M, Rekleity A, Athanassiadou F, DeLutiis MA, Conti P, Catriu D: Serial procalcitonin responses in infection of children with secondary immunodeficiency. Clin Invest Med; 2007;30(2):E75-85
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] Serial procalcitonin responses in infection of children with secondary immunodeficiency.
  • PURPOSE: Procalcitonin has proven to be a sensitive inflammatory marker in non-neutropenic patients.
  • The aim of this study was to determine and compare Procalcitonin with other inflammatory markers in the serum of immunosuppressed children with haematological malignancies; and to assess the predictive value of these mediators in distinguishing between bacterial and non-bacterial infection.
  • METHODS & RESULTS: The study included 37 children with acute lymphoblastic leukaemia undergoing intensive chemotherapy.
  • Group A consisted of 29 neutropenic children with 94 febrile episodes, group B of 20 neutropenic children with 56 afebrile episodes and group C of 13 non-neutropenic children with 58 afebrile episodes.
  • The markers, C-Reactive Protein, Interleukin-6 and NO2/NO3 may not help to identify infections and distinguish the etiology of infection in neutropenic febrile children with acute lymphoblastic leukaemia.
  • [MeSH-major] Bacterial Infections / blood. Calcitonin / blood. Immune Tolerance / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Precursors / blood

  • MedlinePlus Health Information. consumer health - Bacterial Infections.
  • Hazardous Substances Data Bank. Calcitonin .
  • 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 = 17716545.001).
  • [ISSN] 1488-2353
  • [Journal-full-title] Clinical and investigative medicine. Médecine clinique et experimentale
  • [ISO-abbreviation] Clin Invest Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Protein Precursors; 56645-65-9 / procalcitonin; 670-65-5 / Neopterin; 9007-12-9 / Calcitonin; 9007-41-4 / C-Reactive Protein
  •  go-up   go-down


64. Yesilipek MA, Karasu GT, Kupesiz A, Uygun V, Hazar V: Better posttransplant outcome with fludarabine based conditioning in multitransfused fanconi anemia patients who underwent peripheral blood stem cell transplantation. J Pediatr Hematol Oncol; 2009 Jul;31(7):512-5
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.
  • We lost 3 patients in regimen A group and 1 of them from secondary acute myeloid leukemia.

  • Genetic Alliance. consumer health - Fanconi Anemia.
  • Genetic Alliance. consumer health - Anemia.
  • Genetic Alliance. consumer health - Transplantation.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19564748.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  •  go-up   go-down


65. Wiemels JL, Hofmann J, Kang M, Selzer R, Green R, Zhou M, Zhong S, Zhang L, Smith MT, Marsit C, Loh M, Buffler P, Yeh RF: Chromosome 12p deletions in TEL-AML1 childhood acute lymphoblastic leukemia are associated with retrotransposon elements and occur postnatally. Cancer Res; 2008 Dec 1;68(23):9935-44
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromosome 12p deletions in TEL-AML1 childhood acute lymphoblastic leukemia are associated with retrotransposon elements and occur postnatally.
  • This translocation has been detected at a high rate among newborns ( approximately 1%); therefore, the rate-limiting event for leukemia seems to be secondary mutations.
  • Nine del(12p) breakpoints within six leukemia cases were sequenced to explore the etiology of this genetic event, and most involved cryptic sterile translocations.
  • An exploratory assessment of archived neonatal blood cards revealed significantly more long interspersed nuclear element CpG methylations in individuals at birth who were later diagnosed with TEL-AML1 leukemia, compared with individuals who did not contract leukemia (P=0.01).

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2003 Oct 1;102(7):2321-33 [12791663.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4640-1 [12756163.001]
  • [Cites] EMBO J. 2004 Jan 14;23(1):138-49 [14685282.001]
  • [Cites] Nature. 2004 Mar 4;428(6978):88-93 [14999286.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4275-83 [15156184.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 1;101(22):8443-8 [15155899.001]
  • [Cites] Mol Cells. 2004 Apr 30;17(2):217-22 [15179033.001]
  • [Cites] Leukemia. 2004 Sep;18(9):1499-504 [15284860.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Sep 17;322(2):623-30 [15325275.001]
  • [Cites] Clin Cancer Res. 2004 Aug 15;10(16):5355-60 [15328172.001]
  • [Cites] Nucleic Acids Res. 1988 Jun 24;16(12):5533-56 [2838820.001]
  • [Cites] Biochemistry. 1993 Nov 30;32(47):12782-92 [7504526.001]
  • [Cites] Blood. 1996 Apr 1;87(7):2891-9 [8639909.001]
  • [Cites] Mol Cell Biol. 1997 Jun;17(6):3125-36 [9154811.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4584-8 [9539781.001]
  • [Cites] Blood. 1999 Jan 1;93(1):293-9 [9864173.001]
  • [Cites] Leukemia. 1999 Feb;13(2):196-205 [10025893.001]
  • [Cites] Blood. 1999 Aug 1;94(3):1057-62 [10419898.001]
  • [Cites] Cancer Res. 1999 Aug 15;59(16):4075-82 [10463610.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):305-19 [16075461.001]
  • [Cites] Oncogene. 2005 Nov 3;24(48):7213-23 [16170379.001]
  • [Cites] Clin Cancer Res. 2005 Nov 1;11(21):7720-7 [16278392.001]
  • [Cites] Nucleic Acids Res. 2005;33(21):6823-36 [16326863.001]
  • [Cites] Nat Rev Cancer. 2006 Mar;6(3):193-203 [16467884.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Oct 10;103(41):15166-71 [17015828.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1258-66 [17443227.001]
  • [Cites] Oncogene. 2007 Jun 28;26(30):4404-14 [17237815.001]
  • [Cites] Blood. 2008 Jan 15;111(2):776-84 [17890455.001]
  • [Cites] Nucleic Acids Res. 2008 Feb;36(3):770-84 [18084025.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Mar;15(3):578-81 [16537719.001]
  • [Cites] J Mol Biol. 2006 Apr 14;357(5):1383-93 [16490214.001]
  • [Cites] BMC Cancer. 2006;6:100 [16630339.001]
  • [Cites] Lancet. 1999 Oct 30;354(9189):1499-503 [10551495.001]
  • [Cites] Gene. 1999 Nov 29;240(2):297-305 [10580149.001]
  • [Cites] Genes Chromosomes Cancer. 2000 Nov;29(3):219-28 [10992297.001]
  • [Cites] Nature. 2001 Feb 15;409(6822):860-921 [11237011.001]
  • [Cites] Leukemia. 2001 May;15(5):858-9 [11368451.001]
  • [Cites] Blood. 2001 Jul 15;98(2):478-82 [11435320.001]
  • [Cites] Nature. 2001 Jul 19;412(6844):341-6 [11460166.001]
  • [Cites] Blood. 2001 Aug 1;98(3):558-64 [11468150.001]
  • [Cites] Nucleic Acids Res. 2001 Nov 1;29(21):4493-501 [11691937.001]
  • [Cites] Nucleic Acids Res. 2002 Jan 1;30(1):372-4 [11752340.001]
  • [Cites] Genes Dev. 2002 Jan 1;16(1):6-21 [11782440.001]
  • [Cites] Mol Cell Biol. 2002 Apr;22(7):2068-77 [11884595.001]
  • [Cites] Eur J Hum Genet. 2002 Jan;10(1):62-71 [11896457.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8242-7 [12048236.001]
  • [Cites] Oncogene. 2002 Aug 12;21(35):5400-13 [12154403.001]
  • [Cites] Leuk Res. 2003 Feb;27(2):155-64 [12526921.001]
  • [Cites] Genes Chromosomes Cancer. 2003 May;37(1):36-43 [12661004.001]
  • [Cites] Science. 2003 Apr 18;300(5618):489-92 [12702876.001]
  • [Cites] Genes Chromosomes Cancer. 2004 Feb;39(2):156-60 [14695996.001]
  • (PMID = 19047175.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P42-ES04705; United States / NCI NIH HHS / CA / R01 CA089032; United States / NCI NIH HHS / CA / R01 CA089032-04A1; United States / NCI NIH HHS / CA / R01 CA089032-06; United States / NCI NIH HHS / CA / CA89032; United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / R01 ES09137; United States / NCI NIH HHS / CA / CA089032-04A1; United States / NCI NIH HHS / CA / R01 CA089032-05; United States / NIEHS NIH HHS / ES / R01 ES009137
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Retroelements; 0 / TEL-AML1 fusion protein
  • [Other-IDs] NLM/ NIHMS74688; NLM/ PMC2597307
  •  go-up   go-down


66. Forestier E, Andersen MK, Autio K, Blennow E, Borgström G, Golovleva I, Heim S, Heinonen K, Hovland R, Johannsson JH, Kerndrup G, Nordgren A, Rosenquist R, Swolin B, Johansson B, Nordic Society of Pediatric Hematology and Oncology (NOPHO), Swedish Cytogenetic Leukemia Study Group (SCLSG), NOPHO Leukemia Cytogenetic Study Group (NLCSG): Cytogenetic patterns in ETV6/RUNX1-positive pediatric B-cell precursor acute lymphoblastic leukemia: A Nordic series of 245 cases and review of the literature. Genes Chromosomes Cancer; 2007 May;46(5):440-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic patterns in ETV6/RUNX1-positive pediatric B-cell precursor acute lymphoblastic leukemia: A Nordic series of 245 cases and review of the literature.
  • Between 1992 and 2004, 1,140 children (1 to<15 years) were diagnosed with B-cell precursor acute lymphoblastic leukemia (ALL) in the Nordic countries.
  • Secondary chromosomal abnormalities were identified by chromosome banding in 248 (62%) of the 397 ALLs.
  • The numbers of secondary changes varied between 1 and 19, with a median of 2 additional aberrations per cytogenetically abnormal case.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Leukemia, Lymphoid / genetics. Transcription Factors / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • MedlinePlus Health Information. consumer health - Chronic Lymphocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17285576.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [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 / ETV1 protein, human; 0 / RUNX1 protein, human; 0 / Transcription Factors
  •  go-up   go-down


67. Sindt A, Deau B, Brahim W, Staal A, Visanica S, Villarese P, Rault JP, Macintyre E, Delabesse E: Acute monocytic leukemia with coexpression of minor BCR-ABL1 and PICALM-MLLT10 fusion genes along with overexpression of HOXA9. Genes Chromosomes Cancer; 2006 Jun;45(6):575-82
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute monocytic leukemia with coexpression of minor BCR-ABL1 and PICALM-MLLT10 fusion genes along with overexpression of HOXA9.
  • The t(9;22)(q34;q11) translocation occurs in chronic myeloid leukemia (CML) and adult B-cell acute lymphoblastic leukemia (ALL), leading to fusion of BCR to ABL1 and constitutive activation of ABL1 tyrosine kinase activity.
  • We describe here the first case of t(9;22)(q34;q11) associated with t(10;11)(p13;q14) in acute monocytic leukemia.
  • The recurrent t(10;11)(p13;q14) translocation, usually found in acute myeloid leukemia (AML) and T-ALL, merges PICALM to MLLT10.
  • RT-PCR enabled identification of PICALM-MLLT10 and BCR-ABL1 e1-a2 fusion transcripts; in the context of chronic and acute myeloid leukemia, the latter usually has a monocytic presentation.
  • We also identified overexpression of HOXA9, a gene essential to myeloid differentiation that is expressed in PICALM-MLLT10 and MLL-rearranged acute leukemias.
  • This case fits with and extends a recently proposed multistage AML model in which constitutive activation of tyrosine kinases by mutations (BCR-ABL1) are associated with deregulation of transcription factors central to myeloid differentiation (HOXA9 secondary to PICALM-MLLT10).
  • [MeSH-major] Fusion Proteins, bcr-abl / metabolism. Gene Expression Regulation, Neoplastic. Homeodomain Proteins / metabolism. Leukemia, Monocytic, Acute / genetics. Oncogene Proteins, Fusion / metabolism

  • 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
  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16518848.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MLLT10 protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / PICALM-MLLT10 fusion protein, human; 0 / Transcription Factors; 0 / homeobox protein HOXA9; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down


68. Tangen JM, Fløisand Y, Foss-Abrahamsen J, Haukås E, Naess IA, Skjelbakken T: [Survival in adults with acute myelogenous leukemia]. Tidsskr Nor Laegeforen; 2008 May 15;128(10):1164-7
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] [Survival in adults with acute myelogenous leukemia].
  • BACKGROUND: Acute myelogenous leukemia is the most common type of acute leukemia in adults.
  • MATERIAL AND METHODS: Survival data were retrieved from the Norwegian Registry for Acute Leukemias and Lymphoblastic Lymphomas for patients with acute myelogenous leukemia (aged from 16 to 60 years) who were registered in the period 1.1.2000-31.12.2005.
  • Patients with secondary acute myelogenous leukemia were classified as high-risk.
  • RESULTS AND INTERPRETATION: 4-year survival was 94.5% in acute promyelocytic leukemia, 77.7% in other low-risk acute myelogenous leukemia, 39.0% in standard risk patients and 29.1% in high-risk patients.
  • The increase is most probably due to an intensification of chemotherapy after remission and to the implementation of all-trans-retinoic acid in the treatment of promyelocytic leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality
  • [MeSH-minor] Adolescent. Adult. Age Factors. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Female. Humans. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / mortality. Male. Middle Aged. Neoplasm Recurrence, Local / mortality. Norway / epidemiology. Risk Factors. Survival Rate

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Tidsskr Nor Laegeforen. 2008 Aug 14;128(15):1681-2; author reply 1682 [18704137.001]
  • (PMID = 18480864.001).
  • [ISSN] 0807-7096
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Norway
  •  go-up   go-down


69. Jazbec J, Todorovski L, Jereb B: Classification tree analysis of second neoplasms in survivors of childhood cancer. BMC Cancer; 2007;7:27
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.
  • BACKGROUND: Reports on childhood cancer survivors estimated cumulative probability of developing secondary neoplasms vary from 3.3% to 25% at 25 years from diagnosis, and the risk of developing another cancer to several times greater than in the general population.
  • METHODS: In our retrospective study, we have used the classification tree multivariate method on a group of 849 first cancer survivors, to identify childhood cancer patients with the greatest risk for development of secondary neoplasms.
  • RESULTS: In observed group of patients, 34 develop secondary neoplasm after treatment of primary cancer.
  • Analysis of parameters present at the treatment of first cancer, exposed two groups of patients at the special risk for secondary neoplasm.
  • Second group at special risk were male patients with acute lymphoblastic leukemia who were treated at the age between 4.6 and 6.6 years of age.

  • Genetic Alliance. consumer health - Childhood Cancer.
  • MedlinePlus Health Information. consumer health - Cancer in Children.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Cancer Res. 1999 Nov;5(11):3403-10 [10589751.001]
  • [Cites] J Clin Oncol. 1998 Aug;16(8):2848-53 [9704738.001]
  • [Cites] Blood. 2000 May 1;95(9):2770-5 [10779419.001]
  • [Cites] J Natl Cancer Inst. 2001 Apr 18;93(8):618-29 [11309438.001]
  • [Cites] Oncology. 2001;61(4):275-83 [11721174.001]
  • [Cites] Front Radiat Ther Oncol. 2002;37:84-91 [11764672.001]
  • [Cites] J Med Syst. 2002 Oct;26(5):445-63 [12182209.001]
  • [Cites] Cancer Causes Control. 2002 Nov;13(9):813-23 [12462546.001]
  • [Cites] Pediatr Hematol Oncol. 2003 Mar;20(2):89-101 [12554520.001]
  • [Cites] Arch Otolaryngol Head Neck Surg. 2004 Jan;130(1):98-104 [14732777.001]
  • [Cites] Dis Markers. 2003-2004;19(1):33-9 [14757945.001]
  • [Cites] Pediatr Blood Cancer. 2004 Jun;42(7):574-81 [15127411.001]
  • [Cites] J Theor Biol. 2004 Jun 21;228(4):477-96 [15178197.001]
  • [Cites] Acta Radiol Ther Phys Biol. 1973 Apr;12(2):84-106 [4353752.001]
  • [Cites] J Clin Oncol. 1991 Sep;9(9):1639-49 [1651996.001]
  • [Cites] N Engl J Med. 1991 Nov 7;325(19):1330-6 [1922234.001]
  • [Cites] J Clin Oncol. 1995 Mar;13(3):603-9 [7884422.001]
  • [Cites] N Engl J Med. 1996 Mar 21;334(12):745-51 [8592547.001]
  • [Cites] Med Pediatr Oncol. 2000 Apr;34(4):256-8 [10742062.001]
  • (PMID = 17270060.001).
  • [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
  • [Other-IDs] NLM/ PMC1802085
  •  go-up   go-down


70. Kuptsova-Clarkson N, Ambrosone CB, Weiss J, Baer MR, Sucheston LE, Zirpoli G, Kopecky KJ, Ford L, Blanco J, Wetzler M, Moysich KB: XPD DNA nucleotide excision repair gene polymorphisms associated with DNA repair deficiency predict better treatment outcomes in secondary acute myeloid leukemia. Int J Mol Epidemiol Genet; 2010;1(4):278-94
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] XPD DNA nucleotide excision repair gene polymorphisms associated with DNA repair deficiency predict better treatment outcomes in secondary acute myeloid leukemia.
  • We evaluated these polymorphisms and XPD haplotypes in adult de novo (n=214) and secondary (n=79) acute myeloid leukemia (AML) patients treated with cytarabine and anthracycline chemotherapy.
  • Differential responses were observed in secondary, but not de novo, AML.
  • Among secondary AML patients, the odds of achieving complete remission (CR) were higher for the XPD 312Asn/Asn (OR= 11.23; 95% CI, 2.23-56.63) and XPD 751Gln/Gln (OR= 7.07; 95% CI, 1.42-35.18) genotypes.
  • If validated, these findings could support stratification of chemotherapy in secondary AML.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21394217.001).
  • [ISSN] 1948-1756
  • [Journal-full-title] International journal of molecular epidemiology and genetics
  • [ISO-abbreviation] Int J Mol Epidemiol Genet
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA108353-02; United States / NCI NIH HHS / CA / R03 CA108353; United States / NCI NIH HHS / CA / CA108353-01; United States / NCI NIH HHS / CA / R03 CA108353-02; United States / NCI NIH HHS / CA / R03 CA108353-01
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS247623; NLM/ PMC3049908
  • [Keywords] NOTNLM ; Acute Myeloid Leukemia (AML) / DNA repair gene polymorphisms / pharmacogenetics/pharmacogenomics / secondary AML
  •  go-up   go-down


71. Ferrara F, Palmieri S, Izzo T, Criscuolo C, Riccardi C: Continuous sequential infusion of fludarabine and cytarabine for elderly patients with acute myeloid leukaemia secondary to a previously diagnosed myelodysplastic syndrome. Hematol Oncol; 2010 Dec;28(4):202-8
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] Continuous sequential infusion of fludarabine and cytarabine for elderly patients with acute myeloid leukaemia secondary to a previously diagnosed myelodysplastic syndrome.
  • Acute myeloid leukaemia (AML) secondary to myelodysplastic syndrome (MDS) is characterized by poor prognosis, namely in older patients.
  • The combination of fludarabine (F) with cytarabine (ARA-C) ± G-CSF was proven as effective in patients with poor risk AML.
  • The efficacy and toxicity of a regimen including F + ARA-C as sequential continuous infusion (CI-FLA) in 64 untreated patients aged >60 years, in which AML arose after a previous MDS, was investigated.
  • CI-FLA is effective in elderly patients with AML secondary to previously diagnosed MDS.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / complications
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Combined Modality Therapy. Cytarabine / administration & dosage. Cytarabine / adverse effects. Diarrhea / chemically induced. Disease-Free Survival. Female. Humans. Infusions, Intravenous. Male. Middle Aged. Remission Induction. Transplantation, Autologous. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / adverse effects. Vidarabine / analogs & derivatives


72. Allen SL, Kolitz JE, Lundberg AS, Bennett JM, Capizzi RL, Budman DR: Phase I trials of amonafide as monotherapy and in combination with cytarabine in patients with poor-risk acute myeloid leukemia. Leuk Res; 2010 Apr;34(4):487-91
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trials of amonafide as monotherapy and in combination with cytarabine in patients with poor-risk acute myeloid leukemia.
  • Amonafide-l-malate (amonafide) is a unique DNA intercalator that maintains activity in the presence of MDR mechanisms, a frequent cause of treatment-failure in secondary AML.
  • 43 patients with relapsed/refractory or secondary AML or CML blast crisis were enrolled into two phase I dose-escalation studies investigating amonafide as monotherapy or in combination with cytarabine.
  • Between both trials responses occurred in 9/20 patients with secondary AML.
  • Both trials demonstrated an acceptable safety profile and significant antileukemic activity in patients with poor-risk AML, especially those with secondary AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Naphthalimides / administration & dosage

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19748672.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Naphthalimides; 04079A1RDZ / Cytarabine; 1Q8D39N37L / amonafide
  •  go-up   go-down


73. Mittal R, Ramaswamy NV, Pandita R, Al Bahar S, Khalifa N, Omar S: Secondary acute myeloid leukemia after successful treatment for osteosarcoma. Indian J Med Paediatr Oncol; 2010 Jan;31(1):33-5
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] Secondary acute myeloid leukemia after successful treatment for osteosarcoma.
  • Secondary acute myeloid leukemia (sAML) is a rare complication following chemotherapy for osteogenic sarcoma.
  • Eight months after completion of therapy, while on follow-up, he presented with leukocytosis and thrombocytopenia and confirmed to have AML.

  • 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 = 20931020.001).
  • [ISSN] 0975-2129
  • [Journal-full-title] Indian journal of medical and paediatric oncology : official journal of Indian Society of Medical & Paediatric Oncology
  • [ISO-abbreviation] Indian J Med Paediatr Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2941602
  • [Keywords] NOTNLM ; Acute myeloid leukemia / chemotherapy / osteosarcoma / secondary malignancy
  •  go-up   go-down


74. Tavernier E, Le QH, de Botton S, Dhédin N, Bulabois CE, Reman O, Vey N, Lhéritier V, Dombret H, Thomas X: Secondary or concomitant neoplasms among adults diagnosed with acute lymphoblastic leukemia and treated according to the LALA-87 and LALA-94 trials. Cancer; 2007 Dec 15;110(12):2747-55
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary or concomitant neoplasms among adults diagnosed with acute lymphoblastic leukemia and treated according to the LALA-87 and LALA-94 trials.
  • BACKGROUND: Second malignant neoplasms are a serious complication after successful treatment of childhood acute lymphoblastic leukemia (ALL).
  • RESULTS: By February 2005 secondary or concomitant neoplasms were documented in 23 patients, including 9 acute myeloid leukemias (AML) or myelodysplasias (MDS), 4 non-Hodgkin lymphomas (NHL), 5 skin tumors, and 5 other solid tumors (1 lung cancer, 1 tongue carcinoma, 1 thymoma, 1 condrosarcoma, 1 histiocytosis).
  • The overall cumulative risk of secondary neoplasms was 2.1% at 5 years, 4.9% at 10 years, and 9.4% at 15 years.
  • The development of secondary neoplasm was not associated with the use of any specific cytotoxic agent.
  • However, the median OS in patients developing AML/MDS was 5.7 months.
  • The risk of secondary or concomitant neoplasm appeared higher than that of childhood ALL previously reported in the literature.
  • [MeSH-major] Neoplasms, Second Primary / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


75. Buonamici S, Trimarchi T, Ruocco MG, Reavie L, Cathelin S, Mar BG, Klinakis A, Lukyanov Y, Tseng JC, Sen F, Gehrie E, Li M, Newcomb E, Zavadil J, Meruelo D, Lipp M, Ibrahim S, Efstratiadis A, Zagzag D, Bromberg JS, Dustin ML, Aifantis I: CCR7 signalling as an essential regulator of CNS infiltration in T-cell leukaemia. Nature; 2009 Jun 18;459(7249):1000-4
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.
  • T-cell acute lymphoblastic leukaemia (T-ALL) is a blood malignancy afflicting mainly children and adolescents.
  • Such complications include secondary tumours, neurocognitive deficits, endocrine disorders and growth impairment.

  • COS Scholar Universe. author profiles.
  • 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).
  • 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] Nature. 2001 Mar 1;410(6824):50-6 [11242036.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Feb 17;106(7):2359-64 [19174523.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8389-94 [12829791.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):451-61 [14706337.001]
  • [Cites] Nature. 2004 Jan 8;427(6970):154-9 [14712275.001]
  • [Cites] Ann Neurol. 2004 May;55(5):627-38 [15122702.001]
  • [Cites] Curr Opin Immunol. 2004 Aug;16(4):406-17 [15245733.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11400-6 [8876147.001]
  • [Cites] J Exp Med. 1999 Feb 1;189(3):451-60 [9927507.001]
  • [Cites] Cell. 1999 Oct 1;99(1):23-33 [10520991.001]
  • [Cites] Annu Rev Immunol. 2005;23:127-59 [15771568.001]
  • [Cites] Nat Immunol. 2005 Jul;6(7):707-14 [15924144.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] N Engl J Med. 2006 Feb 9;354(6):610-21 [16467548.001]
  • [Cites] Nat Rev Cancer. 2006 May;6(5):347-59 [16612405.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 2;103(18):7006-11 [16641096.001]
  • [Cites] J Nucl Med. 2006 Jul;47(7):1136-43 [16818948.001]
  • [Cites] Nat Med. 2007 Jan;13(1):70-7 [17173050.001]
  • [Cites] Cancer Cell. 2007 Jun;11(6):526-38 [17560334.001]
  • [Cites] N Engl J Med. 2007 Jun 21;356(25):2622-9 [17582072.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Lancet Oncol. 2008 Mar;9(3):257-68 [18308251.001]
  • [Cites] Nat Rev Immunol. 2008 May;8(5):362-71 [18379575.001]
  • [Cites] Nat Rev Immunol. 2008 May;8(5):380-90 [18421304.001]
  • [Cites] J Leukoc Biol. 2008 Sep;84(3):587-94 [18467654.001]
  • [Cites] J Leukoc Biol. 2003 May;73(5):584-90 [12714572.001]
  • (PMID = 19536265.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016087; United States / NCI NIH HHS / CA / P01 CA097403; United States / NCI NIH HHS / CA / R01 CA133379; United States / NIAID NIH HHS / AI / R56AI070310; United States / NCI NIH HHS / CA / R01CA133379; United States / NIAID NIH HHS / AI / R01 AI062765; United States / NCI NIH HHS / CA / R01 CA149655; United States / NCI NIH HHS / CA / R01 CA105129; United States / NIAID NIH HHS / AI / R01AI072039; United States / NIAID NIH HHS / AI / R01 AI072039; United States / NCI NIH HHS / CA / R21 CA141399; United States / NIAID NIH HHS / AI / R56 AI041428; United States / NIAID NIH HHS / AI / R56 AI072039; United States / NIAID NIH HHS / AI / R01 AI041428; United States / NIAID NIH HHS / AI / R01AI41428; United States / NCI NIH HHS / CA / R01CA105129; United States / NIAID NIH HHS / AI / R56 AI070310; United States / NCI NIH HHS / CA / P30CA016087; United States / NCI NIH HHS / CA / 1 P01 CA97403; United States / NIAID NIH HHS / AI / R21 AI041428
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCR7 protein, human; 0 / Ccl19 protein, mouse; 0 / Ccr7 protein, mouse; 0 / Chemokine CCL19; 0 / Chemokine CCL21; 0 / Receptor, Notch1; 0 / Receptors, CCR7
  • [Other-IDs] NLM/ NIHMS488881; NLM/ PMC3750496
  •  go-up   go-down


76. Wong SF: New dosing schedules of dasatinib for CML and adverse event management. J Hematol Oncol; 2009;2:10
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.
  • Resistance to imatinib in patients with chronic myelogenous leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) has emerged as a significant clinical issue.
  • Dasatinib is a tyrosine kinase inhibitor that has 325-fold greater in vitro activity against native BCR-ABL (breakpoint cluster region-Abelson leukemia virus) compared with imatinib and can overcome primary (intrinsic) and secondary (acquired) imatinib resistance.
  • [MeSH-major] Drug-Related Side Effects and Adverse Reactions / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Pyrimidines / administration & dosage. Pyrimidines / adverse effects. Thiazoles / administration & dosage. Thiazoles / adverse effects

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Drug Reactions.
  • COS Scholar Universe. author profiles.
  • Chapman University Digital Commons. Full Text from .
  • 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
  • [Cites] Leukemia. 2002 Nov;16(11):2190-6 [12399961.001]
  • [Cites] Oncogene. 2002 Nov 21;21(53):8075-88 [12444544.001]
  • [Cites] Blood. 2003 Jan 15;101(2):473-5 [12393385.001]
  • [Cites] Blood. 2003 Jan 15;101(2):690-8 [12509383.001]
  • [Cites] N Engl J Med. 2003 Mar 13;348(11):994-1004 [12637609.001]
  • [Cites] J Clin Oncol. 2003 Jun 1;21(11):2138-46 [12775739.001]
  • [Cites] Clin Cancer Res. 2003 Jun;9(6):2092-7 [12796373.001]
  • [Cites] Cancer. 2004 Jun 15;100(12):2592-7 [15197801.001]
  • [Cites] Science. 2004 Jul 16;305(5682):399-401 [15256671.001]
  • [Cites] Nat Med. 1996 May;2(5):561-6 [8616716.001]
  • [Cites] N Engl J Med. 1999 Apr 29;340(17):1330-40 [10219069.001]
  • [Cites] N Engl J Med. 1999 Jul 15;341(3):164-72 [10403855.001]
  • [Cites] J Med Chem. 2004 Dec 30;47(27):6658-61 [15615512.001]
  • [Cites] Cancer. 2005 Apr 15;103(8):1659-69 [15747376.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4500-5 [15930265.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9185-9 [16230377.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2005;:118-22 [16304368.001]
  • [Cites] Cancer Res. 2006 Jan 1;66(1):473-81 [16397263.001]
  • [Cites] CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30 [16514137.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2531-41 [16775234.001]
  • [Cites] Blood. 2006 Jul 15;108(2):465-72 [16556888.001]
  • [Cites] Expert Opin Emerg Drugs. 2006 Nov;11(4):651-64 [17064224.001]
  • [Cites] N Engl J Med. 2006 Dec 7;355(23):2408-17 [17151364.001]
  • [Cites] Clin Cancer Res. 2006 Dec 15;12(24):7374-9 [17189410.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2303-9 [17138817.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3207-13 [17185463.001]
  • [Cites] Curr Opin Hematol. 2002 Jul;9(4):303-7 [12042704.001]
  • [Cites] Science. 2001 Aug 3;293(5531):876-80 [11423618.001]
  • [Cites] Blood. 2007 May 15;109(10):4143-50 [17264298.001]
  • [Cites] Hematol Oncol Clin North Am. 2001 Feb;15(1):21-36 [11258387.001]
  • [Cites] J Hematol Oncol. 2008;1:15 [18828913.001]
  • [Cites] Drug Metab Dispos. 2008 Jul;36(7):1357-64 [18420784.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5505-8 [18322153.001]
  • [Cites] Cancer Chemother Pharmacol. 2008 Mar;61(3):365-76 [17429625.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5143-50 [17317857.001]
  • [Cites] Cancer. 2007 Jun 1;109(11):2171-81 [17431887.001]
  • (PMID = 19236716.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
  • [Number-of-references] 57
  • [Other-IDs] NLM/ PMC2649947
  •  go-up   go-down


77. Lichtman MA: Is there an entity of chemically induced BCR-ABL-positive chronic myelogenous leukemia? Oncologist; 2008 Jun;13(6):645-54
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] Is there an entity of chemically induced BCR-ABL-positive chronic myelogenous leukemia?
  • Advances in the therapy of malignancy have been accompanied by an increased frequency of cases of secondary acute myelogenous leukemia and related clonal cytopenias and oligoblastic (subacute) myelogenous leukemia (myelodysplastic syndromes).
  • The acute myelogenous leukemia incidence can be increased by high-dose acute ionizing radiation exposure, alkylating agents, topoisomerase II inhibitors, possibly other DNA-damaging therapeutic agents, heavy, prolonged cigarette smoking, and high dose-time exposure to benzene, the latter less frequently seen in industrialized countries with worksite regulations.
  • Acute myelogenous leukemia and myelodysplastic syndromes may result from innumerable primary types of chromosome damage.
  • In the case of chronic myelogenous leukemia, a specific break in chromosome bands 9q34 and 22q11 must occur to result in the causal fusion oncogene (BCR-ABL).
  • A review of 11 studies of the chromosomal abnormalities found in presumptive cases of cytotoxic therapy-induced leukemia and of 40 studies of the subtypes of leukemia that occur following cytotoxic therapy for other cancers has not provided evidence of an increased risk for chemically induced BCR-ABL-positive chronic myelogenous leukemia.
  • Studies of the effects of alkylating agents, topoisomerase inhibitors, and benzene on chromosomes of hematopoietic cells in vitro, coupled with the aforementioned epidemiological studies of secondary leukemia after cytotoxic therapy or of persons exposed to high dose-time concentrations of benzene in the workplace, do not indicate a relationship among chemical exposure, injury to chromosome bands 9q34 and 22q11, and an increased risk for BCR-ABL-positive chronic myelogenous leukemia.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Chromosome Aberrations. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / chemically induced

  • 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 = 18586919.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 113
  •  go-up   go-down


78. Zuna J, Cavé H, Eckert C, Szczepanski T, Meyer C, Mejstrikova E, Fronkova E, Muzikova K, Clappier E, Mendelova D, Boutard P, Schrauder A, Sterba J, Marschalek R, van Dongen JJ, Hrusak O, Stary J, Trka J: Childhood secondary ALL after ALL treatment. Leukemia; 2007 Jul;21(7):1431-5
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] Childhood secondary ALL after ALL treatment.
  • Data on secondary acute lymphoblastic leukaemia (sALL) following ALL treatment are very rare.
  • Our proposal for the 'secondary ALL after ALL' diagnostic criteria is as follows: (A) No clonal relationship between diagnosis and recurrence;.
  • Finally, we propose a treatment strategy for the patients with secondary disease.
  • [MeSH-major] Molecular Diagnostic Techniques / methods. Neoplasms, Second Primary / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17460701.001).
  • [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 / Antineoplastic Agents
  •  go-up   go-down


79. Sabnis AJ, Cheung LS, Dail M, Kang HC, Santaguida M, Hermiston ML, Passegué E, Shannon K, Braun BS: Oncogenic Kras initiates leukemia in hematopoietic stem cells. PLoS Biol; 2009 Mar 17;7(3):e59
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] Oncogenic Kras initiates leukemia in hematopoietic stem cells.
  • MPD could be initiated by Kras(G12D) expression in a highly restricted population enriched for hematopoietic stem cells (HSCs), but not in common myeloid progenitors.
  • Transplanted Kras(G12D) HSCs efficiently initiated acute T-lineage leukemia/lymphoma, which was associated with secondary Notch1 mutations in thymocytes.
  • [MeSH-major] Hematopoietic Stem Cells / pathology. Leukemia, Experimental / pathology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Proto-Oncogene Proteins p21(ras) / metabolism

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • 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) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2008 Jun 15;111(12):5562-70 [18424665.001]
  • [Cites] Genes Dev. 2001 Dec 15;15(24):3243-8 [11751630.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4243-50 [14982883.001]
  • [Cites] Cell. 2004 Aug 20;118(4):477-91 [15315760.001]
  • [Cites] Genes Dev. 2004 Oct 1;18(19):2336-41 [15371326.001]
  • [Cites] Blood. 2002 Feb 1;99(3):840-9 [11806985.001]
  • [Cites] Blood. 2000 Sep 15;96(6):2310-3 [10979983.001]
  • [Cites] Nature. 2006 Aug 17;442(7104):818-22 [16862118.001]
  • [Cites] Nucleic Acids Res. 2004;32(11):e92 [15247325.001]
  • [Cites] Cancer Cell. 2004 Dec;6(6):587-96 [15607963.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):295-308 [17384584.001]
  • [Cites] Nature. 2005 Jul 14;436(7048):221-6 [16015321.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Cell Cycle. 2007 Mar 1;6(5):550-66 [17351342.001]
  • [Cites] Blood. 1999 Mar 15;93(6):2043-56 [10068678.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 May 14;93(10):4683-7 [8643464.001]
  • [Cites] Br J Haematol. 2005 Jul;130(1):51-7 [15982344.001]
  • [Cites] Nature. 2000 Mar 9;404(6774):193-7 [10724173.001]
  • [Cites] Oncogene. 2005 Oct 27;24(47):7114-9 [16103884.001]
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] Cell. 2005 Jun 17;121(6):823-35 [15960971.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2540-3 [16282337.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Sep 19;103(38):14122-7 [16959882.001]
  • [Cites] Blood. 2006 Jan 15;107(2):781-5 [16166587.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4185-93 [11110690.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3181-94 [18677410.001]
  • [Cites] Blood. 2008 Oct 15;112(8):3373-82 [18663146.001]
  • [Cites] BMC Dev Biol. 2001;1:4 [11299042.001]
  • [Cites] Nature. 2001 Apr 26;410(6832):1111-6 [11323676.001]
  • [Cites] Carcinogenesis. 2003 Jul;24(7):1257-68 [12807718.001]
  • [Cites] Blood. 2001 Aug 1;98(3):627-35 [11468160.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1532-42 [12176867.001]
  • [Cites] Cell Stem Cell. 2007 Sep 13;1(3):324-37 [18371366.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Dec 4;98(25):14541-6 [11724967.001]
  • [Cites] Pediatr Blood Cancer. 2006 May 1;46(5):579-85 [16261595.001]
  • [Cites] Blood. 1996 Oct 1;88(7):2655-64 [8839860.001]
  • [Cites] Cancer Cell. 2003 Aug;4(2):111-20 [12957286.001]
  • [Cites] Leuk Res. 2005 Sep;29(9):1069-72 [16038733.001]
  • [Cites] Blood. 2007 May 1;109(9):3945-52 [17192389.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [Cites] Cell. 2007 Jun 1;129(5):865-77 [17540168.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 May 22;104(21):8953-8 [17517660.001]
  • [Cites] Cell. 1990 Jun 1;61(5):759-67 [2188735.001]
  • [Cites] N Engl J Med. 2004 Aug 12;351(7):657-67 [15306667.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Nov;87(22):8736-40 [2247442.001]
  • [Cites] J Cell Biol. 1993 Aug;122(4):897-902 [8349737.001]
  • [Cites] Blood. 1996 Dec 1;88(11):4314-20 [8943868.001]
  • [Cites] Cell. 2004 Oct 29;119(3):431-43 [15507213.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jan 13;101(2):597-602 [14699048.001]
  • [Cites] Nat Rev Cancer. 2003 Jan;3(1):11-22 [12509763.001]
  • [Cites] Nature. 1983 Aug 18-24;304(5927):596-602 [6308472.001]
  • [Cites] Blood. 1990 Sep 15;76(6):1214-9 [2205309.001]
  • [Cites] Cytometry. 2000 Feb 1;39(2):108-16 [10679728.001]
  • [Cites] Nat Med. 2004 Aug;10(8):849-57 [15273746.001]
  • [Cites] Ann N Y Acad Sci. 2005 Jun;1044:1-5 [15958691.001]
  • [Cites] Am J Hematol. 1984 Apr;16(3):277-86 [6711557.001]
  • [Cites] Nature. 2001 Jun 28;411(6841):1017-21 [11429595.001]
  • [Cites] Eur J Immunol. 1988 Sep;18(9):1343-50 [3262519.001]
  • [Cites] Curr Opin Cell Biol. 1999 Dec;11(6):732-6 [10600705.001]
  • [Cites] N Engl J Med. 1988 Sep 1;319(9):525-32 [2841597.001]
  • [Cites] J Exp Med. 2005 Dec 5;202(11):1599-611 [16330818.001]
  • [Cites] J Exp Med. 1997 May 5;185(9):1549-56 [9151892.001]
  • [Cites] Science. 1995 Sep 8;269(5229):1427-9 [7660125.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 2005;70:65-72 [16869739.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):6964-9 [18056171.001]
  • [Cites] J Clin Invest. 2001 Sep;108(5):709-15 [11544276.001]
  • [Cites] J Exp Med. 1998 Jul 20;188(2):393-8 [9670051.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3029-35 [14701873.001]
  • [Cites] Cancer Cell. 2004 Dec;6(6):547-52 [15607959.001]
  • [Cites] Stem Cells. 1996 Nov;14(6):690-701 [8948026.001]
  • [Cites] J Clin Invest. 2004 Feb;113(4):528-38 [14966562.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1380-7 [10942381.001]
  • [Cites] Cancer Cell. 2002 Dec;2(6):507-14 [12498719.001]
  • [Cites] Nature. 2006 May 25;441(7092):518-22 [16633340.001]
  • [Cites] Nature. 2006 May 25;441(7092):475-82 [16598206.001]
  • (PMID = 19296721.001).
  • [ISSN] 1545-7885
  • [Journal-full-title] PLoS biology
  • [ISO-abbreviation] PLoS Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / R37 CA72614; United States / NCI NIH HHS / CA / R37 CA072614; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / K08 CA103868; United States / NCI NIH HHS / CA / U01 CA84221
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ PMC2656550
  •  go-up   go-down


80. Kuendgen A, Schmid M, Schlenk R, Knipp S, Hildebrandt B, Steidl C, Germing U, Haas R, Dohner H, Gattermann N: The histone deacetylase (HDAC) inhibitor valproic acid as monotherapy or in combination with all-trans retinoic acid in patients with acute myeloid leukemia. Cancer; 2006 Jan 1;106(1):112-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The histone deacetylase (HDAC) inhibitor valproic acid as monotherapy or in combination with all-trans retinoic acid in patients with acute myeloid leukemia.
  • BACKGROUND: Valproic acid (VPA) inhibits histone deacetylase activity and, synergizing with all-trans retinoic acid (ATRA), achieves differentiation induction of myeloid blast cells in vitro.
  • METHODS: We used VPA in 58 patients with acute myeloid leukemia (AML) who were too old and/or medically unfit to receive intensive chemotherapy (32 AML secondary to myelodysplastic syndrome [MDS], 22 de novo AML, 4 AML secondary to myeloproliferative syndrome).
  • RESULTS: The response rate was only 5% according to International Working Group (IWG) criteria for AML but was 16% when IWG response criteria for MDS were used, which capture hematologic improvement and stabilization of the disease.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Histone Deacetylase Inhibitors. Leukemia, Myeloid / drug therapy. Tretinoin / therapeutic use. Valproic Acid / therapeutic use
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Male. Middle Aged. Treatment Outcome


81. Pyatt DW, Hays SM, Cushing CA: Do children have increased susceptibility for developing secondary acute myelogenous leukemia? Chem Biol Interact; 2005 May 30;153-154:223-9
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] Do children have increased susceptibility for developing secondary acute myelogenous leukemia?
  • This study was undertaken to evaluate the effects of age on a child's susceptibility to developing leukemia following exposure to known leukemogenic agents.
  • The clinical literature describing the risk of developing acute myelogenous leukemia (AML) following treatment with alkylating agents or topoisomerase reactive drugs (known leukemogens) was used as a basis for this investigation.
  • Although the number of studies and cases was very small, the available scientific and medical literature does not support the hypothesis that children will necessarily have an altered susceptibility or increased risk of developing chemotherapy-induced AML.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Leukemia, Myeloid, Acute / epidemiology. Neoplasms, Second Primary / epidemiology

  • 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
  • [ErratumIn] Chem Biol Interact. 2005 Aug 15;155(3):191
  • (PMID = 15878160.001).
  • [ISSN] 0009-2797
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Topoisomerase II Inhibitors
  •  go-up   go-down


82. Ravoet C, Mineur P, Robin V, Debusscher L, Bosly A, André M, El Housni H, Soree A, Bron D, Martiat P: Farnesyl transferase inhibitor (lonafarnib) in patients with myelodysplastic syndrome or secondary acute myeloid leukaemia: a phase II study. Ann Hematol; 2008 Nov;87(11):881-5
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] Farnesyl transferase inhibitor (lonafarnib) in patients with myelodysplastic syndrome or secondary acute myeloid leukaemia: a phase II study.
  • We prospectively studied efficiency and tolerance of lonafarnib, a compound able to inhibit Ras signalling pathway through an inhibition of farnesyl transferase, in patients with MDS or secondary acute myeloid leukaemia (sAML).
  • Sixteen patients were included: FAB/RAEB (n = 10), RAEB-T (n = 2), sAML (n = 2) and chronic myelomonocytic leukaemia (CMML; n = 2); WHO/RAEB-1 (n = 4), RAEB-2 (n = 5), AML (n = 5), CMML (n = 2).
  • Lonafarnib alone, administered following our schedule, has shown limited activity in patients with MDS or secondary AML.
  • [MeSH-major] Farnesyltranstransferase / antagonists & inhibitors. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Piperidines / adverse effects. Pyridines / adverse effects


83. Greaves M: Darwin and evolutionary tales in leukemia. The Ham-Wasserman Lecture. Hematology Am Soc Hematol Educ Program; 2009;:3-12
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] Darwin and evolutionary tales in leukemia. The Ham-Wasserman Lecture.
  • The evolutionary, natural history of childhood acute lymphoblastic leukemia (ALL) is almost entirely covert, clinically silent and well advanced by the point of diagnosis.
  • (ii) archived neonatal blood spots or Guthrie cards from individuals who later developed leukemia; and (iii) stored, viable cord blood cells.
  • These studies indicate prenatal initiation of leukemia by chromosome translocation and gene fusion (or hyperdiploidy) and the post-natal acquisition of multiple, gene copy number alterations (CNAs), mostly deletions.
  • The acquisition of the critical, secondary CNAs requires some Darwinian selective advantage to expand numbers of cells at risk, and the cytokine TGF beta is able to exercise this function.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20008176.001).
  • [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] Lectures; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
  •  go-up   go-down


84. Karp JE, Smith BD, Gojo I, Lancet JE, Greer J, Klein M, Morris L, Levis MJ, Gore SD, Wright JJ, Garrett-Mayer E: Phase II trial of tipifarnib as maintenance therapy in first complete remission in adults with acute myelogenous leukemia and poor-risk features. Clin Cancer Res; 2008 May 15;14(10):3077-82
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] Phase II trial of tipifarnib as maintenance therapy in first complete remission in adults with acute myelogenous leukemia and poor-risk features.
  • PURPOSE: Acute myelogenous leukemia (AML) does not have a high cure rate, particularly in patients with poor-risk features.
  • Tipifarnib is an oral farnesyltransferase inhibitor with activity in AML.
  • We conducted a phase II trial of maintenance tipifarnib monotherapy for 48 adults with poor-risk AML in first CR.
  • Comparison of CR durations for 25 patients who received two-cycle timed sequential therapy followed by tipifarnib maintenance with 23 historically similar patients who did not receive tipifarnib showed that tipifarnib was associated with DFS prolongation for patients with secondary AML and adverse cytogenetics.
  • CONCLUSIONS: This study suggests that some patients with poor-risk AML, including patients with secondary AML and adverse cytogenetics, may benefit from tipifarnib maintenance therapy.

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3835-49 [10577857.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1964-70 [17581608.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3361-9 [11369625.001]
  • [Cites] Blood. 2001 Aug 1;98(3):548-53 [11468148.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1302-11 [11520775.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1312-20 [11520776.001]
  • [Cites] Leuk Res. 2003 Apr;27(4):313-21 [12531222.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1692-7 [12411300.001]
  • [Cites] Am J Clin Pathol. 2003 May;119(5):672-80 [12760285.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3880-9 [12920034.001]
  • [Cites] Blood. 2003 Dec 15;102(13):4527-34 [12947010.001]
  • [Cites] Blood Rev. 2004 Mar;18(1):39-63 [14684148.001]
  • [Cites] J Clin Oncol. 2004 Apr 1;22(7):1287-92 [15051776.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1605-16 [15084693.001]
  • [Cites] Blood. 1989 Oct;74(5):1499-506 [2676014.001]
  • [Cites] Blood. 1992 Apr 15;79(8):1924-30 [1562720.001]
  • [Cites] Blood. 1997 Oct 15;90(8):2952-61 [9376575.001]
  • [Cites] J Clin Oncol. 1998 Mar;16(3):872-81 [9508168.001]
  • [Cites] Leukemia. 1999 Jun;13(6):843-9 [10360370.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1969-78 [15632409.001]
  • [Cites] Eur J Haematol. 2005 May;74(5):418-23 [15813916.001]
  • [Cites] J Clin Oncol. 2006 Jun 1;24(16):2480-9 [16735702.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1677-83 [16670265.001]
  • [Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1387-94 [17082323.001]
  • [Cites] Blood. 2007 May 15;109(10):4158-63 [17264294.001]
  • [Cites] J Clin Oncol. 2007 May 10;25(14):1908-15 [17488990.001]
  • [Cites] Hematol Oncol Clin North Am. 2000 Feb;14(1):251-67 [10680081.001]
  • (PMID = 18483374.001).
  • [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 69854; United States / NCI NIH HHS / CA / U01 CA069854-07; United States / NCI NIH HHS / CA / U01 CA069854; United States / NCI NIH HHS / CA / U01 CA70095; United States / NCI NIH HHS / CA / U01 CA070095
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinolones; 192185-72-1 / tipifarnib
  • [Other-IDs] NLM/ NIHMS281726; NLM/ PMC3074480
  •  go-up   go-down


85. Figueroa ME, Skrabanek L, Li Y, Jiemjit A, Fandy TE, Paietta E, Fernandez H, Tallman MS, Greally JM, Carraway H, Licht JD, Gore SD, Melnick A: MDS and secondary AML display unique patterns and abundance of aberrant DNA methylation. Blood; 2009 Oct 15;114(16):3448-58
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] MDS and secondary AML display unique patterns and abundance of aberrant DNA methylation.
  • Increasing evidence shows aberrant hypermethylation of genes occurring in and potentially contributing to pathogenesis of myeloid malignancies.
  • To determine the extent of promoter hypermethylation in such tumors, we compared the distribution of DNA methylation of 14 000 promoters in MDS and secondary acute myeloid leukemia (AML) patients enrolled in a phase 1 trial of 5-azacytidine and the histone deacetylase inhibitor entinostat against de novo AML patients and normal CD34(+) bone marrow cells.
  • The MDS and secondary AML patients displayed more extensive aberrant DNA methylation involving thousands of genes than did the normal CD34(+) bone marrow cells or de novo AML blasts.
  • Aberrant methylation in MDS and secondary AML tended to affect particular chromosomal regions, occurred more frequently in Alu-poor genes, and included prominent involvement of genes involved in the WNT and MAPK signaling pathways.
  • [MeSH-major] Azacitidine / administration & dosage. DNA Methylation / drug effects. DNA, Neoplasm / metabolism. Enzyme Inhibitors / administration & dosage. Leukemia, Myeloid, Acute. Myelodysplastic Syndromes. Neoplasms, Second Primary / drug therapy. Neoplasms, Second Primary / metabolism

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • Hazardous Substances Data Bank. AZACITIDINE .
  • 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] Mol Pharmacol. 2001 Apr;59(4):751-7 [11259619.001]
  • [Cites] Lancet Oncol. 2009 Mar;10(3):223-32 [19230772.001]
  • [Cites] Blood. 2009 Feb 5;113(6):1315-25 [18832655.001]
  • [Cites] Blood. 2009 Sep 24;114(13):2764-73 [19546476.001]
  • [Cites] Nucleic Acids Res. 2002 Jan 1;30(1):207-10 [11752295.001]
  • [Cites] J Clin Oncol. 2002 May 15;20(10):2429-40 [12011120.001]
  • [Cites] Nat Rev Genet. 2002 Jun;3(6):415-28 [12042769.001]
  • [Cites] Hum Mol Genet. 2002 Oct 1;11(20):2479-88 [12351584.001]
  • [Cites] Leukemia. 2003 May;17(5):910-8 [12750705.001]
  • [Cites] Leukemia. 2003 Sep;17(9):1813-9 [12970781.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2042-54 [14627790.001]
  • [Cites] J Biol Chem. 2004 Apr 9;279(15):15161-6 [14722112.001]
  • [Cites] Nat Med. 2004 May;10(5):481-3 [15048110.001]
  • [Cites] Genome Biol. 2004;5(10):R80 [15461798.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):103-7 [9916800.001]
  • [Cites] Bioinformatics. 2005 Jun 1;21(11):2789-90 [15797915.001]
  • [Cites] Br J Haematol. 2005 Jul;130(2):209-17 [16029449.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7086-90 [16103056.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):305-19 [16075461.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 1;102(44):15785-90 [16243968.001]
  • [Cites] Nat Clin Pract Oncol. 2005 Dec;2 Suppl 1:S36-44 [16341239.001]
  • [Cites] Eur J Haematol. 2006 Jan;76(1):23-32 [16343268.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6361-9 [16778214.001]
  • [Cites] BMC Genomics. 2006;7:133 [16740159.001]
  • [Cites] Genome Res. 2006 Aug;16(8):1046-55 [16809668.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3895-903 [16921040.001]
  • [Cites] Blood. 2007 Jan 1;109(1):52-7 [16882708.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1937-44 [17611569.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):8248-54 [17804739.001]
  • [Cites] Mol Cell. 2007 Oct 26;28(2):337-50 [17964271.001]
  • [Cites] Mol Cell Biol. 2008 Jan;28(2):752-71 [17991895.001]
  • [Cites] Semin Hematol. 2008 Jan;45(1):23-30 [18179966.001]
  • [Cites] Nucleic Acids Res. 2008 Jan;36(Database issue):D773-9 [18086701.001]
  • [Cites] PLoS One. 2008;3(3):e1882 [18365023.001]
  • [Cites] Bioinformatics. 2008 May 1;24(9):1161-7 [18353789.001]
  • [Cites] Mol Cancer Ther. 2008 Sep;7(9):2998-3005 [18790780.001]
  • [CommentIn] Blood. 2009 Oct 15;114(16):3363-4 [19833849.001]
  • (PMID = 19652201.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00101179
  • [Grant] United States / NCI NIH HHS / CA / R21 CA110507; United States / NCI NIH HHS / CA / U10 CA021115; United States / NCI NIH HHS / CA / U54 CA143876-01; United States / NCI NIH HHS / CA / K24 CA111717; United States / NCI NIH HHS / CA / R01 CA125635; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCI NIH HHS / CA / U54 CA143876; United States / NICHD NIH HHS / HD / R01 HD044078; United States / NCI NIH HHS / CA / CA21115; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / R01 CA104348; United States / NCI NIH HHS / CA / U01CA70095
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / DNA, Neoplasm; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Wnt Proteins; EC 3.5.1.98 / Histone Deacetylases; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC2765680
  •  go-up   go-down


86. de Witte T, Hagemeijer A, Suciu S, Belhabri A, Delforge M, Kobbe G, Selleslag D, Schouten HC, Ferrant A, Biersack H, Amadori S, Muus P, Jansen JH, Hellström-Lindberg E, Kovacsovics T, Wijermans P, Ossenkoppele G, Gratwohl A, Marie JP, Willemze R: Value of allogeneic versus autologous stem cell transplantation and chemotherapy in patients with myelodysplastic syndromes and secondary acute myeloid leukemia. Final results of a prospective randomized European Intergroup Trial. Haematologica; 2010 Oct;95(10):1754-61
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Value of allogeneic versus autologous stem cell transplantation and chemotherapy in patients with myelodysplastic syndromes and secondary acute myeloid leukemia. Final results of a prospective randomized European Intergroup Trial.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mod Pathol. 2000 Feb;13(2):193-207 [10697278.001]
  • [Cites] Br J Haematol. 2000 Sep;110(3):620-30 [10997974.001]
  • [Cites] Blood. 2001 Oct 15;98(8):2326-31 [11588026.001]
  • [Cites] Br J Haematol. 2002 Aug;118(2):385-400 [12139722.001]
  • [Cites] Blood. 2002 Aug 15;100(4):1201-7 [12149198.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1997-2004 [12200358.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1615-21 [12200672.001]
  • [Cites] Leukemia. 2003 May;17(5):859-68 [12750698.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1232-40 [12714526.001]
  • [Cites] Blood. 2004 Apr 15;103(8):2908-13 [15070662.001]
  • [Cites] Blood. 2004 Jul 15;104(2):579-85 [15039286.001]
  • [Cites] Ann Hematol. 2004 Aug;83(8):498-503 [15156346.001]
  • [Cites] Br J Haematol. 1985 Mar;59(3):425-33 [3970861.001]
  • [Cites] Br J Haematol. 1991 Apr;77(4):497-501 [2025575.001]
  • [Cites] Blood. 1995 Nov 15;86(10):3660-7 [7579331.001]
  • [Cites] Leukemia. 1995 Nov;9(11):1805-11 [7475266.001]
  • [Cites] Leukemia. 1996 Oct;10(10):1648-52 [8847900.001]
  • [Cites] Blood. 1997 Mar 15;89(6):2079-88 [9058730.001]
  • [Cites] Blood. 1997 Nov 15;90(10):3853-7 [9354651.001]
  • [Cites] Br J Haematol. 1997 Dec;99(4):939-44 [9432047.001]
  • [Cites] Br J Haematol. 1998 Sep;102(4):1015-24 [9734653.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Leukemia. 1999 Apr;13(4):524-9 [10214857.001]
  • [Cites] Ann Oncol. 1999 Jul;10(7):825-9 [10470430.001]
  • [Cites] Leukemia. 2005 Mar;19(3):396-401 [15674354.001]
  • [Cites] Bone Marrow Transplant. 2006 Jan;37(2):183-9 [16299545.001]
  • [Cites] Haematologica. 2006 Mar;91(3):373-6 [16531261.001]
  • [Cites] Blood. 2007 May 1;109(9):3658-66 [17213292.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1945-51 [17611571.001]
  • [Cites] Br J Haematol. 1982 Jun;51(2):189-99 [6952920.001]
  • [CommentIn] Haematologica. 2010 Oct;95(10):1623-7 [20884716.001]
  • (PMID = 20494931.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00002926
  • [Grant] United States / NCI NIH HHS / CA / 5U10 CA11488-32; United States / NCI NIH HHS / CA / 5U10 CA11488-27; United States / NCI NIH HHS / CA / 5U10 CA11488-38; United States / NCI NIH HHS / CA / 5U10 CA11488-28; United States / NCI NIH HHS / CA / 5U10 CA11488-35; United States / NCI NIH HHS / CA / 5U10 CA11488-31; United States / NCI NIH HHS / CA / 5U10 CA11488-26; United States / NCI NIH HHS / CA / 5U10 CA11488-37; United States / NCI NIH HHS / CA / U10 CA011488; United States / NCI NIH HHS / CA / 5U10 CA11488-29; United States / NCI NIH HHS / CA / 5U10 CA11488-36; United States / NCI NIH HHS / CA / 5U10 CA11488-33; United States / NCI NIH HHS / CA / 5U10 CA11488-34; United States / NCI NIH HHS / CA / 5U10 CA11488-30
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2948102
  •  go-up   go-down


87. Gupta V, Chun K, Yi QL, Minden M, Schuh A, Wells R, Brandwein J: Disease biology rather than age is the most important determinant of survival of patients &gt; or = 60 years with acute myeloid leukemia treated with uniform intensive therapy. Cancer; 2005 May 15;103(10):2082-90
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disease biology rather than age is the most important determinant of survival of patients > or = 60 years with acute myeloid leukemia treated with uniform intensive therapy.
  • BACKGROUND: The objectives of the current study were to evaluate the outcome of patients > or = 60 years with acute myeloid leukemia (AML) treated uniformly with high-dose daunorubicin containing induction and modified high-dose cytosine arabinoside containing postremission therapy, and to identify factors predictive of complete disease remission (CR) and survival.
  • METHODS: Between 1998 and 2002, the authors treated 117 newly diagnosed patients (acute promyelocytic leukemia excluded) with AML > or = 60 years (median, 67 years; range, 60-82 years).
  • A normal karyotype was seen in 41 patients and 40 (34%) had secondary AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Age Factors. Aged. Aged, 80 and over. Antibiotics, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / administration & dosage. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Disease-Free Survival. Female. Follow-Up Studies. Hematologic Diseases / complications. Humans. Karyotyping. L-Lactate Dehydrogenase / analysis. Leukocyte Count. Male. Middle Aged. Myelodysplastic Syndromes / complications. Remission Induction. Retrospective Studies. Survival Rate. Treatment Outcome

  • 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 = 15830348.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 1.1.1.27 / L-Lactate Dehydrogenase; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


88. Bonilla M, Gupta S, Vasquez R, Fuentes SL, deReyes G, Ribeiro R, Sung L: Predictors of outcome and methodological issues in children with acute lymphoblastic leukaemia in El Salvador. Eur J Cancer; 2010 Dec;46(18):3280-6
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] Predictors of outcome and methodological issues in children with acute lymphoblastic leukaemia in El Salvador.
  • BACKGROUND: Most children with cancer live in low-income countries (LICs) where risk factors in paediatric acute lymphoblastic leukaemia (ALL) developed in high-income countries may not apply.
  • Among standard-risk children, socioeconomic variables such as higher monthly income (hazard ratio [HR] per $100 = 0.84 [95% confidence interval (CI) 0.70-0.99; P=0.04]) and parental secondary education (HR = 0.49, 95% CI 0.29-0.84; P = 0.01) were associated with better EFS.
  • The difference in EFS and OS appeared related to overestimating OS secondary to poor follow-up after abandonment/relapse.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20674335.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


89. Christie L, Kernohan N, Levison D, Sales M, Cunningham J, Gillespie K, Batstone P, Meiklejohn D, Goodlad J: C-MYC translocation in t(14;18) positive follicular lymphoma at presentation: An adverse prognostic indicator? Leuk Lymphoma; 2008 Mar;49(3):470-6
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.
  • Follicular lymphoma (FL) is a common subtype of low grade B-cell non-Hodgkin lymphoma (NHL).
  • Although, the t(14;18) in itself does not affect outcome in cases of FL, secondary abnormalities that occur in a complex polyploid karyotype may identify cases with a poor prognosis.
  • It is unusual to find both t(14;18) and C-MYC translocation in the same tumour; those cases in which it has been described include examples of high-grade B-cell NHL (either de novo or transformed FL) or B-cell acute lymphoblastic lymphoma.

  • Genetic Alliance. consumer health - Follicular Lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Leuk Lymphoma. 2008 Mar;49(3):377-80 [18297511.001]
  • (PMID = 18297523.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myc
  •  go-up   go-down


90. Krapf G, Kaindl U, Kilbey A, Fuka G, Inthal A, Joas R, Mann G, Neil JC, Haas OA, Panzer-Grümayer ER: ETV6/RUNX1 abrogates mitotic checkpoint function and targets its key player MAD2L1. Oncogene; 2010 Jun 03;29(22):3307-12
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Approximately 25% of childhood B-cell precursor acute lymphoblastic leukemia have an ETV6/RUNX1 (E/R) gene fusion that results from a t(12;21).
  • This genetic subgroup of leukemia is associated with near-triploidy, near-tetraploidy, and trisomy 21 as rather specific types of secondary changes.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2003 Oct 15;102(8):2951-9 [12730115.001]
  • [Cites] Nat Rev Cancer. 2002 Jul;2(7):502-13 [12094236.001]
  • [Cites] Biochem Biophys Res Commun. 2004 May 14;317(4):1128-37 [15094386.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4275-83 [15156184.001]
  • [Cites] Leukemia. 2004 Oct;18(10):1611-6 [15356655.001]
  • [Cites] Cell Cycle. 2004 Aug;3(8):990-2 [15254432.001]
  • [Cites] Mol Cell Biol. 1996 Apr;16(4):1349-55 [8657108.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):166-75 [10508512.001]
  • [Cites] Cancer Cell. 2005 Jul;8(1):7-12 [16023594.001]
  • [Cites] Nat Rev Cancer. 2005 Oct;5(10):773-85 [16195750.001]
  • [Cites] Trends Cell Biol. 2006 Jan;16(1):55-63 [16337124.001]
  • [Cites] Genes Chromosomes Cancer. 2006 Jun;45(6):608-11 [16552772.001]
  • [Cites] Oncogene. 2006 Jun 15;25(25):3598-605 [16449973.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Aug;169(1):50-7 [16875937.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):9-23 [17189715.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2607-10 [17095626.001]
  • [Cites] Nature. 2007 Apr 19;446(7138):868-9 [17443175.001]
  • [Cites] Blood. 2007 May 1;109(9):3963-71 [17197431.001]
  • [Cites] J Biol Chem. 2003 Aug 29;278(35):33088-96 [12807882.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Carcinogenesis. 2007 May;28(5):899-912 [17259655.001]
  • [Cites] Oncogene. 2007 Jun 28;26(30):4404-14 [17237815.001]
  • [Cites] Cancer Res. 2007 Aug 1;67(15):7155-64 [17671183.001]
  • [Cites] Science. 2008 Jan 18;319(5861):336-9 [18202291.001]
  • [Cites] Nature. 2008 Mar 20;452(7185):365-9 [18354482.001]
  • [Cites] Oncogene. 2008 Oct 2;27(44):5856-66 [18560354.001]
  • [Cites] Blood. 2009 Mar 26;113(13):3070-9 [19179469.001]
  • [Cites] J Clin Invest. 2009 Apr;119(4):826-36 [19287094.001]
  • [Cites] Oncogene. 2009 Jul 9;28(27):2502-12 [19448675.001]
  • [Cites] Leukemia. 1999 Dec;13(12):1932-42 [10602413.001]
  • [Cites] J Biol Chem. 2000 Feb 4;275(5):3438-45 [10652337.001]
  • [Cites] Oncogene. 2000 May 18;19(22):2695-703 [10851069.001]
  • (PMID = 20190817.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / P 17551
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Cell Cycle Proteins; 0 / Core Binding Factor Alpha 2 Subunit; 0 / MAD2L1 protein, human; 0 / Mad2 Proteins; 0 / Oncogene Proteins, Fusion; 0 / Repressor Proteins; 0 / TEL-AML1 fusion protein
  • [Other-IDs] NLM/ EMS32872; NLM/ PMC4194424
  •  go-up   go-down


91. Liu KY, Chen YH, Liu DH, Xu LP, Huang XJ: A pilot study of low-dose recombinant interleukin-2 for acute lymphoblastic malignancy after unmanipulated allogeneic blood and marrow transplantation. Bone Marrow Transplant; 2008 Oct;42(8):535-9
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] A pilot study of low-dose recombinant interleukin-2 for acute lymphoblastic malignancy after unmanipulated allogeneic blood and marrow transplantation.
  • The objective of this study was to determine the efficacy and safety of low-dose recombinant interleukin-2(IL-2) administered to patients with acute lymphoblastic malignancy at high-risk of relapse after unmanipulated HLA-identical or HLA-haploidentical allogeneic hematopoietic stem cell transplantation (allo-HSCT).
  • We studied 19 patients with acute lymphoblastic malignancy who underwent IL-2 treatment for a high probability of disease recurrence after allo-HSCT between July 2004 and June 2006 at Peking University Institute of Hematology.
  • In conclusion, low-dose IL-2 subcutaneous administration from 100 days for a prolonged period could be a safe and effective strategy to prevent relapse in acute lymphoblastic malignancy patients with high risk of recurrence after unmanipulated allo-HSCT.
  • [MeSH-major] Interleukin-2 / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / prevention & control
  • [MeSH-minor] Adolescent. Adult. Blood Transfusion. Child. Child, Preschool. Female. Follow-Up Studies. Graft vs Host Disease / mortality. Graft vs Host Disease / therapy. Humans. Injections, Subcutaneous. Male. Pilot Projects. Risk Factors. Secondary Prevention. Young Adult

  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18641681.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / IL2 protein, human; 0 / Interleukin-2
  •  go-up   go-down


92. D'Andrea AD: Targeting DNA repair pathways in AML. Best Pract Res Clin Haematol; 2010 Dec;23(4):469-73
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] Targeting DNA repair pathways in AML.
  • DNA repair inhibitors, such as poly-ADP-ribose polymerase (PARP) inhibitors, may be useful in a small subset of acute myeloid leukemia (AML) patients, especially those who have complex karyotypes or those with secondary AML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. DNA Repair / drug effects. Enzyme Inhibitors / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21130409.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Enzyme Inhibitors; 0 / Poly(ADP-ribose) Polymerase Inhibitors; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
  •  go-up   go-down


93. Karp JE, Smith BD, Levis MJ, Gore SD, Greer J, Hattenburg C, Briel J, Jones RJ, Wright JJ, Colevas AD: Sequential flavopiridol, cytosine arabinoside, and mitoxantrone: a phase II trial in adults with poor-risk acute myelogenous leukemia. Clin Cancer Res; 2007 Aug 1;13(15 Pt 1):4467-73
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] Sequential flavopiridol, cytosine arabinoside, and mitoxantrone: a phase II trial in adults with poor-risk acute myelogenous leukemia.
  • In a phase I study of flavopiridol followed by 1-beta-d-arabinofuranosylcytosine (ara-C) and mitoxantrone, overall response rate for adults with relapsed and refractory acute myelogenous leukemias (AML) was 31%.
  • We have now completed a phase II study of sequential flavopiridol, ara-C, and mitoxantrone in 62 adults with poor-risk AML.
  • Complete remissions (CR) were achieved in 12 of 15 (75%) newly diagnosed secondary AML, 18 of 24 (75%) first relapse after short CR (median CR, 9 months, including prior allotransplant), and 2 of 13 (15%) primary refractory but 0 of 10 multiply refractory AML.
  • CONCLUSIONS: Flavopiridol has anti-AML activity directly and in combination with ara-C and mitoxantrone.
  • This timed sequential regimen induces durable CRs in a significant proportion of adults with newly diagnosed secondary AML (including complex cytogenetics) and adults with AML in first relapse after short first CR.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17671131.001).
  • [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 / NCRR NIH HHS / RR / M01-RR0052; United States / NCI NIH HHS / CA / U01 CA70095
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Piperidines; 04079A1RDZ / Cytarabine; 45AD6X575G / alvocidib; BZ114NVM5P / Mitoxantrone
  •  go-up   go-down


94. Roboz GJ, Giles FJ, List AF, Cortes JE, Carlin R, Kowalski M, Bilic S, Masson E, Rosamilia M, Schuster MW, Laurent D, Feldman EJ: Phase 1 study of PTK787/ZK 222584, a small molecule tyrosine kinase receptor inhibitor, for the treatment of acute myeloid leukemia and myelodysplastic syndrome. Leukemia; 2006 Jun;20(6):952-7
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] Phase 1 study of PTK787/ZK 222584, a small molecule tyrosine kinase receptor inhibitor, for the treatment of acute myeloid leukemia and myelodysplastic syndrome.
  • The objective of this Phase I study was to evaluate the safety, tolerability, biologic activity and pharmacologic profile of PTK/ZK administered orally, twice daily, on a continuous dosing schedule in patients with primary refractory or relapsed acute myeloid leukemia (AML), secondary AML, poor-prognosis de novo AML or advanced myelodysplastic syndrome (MDS).
  • Acute myeloid leukemia patients for whom PTK/ZK monotherapy was ineffective could receive PTK/ZK combined with standard induction chemotherapy.
  • Complete remission was observed in five of 17 AML patients treated with PTK/ZK combined with chemotherapy.
  • The drug is generally well tolerated and can be given in combination with chemotherapy for patients with MDS and AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. Phthalazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyridines / therapeutic use
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Cell Proliferation / drug effects. Cohort Studies. Dose-Response Relationship, Drug. Drug Therapy, Combination. Female. Humans. Male. Middle Aged. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Treatment Outcome. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors


95. Bug G, Ritter M, Wassmann B, Schoch C, Heinzel T, Schwarz K, Romanski A, Kramer OH, Kampfmann M, Hoelzer D, Neubauer A, Ruthardt M, Ottmann OG: Clinical trial of valproic acid and all-trans retinoic acid in patients with poor-risk acute myeloid leukemia. Cancer; 2005 Dec 15;104(12):2717-25
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.
  • [Title] Clinical trial of valproic acid and all-trans retinoic acid in patients with poor-risk acute myeloid leukemia.
  • BACKGROUND: Valproic acid (VPA), a histone deacetylase (HDAC) inhibitor, induced in vitro differentiation of primary acute myeloid leukemia (AML) blasts, an effect enhanced by all-trans retinoic acid (ATRA).
  • Herein, the authors have described results of a clinical trial with VPA plus ATRA in 26 patients with poor-risk AML.
  • No patient achieved complete remission, one with de novo AML had a minor response, and two patients with secondary AML arising from myeloproliferative disorder (MPD) achieved a partial remission and clearance of PB blasts, respectively.
  • The latter responses were accompanied by profound granulocytosis and erythrocytosis in both patients, reminiscent of the response pattern known from ATRA treatment of acute promyelocytic leukemia.
  • CONCLUSIONS: Treatment with VPA/ATRA results in transient disease control in a subset of patients with AML that has evolved from a myeloproliferative disorder but not in patients with a primary or MDS-related AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / drug therapy. Tretinoin / administration & dosage. Valproic Acid / administration & dosage