[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 149
1. 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


2. 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


3. 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


Advertisement
4. 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


5. 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


6. 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


7. 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


8. 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.


9. 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


10. 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


11. 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


12. 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


13. 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


14. 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


15. 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


16. 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


17. 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


18. 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


19. 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


20. 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


21. 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.


22. 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


23. Reiter A, Walz C, Watmore A, Schoch C, Blau I, Schlegelberger B, Berger U, Telford N, Aruliah S, Yin JA, Vanstraelen D, Barker HF, Taylor PC, O'Driscoll A, Benedetti F, Rudolph C, Kolb HJ, Hochhaus A, Hehlmann R, Chase A, Cross NC: The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2. Cancer Res; 2005 Apr 1;65(7):2662-7
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] The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2.
  • We have identified a t(8;9)(p21-23;p23-24) in seven male patients (mean age 50, range 32-74) with diverse hematologic malignancies and clinical outcomes: atypical chronic myeloid leukemia/chronic eosinophilic leukemia (n = 5), secondary acute myeloid leukemia (n = 1), and pre-B-cell acute lymphoblastic leukemia (n = 1).
  • [MeSH-major] Cell Cycle Proteins / genetics. Chromosomes, Human, Pair 8 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Aged. Amino Acid Sequence. Autoantigens. Base Sequence. Humans. Janus Kinase 2. Male. Middle Aged. Molecular Sequence Data. Reverse Transcriptase Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • 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
  • (PMID = 15805263.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantigens; 0 / Cell Cycle Proteins; 0 / Oncogene Proteins, Fusion; 0 / PCM1 protein, human; 0 / PCM1-JAK2 fusion protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


24. 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


25. 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


26. 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


27. 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


28. 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


29. 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


30. 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


31. 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


32. 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


33. 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


34. 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


35. 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.


36. 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


37. 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


38. 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


39. 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


40. 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


41. 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


42. 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


43. 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


44. 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


45. Shah A, Stiller CA, Kenward MG, Vincent T, Eden TO, Coleman MP: Childhood leukaemia: long-term excess mortality and the proportion 'cured'. Br J Cancer; 2008 Jul 8;99(1):219-23
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.
  • Average time to cure increased from 12 years (95% confidence interval (CI): 11-14) to 19 years (95% CI: 14-26) for lymphoid leukaemia (average annual increase of 0.3 years; P<0.001), but remained at about 5 years for acute nonlymphoblastic leukaemia.
  • The proportion of children cured of leukaemia has risen dramatically, but the period of excess mortality associated with lymphoid leukaemia has also increased, possibly because of late relapse, secondary malignancy and toxicity from treatment.

  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 1998 Oct 1;92(7):2334-7 [9746771.001]
  • [Cites] J Natl Cancer Inst. 1996 Mar 6;88(5):270-8 [8614005.001]
  • [Cites] Br J Cancer. 2004 Nov 29;91(11):1905-10 [15534607.001]
  • [Cites] Br J Haematol. 2005 Jul;130(1):67-75 [15982346.001]
  • [Cites] J Clin Oncol. 2005 Nov 1;23(31):7936-41 [16258093.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2130-8 [16304572.001]
  • [Cites] N Engl J Med. 2006 Oct 12;355(15):1572-82 [17035650.001]
  • [Cites] Br J Cancer. 2007 Apr 10;96(7):1147-52 [17342086.001]
  • [Cites] Br J Haematol. 2000 Mar;108(3):531-43 [10759711.001]
  • [Cites] Blood. 2000 May 1;95(9):2770-5 [10779419.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2307-20 [11187922.001]
  • [Cites] J Clin Oncol. 2001 Jul 1;19(13):3163-72 [11432882.001]
  • [Cites] J Clin Oncol. 2001 Jul 1;19(13):3173-81 [11432883.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4257-64 [12036851.001]
  • [Cites] Br J Haematol. 2003 Aug;122(3):345-59 [12877662.001]
  • [Cites] N Engl J Med. 2003 Aug 14;349(7):640-9 [12917300.001]
  • [Cites] Br J Haematol. 2004 Jan;124(1):33-46 [14675406.001]
  • [Cites] Pediatr Blood Cancer. 2004 Jun;42(7):563-73 [15127410.001]
  • [Cites] Lancet. 1986 Feb 22;1(8478):408-11 [2868339.001]
  • [Cites] Arch Dis Child. 1989 Jun;64(6):798-807 [2774614.001]
  • [Cites] J Clin Epidemiol. 1997 Feb;50(2):211-6 [9120515.001]
  • [Cites] Int J Cancer. 1998 Jul 29;77(3):322-9 [9663589.001]
  • [Cites] J Clin Oncol. 1998 Aug;16(8):2848-53 [9704738.001]
  • [Cites] N Engl J Med. 1991 Nov 7;325(19):1330-6 [1922234.001]
  • [Cites] BMJ. 1994 Jul 16;309(6948):162-6 [8044095.001]
  • [Cites] IARC Sci Publ. 1994;(128):1-302 [7698823.001]
  • [Cites] Stat Med. 1999 Feb 28;18(4):441-54 [10070685.001]
  • (PMID = 18594545.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Department of Health / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2453011
  •  go-up   go-down


46. 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


47. 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


48. 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


49. 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


50. 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


51. 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


52. 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


53. 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


54. 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


55. Wadehra N, Farag S, Bolwell B, Elder P, Penza S, Kalaycio M, Avalos B, Pohlman B, Marcucci G, Sobecks R, Lin T, Andrèsen S, Copelan E: Long-term outcome of Hodgkin disease patients following high-dose busulfan, etoposide, cyclophosphamide, and autologous stem cell transplantation. Biol Blood Marrow Transplant; 2006 Dec;12(12):1343-9
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.
  • Five patients died between 5.3 and 9.3 years of late complications, including secondary myelodysplasia or acute myeloid leukemia, secondary solid malignancies, and pulmonary toxicity.

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Hodgkin Disease.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. BUSULFAN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Biol Blood Marrow Transplant. 2007 Jun;13(6):746-7 [17531785.001]
  • (PMID = 17162217.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; G1LN9045DK / Busulfan
  •  go-up   go-down


56. Suzuki K, Ohishi K, Sekine T, Masuya M, Katayama N: Selective blast cell reduction in elderly patients with acute myeloid leukemia secondary to myelodysplastic syndrome treated with methylprednisolone. Int J Hematol; 2007 May;85(4):344-9
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] Selective blast cell reduction in elderly patients with acute myeloid leukemia secondary to myelodysplastic syndrome treated with methylprednisolone.
  • The management of elderly patients with acute myeloid leukemia (AML) and a poor performance status is challenging.
  • An 89-year-old man with AML secondary to myelodysplastic syndrome (MDS) and a poor performance status (4) underwent treatment with methylprednisolone (mPSL) (125 mg/body), which resulted in a remarkable reduction of blast cells in the peripheral blood.
  • On the basis of this experience, we gave the same mPSL dose to other elderly patients with MDS/AML (n=5) or AML-M4 (n=1) who had a poor performance status (3 or higher) and appeared unable to tolerate standard cytotoxic chemotherapies.
  • Selective and significant blast cell reduction was observed in 4 of the 5 patients with MDS/AML, whereas no effects were seen in the AML patient.
  • Although our experience is limited, these findings may provide a clue to understanding the mechanisms regulating the survival of blast cells of MDS/AML and indicate that mPSL may provide a benefit to a subset of these patients.
  • [MeSH-major] Blast Crisis / drug therapy. Blast Crisis / etiology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / etiology. Methylprednisolone / administration & dosage. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / drug therapy


57. Infante-Rivard C, Vermunt JK, Weinberg CR: Excess transmission of the NAD(P)H:quinone oxidoreductase 1 (NQO1) C609T polymorphism in families of children with acute lymphoblastic leukemia. Am J Epidemiol; 2007 Jun 1;165(11):1248-54
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] Excess transmission of the NAD(P)H:quinone oxidoreductase 1 (NQO1) C609T polymorphism in families of children with acute lymphoblastic leukemia.
  • Topoisomerase II is a DNA-processing enzyme, and secondary acute myeloid leukemia has been associated with exposure to drugs that inhibit its action.
  • Hence, prenatal exposure to chemicals that inhibit topoisomerase II could plausibly contribute to the incidence of childhood leukemia.
  • To assess its role in the etiology of childhood acute lymphoblastic leukemia, the authors studied transmission of the variant T allele in the families (parents and grandparents) of 657 affected children in Québec, Canada (1980-2000).
  • [MeSH-major] Family Health. Inheritance Patterns. NAD(P)H Dehydrogenase (Quinone) / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. BENZENE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Crit Rev Toxicol. 2002 May;32(3):155-210 [12071572.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4590-3 [12393620.001]
  • [Cites] Am J Epidemiol. 2003 Jan 15;157(2):176-82 [12522025.001]
  • [Cites] Am J Hum Genet. 2003 Feb;72(2):438-47 [12533786.001]
  • [Cites] J Biol Chem. 2003 Mar 21;278(12):10368-73 [12529318.001]
  • [Cites] Int J Epidemiol. 2003 Feb;32(1):1-22 [12689998.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):639-49 [12951583.001]
  • [Cites] Methods Enzymol. 2004;382:115-44 [15047100.001]
  • [Cites] Mutat Res. 2004 Mar;566(2):99-130 [15164977.001]
  • [Cites] Pediatr Blood Cancer. 2004 Oct;43(5):568-70 [15382274.001]
  • [Cites] Nature. 1993 May 27;363(6427):358-60 [8497319.001]
  • [Cites] Am J Hum Genet. 1993 Nov;53(5):1114-26 [8213835.001]
  • [Cites] Biotechniques. 1998 Feb;24(2):206-8, 210, 212 [9494715.001]
  • [Cites] Am J Hum Genet. 1998 Apr;62(4):969-78 [9529360.001]
  • [Cites] Am J Epidemiol. 1998 Nov 1;148(9):893-901 [9801020.001]
  • [Cites] Annu Rev Genet. 1998;32:495-519 [9928489.001]
  • [Cites] Am J Hum Genet. 1999 Apr;64(4):1186-93 [10090904.001]
  • [Cites] Pharmacogenetics. 1999 Feb;9(1):113-21 [10208650.001]
  • [Cites] Lancet. 1999 May 29;353(9167):1816-7 [10359403.001]
  • [Cites] Cancer Res. 1999 Aug 15;59(16):4095-9 [10463613.001]
  • [Cites] Epidemiology. 1999 Sep;10(5):481-7 [10468419.001]
  • [Cites] Haematologica. 2004 Dec;89(12):1492-7 [15590400.001]
  • [Cites] Eur J Hum Genet. 2005 Jan;13(1):79-85 [15470368.001]
  • [Cites] Leukemia. 2005 Feb;19(2):214-6 [15618957.001]
  • [Cites] Environ Health Perspect. 2005 Jun;113(6):787-92 [15929905.001]
  • [Cites] Chem Biol Interact. 2005 May 30;153-154:137-46 [15935810.001]
  • [Cites] Haematologica. 2005 Nov;90(11):1511-5 [16266898.001]
  • [Cites] J Biol Chem. 2006 Jul 21;281(29):19798-808 [16682409.001]
  • [Cites] Am J Hum Genet. 2000 Jan;66(1):251-61 [10631155.001]
  • [Cites] Am J Hum Genet. 2000 Jan;66(1):335-8 [10631165.001]
  • [Cites] Cancer Causes Control. 2000 Jul;11(6):547-53 [10880037.001]
  • [Cites] Am J Epidemiol. 2000 Sep 1;152(5):480-6 [10981463.001]
  • [Cites] Br J Cancer. 2000 Dec;83(11):1559-64 [11076669.001]
  • [Cites] Epidemiology. 2001 Jan;12(1):13-9 [11138808.001]
  • [Cites] Cancer Chemother Biol Response Modif. 2001;19:129-47 [11686011.001]
  • [Cites] Int J Cancer. 2002 Jan 10;97(2):230-6 [11774269.001]
  • [Cites] BMJ. 2002 Feb 2;324(7332):283-7 [11823363.001]
  • (PMID = 17332311.001).
  • [ISSN] 0002-9262
  • [Journal-full-title] American journal of epidemiology
  • [ISO-abbreviation] Am. J. Epidemiol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 ES045005-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; J64922108F / Benzene
  • [Other-IDs] NLM/ NIHMS33454; NLM/ PMC2080583
  •  go-up   go-down


58. Gyurkocza B, Storb R, Storer BE, Chauncey TR, Lange T, Shizuru JA, Langston AA, Pulsipher MA, Bredeson CN, Maziarz RT, Bruno B, Petersen FB, Maris MB, Agura E, Yeager A, Bethge W, Sahebi F, Appelbaum FR, Maloney DG, Sandmaier BM: Nonmyeloablative allogeneic hematopoietic cell transplantation in patients with acute myeloid leukemia. J Clin Oncol; 2010 Jun 10;28(17):2859-67
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] Nonmyeloablative allogeneic hematopoietic cell transplantation in patients with acute myeloid leukemia.
  • PURPOSE: Allogeneic hematopoietic cell transplantation (HCT) after high-dose conditioning regimens imposes prohibitively high risks of morbidity and mortality for patients with high-risk acute myeloid leukemia (AML) who are older or have comorbid conditions.
  • PATIENTS AND METHODS: Two hundred seventy-four patients (median age, 60 years) with de novo or secondary AML underwent allogeneic HCT from related (n = 118) or unrelated donors (n = 156) after conditioning with 2 Gy of total-body irradiation (TBI) with or without fludarabine.
  • The cumulative incidences of grades 2, 3, and 4 acute graft-versus-host disease (GVHD) were 38%, 9%, and 5%, respectively.
  • CONCLUSION: Allogeneic HCT from related or unrelated donors after conditioning with low-dose TBI and fludarabine, relying almost exclusively on graft-versus-leukemia effects, can result in long-term remissions in older or medically infirm patients with AML.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2009 Mar 26;113(13):3110-8 [19059878.001]
  • [Cites] J Clin Oncol. 2008 Feb 1;26(4):577-84 [18086801.001]
  • [Cites] Blood. 2009 Sep 10;114(11):2220-31 [19587375.001]
  • [Cites] N Engl J Med. 2009 Sep 24;361(13):1235-48 [19776405.001]
  • [Cites] J Clin Oncol. 2009 Sep 20;27(27):4570-7 [19652066.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4075-83 [11110676.001]
  • [Cites] Blood. 2002 Dec 1;100(12):3869-76 [12393614.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1620-9 [12393457.001]
  • [Cites] Bone Marrow Transplant. 2003 Jun;31(12):1089-95 [12796788.001]
  • [Cites] Biol Blood Marrow Transplant. 2003 Aug;9(8):489-95 [12931117.001]
  • [Cites] Blood. 2003 Sep 15;102(6):2021-30 [12791654.001]
  • [Cites] Blood. 2003 Nov 1;102(9):3447-54 [12855572.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4642-9 [14673054.001]
  • [Cites] Blood. 2004 Aug 1;104(3):865-72 [15090449.001]
  • [Cites] Blood. 1988 Oct;72(4):1300-4 [3048439.001]
  • [Cites] Blood. 1991 Apr 15;77(8):1666-74 [2015395.001]
  • [Cites] N Engl J Med. 1994 Oct 6;331(14):896-903 [8078551.001]
  • [Cites] Blood. 1994 Nov 15;84(10):3558-66 [7524741.001]
  • [Cites] Blood. 1995 Dec 1;86(11):4376-81 [7492799.001]
  • [Cites] Bone Marrow Transplant. 1995 Jun;15(6):825-8 [7581076.001]
  • [Cites] Leukemia. 1996 Jan;10(1):13-9 [8558917.001]
  • [Cites] Blood. 1996 Mar 1;87(5):1710-7 [8634416.001]
  • [Cites] Blood. 1997 Apr 15;89(8):3048-54 [9108426.001]
  • [Cites] Blood. 1998 May 15;91(10):3607-15 [9572995.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3515-20 [9808542.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1969-78 [15632409.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Apr;11(4):272-9 [15812392.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3439-46 [15824415.001]
  • [Cites] Leukemia. 2005 Jun;19(6):990-7 [15800667.001]
  • [Cites] Leukemia. 2005 Jun;19(6):916-20 [15843817.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5728-38 [16009946.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2912-9 [15994282.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Dec;11(12):945-56 [16338616.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9387-93 [16314618.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):444-53 [16344316.001]
  • [Cites] Leukemia. 2006 Feb;20(2):322-8 [16307018.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3959-66 [16880451.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 Oct;12(10):1047-55 [17067911.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2744-8 [17595333.001]
  • [Cites] Br J Haematol. 2009 Jun;145(5):598-605 [19344426.001]
  • (PMID = 20439626.001).
  • [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 / NCI NIH HHS / CA / CA18029; United States / NHLBI NIH HHS / HL / HL36444; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / P30 CA015704; United States / NCI NIH HHS / CA / CA78902; United States / NCI NIH HHS / CA / R21 CA106177; United States / NCI NIH HHS / CA / CA15704; United States / NHLBI NIH HHS / HL / P01 HL036444; United States / NCI NIH HHS / CA / CA106177; United States / NCI NIH HHS / CA / P01 CA078902
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2903320
  •  go-up   go-down


59. Larson RA: Is secondary leukemia an independent poor prognostic factor in acute myeloid leukemia? Best Pract Res Clin Haematol; 2007 Mar;20(1):29-37
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] Is secondary leukemia an independent poor prognostic factor in acute myeloid leukemia?
  • Secondary leukemia is a poorly defined term that often refers to the development of acute myeloid leukemia (AML) following the history of a previous disease, such as a myelodysplastic syndrome or a chronic myeloproliferative disorder.
  • Secondary leukemia can also be a consequence of treatment with chemotherapy, including alkylating agents and topoisomerase II inhibitors, and/or radiotherapy, or due to exposure to environmental carcinogens.
  • Outcomes for this large and variable group of patients with secondary AML have been poor compared to people who develop AML de novo.
  • The question arises whether a diagnosis of secondary leukemia per se indicates a poor prognosis or whether their bad outcomes result from an association with certain morphologic and biologic characteristics.
  • Morphologic dysplasia in de novo AML is related to unfavorable cytogenetics, but has no independent prognostic relevance under the conditions of intensive chemotherapy.
  • While there is no significant correlation between cytogenetic risk groups and dysplasia, cytogenetic features do have an impact on outcome among both de novo and secondary AML patients.
  • In various subgroups of secondary AML, the spectrum of cytogenetic abnormalities is similar to de novo AML, but the frequency of abnormalities associated with unfavorable and intermediate risk cytogenetics, such as a complex karyotype, trisomy 8, monosomy 7, and others, is higher in secondary AML.
  • The survival of patients with therapy-related myeloid leukemia (t-AML) is generally shorter than for those with de novo AML within the same cytogenetic risk group.
  • Across the population of t-AML, however, survival varies according to cytogenetic risk group, with longer survival in patients with favorable-risk karyotypes.
  • The term secondary AML is too broad and imprecise to be of importance and should not be used.
  • These AML patients should be enrolled on front-line chemotherapy trials and should be stratified by pretreatment disease status and exposure history, if necessary.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Humans. Myelodysplastic Syndromes. Myeloproliferative Disorders. Neoplasms, Second Primary / drug therapy. Neoplasms, Second Primary / genetics. Prognosis. Survival Analysis

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17336252.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 23
  •  go-up   go-down


60. Al-Ali HK, Brand R, van Biezen A, Finke J, Boogaerts M, Fauser AA, Egeler M, Cahn JY, Arnold R, Biersack H, Niederwieser D, de Witte T: A retrospective comparison of autologous and unrelated donor hematopoietic cell transplantation in myelodysplastic syndrome and secondary acute myeloid leukemia: a report on behalf of the Chronic Leukemia Working Party of the European Group for Blood and Marrow Transplantation (EBMT). Leukemia; 2007 Sep;21(9):1945-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A retrospective comparison of autologous and unrelated donor hematopoietic cell transplantation in myelodysplastic syndrome and secondary acute myeloid leukemia: a report on behalf of the Chronic Leukemia Working Party of the European Group for Blood and Marrow Transplantation (EBMT).
  • Hematopoietic cell transplantation (HCT) is an effective treatment for myelodysplasia (MDS) and secondary acute myeloid leukemia (sAML).
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / mortality. Leukemia, Myeloid / mortality. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / mortality. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Distribution. Aged. Disease-Free Survival. Female. Humans. Incidence. Male. Middle Aged. Recurrence. Retrospective Studies. Survival Analysis. Tissue Donors. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome


61. Preudhomme C, Renneville A, Bourdon V, Philippe N, Roche-Lestienne C, Boissel N, Dhedin N, André JM, Cornillet-Lefebvre P, Baruchel A, Mozziconacci MJ, Sobol H: High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder. Blood; 2009 May 28;113(22):5583-7
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] High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder.
  • Familial platelet disorder (FPD), a rare autosomal dominant disorder characterized by quantitative and qualitative platelet abnormalities, is considered as a model of genetic predisposition to acute myeloid leukemia (AML).
  • So far, monoallelic RUNX1 germline mutations have been found in 19 of 20 families with reported FPD, and the analysis of blast cells from only 5 patients at acute leukemia (AL) stage has shown no additional RUNX1 abnormality.
  • In addition to the germline RUNX1 mutation, we identified a second RUNX1 alteration in 6 AML cases (acquired point mutations in 4 cases and duplication of the altered RUNX1 allele associated with acquired trisomy 21 in 2 other cases).
  • Although haploinsufficiency of RUNX1 causes FPD, our findings suggest that a second genetic event involving RUNX1 is often associated with progression to AML.
  • [MeSH-major] Blood Platelet Disorders / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics


62. Pulsoni A, Pagano L: Treatment of secondary acute myeloid leukemia. J Clin Oncol; 2005 Feb 1;23(4):926-7
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] Treatment of secondary acute myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Neoplasms, Second Primary / therapy

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] J Clin Oncol. 2004 Jun 15;22(12):2510-1 [15197216.001]
  • (PMID = 15681547.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  •  go-up   go-down


63. Marcucci G, Mrózek K, Ruppert AS, Maharry K, Kolitz JE, Moore JO, Mayer RJ, Pettenati MJ, Powell BL, Edwards CG, Sterling LJ, Vardiman JW, Schiffer CA, Carroll AJ, Larson RA, Bloomfield CD: Prognostic factors and outcome of core binding factor acute myeloid leukemia patients with t(8;21) differ from those of patients with inv(16): a Cancer and Leukemia Group B study. J Clin Oncol; 2005 Aug 20;23(24):5705-17
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 outcome of core binding factor acute myeloid leukemia patients with t(8;21) differ from those of patients with inv(16): a Cancer and Leukemia Group B study.
  • PURPOSE: Because both t(8;21) and inv(16) disrupt core binding factor (CBF) in acute myeloid leukemia (AML) and confer relatively favorable prognoses, these cytogenetic groups are often treated similarly.
  • PATIENTS AND METHODS: We analyzed 144 consecutive adults with t(8;21) and 168 with inv(16) treated on Cancer and Leukemia Group B front-line studies.
  • RESULTS: With a median follow-up of 6.4 years, for CBF AML as a whole, the CR rate was 88%, 5-year OS was 50% and CIR was 53%.
  • Unexpectedly, race was an important predictor for t(8;21) AML, in that nonwhites failed induction more often (odds ratio = 5.7; P = .006) and had shorter OS than whites when certain secondary cytogenetic abnormalities were present.
  • For inv(16) AML, secondary cytogenetic abnormalities (especially +22) and male sex predicted better outcome.
  • CONCLUSION: When the prognostic impact of race, secondary cytogenetic abnormalities, sex, and response to salvage treatment is considered, t(8;21) and inv(16) AMLs seem to be distinct clinical entities and should be stratified and reported separately.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Aged. Aziridines / administration & dosage. Benzoquinones / administration & dosage. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Etoposide / administration & dosage. Female. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Prognosis. Proportional Hazards Models. Prospective Studies. Remission Induction. Statistics, Nonparametric. Survival Analysis

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16110030.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / CA31946; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / K08-CA90469; United States / NCI NIH HHS / CA / P30-CA16058
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aziridines; 0 / Benzoquinones; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; FQL5EUP13W / diaziquone; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


64. 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


65. Kornblau SM, Minden MD, Rosen DB, Putta S, Cohen A, Covey T, Spellmeyer DC, Fantl WJ, Gayko U, Cesano A: Dynamic single-cell network profiles in acute myelogenous leukemia are associated with patient response to standard induction therapy. Clin Cancer Res; 2010 Jul 15;16(14):3721-33
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] Dynamic single-cell network profiles in acute myelogenous leukemia are associated with patient response to standard induction therapy.
  • PURPOSE: Complete response to induction chemotherapy is observed in approximately 60% of patients with newly diagnosed non-M3 acute myelogenous leukemia (AML).
  • However, no methods exist to predict with high accuracy at the individual patient level the response to standard AML induction therapy.
  • EXPERIMENTAL DESIGN: We applied single-cell network profiling (SCNP) using flow cytometry, a tool that allows a comprehensive functional assessment of intracellular signaling pathways in heterogeneous tissues, to two training cohorts of AML samples (n = 34 and 88) to predict the likelihood of response to induction chemotherapy.
  • Results were independent of cytogenetics, FLT3 mutational status, and diagnosis of secondary AML.
  • SCNP provides information distinct from other known prognostic factors such as age, secondary AML, cytogenetics, and molecular alterations and is potentially combinable with the latter to improve clinical decision making.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism


66. Monreal MB, Pardo ML, Pavlovsky MA, Fernandez I, Corrado CS, Giere I, Sapia S, Pavlovsky S: Increased immature hematopoietic progenitor cells CD34+/CD38dim in myelodysplasia. Cytometry B Clin Cytom; 2006 Mar;70(2):63-70
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: We analyzed the expression of CD38 and HLA-DR on CD34+ cells by flow cytometry in 36 patients with MDS, as well as in healthy donors (n = 12) and patients with other hematological disorders: non-Hodgkin lymphomas and multiple myeloma, both in complete remission (CR) (n = 32); acute lymphoblastic leukemia in CR (n = 17); de novo acute myeloblastic leukemia (AML) at diagnosis (n = 22) and in CR (n = 37); and AML secondary to MDS at diagnosis (n = 19).
  • RESULTS: Compared to normal BM, the fraction of immature HPC, characterized as CD34+bright, intermediate FSC/SSC, and CD38dim, was significantly increased in high risk MDS and secondary AML, but not in low risk MDS, (P < or = 0.001, P = 0.03, and P = 0.7).
  • De novo AML showed decreased immature HPC.
  • Increased immature HPC in high risk MDS and secondary AML may reflect blocked differentiation of CD34+ cells in these diseases.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation. Disease Progression. Female. Flow Cytometry. HLA-DR Antigens / immunology. Humans. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / immunology. Male. Middle Aged. Multiple Myeloma / diagnosis. Multiple Myeloma / immunology. Observer Variation. Phenotype. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Prognosis. Reproducibility of Results. Risk Factors

  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • 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 2005 International Society for Analytical Cytology.
  • (PMID = 16470534.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / HLA-DR Antigens; EC 3.2.2.5 / Antigens, CD38
  •  go-up   go-down


67. Mihailov G, Ganeva P, Vassileva N, Guenova M, Balacenko G, Toshkov S, Hodjadjik D: Secondary acute myeloid leukemia early after therapy for Hodgkin's disease--a case report. J BUON; 2007 Jul-Sep;12(3):403-6
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] Secondary acute myeloid leukemia early after therapy for Hodgkin's disease--a case report.
  • A case of acute myeloid leukemia (AML) after successful therapy for Hodgkin's disease (HD) is reported.
  • Seven months after the CR was obtained the patient developed AML.
  • Knowing that the prognosis of patients with secondary AML (sAML) after primary HD is poor we decided to perform autologous peripheral stem cells' transplantation.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / surgery. Neoplasms, Second Primary / diagnosis. Neoplasms, Second Primary / surgery

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17918297.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  •  go-up   go-down


68. Bakanay ŞM, Topçuoğlu P, Uğur Bilgin A, Yararbaş K, Berker Karaüzüm S, Özcan M, Arat M, Ündar L, Ilhan O: Clonal evolution of monosomy 7 in acquired severe aplastic anemia: Two cases treated with allogeneic hematopoietic stem cell transplantation. Turk J Haematol; 2008 Jun 5;25(2):94-7
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.
  • Aplastic anemia (AA) may evolve into clonal diseases like myelodysplastic syndrome (MDS) and acute myeloblastic leuke¬mia (AML).
  • Monosomy 7 is a poor prognostic chromosomal abnormality commonly associated with therapy related MDS and secondary AML.
  • Both patients had received immunosuppressive therapy (IST) as first line treatment and had monosomy 7 positive clone at transformation to MDS with refractory anemia and excess of blast (RAEB-II) and AML, respectively.

  • 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 = 27264447.001).
  • [ISSN] 1300-7777
  • [Journal-full-title] Turkish journal of haematology : official journal of Turkish Society of Haematology
  • [ISO-abbreviation] Turk J Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
  •  go-up   go-down


69. Abdel-Wahab O, Manshouri T, Patel J, Harris K, Yao J, Hedvat C, Heguy A, Bueso-Ramos C, Kantarjian H, Levine RL, Verstovsek S: Genetic analysis of transforming events that convert chronic myeloproliferative neoplasms to leukemias. Cancer Res; 2010 Jan 15;70(2):447-52
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The oncogenetic events that transform chronic myeloproliferative neoplasms (MPN) to acute myeloid leukemias (AML) are not well characterized.
  • We investigated the role of several genes implicated in leukemic transformation by mutational analysis of 63 patients with AML secondary to a preexisting MPN (sAML).
  • In contrast, ASXL1 mutations were almost always detected in both the MPN and AML clones from individual patients.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • 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 .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 1994 Apr;8 Suppl 1:S27-9 [8152300.001]
  • [Cites] Cancer Res. 2010 Jul 15;70(14):5901-11 [20570890.001]
  • [Cites] Blood. 2005 Feb 1;105(3):973-7 [15388582.001]
  • [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] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Blood. 2006 May 15;107(10):4139-41 [16434490.001]
  • [Cites] Nat Med. 2006 Jul;12(7):852-5 [16799556.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3548-55 [16873677.001]
  • [Cites] N Engl J Med. 2006 Dec 7;355(23):2452-66 [17151367.001]
  • [Cites] Blood. 2007 Jul 1;110(1):375-9 [17363731.001]
  • [Cites] N Engl J Med. 2009 Feb 19;360(8):765-73 [19228619.001]
  • [Cites] N Engl J Med. 2009 May 28;360(22):2289-301 [19474426.001]
  • [Cites] Blood. 2009 Jul 2;114(1):144-7 [19420352.001]
  • [Cites] N Engl J Med. 2009 Sep 10;361(11):1058-66 [19657110.001]
  • [Cites] Leukemia. 2009 Nov;23(11):2183-6 [19609284.001]
  • [Cites] Semin Hematol. 1997 Jan;34(1):6-16 [9025157.001]
  • (PMID = 20068184.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K08 HL082677; United States / NCI NIH HHS / CA / P30 CA008748; United States / NHLBI NIH HHS / HL / K08 HL082677-01A1; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / R01 CA151949; United States / NHLBI NIH HHS / HL / HL082677-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ASXL1 protein, human; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / TET2 protein, human; 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
  • [Other-IDs] NLM/ NIHMS162374; NLM/ PMC2947340
  •  go-up   go-down


70. Xu LP, Huang XJ, Liu KY, Chen H, Liu DH, Han W, Chen YH, Gao ZY, Lu J, Wang JZ, Lu DP: [Allogenic stem cell transplantation from genotypically HLA-identical siblings for 30 patients with myelodysplastic syndromes]. Zhonghua Xue Ye Xue Za Zhi; 2006 Aug;27(8):518-21
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.
  • On HSCT, 4 patients had refractory anemia (RA) , 2 RA with ringed sideroblasts (RARS) , 7 RA with excess blasts(RAEB) , 14 RAEB in transformation (RAEB-t) , 3 already progressed to secondary AML.
  • RESULTS: The 3-year expected overall survival (OS) was 63.61%, 3-year expected disease-free survival ( DFS) 61.41%, and relapse rate 5.26%; OS for RA/ RAS, RAEB and RAEB-t/AML subgroup was 83.33%, 34.29% and 66.67% , respectively, and all had no statistic difference among them.


71. Burcu M, O'Loughlin KL, Ford LA, Baer MR: Amonafide L-malate is not a substrate for multidrug resistance proteins in secondary acute myeloid leukemia. Leukemia; 2008 Nov;22(11):2110-5
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] Amonafide L-malate is not a substrate for multidrug resistance proteins in secondary acute myeloid leukemia.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. ATP-Binding Cassette, Sub-Family B, Member 1 / metabolism. Antineoplastic Agents / pharmacokinetics. Drug Resistance, Multiple. Leukemia, Myeloid, Acute / metabolism. Naphthalimides / pharmacokinetics. Neoplasm Proteins / metabolism

  • 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 = 18418409.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Antineoplastic Agents; 0 / Cyclosporins; 0 / Enzyme Inhibitors; 0 / Naphthalimides; 0 / Neoplasm Proteins; 0 / Topoisomerase II Inhibitors; LI06Q37TEG / xanafide; Q7ZP55KF3X / valspodar
  •  go-up   go-down


72. Soares EM, Santos N, de Araújo Silva Amaral B, Silva ML, Leite EP, Silva MO, Muniz MT, Ribeiro RC, de Morais VL, de Jesus Marques Salles T: Secondary acute myeloid leukemia with a t(1;11)(q23;p15) in an adolescent treated for testicular sarcoma. Cancer Genet Cytogenet; 2006 Aug;169(1):83-5
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] Secondary acute myeloid leukemia with a t(1;11)(q23;p15) in an adolescent treated for testicular sarcoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 11. Leukemia, Myeloid / genetics. Sarcoma / genetics. Testicular Neoplasms / drug therapy. Testicular Neoplasms / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Humans. Karyotyping. Male


73. Sonneck K, Mannhalter C, Krauth MT, Sperr WR, Schwarzinger I, Fonatsch C, Haas O, Geissler K, Valent P: An unusual case of myelodysplastic syndrome with prolonged clonal stability, indolent clinical course over a decade, and spontaneous regression of AML in the terminal phase. Eur J Haematol; 2005 Jul;75(1):73-7
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] An unusual case of myelodysplastic syndrome with prolonged clonal stability, indolent clinical course over a decade, and spontaneous regression of AML in the terminal phase.
  • An unusual case of secondary acute myeloid leukemia (AML) with indolent clinical course is described.
  • In 2001, transformation to secondary AML with an increase in bone marrow blasts (>20%) and thrombocytopenia, was found.
  • However, the bone marrow still showed AML with >20% blasts.
  • [MeSH-major] Leukemia, Myeloid, Acute / physiopathology. Myelodysplastic Syndromes / complications


74. Takei N, Suzukawa K, Mukai HY, Itoh T, Okoshi Y, Yoda Y, Nagasawa T: Therapy-related acute myeloid leukemia 6 years after clonal detection of inv(11)(q21q23) and MLL gene rearrangement. Int J Hematol; 2006 Apr;83(3):247-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related acute myeloid leukemia 6 years after clonal detection of inv(11)(q21q23) and MLL gene rearrangement.
  • Results of recent studies with animal models suggest that expression of MLL fusion proteins promotes acute leukemogenesis.
  • However, the most potent MLL fusion proteins are not sufficient for the development of acute myeloid leukemia (AML).
  • The clinical data on the pathogenesis of this type of leukemia are limited.
  • We analyzed the case of a patient with therapy-related AML with MLL rearrangement.
  • The patient initially developed AML with t(8;21).
  • After 6-year persistence of a clone with the inversion 11 karyotype in the bone marrow, secondary AML developed.
  • One was that MLL rearrangement was not sufficient for the development of leukemia.
  • [MeSH-major] Chromosome Inversion / genetics. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics
  • [MeSH-minor] Antigens, CD13 / biosynthesis. Antigens, CD34 / biosynthesis. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Female. Humans. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Semin Hematol. 2003 Oct;40(4):268-73 [14582077.001]
  • [Cites] Hematol Oncol Clin North Am. 1997 Oct;11(5):963-73 [9336725.001]
  • [Cites] Cancer. 1993 Jun 15;71(12):3888-95 [8508355.001]
  • [Cites] Genes Dev. 2004 May 1;18(9):965-74 [15132992.001]
  • [Cites] Med Pediatr Oncol. 2001 May;36(5):525-35 [11340607.001]
  • [Cites] J Clin Oncol. 1991 Jan;9(1):25-38 [1702144.001]
  • [Cites] Leukemia. 1999 Dec;13(12):2116-8 [10602439.001]
  • [Cites] Blood. 2005 May 15;105(10):4151-2 [15867425.001]
  • [Cites] Blood. 1992 Jul 1;80(1):217-24 [1611087.001]
  • [Cites] Best Pract Res Clin Haematol. 2001 Mar;14(1):119-37 [11355927.001]
  • [Cites] Leukemia. 1991 Oct;5(10):908-11 [1961025.001]
  • [Cites] Med Pediatr Oncol. 1994;23(2):86-98 [8202047.001]
  • [Cites] Int J Hematol. 2000 Apr;71(3):238-44 [10846828.001]
  • [Cites] Blood. 1998 Oct 15;92(8):2886-92 [9763574.001]
  • [Cites] Oncogene. 2001 Sep 10;20(40):5695-707 [11607819.001]
  • [Cites] Leukemia. 1998 May;12(5):811-22 [9593286.001]
  • [Cites] Blood. 1997 Jul 15;90(2):535-41 [9226152.001]
  • [Cites] FASEB J. 2004 Jan;18(1):173-5 [14630694.001]
  • [Cites] Leuk Lymphoma. 2001 Apr;41(3-4):255-76 [11378539.001]
  • [Cites] Semin Cancer Biol. 2005 Jun;15(3):175-88 [15826832.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3029-35 [14701873.001]
  • [Cites] Blood. 2005 Mar 1;105(5):2124-31 [15528316.001]
  • (PMID = 16720556.001).
  • [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
  • [Chemical-registry-number] 0 / Antigens, CD34; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.4.11.2 / Antigens, CD13
  •  go-up   go-down


75. Ooi J: The efficacy of unrelated cord blood transplantation for adult myelodysplastic syndrome. Leuk Lymphoma; 2006 Apr;47(4):599-602
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Diagnosis at transplantation included refractory anemia (RA) (n = 3), refractory anemia with excess blasts (RAEB) (n = 2), RAEB-t (n = 2), and MDS-related secondary acute myeloid leukemia (AML) (n = 15).
  • Twenty one patients had myeloid reconstitution and the median time to more than 0.5 x 10(9)/l absolute neutrophil count was 22.5 days.
  • Acute GVHD above grade II occurred in seven of 21 evaluable patients and chronic GVHD in 16 of 19 evaluable patients.


76. Hallemeier CL, Girgis MD, Blum WG, Brown RA, Khoury HJ, Devine SM, Vij R, Lin HS, DiPersio JF, Adkins DR: Long-term remissions in patients with myelodysplastic syndrome and secondary acute myelogenous leukemia undergoing allogeneic transplantation following a reduced intensity conditioning regimen of 550 cGy total body irradiation and cyclophosphamide. Biol Blood Marrow Transplant; 2006 Jul;12(7):749-57
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] Long-term remissions in patients with myelodysplastic syndrome and secondary acute myelogenous leukemia undergoing allogeneic transplantation following a reduced intensity conditioning regimen of 550 cGy total body irradiation and cyclophosphamide.
  • We analyzed outcomes of patients with myelodysplastic syndrome (MDS) or secondary acute myelogenous leukemia (sAML) that were treated at our institution with a reduced intensity conditioning (RIC) regimen of 550-cGy total body irradiation and cyclophosphamide followed by related donor (RD) or unrelated donor (URD) transplantation.
  • [MeSH-major] Bone Marrow Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Neoplasms, Second Primary / therapy. Peripheral Blood Stem Cell Transplantation / methods. Transplantation Conditioning / methods


77. Balgobind BV, Lugthart S, Hollink IH, Arentsen-Peters ST, van Wering ER, de Graaf SS, Reinhardt D, Creutzig U, Kaspers GJ, de Bont ES, Stary J, Trka J, Zimmermann M, Beverloo HB, Pieters R, Delwel R, Zwaan CM, van den Heuvel-Eibrink MM: EVI1 overexpression in distinct subtypes of pediatric acute myeloid leukemia. Leukemia; 2010 May;24(5):942-9
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] EVI1 overexpression in distinct subtypes of pediatric acute myeloid leukemia.
  • Overexpression of the ecotropic virus integration-1 (EVI1) gene (EVI1+), localized at chromosome 3q26, is associated with adverse outcome in adult acute myeloid leukemia (AML).
  • In pediatric AML, 3q26 abnormalities are rare, and the role of EVI1 is unknown.
  • We studied 228 pediatric AML samples for EVI1+ using gene expression profiling and RQ-PCR.
  • EVI1+ was found in 20/213 (9%) of children with de novo AML, and in 4/8 with secondary AML.
  • It was predominantly found in MLL-rearranged AML (13/47), monosomy 7 (2/3), or FAB M6/7 (6/10), and mutually exclusive with core-binding factor AML, t(15;17), and NPM1 mutations.
  • Although significant differences in 4 years pEFS for EVI1+ and EVI1- pediatric AML were observed (28%+/-11 vs 44%+/-4, P=0.04), multivariate analysis did not identify EVI1+ as an independent prognostic factor.
  • We conclude that EVI1+ can be found in approximately 10% of pediatric AML.
  • Although EVI1+ was not an independent prognostic factor, it was predominantly found in subtypes of pediatric AML that are related with an intermediate to unfavorable prognosis.
  • Remarkably, no 3q26 abnormalities were identified in EVI1+ pediatric AML.
  • [MeSH-major] Biomarkers, Tumor / genetics. Chromosomes, Human, Pair 3 / genetics. DNA-Binding Proteins / genetics. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20357826.001).
  • [ISSN] 1476-5551
  • [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 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / RNA, Messenger; 0 / Transcription Factors
  •  go-up   go-down


78. Cilloni D, Messa E, Messa F, Carturan S, Defilippi I, Arruga F, Rosso V, Catalano R, Bracco E, Nicoli P, Saglio G: Genetic abnormalities as targets for molecular therapies in myelodysplastic syndromes. Ann N Y Acad Sci; 2006 Nov;1089:411-23
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent advances in molecular genetics have increased knowledge regarding the mechanisms leading to myelodysplastic syndrome (MDS), secondary acute myeloid leukemia (AML), and therapy-induced MDS.
  • Many genetic defects underlying MDS and AML have been identified thereby allowing the development of new molecular-targeted therapies.
  • These agents have been tested in patients with solid tumors and hematologic malignancies such as AML and MDS.

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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 = 17261784.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / MECOM protein, human; 0 / Transcription Factors; 0 / WT1 Proteins; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Number-of-references] 76
  •  go-up   go-down


79. Nemoto N, Suzukawa K, Shimizu S, Shinagawa A, Takei N, Taki T, Hayashi Y, Kojima H, Kawakami Y, Nagasawa T: Identification of a novel fusion gene MLL-MAML2 in secondary acute myelogenous leukemia and myelodysplastic syndrome with inv(11)(q21q23). Genes Chromosomes Cancer; 2007 Sep;46(9):813-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of a novel fusion gene MLL-MAML2 in secondary acute myelogenous leukemia and myelodysplastic syndrome with inv(11)(q21q23).
  • We have identified a novel fusion partner of MLL, namely the mastermind like 2 (MAML2 gene), in secondary acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) with inv(11)(q21q23).
  • RT-PCR and sequencing revealed that exon 7 of MLL was fused to exon 2 of MAML2 in the AML and MDS cells.
  • MLL-MAML2 in secondary AML/MDS and MECT1-MAML2 in mucoepithelioid carcinoma, benign Wartin's tumor, and clear cell hidradenoma consist of the same COOH-terminal part of MAML2.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. Transcription Factors / genetics


80. Natelson EA: Benzene-induced acute myeloid leukemia: a clinician's perspective. Am J Hematol; 2007 Sep;82(9):826-30
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] Benzene-induced acute myeloid leukemia: a clinician's perspective.
  • Benzene-induced acute myeloid leukemia (AML) is considered a secondary form of AML, based both in theory and on limited cohort observations.
  • Its latency, cytogenetic aberrations, and clinical features are thought similar to, or identical with, AML resulting from the use of modern day cytotoxic agents for chemotherapy and immunotherapy.
  • Although distinction between secondary AML and the far more common de novo AML is difficult to establish with certainty in any given case, latency from toxic therapeutic and environmental exposure and certain clinical and pathological features generally separate these two entities.
  • AML is the only human neoplasm proven to be potentially caused by benzene, which actually is an obsolete form of chemotherapy.
  • A review of benzene-induced AML suggests that, in developed countries, this entity should no longer merit serious consideration among workers in the modern petrochemical industry and related fields.
  • [MeSH-major] Attitude of Health Personnel. Benzene / adverse effects. Developed Countries. Drug-Related Side Effects and Adverse Reactions. Leukemia, Myeloid / etiology
  • [MeSH-minor] Acute Disease. Chromosome Aberrations / chemically induced. Chromosome Inversion. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Humans. Occupational Diseases / chemically induced. Occupational Diseases / epidemiology. Occupational Exposure / adverse effects. Occupational Exposure / analysis. Petroleum / adverse effects. Translocation, Genetic

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Drug Reactions.
  • Hazardous Substances Data Bank. BENZENE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2007 Wiley-Liss, Inc
  • (PMID = 17506065.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Petroleum; J64922108F / Benzene
  • [Number-of-references] 79
  •  go-up   go-down


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

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


82. Hussein K, Bock O, Theophile K, Schulz-Bischof K, Porwit A, Schlue J, Jonigk D, Kreipe H: MPLW515L mutation in acute megakaryoblastic leukaemia. Leukemia; 2009 May;23(5):852-5
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] MPLW515L mutation in acute megakaryoblastic leukaemia.
  • A series of primary and secondary acute myeloid leukaemias (AML) with megakaryoblastic phenotype and myelofibrosis unrelated to PMF (n=12) was analysed for the MPL(W515K/L) mutation by pyrosequencing.
  • None of the secondary AML cases evolving from pre-existing PMF showed MPL(W515K/L) (n=4).
  • We conclude that MPL(W515L) occurs in a considerable proportion of acute megakaryoblastic leukaemias with myelofibrosis unrelated to PMF.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mutation / genetics. Primary Myelofibrosis / genetics. Receptors, Thrombopoietin / genetics

  • 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
  • [CommentIn] Leukemia. 2009 Nov;23(11):2159-60 [19657363.001]
  • (PMID = 19194467.001).
  • [ISSN] 1476-5551
  • [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 / Receptors, Thrombopoietin; 143641-95-6 / MPL protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


83. Schroeder T, Czibere A, Zohren F, Aivado M, Gattermann N, Germing U, Haas R: Meningioma 1 gene is differentially expressed in CD34 positive cells from bone marrow of patients with myelodysplastic syndromes with the highest expression in refractory anemia with excess of blasts and secondary acute myeloid leukemia. Leuk Lymphoma; 2009 Jun;50(6):1043-6
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] Meningioma 1 gene is differentially expressed in CD34 positive cells from bone marrow of patients with myelodysplastic syndromes with the highest expression in refractory anemia with excess of blasts and secondary acute myeloid leukemia.
  • [MeSH-major] Anemia / genetics. Antigens, CD34 / blood. Bone Marrow Cells / metabolism. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Disease Progression. Female. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Humans. Male. Middle Aged. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction


84. Klepin HD, Balducci L: Acute myelogenous leukemia in older adults. Oncologist; 2009 Mar;14(3):222-32
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myelogenous leukemia in older adults.
  • The incidence of acute myelogenous leukemia (AML) increases with age.
  • Older AML patients, generally defined by age > or = 60 years, have worse treatment outcomes than younger patients.
  • Older patients are more likely to present with unfavorable cytogenetic abnormalities, multidrug resistance phenotypes, and secondary AML.
  • Investigations of hypomethylating agents and signal transduction inhibitors hold promise for the treatment of AML patients.
  • [MeSH-major] Geriatrics / methods. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy


85. Bacher U, Haferlach T, Schoch C: Gain of 9p due to an unbalanced rearrangement der(9;18): a recurrent clonal abnormality in chronic myeloproliferative disorders. Cancer Genet Cytogenet; 2005 Jul 15;160(2):179-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Three cases were diagnosed as polycythemia vera; one case presented with secondary acute myeloid leukemia following idiopathic osteomyelofibrosis.

  • Genetic Alliance. consumer health - Chronic Myeloproliferative Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15993276.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


86. Park TS, Choi JR, Yoon SH, Song J, Kim J, Kim SJ, Kwon O, Min YH: Acute promyelocytic leukemia relapsing as secondary acute myelogenous leukemia with translocation t(3;21)(q26;q22) and RUNX1-MDS1-EVI1 fusion transcript. Cancer Genet Cytogenet; 2008 Dec;187(2):61-73
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] Acute promyelocytic leukemia relapsing as secondary acute myelogenous leukemia with translocation t(3;21)(q26;q22) and RUNX1-MDS1-EVI1 fusion transcript.
  • Acute promyelocytic leukemia (APL) is a subtype of acute myelogenous leukemia (AML) that is characterized by peculiar clinical and biologic features, including severe hemorrhagic diathesis, specific recurrent chromosomal aberration, and distinct morphologic features with predominant pathologic promyelocytes.
  • A reciprocal translocation involving chromosomes 15 and 17, t(15;17)(q22;q21), is a characteristic feature of APL that represents approximately 5-8% of AML.
  • In contrast to other AML subtypes, APL is particularly sensitive to treatment with all trans-retinoic acid (ATRA) combined with chemotherapy, converting this once fatal leukemia to a highly curable disease.
  • Nonetheless, therapy-related myelodysplastic syndrome-acute myelogenous leukemia (t-MDS/AML) has been reported as a rare complication of chemotherapy in APL.
  • Of 30 APL cases described as t-MDS/AML in the literature, only 1 case relapsed as acute leukemia with t(3;21)(q26;q22).
  • Here we describe a rare case of APL relapsing as secondary AML with t(3;21)(q26;q22) and clinically characterize this patient using the RUNX1 (previously AML1)-MDS1-EVI1 fusion transcript (with follow-up for 55 months), and review the relevant literature.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Promyelocytic, Acute / genetics. Neoplasms, Second Primary / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic


87. Shao B, Gao YR, Wang C, Yan SK, Cai Q, Jiang JL, Yang J, Bai HT, Zhao M, Zhao CX: [Prognostic factor analysis of 77 old patients with acute myelogenous leukemia]. Ai Zheng; 2006 Aug;25(8):1007-12
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] [Prognostic factor analysis of 77 old patients with acute myelogenous leukemia].
  • BACKGROUND & OBJECTIVE: The manifestations of old acute myelogenous (AML) patients have their special biological and clinical characteristics, with lower response rate to therapy and shorter survival time.
  • This study was to investigate the prognostic factors of elderly patients with AML retrospectively.
  • METHODS: 77 patients aged> or =60 years with AML from 1994 to 2005 were admitted to our study and all the possible prognostic factors were analyzed with Kaplan-Meier survival analysis.
  • The patients with primary AML (median survival time was 98 days) had significantly longer survival time than those with secondary AML (median survival time was 32 days)(P=0.007), which their CR ratios were 50% and 0% (P=0.023).
  • CONCLUSIONS: Factors, including age >70, PS 2 to 4, percentage of blasts in bone marrow >50%, secondary AML, unfavorable karyotype, expression of CD34, lower dosage.
  • [MeSH-major] Anthracyclines / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

  • 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
  • (PMID = 16965684.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antigens, CD34
  •  go-up   go-down


88. Chaoui D, Peffault De Latour R, Legrand O, Marie JP: Acute myeloid leukemia in the elderly: etoposide when anthracyclins are contraindicated. Leuk Lymphoma; 2005 Mar;46(3):401-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia in the elderly: etoposide when anthracyclins are contraindicated.
  • We investigated whether etoposide might be a suitable alternative to anthracyclins for the treatment of elderly patients with acute myeloid leukemia (AML) in whom anthracyclins are contraindicated.
  • In total, 88 patients over 60 years old were treated in our department between 1988 and 2000 for de novo or secondary AML.
  • Etoposide combined with a standard dose of cytosine arabinoside is relatively safe and effective in elderly patients with AML and offers an alternative approach to patients with cardiac contraindications to anthracyclin treatment.
  • [MeSH-major] Anthracyclines / contraindications. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Etoposide / administration & dosage. Leukemia, Myeloid, Acute / drug therapy

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15621830.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracyclines; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


89. Wang H, Wang XQ, Xu XP, Lin GW: ID4 methylation predicts high risk of leukemic transformation in patients with myelodysplastic syndrome. Leuk Res; 2010 May;34(5):598-604
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.
  • Epigenetic gene silencing due to promoter methylation is observed in human cancers like acute myeloid leukemia (AML).
  • Little is known about aberrant methylation in myelodysplastic syndrome (MDS), a heterogeneous clonal stem cell disorder with a approximately 30% risk of transformation into secondary AML.
  • Multivariate analysis indicated that ID4 methylation status was the independent factor that impacted leukemia-free survival (LFS).
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. DNA Methylation / genetics. Inhibitor of Differentiation Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


90. Shono Y, Toubai T, Ota S, Ibata M, Mashiko S, Hirate D, Miura Y, Umehara S, Toyoshima N, Tanaka J, Asaka M, Imamura M: Abnormal expansion of naïve B lymphocytes after unrelated cord blood transplantation--a case report. Clin Lab Haematol; 2006 Oct;28(5):351-4
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.
  • A 33-year-old woman underwent unrelated cord blood transplantation (U-CBT) for myelodysplastic syndrome (MDS)-related secondary AML.
  • [MeSH-minor] Adult. Female. Humans. Immunophenotyping / methods. Leukemia, Myeloid, Acute / therapy. Lymphocyte Activation / immunology. Myelodysplastic Syndromes / therapy. Transplantation, Homologous


91. Wadhwa PD, Fu P, Koc ON, Cooper BW, Fox RM, Creger RJ, Bajor DL, Bedi T, Laughlin MJ, Payne J, Gerson SL, Lazarus HM: High-dose carmustine, etoposide, and cisplatin for autologous stem cell transplantation with or without involved-field radiation for relapsed/refractory lymphoma: an effective regimen with low morbidity and mortality. Biol Blood Marrow Transplant; 2005 Jan;11(1):13-22
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.
  • Over a 10-year period (January 1993 to October 2002), 101 relapsed or refractory non-Hodgkin lymphoma patients were treated at our center with high-dose chemotherapy and autologous transplantation.
  • Thirty-two patients had indolent (low-grade), 42 had aggressive (intermediate-grade), and 27 had very aggressive (high-grade) non-Hodgkin lymphoma.
  • Two patients (2%) developed interstitial pneumonitis most likely secondary to high-dose BCNU.
  • Three cases (3%) of secondary acute myelogenous leukemia occurred.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Lymphoma, Non-Hodgkin / therapy. Peripheral Blood Stem Cell Transplantation / methods

  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Carmustine .
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15625540.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin; U68WG3173Y / Carmustine
  •  go-up   go-down


92. Jekarl DW, Kim M, Lim J, Kim Y, Han K, Lee AW, Kim HJ, Min WS: CD56 antigen expression and hemophagocytosis of leukemic cells in acute myeloid leukemia with t(16;21)(p11;q22). Int J Hematol; 2010 Sep;92(2):306-13
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD56 antigen expression and hemophagocytosis of leukemic cells in acute myeloid leukemia with t(16;21)(p11;q22).
  • The translocation t(16;21)(p11;q22) is rare, occurs with an incidence of 1%, in acute myeloid leukemia (AML), forming TLS/FUS-ERG fusion transcript, and it is known to cause the hemophagocytosis and vacuolation of leukemic cells.
  • As previously reported cases numbered less than 60, we aimed to identify the clinical and genetic aspects of AML with t(16;21).
  • Among 1,277 patients diagnosed with de novo and secondary AML, 12 AML patients with t(16;21) were retrospectively evaluated (0.94%, 12/1,277).
  • AML with t(16;21) expressed CD56 with a median value of 45% (7.8-87%), and the rate of hemophagocytosis plus vacuolation of leukemic cells was 2.9% (2.0-9.0%).
  • AML with t(16;21) expressed CD13, CD33, CD34, CD117, CD56, HLA-DR, and cytoplasmic myeloperoxidase.
  • RUNX1, which regulates a gene for hematopoiesis, is frequently mutated in AML and, in this study, one out of three patients showed the mutation R174Q in RUNX1.
  • AML with t(16;21) showed a very low rate of complete remission after induction chemotherapy (8.3%), and high relapse (75%) and mortality (75%) rates.
  • AML with t(16;21) exhibited a distinct morphology with frequent CD56 expression and a poor prognosis.
  • [MeSH-major] Antigens, CD56 / analysis. Cytophagocytosis. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Translocation, Genetic

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Scand J Haematol. 1978 Jan;20(1):85-8 [272729.001]
  • [Cites] Leukemia. 2009 Jan;23(1):78-84 [18830253.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):166-75 [10508512.001]
  • [Cites] Blood. 1997 Aug 1;90(3):1192-9 [9242552.001]
  • [Cites] Haematologica. 2002 Mar;87(3):250-6 [11869936.001]
  • [Cites] Int J Hematol. 1991 Oct;54(5):395-403 [1721853.001]
  • [Cites] Scand J Haematol. 1973;11(3):253-6 [4128872.001]
  • [Cites] Leukemia. 2008 Aug;22(8):1567-75 [18528428.001]
  • [Cites] Br J Haematol. 1999 Jun;105(3):711-9 [10354136.001]
  • [Cites] Leukemia. 2001 Aug;15(8):1161-4 [11480556.001]
  • [Cites] EMBO J. 2007 Feb 21;26(4):1163-75 [17290219.001]
  • [Cites] West J Med. 1977 Feb;126(2):139-41 [265650.001]
  • [Cites] Blood. 1997 Aug 15;90(4):1643-8 [9269784.001]
  • [Cites] Blood. 2009 Dec 17;114(26):5352-61 [19808697.001]
  • [Cites] Leuk Lymphoma. 2004 May;45(5):1061-4 [15291368.001]
  • [Cites] Leukemia. 2003 Jan;17(1):9-16 [12529654.001]
  • [Cites] Cancer Genet Cytogenet. 2009 Oct 15;194(2):111-8 [19781443.001]
  • [Cites] Blood. 1977 Jan;49(1):19-27 [299732.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1308-16 [17485549.001]
  • [Cites] Haematologica. 2007 Jun;92(6):861-2 [17550866.001]
  • [Cites] Cancer. 2000 Apr 15;88(8):1970-5 [10760776.001]
  • [Cites] Blood. 2001 Feb 1;97(3):805-8 [11157501.001]
  • [Cites] Cancer Genet Cytogenet. 1991 May;53(1):83-90 [2036642.001]
  • (PMID = 20694842.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD56
  •  go-up   go-down


93. Lim Z, Brand R, Martino R, van Biezen A, Finke J, Bacigalupo A, Beelen D, Devergie A, Alessandrino E, Willemze R, Ruutu T, Boogaerts M, Falda M, Jouet JP, Niederwieser D, Kroger N, Mufti GJ, De Witte TM: Allogeneic hematopoietic stem-cell transplantation for patients 50 years or older with myelodysplastic syndromes or secondary acute myeloid leukemia. J Clin Oncol; 2010 Jan 20;28(3):405-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic hematopoietic stem-cell transplantation for patients 50 years or older with myelodysplastic syndromes or secondary acute myeloid leukemia.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy


94. Gondek LP, Dunbar AJ, Szpurka H, McDevitt MA, Maciejewski JP: SNP array karyotyping allows for the detection of uniparental disomy and cryptic chromosomal abnormalities in MDS/MPD-U and MPD. PLoS One; 2007 Nov 21;2(11):e1225
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 applied single nucleotide polymorphism arrays (SNP-A) to study karyotypic abnormalities in patients with atypical myeloproliferative syndromes (MPD), including myeloproliferative/myelodysplastic syndrome overlap both positive and negative for the JAK2 V617F mutation and secondary acute myeloid leukemia (AML).
  • Transformation to AML was observed in 8/30 patients.
  • In 5 V617F+ patients who progressed to AML, we show that SNP-A can allow for the detection of two modes of transformation: leukemic blasts evolving from either a wild-type jak2 precursor carrying other acquired chromosomal defects, or from a V617F+ mutant progenitor characterized by UPD9p.

  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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] Blood. 2008 Feb 1;111(3):1534-42 [17954704.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3365-73 [17634407.001]
  • [Cites] Nat Biotechnol. 2000 Sep;18(9):1001-5 [10973224.001]
  • [Cites] Am J Pathol. 2001 Apr;158(4):1253-62 [11290543.001]
  • [Cites] Nucleic Acids Res. 2001 Sep 1;29(17):E88-8 [11522844.001]
  • [Cites] Blood. 2002 Jan 1;99(1):375-7 [11756195.001]
  • [Cites] Exp Hematol. 2002 Mar;30(3):229-36 [11882360.001]
  • [Cites] Br J Haematol. 2002 Nov;119(2):558-66 [12406101.001]
  • [Cites] Hematol Oncol Clin North Am. 2003 Oct;17(5):1129-49 [14560778.001]
  • [Cites] Nat Genet. 2004 Sep;36(9):949-51 [15286789.001]
  • [Cites] Cancer Res. 2005 Jan 15;65(2):375-8 [15695375.001]
  • [Cites] Leuk Res. 2005 Apr;29(4):365-70 [15725469.001]
  • [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] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6071-9 [16024607.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1207-9 [15860661.001]
  • [Cites] Biochem J. 2005 Aug 15;390(Pt 1):359-66 [15833084.001]
  • [Cites] Blood. 2005 Sep 15;106(6):2162-8 [15920007.001]
  • [Cites] Cancer. 2005 Oct 15;104(8):1656-60 [16104040.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3377-9 [16081687.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1242-3 [16434499.001]
  • [Cites] Oncogene. 2006 Mar 2;25(9):1434-6 [16247455.001]
  • [Cites] Cancer. 2006 May 1;106(9):1985-9 [16568439.001]
  • [Cites] Leukemia. 2006 Jun;20(6):971-8 [16598306.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1865-7 [16728702.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Oct 1;170(1):65-8 [16965958.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2173-81 [16741247.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3548-55 [16873677.001]
  • [Cites] Carcinogenesis. 2007 Jan;28(1):38-48 [16774939.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1678-86 [17038539.001]
  • [Cites] Am J Hum Genet. 2007 Jul;81(1):114-26 [17564968.001]
  • [Cites] Blood. 2007 Jul 1;110(1):375-9 [17363731.001]
  • [Cites] Leukemia. 2007 Aug;21(8):1648-57 [17554386.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2058-61 [17525728.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3835-49 [10577857.001]
  • (PMID = 18030353.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [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
  • [Chemical-registry-number] 0 / DNA Primers
  • [Other-IDs] NLM/ PMC2075364
  •  go-up   go-down


95. Rohatiner AZ, Nadler L, Davies AJ, Apostolidis J, Neuberg D, Matthews J, Gribben JG, Mauch PM, Lister TA, Freedman AS: Myeloablative therapy with autologous bone marrow transplantation for follicular lymphoma at the time of second or subsequent remission: long-term follow-up. J Clin Oncol; 2007 Jun 20;25(18):2554-9
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.
  • However, use of CY+TBI was associated with a significant risk of secondary myelodysplasia and secondary acute myeloblastic leukemia, resulting in 15 patient deaths.


96. Ducastelle S, Adès L, Gardin C, Dombret H, Prébet T, Deconinck E, Rio B, Thomas X, Debotton S, Guerci A, Gratecos N, Stamatoullas A, Fegueux N, Dreyfus F, Fenaux P, Wattel E: Long-term follow-up of autologous stem cell transplantation after intensive chemotherapy in patients with myelodysplastic syndrome or secondary acute myeloid leukemia. Haematologica; 2006 Mar;91(3):373-6
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] Long-term follow-up of autologous stem cell transplantation after intensive chemotherapy in patients with myelodysplastic syndrome or secondary acute myeloid leukemia.
  • We report on the outcomes of 53 patients with myelodysplastic syndromes (MDS) or acute myeloid leukemia secondary to MDS, autografted in first complete remission.
  • [MeSH-major] Leukemia, Myeloid, Acute / surgery. Myelodysplastic Syndromes / surgery. Stem Cell Transplantation


97. Crump M, Hedley D, Kamel-Reid S, Leber B, Wells R, Brandwein J, Buckstein R, Kassis J, Minden M, Matthews J, Robinson S, Turner R, McIntosh L, Eisenhauer E, Seymour L: A randomized phase I clinical and biologic study of two schedules of sorafenib in patients with myelodysplastic syndrome or acute myeloid leukemia: a NCIC (National Cancer Institute of Canada) Clinical Trials Group Study. Leuk Lymphoma; 2010 Feb;51(2):252-60
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A randomized phase I clinical and biologic study of two schedules of sorafenib in patients with myelodysplastic syndrome or acute myeloid leukemia: a NCIC (National Cancer Institute of Canada) Clinical Trials Group Study.
  • In this randomized phase I study, eligible patients had relapsed/refractory acute myeloid leukemia (AML), and one prior induction regimen, or were age >65 with untreated myelodysplastic syndrome (MDS) or secondary AML.
  • One CR was seen in a patient with AML with FLT3-ITD.
  • The recommended phase II dose in AML is 300 mg BID continuously, and testing in combination and in FLT3-ITD AML is warranted.
  • [MeSH-major] Benzenesulfonates / therapeutic use. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. Pyridines / therapeutic use
  • [MeSH-minor] Abdominal Pain / chemically induced. Acute Disease. Adult. Aged. Aged, 80 and over. Area Under Curve. Diarrhea / chemically induced. Dose-Response Relationship, Drug. Drug Administration Schedule. Extracellular Signal-Regulated MAP Kinases / metabolism. Female. Humans. Male. Metabolic Clearance Rate. Middle Aged. Nausea / chemically induced. Niacinamide / analogs & derivatives. Phenylurea Compounds. Phosphorylation / drug effects. Protein Kinase Inhibitors / adverse effects. Protein Kinase Inhibitors / pharmacokinetics. Protein Kinase Inhibitors / therapeutic use. Treatment Outcome


98. Lu GH: Clinical cytogenetic diagnosis of therapy-related acute myeloid leukemia. Beijing Da Xue Xue Bao; 2005 Feb 18;37(1):10-3
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 cytogenetic diagnosis of therapy-related acute myeloid leukemia.
  • Therapy-related acute myeloid leukemia (tAML) is one of the two forms of secondary acute myeloid leukemia, with one derived from de novo myelodysplastic syndrome (MDS) and the other from exposure to environmental or therapeutic agents such as radiation and toxins.
  • There has been a marked increase in the number of incidences of therapy-related acute myeloid leukemia.
  • In this study, an interesting case with therapy-related myelodysplastic syndrome and acute myeloid leukemia (tMDS/tAML) will be presented.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / diagnosis. Lymphoma, B-Cell / drug therapy. Neoplasms, Second Primary / diagnosis


99.