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1. Belgaumi AF, Al-Shehri A, Ayas M, Al-Mahr M, Al-Seraihy A, Al-Ahmari A, El-Solh H: Clinical characteristics and treatment outcome of pediatric patients with chronic myeloid leukemia. Haematologica; 2010 Jul;95(7):1211-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical characteristics and treatment outcome of pediatric patients with chronic myeloid leukemia.
  • As chronic myeloid leukemia is rare in children, most data on imatinib mesylate therapy is derived from adult studies.
  • We retrospectively evaluated pediatric (<14 years) patients with Ph+ chronic myeloid leukemia treated with imatinib mesylate, from January 2003 through June 2008.
  • Of the 12 chronic myeloid leukemia patients (2% of all leukemias) 11 were in chronic phase while one had myeloid blast crisis.
  • Five patients had grade 3-4 arthralgia requiring therapy alteration.
  • Imatinib mesylate is effective therapy for children with chronic myeloid leukemia.
  • Acute toxicity of imatinib mesylate is tolerable, but long-term effects on growing children are unknown.
  • Pediatric patients with chronic myeloid leukemia should undergo stem cell transplantation when appropriate related donors are available.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy


2. Thall PF, Cook JD, Estey EH: Adaptive dose selection using efficacy-toxicity trade-offs: illustrations and practical considerations. J Biopharm Stat; 2006;16(5):623-38
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  • We next describe an application to a trial of a biologic agent for treatment of acute myelogenous leukemia, including a computer simulation study to assess the design's average behavior.
  • [MeSH-minor] Algorithms. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bayes Theorem. Computer Simulation. Drug-Related Side Effects and Adverse Reactions. Humans. Leukemia, Myeloid, Acute / drug therapy. Models, Statistical. Treatment Outcome

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  • (PMID = 17037262.001).
  • [ISSN] 1054-3406
  • [Journal-full-title] Journal of biopharmaceutical statistics
  • [ISO-abbreviation] J Biopharm Stat
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 83932
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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3. Yin CC, Cortes J, Barkoh B, Hayes K, Kantarjian H, Jones D: t(3;21)(q26;q22) in myeloid leukemia: an aggressive syndrome of blast transformation associated with hydroxyurea or antimetabolite therapy. Cancer; 2006 Apr 15;106(8):1730-8
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  • [Title] t(3;21)(q26;q22) in myeloid leukemia: an aggressive syndrome of blast transformation associated with hydroxyurea or antimetabolite therapy.
  • RESULTS: In all 16 patients with chronic myeloproliferative disorders, including 14 with chronic myelogenous leukemia (CML), the occurrence of t(3;21) heralded myeloid blast transformation.
  • Among 10 cases of t(3;21)-associated acute myeloid leukemia, 8 were secondary tumors after chemotherapy for other neoplasms that had been treated with regimens including fludarabine and 5-fluorouracil in 3 patients each and etoposide in 2 patients.
  • Among patients with acute myeloid leukemia/myelodysplastic syndrome, 7 died of disease (at a median of 2 mos) and 2 had persistent leukemia with short follow-up.
  • CONCLUSIONS: Activation of AME through t(3;21) defines a highly aggressive, therapy-related leukemic blast syndrome.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Antineoplastic Agents / adverse effects. Chromosomes, Human, Pair 21 / drug effects. Chromosomes, Human, Pair 3 / drug effects. Hydroxyurea / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / genetics. Lymphocyte Activation / drug effects. Myeloproliferative Disorders / drug therapy. Oncogene Proteins, Fusion / analysis. Translocation, Genetic / drug effects

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  • [Copyright] 2006 American Cancer Society
  • (PMID = 16532439.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672
  • [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 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human; 0 / Transcription Factors; X6Q56QN5QC / Hydroxyurea
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4. Jabbour E, Cortes J, Kantarjian H, Giralt S, Andersson BS, Giles F, Shpall E, Kebriaei P, Champlin R, de Lima M: Novel tyrosine kinase inhibitor therapy before allogeneic stem cell transplantation in patients with chronic myeloid leukemia: no evidence for increased transplant-related toxicity. Cancer; 2007 Jul 15;110(2):340-4
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  • [Title] Novel tyrosine kinase inhibitor therapy before allogeneic stem cell transplantation in patients with chronic myeloid leukemia: no evidence for increased transplant-related toxicity.
  • BACKGROUND: Patients undergoing allogeneic hematopoietic stem cell transplantation (HSCT) for chronic myeloid leukemia (CML) are increasingly likely to have received a novel tyrosine kinase inhibitor (NTKI) after failing imatinib mesylate.
  • It is unknown whether the use of these NTKIs before HSCT increases transplant-related toxicity.
  • RESULTS: The median time on treatment was 134 days, and the median time from the end of NTKI therapy to HSCT was 34 days.
  • There was no significant early transplant-related toxicity.
  • Acute and chronic graft-versus-host disease (GVHD) was observed in 7 and 6 patients, respectively.
  • CONCLUSIONS: Previous treatment with NTKI did not increase transplant-related toxicity in this preliminary experience.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Combined Modality Therapy. Dasatinib. Female. Humans. Male. Middle Aged


5. Majhail NS, Brunstein CG, Tomblyn M, Thomas AJ, Miller JS, Arora M, Kaufman DS, Burns LJ, Slungaard A, McGlave PB, Wagner JE, Weisdorf DJ: Reduced-intensity allogeneic transplant in patients older than 55 years: unrelated umbilical cord blood is safe and effective for patients without a matched related donor. Biol Blood Marrow Transplant; 2008 Mar;14(3):282-9
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  • [Title] Reduced-intensity allogeneic transplant in patients older than 55 years: unrelated umbilical cord blood is safe and effective for patients without a matched related donor.
  • Unrelated umbilical cord blood (UCB) has been investigated as an alternative stem cell source to suitably HLA matched related (MRD) and adult volunteer unrelated donors.
  • We hypothesized that RIC HCT using UCB would be safe and efficacious in older patients, and compared the treatment-related mortality (TRM) and overall survival (OS) of RIC HCT in patients older than 55 years using either MRD (n = 47) or, in patients with no 5 of 6 or 6 of 6 HLA compatible related donors, UCB (n = 43).
  • The median age of MRD and UCB cohorts was 58 (range, 55-70) and 59 (range, 55-69) years, respectively. acute myelogenous leukemia/myelodysplastic syndrome (AML/MDS) (50%) was the most common diagnosis.
  • The cumulative incidence of grade II-IV acute graft-versus-host (aGVHD) disease (42% versus 49%, P = .20) and TRM at 180-days (23% versus 28%, P = .36) were comparable.
  • The use of RIC and UCB extends the availability of transplant therapy to older patients previously excluded on the basis of age and lack of a suitable MRD.

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  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1993-2003 [15774790.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2912-9 [15994282.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1343-7 [15466923.001]
  • [Cites] Leukemia. 2005 Jan;19(1):7-12 [15526016.001]
  • [Cites] N Engl J Med. 2004 Nov 25;351(22):2276-85 [15564544.001]
  • [Cites] Stat Med. 1997 Apr 30;16(8):901-10 [9160487.001]
  • [Cites] Bone Marrow Transplant. 1995 Jun;15(6):825-8 [7581076.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Oct 24;92(22):10119-22 [7479737.001]
  • [Cites] Blood. 1995 Aug 15;86(4):1636-42 [7632974.001]
  • [Cites] Blood. 1995 Apr 1;85(7):1954-63 [7703498.001]
  • [Cites] Semin Hematol. 1991 Jul;28(3):250-9 [1887253.001]
  • [Cites] Blood. 2003 Sep 15;102(6):2021-30 [12791654.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1915-9 [12738676.001]
  • [Cites] Transplantation. 2003 Jun 27;75(12):2135-43 [12829926.001]
  • [Cites] J Hematother Stem Cell Res. 2002 Aug;11(4):731-7 [12201962.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1611-8 [12176879.001]
  • [Cites] Bone Marrow Transplant. 2002 Feb;29(3):243-8 [11859397.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3390-400 [11369628.001]
  • [Cites] Blood. 2001 May 15;97(10):2962-71 [11342418.001]
  • [Cites] Blood. 2001 May 15;97(10):2957-61 [11342417.001]
  • [Cites] Clin Transpl. 1999;:121-7 [11038630.001]
  • [Cites] Hum Immunol. 2000 Aug;61(8):834-40 [10980395.001]
  • [Cites] N Engl J Med. 2000 Jun 22;342(25):1846-54 [10861319.001]
  • [Cites] Blood. 2007 Oct 15;110(8):3064-70 [17569820.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Oct;13(10):1145-52 [17889350.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Jul;13(7):844-52 [17580263.001]
  • [Cites] Curr Opin Immunol. 2006 Oct;18(5):571-5 [16895752.001]
  • [Cites] Bone Marrow Transplant. 2006 Jul;38(2):83-93 [16751788.001]
  • [Cites] Haematologica. 2006 Jun;91(6):852-5 [16769592.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 May;12(5):560-5 [16635791.001]
  • [Cites] Blood. 2006 May 1;107(9):3804-7 [16384924.001]
  • [Cites] Bone Marrow Transplant. 2006 Feb;37(4):339-44 [16415898.001]
  • (PMID = 18275894.001).
  • [ISSN] 1523-6536
  • [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
  • [Grant] United States / NCI NIH HHS / CA / P01 CA065493-110009; United States / NCI NIH HHS / CA / P01 CA065493; United States / NCI NIH HHS / CA / P01 CA065493-120009; United States / NCI NIH HHS / CA / P01CA65493; United States / NCI NIH HHS / CA / CA065493-120009; United States / NCI NIH HHS / CA / CA065493-110009
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Myeloablative Agonists
  • [Other-IDs] NLM/ NIHMS41246; NLM/ PMC2674378
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6. Mustjoki S, Ekblom M, Arstila TP, Dybedal I, Epling-Burnette PK, Guilhot F, Hjorth-Hansen H, Höglund M, Kovanen P, Laurinolli T, Liesveld J, Paquette R, Pinilla-Ibarz J, Rauhala A, Shah N, Simonsson B, Sinisalo M, Steegmann JL, Stenke L, Porkka K: Clonal expansion of T/NK-cells during tyrosine kinase inhibitor dasatinib therapy. Leukemia; 2009 Aug;23(8):1398-405
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  • [Title] Clonal expansion of T/NK-cells during tyrosine kinase inhibitor dasatinib therapy.
  • We identified 22 patients with marked lymphoproliferation in blood while on dasatinib therapy.
  • Clonality and immunophenotype were analyzed and related clinical information was collected.
  • An abrupt lymphocytosis (peak count range 4-20 x 10(9)/l) with large granular lymphocyte (LGL) morphology was observed after a median of 3 months from the start of therapy and it persisted throughout the therapy.
  • Responses to dasatinib were good and included complete, unexpectedly long-lasting remissions in patients with advanced leukemia.
  • In a phase II clinical study on 46 Philadelphia chromosome-positive acute lymphoblastic leukemia, patients with lymphocytosis had superior survival compared with patients without lymphocytosis.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Killer Cells, Natural / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Lymphocytosis / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / pharmacology. Pyrimidines / pharmacology. T-Lymphocyte Subsets / drug effects. T-Lymphocytes, Cytotoxic / drug effects. Thiazoles / pharmacology

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  • [CommentIn] Acta Haematol. 2016;136(4):219-228 [27656875.001]
  • (PMID = 19295545.001).
  • [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 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
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7. Halim TY, Song KW, Barnett MJ, Forrest DL, Hogge DE, Nantel SH, Nevill TJ, Shepherd JD, Smith CA, Sutherland HJ, Toze CL, Lavoie JC: Positive impact of selective outpatient management of high-risk acute myelogenous leukemia on the incidence of septicemia. Ann Oncol; 2007 Jul;18(7):1246-52
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  • [Title] Positive impact of selective outpatient management of high-risk acute myelogenous leukemia on the incidence of septicemia.
  • BACKGROUND: Curative intent chemotherapy for acute myelogenous leukemia (AML) leads to prolonged severe neutropenia, during which patients are highly susceptible to infection.
  • Our center recently implemented a selective ambulatory management policy for AML patients undergoing chemotherapy.
  • MATERIALS AND METHODS: A retrospective analysis was conducted to assess the occurrence of septicemia in AML patients treated over a 5 years period with curative intent chemotherapy.
  • This review encompasses a change in policy from primarily inpatient care to selective outpatient management coupled with prophylactic antibiotic therapy.
  • No significant emerging resistance and no septicemia-related mortality were noted in the outpatient cohort.
  • CONCLUSION: The observed decrease in the incidence of septicemia in the ambulatory cohort adds supportive evidence to the feasibility of selective outpatient management of AML patients with respect to infectious complications.


8. Introna M, Borleri G, Conti E, Franceschetti M, Barbui AM, Broady R, Dander E, Gaipa G, D'Amico G, Biagi E, Parma M, Pogliani EM, Spinelli O, Baronciani D, Grassi A, Golay J, Barbui T, Biondi A, Rambaldi A: Repeated infusions of donor-derived cytokine-induced killer cells in patients relapsing after allogeneic stem cell transplantation: a phase I study. Haematologica; 2007 Jul;92(7):952-9
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  • DESIGN AND METHODS: Eleven patients with acute myelogenous leukemia (n=4), Hodgkin's disease (n=3), chronic myelomonocytic leukemia, (n=1), pre-B acute lymphoblastic leukemia (n=1) and myelodysplasia (n=2), all of whom had relapsed after sibling (n=6) or matched unrelated donor (n=5) HSCT, entered this study.
  • The infusions were well tolerated and no acute or late infusion-related reactions were recorded.
  • Acute GVHD (grade I and II) was observed in four patients, 30 days after the last CIK infusion, and progressed into extensive chronic GVHD in two cases.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Killer Cells, Natural / transplantation. Lymphocyte Transfusion / methods. Salvage Therapy / methods
  • [MeSH-minor] Adult. Cytokines / pharmacology. Female. Hematologic Neoplasms / therapy. Humans. Male. Middle Aged. Recurrence. Transplantation, Homologous

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  • (PMID = 17606446.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Cytokines
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9. Barr RD: Imatinib mesylate in children and adolescents with cancer. Pediatr Blood Cancer; 2010 Jul 15;55(1):18-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Imatinib is an inhibitor of the BCR-ABL fusion gene product that characterizes chronic myeloid leukemia (CML), and of the related tyrosine kinases c-KIT and platelet-derived growth factor (PDGF) receptor.
  • The drug is now included as front-line therapy for CML and Philadelphia chromosome-positive acute lymphoblastic leukemia in children and adolescents, though valid concerns about serious late sequelae remain unresolved and are important issues for further study.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Philadelphia Chromosome. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / therapeutic use

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  • (PMID = 20486169.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 116
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10. Faller BA, Robu VG, Borghaei H: Therapy-related acute myelogenous leukemia with an 11q23/MLL translocation following adjuvant cisplatin and vinorelbine for non-small-cell lung cancer. Clin Lung Cancer; 2009 Nov;10(6):438-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related acute myelogenous leukemia with an 11q23/MLL translocation following adjuvant cisplatin and vinorelbine for non-small-cell lung cancer.
  • We present a case of acute myelogenous leukemia with an 11q23/MLL rearrangement diagnosed 1 year after the completion of 4 cycles of cisplatin and vinorelbine for resected NSCLC.
  • To our knowledge, this is the first case of therapy-related acute myelogenous leukemia (t-AML) associated with this chemotherapy combination.
  • The literature on t-AML with the 11q23/MLL rearrangement is reviewed.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Translocation, Genetic / drug effects
  • [MeSH-minor] Aged. Carcinoma, Non-Small-Cell Lung / drug therapy. Chromosomes, Human, Pair 11. Cisplatin / administration & dosage. Follow-Up Studies. Histone-Lysine N-Methyltransferase. Humans. Lung Neoplasms / drug therapy. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Vinblastine / administration & dosage. Vinblastine / analogs & derivatives


11. 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
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  • [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


12. Robin M, Porcher R, De Castro Araujo R, de Latour RP, Devergie A, Rocha V, Larghero J, Adès L, Ribaud P, Mary JY, Socié G: Risk factors for late infections after allogeneic hematopoietic stem cell transplantation from a matched related donor. Biol Blood Marrow Transplant; 2007 Nov;13(11):1304-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk factors for late infections after allogeneic hematopoietic stem cell transplantation from a matched related donor.
  • Late infection incidence and risk factors were retrospectively determined in 196 long-term survivors after HLA matched related HSCT.
  • Patients transplanted for aplastic anemia, chronic myelogenous leukemia (CML), and acute myelogenous leukemia (AML) were included.
  • Extensive cGVHD was the only risk factor for non-HCV viral infections in patients transplanted for AML or CML (HR: 2.7, 95%CI: 1.4-5.1, P = .002).
  • [MeSH-minor] Adolescent. Adult. Anemia, Aplastic / therapy. Female. France / epidemiology. Graft vs Host Disease. Humans. Incidence. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / therapy. Male. Retrospective Studies. Risk Factors. Transplantation, Homologous / adverse effects


13. Claxton DF, Ehmann C, Rybka W: Control of advanced and refractory acute myelogenous leukaemia with sirolimus-based non-myeloablative allogeneic stem cell transplantation. Br J Haematol; 2005 Jul;130(2):256-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Control of advanced and refractory acute myelogenous leukaemia with sirolimus-based non-myeloablative allogeneic stem cell transplantation.
  • A total of 23 patients with acute myelogenous leukaemia (AML) were treated, with a median age of 59 years (range: 28-72) at transplant.
  • Nine patients were in chemotherapy-refractory progression and seven were primarily refractory to induction therapy.
  • Only two, both recipients of haploidentical cells, have died from transplant-related causes.
  • Although follow up is short, this data suggests that non-myeloablative haematopoietic cell transplantation with sirolimus (rapamycin)-based immunosuppression may provide disease control over several years in some patients with advanced and poor prognosis AML.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Immunosuppressive Agents / administration & dosage. Leukemia, Myeloid, Acute / therapy. Sirolimus / administration & dosage

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  • (PMID = 16029454.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Immunosuppressive Agents; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; W36ZG6FT64 / Sirolimus
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14. Solomon SR, Savani BN, Childs R, Montero A, Boss C, Read EJ, Leitman SF, Barrett AJ: Improved outcome for peripheral blood stem cell transplantation for advanced primary myelodysplastic syndrome. Biol Blood Marrow Transplant; 2005 Aug;11(8):619-26
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  • Stem cell transplantation for myelodysplastic syndrome (MDS) is characterized by high transplant-related mortality (TRM), especially in older patients and those with more advanced disease.
  • Thirty-seven (86%) had advanced disease (refractory anemia with excess blasts [n = 9], refractory anemia with excess blasts in transformation [n = 6], acute myelogenous leukemia [n = 13], or treatment-related MDS [n = 9]); 6 had low-risk MDS (refractory anemia or refractory anemia with ringed sideroblasts).
  • Although outcomes for all stages of primary MDS were improved, that for therapy-related MDS remained dismal, with 11% OS, because of a high relapse rate (89%).
  • [MeSH-major] Anemia, Refractory, with Excess of Blasts / mortality. Anemia, Refractory, with Excess of Blasts / therapy. Peripheral Blood Stem Cell Transplantation / mortality


15. Silverman LR: Clinical roundtable monograph. Overall survival and maintenance of MDS patients. Clin Adv Hematol Oncol; 2009 Jul;7(7):S3-5
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  • The disease is marked by gradually worsening cytopenias and a variable risk for the eventual transformation to acute myelogenous leukemia (AML).
  • The International Prognostic Scoring System (IPSS) was developed to aid in determining the prognosis of patients with MDS; this system categorizes patients into four risk groups for both overall survival and transformation to AML: low, intermediate-1, intermediate-2, and high.
  • The management of MDS is based on the goal of controlling cytopenia-related symptoms, improving survival, improving quality of life, and decreasing risk of progression to AML.
  • However, selecting the appropriate therapy for each individual patient is critical to optimize clinical benefit.
  • This monograph discusses treatment selection for the MDS patient,including a discussion of the overall survival and maintenance of MDS patients, how an appropriate therapy should be chosen in the community setting, and how MDS classification and risk stratification impacts treatment decisions.
  • [MeSH-major] Azacitidine / analogs & derivatives. Azacitidine / therapeutic use. DNA Modification Methylases / antagonists & inhibitors. Myelodysplastic Syndromes / drug therapy

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  • (PMID = 19708287.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
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16. Middeldorf I, Galm O, Osieka R, Jost E, Herman JG, Wilop S: Sequence of administration and methylation of SOCS3 may govern response to gemtuzumab ozogamicin in combination with conventional chemotherapy in patients with refractory or relapsed acute myelogenous leukemia (AML). Am J Hematol; 2010 Jul;85(7):477-81
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  • [Title] Sequence of administration and methylation of SOCS3 may govern response to gemtuzumab ozogamicin in combination with conventional chemotherapy in patients with refractory or relapsed acute myelogenous leukemia (AML).
  • In older patients suffering from acute myelogenous leukemia (AML), aggressive chemotherapy is accompanied with high treatment-related morbidity and mortality.
  • Consequently, a variable response of AML cells to anti-CD33-targeted therapy may be caused by modulation of SOCS3 expression.
  • Twenty-four patients with refractory or relapsed CD33-positive AML received GO as a single agent before or after conventional chemotherapy.
  • Response (RR) and overall survival (OS) were significantly higher in 16 patients receiving chemotherapy before GO (RR 81%, OS 14.8 months) compared to three patients who received GO single agent therapy (RR 33%, OS 7.2 months) or 16 with GO before chemotherapy (RR 0% OS 2.2 months, P = 0.01 for RR and P < 0.001 for OS).
  • [MeSH-major] Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. DNA Methylation. Leukemia, Myeloid, Acute / drug therapy. Salvage Therapy / methods. Suppressor of Cytokine Signaling Proteins / genetics

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20575043.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / SOCS3 protein, human; 0 / Suppressor of Cytokine Signaling Proteins; 0 / gemtuzumab
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17. Jameel A, Jamil SN: Safety of cytotoxic chemotherapy during pregnancy. J Pak Med Assoc; 2007 Sep;57(9):449-52
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  • Six patients (33%) had breast cancer, four (22%) had chronic myeloid leukaemia, two (11%) had Hodgkin's disease, two (11%) had acute myeloid leukaemia and one each had recurrent ovarian carcinoma (5.7%), soft-tissue sarcoma (5.7%), acute lymphoblastic leukaemia (5.7%) and non-Hodgkin's lymphoma (5.7%).
  • [MeSH-major] Antineoplastic Agents / adverse effects. Cytotoxins / adverse effects. Drug-Related Side Effects and Adverse Reactions. Pregnancy Complications. Pregnancy Outcome
  • [MeSH-minor] Adult. Breast Neoplasms / drug therapy. Female. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Neoplasms / drug therapy. Pregnancy. Pregnancy Trimester, Second. Prospective Studies. Time Factors

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  • (PMID = 18072640.001).
  • [ISSN] 0030-9982
  • [Journal-full-title] JPMA. The Journal of the Pakistan Medical Association
  • [ISO-abbreviation] J Pak Med Assoc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytotoxins
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18. 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
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  • [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).
  • The patients received chemotherapy (50%) had significantly higher CR ratio than those received supportive therapy (0%)(P=0.001).
  • In the stepwise COX proportional hazard regression model, all the seven factors related to OS remained independent and significant.
  • 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

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  • (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
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19. Or R, Hadar E, Bitan M, Resnick IB, Aker M, Ackerstein A, Samuel S, Tsirigotis P, Gesundheit B, Slavin S, Shapira MY: Safety and efficacy of donor lymphocyte infusions following mismatched stem cell transplantation. Biol Blood Marrow Transplant; 2006 Dec;12(12):1295-301
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  • The use of a mismatched allograft necessitates T cell depletion for prevention of uncontrolled graft-versus-host disease (GVHD), thus impairing a graft-versus-leukemia effect.
  • Death was frequent and usually related to the basic disease rather than to DLI complications.
  • Future developments using cell therapy with selective or targeted anticancer activity are warranted, with special attention to prophylactic treatment of T cell depleted mismatched allografts recipients.
  • [MeSH-major] Graft Enhancement, Immunologic. Leukemia, Myeloid / surgery. Lymphocyte Transfusion. Peripheral Blood Stem Cell Transplantation
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Child, Preschool. Feasibility Studies. Female. Graft vs Host Disease / mortality. Graft vs Host Disease / prevention & control. Graft vs Leukemia Effect. HLA Antigens / immunology. Histocompatibility. Humans. Kaplan-Meier Estimate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Leukocyte Reduction Procedures. Lymphoma / surgery. Male. Middle Aged. Myelodysplastic Syndromes / surgery. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery. Remission Induction. Survival Analysis. Tissue Donors. Transplantation Conditioning. Tumor Burden

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  • (PMID = 17162211.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA Antigens
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20. Carpenter PA, Snyder DS, Flowers ME, Sanders JE, Gooley TA, Martin PJ, Appelbaum FR, Radich JP: Prophylactic administration of imatinib after hematopoietic cell transplantation for high-risk Philadelphia chromosome-positive leukemia. Blood; 2007 Apr 1;109(7):2791-3
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  • [Title] Prophylactic administration of imatinib after hematopoietic cell transplantation for high-risk Philadelphia chromosome-positive leukemia.
  • Relapse occurs frequently after allogeneic hematopoietic cell transplantation (HCT) for treatment of high-risk Philadelphia chromosome-positive (Ph+) leukemia.
  • Administration of imatinib early after HCT might provide an effective approach for preventing recurrent Ph+ leukemia, but the feasibility of this approach has not been systematically tested.
  • Twenty-two patients, 15 with Ph+ acute lymphoblastic leukemia and 7 with high-risk chronic myelogenous leukemia, were enrolled in a prospective study and given imatinib from the time of engraftment until 365 days after HCT.
  • The most common adverse events related to imatinib administration were grade 1-3 nausea, emesis, and serum transaminase elevations.
  • We conclude that imatinib can be safely administered early after myeloablative allogeneic HCT at a dose intensity comparable to that used in primary therapy.

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  • [Cites] Hematol Oncol Clin North Am. 2001 Feb;15(1):21-36 [11258387.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1469-77 [16638934.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1965-71 [12200353.001]
  • [Cites] Haematologica. 2003 Feb;88(2):227-9 [12604417.001]
  • [Cites] N Engl J Med. 2003 Mar 13;348(11):994-1004 [12637609.001]
  • [Cites] Biol Blood Marrow Transplant. 2003 Mar;9(3):206-12 [12652472.001]
  • [Cites] Leukemia. 2003 Sep;17(9):1707-12 [12970768.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):685-702, x [15271400.001]
  • [Cites] J Clin Invest. 2004 Aug;114(3):379-88 [15286804.001]
  • [Cites] Blood. 1995 May 1;85(9):2632-8 [7727789.001]
  • [Cites] Blood. 1997 Apr 1;89(7):2602-9 [9116308.001]
  • [Cites] Blood. 1997 Aug 15;90(4):1410-4 [9269758.001]
  • [Cites] Biol Blood Marrow Transplant. 2004 Dec;10(12):883-4 [15570257.001]
  • [Cites] Blood. 2005 Jul 15;106(2):458-63 [15817679.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):460-6 [16344315.001]
  • [Cites] Nat Med. 2006 Feb;12(2):214-9 [16444265.001]
  • [Cites] Nat Med. 2006 Feb;12(2):207-13 [16444266.001]
  • [Cites] N Engl J Med. 2006 May 25;354(21):2282-4 [16723621.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1590-5 [12176876.001]
  • (PMID = 17119111.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / CA18029
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC1852215
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21. Wang XS, Shi Q, Williams LA, Cleeland CS, Mobley GM, Reuben JM, Lee BN, Giralt SA: Serum interleukin-6 predicts the development of multiple symptoms at nadir of allogeneic hematopoietic stem cell transplantation. Cancer; 2008 Oct 15;113(8):2102-9
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  • BACKGROUND: During the time of lowest white blood cell count (nadir) of allogeneic hematopoietic stem cell transplantation (allo-HSCT), cancer patients suffer from tremendous symptom burden related to therapy that requires intensive patient care.
  • METHODS: To explore the role of inflammatory cytokines in the development of treatment-related symptoms, we studied dynamic changes in symptoms and in serum concentrations of inflammatory cytokines (interleukin [IL]-6, IL-8, soluble tumor necrosis factor receptor 1 [sTNF-R1], IL-1 receptor antagonist, and IL-12p40p70) from pretherapy throughout the first 30 days of allo-HSCT in 30 patients with acute myelogenous leukemia or myelodysplastic syndrome.
  • CONCLUSIONS: These results suggest that release of systemic inflammatory cytokines, mainly IL-6, corresponds to an increase in treatment-related multiple-symptom burden during the nadir period of allo-HSCT.

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  • [Copyright] (c) 2008 American Cancer Society.
  • [Cites] Curr Opin Immunol. 1993 Oct;5(5):794-9 [8240742.001]
  • [Cites] Stat Methods Med Res. 1992;1(3):225-47 [1341659.001]
  • [Cites] Blood. 1994 Apr 15;83(8):2360-7 [8161803.001]
  • [Cites] Semin Oncol Nurs. 1994 Feb;10(1):42-57 [8165378.001]
  • [Cites] Cancer. 2006 Jun 1;106(11):2437-44 [16615096.001]
  • [Cites] Am J Hematol. 2007 Jan;82(1):45-52 [16937391.001]
  • [Cites] Brain Behav Immun. 2007 May;21(4):413-27 [17178209.001]
  • [Cites] Oncologist. 2007;12 Suppl 1:22-34 [17573453.001]
  • [Cites] J Natl Cancer Inst Monogr. 2007;(37):16-21 [17951226.001]
  • [Cites] J Clin Oncol. 2008 Feb 20;26(6):971-82 [18281672.001]
  • [Cites] Cancer. 2000 Oct 1;89(7):1634-46 [11013380.001]
  • [Cites] Exp Hematol. 2001 Mar;29(3):259-77 [11274753.001]
  • [Cites] Cancer. 2001 Sep 15;92(6 Suppl):1684-8 [11598887.001]
  • [Cites] Eur J Cancer Care (Engl). 2001 Jun;10(2):124-30 [11829045.001]
  • [Cites] Med Sci Monit. 2002 May;8(5):HY1-9 [12011758.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Oct 4;297(4):700-13 [12359210.001]
  • [Cites] Brain Behav Immun. 2003 Feb;17 Suppl 1:S112-8 [12615196.001]
  • [Cites] Cancer. 2003 Jun 1;97(11):2919-25 [12767108.001]
  • [Cites] Clin Cancer Res. 2003 Oct 15;9(13):4653-65 [14581334.001]
  • [Cites] Cytokine. 2004 Feb 7;25(3):94-102 [14698135.001]
  • [Cites] JAMA. 2004 May 19;291(19):2335-43 [15150205.001]
  • [Cites] Neuroimmunomodulation. 2004;11(5):279-92 [15316238.001]
  • [Cites] Blood. 2004 Oct 1;104(7):2194-200 [15198954.001]
  • [Cites] Blood. 1990 Feb 15;75(4):1011-6 [2405918.001]
  • [Cites] N Engl J Med. 1991 Mar 7;324(10):667-74 [1994250.001]
  • [Cites] Bone Marrow Transplant. 1991 Apr;7(4):311-6 [2070138.001]
  • [Cites] J Immunol Methods. 1992 Aug 30;153(1-2):115-24 [1381403.001]
  • [Cites] Eur J Cancer. 1995;31A(2):163-73 [7718320.001]
  • [Cites] Bone Marrow Transplant. 1995 Jan;15(1):99-104 [7742764.001]
  • [Cites] Br J Cancer. 1995 Jun;71(6):1322-9 [7779732.001]
  • [Cites] Pain. 1995 Apr;61(1):69-79 [7644251.001]
  • [Cites] Ann N Y Acad Sci. 1995 Dec 29;770:227-36 [8597363.001]
  • [Cites] Cancer Nurs. 1996 Jun;19(3):170-6 [8674025.001]
  • [Cites] Bone Marrow Transplant. 1996 Jun;17(6):1133-42 [8807126.001]
  • [Cites] Oncol Nurs Forum. 1999 Apr;26(3):575-82 [10214598.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Sep;11(9):706-12 [16125641.001]
  • [Cites] Bone Marrow Transplant. 2005 Nov;36(9):771-9 [16113665.001]
  • [Cites] Eur J Haematol. 2006 Feb;76(2):93-101 [16405429.001]
  • [Cites] Trends Immunol. 2006 Jan;27(1):24-31 [16316783.001]
  • [Cites] J Clin Oncol. 2006 Apr 20;24(12):1852-9 [16622259.001]
  • [Cites] Oncol Nurs Forum. 2006 May;33(3):535-42 [16676010.001]
  • (PMID = 18792065.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA026582-25; United States / NCI NIH HHS / CA / R01 CA026582; United States / NCI NIH HHS / CA / R21 CA132109; United States / NCI NIH HHS / CA / R01 CA026582-25
  • [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 / Biomarkers; 0 / Cytokines; 0 / Interleukin-6
  • [Other-IDs] NLM/ NIHMS70711; NLM/ PMC2633777
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22. Niedzielska E, Wójcik D, Barg E, Pietras W, Sega-Pondel D, Doroszko A, Niedzielska M, Skarzyńska M, Chybicka A: [Evaluation of selected endocrine complications in patients treated with auto- and allo-haematopoietic stem cell transplantation]. Med Wieku Rozwoj; 2008 Jul-Sep;12(3):761-6
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  • MATERIAL AND METHODS: The investigated group consisted of: I. 16 patients after auto-HSCT (6 girls, 10 boys) aged 3-20 years (average 10,8+/-) because of acute myelogenous leukaemia (n=5), non Hodgkin lymphoma (n=3), neuroblastoma (n=3), embryonal cancer (n=2), medulloblastoma (n=1), Ewing's sarcoma/PNET (n=1), hyper eosinophilic syndrome (n=1).
  • Indication for HSCT was acute lymphoblastic leukaemia (n=11), acute myelogenous leukaemia (n=5), chronic myeloid leukaemia-CML (n=6), myelodysplastic syndromes (n=2), non Hodgkin lymphoma (n=1), juvenile myelomonocytic leukemia (n=1), severe aplastic anaemia (n=1), Blackfan-Diamond anaemia (n=1), severe combined immune deficiency (n=1), rhabdomyosarcoma (n=1).
  • The patients underwent the following types of transplantation: HSCT of matched sibling donor (n=13), HSCT of matched unrelated donor (n=11) and HLA-mismatched related donor (n=6).
  • [MeSH-major] Endocrine System Diseases / etiology. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia / therapy
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Combined Modality Therapy. Female. Humans. Hypogonadism / etiology. Hypoparathyroidism / etiology. Hypothyroidism / etiology. Male. Poland. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome. Young Adult


23. Kaufmann SH, Steensma DP: On the TRAIL of a new therapy for leukemia. Leukemia; 2005 Dec;19(12):2195-202
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  • [Title] On the TRAIL of a new therapy for leukemia.
  • The cytokine TRAIL (tumor necrosis factor alpha-related apoptosis-inducing ligand) as well as agonistic antibodies that bind to the TRAIL receptors, death receptor 4 (DR4) and DR5, are undergoing preclinical and early clinical evaluation as potential therapeutic agents for a variety of hematological and nonhematological malignancies.
  • Here, we briefly review the normal biological function of TRAIL, the mechanism of cytotoxicity of TRAIL receptor ligands, and their effects on normal myeloid progenitors, myelodysplastic marrow and leukemic cells, including acute myelogenous leukemia (AML) and chronic lymphocytic leukemia (CLL), in vitro.
  • [MeSH-major] Apoptosis Regulatory Proteins / physiology. Leukemia / pathology. Membrane Glycoproteins / physiology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Apoptosis. Humans. Ligands. Receptors, Tumor Necrosis Factor / physiology. TNF-Related Apoptosis-Inducing Ligand

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  • (PMID = 16224489.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA69008
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Ligands; 0 / Membrane Glycoproteins; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 121
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24. Lee SJ, Kukreja M, Wang T, Giralt SA, Szer J, Arora M, Woolfrey AE, Cervantes F, Champlin RE, Gale RP, Halter J, Keating A, Marks DI, McCarthy PL, Olavarria E, Stadtmauer EA, Abecasis M, Gupta V, Khoury HJ, George B, Hale GA, Liesveld JL, Rizzieri DA, Antin JH, Bolwell BJ, Carabasi MH, Copelan E, Ilhan O, Litzow MR, Schouten HC, Zander AR, Horowitz MM, Maziarz RT: Impact of prior imatinib mesylate on the outcome of hematopoietic cell transplantation for chronic myeloid leukemia. Blood; 2008 Oct 15;112(8):3500-7
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  • [Title] Impact of prior imatinib mesylate on the outcome of hematopoietic cell transplantation for chronic myeloid leukemia.
  • Imatinib mesylate (IM, Gleevec) has largely supplanted allogeneic hematopoietic cell transplantation (HCT) as first line therapy for chronic myeloid leukemia (CML).
  • Nevertheless, many people with CML eventually undergo HCT, raising the question of whether prior IM therapy impacts HCT success.
  • Among patients in first chronic phase, IM therapy before HCT was associated with better survival but no statistically significant differences in treatment-related mortality, relapse, and leukemia-free survival.
  • Better HLA-matched donors, use of bone marrow, and transplantation within one year of diagnosis were also associated with better survival.
  • Among patients transplanted with advanced CML, use of IM before HCT was not associated with treatment-related mortality, relapse, leukemia-free survival, or survival.
  • Acute graft-versus-host disease rates were similar between IM(+) and IM(-) groups regardless of leukemia phase.


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

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • [CommentIn] Pediatr Blood Cancer. 2007 Jun 15;48(7):649-50 [17318875.001]
  • (PMID = 17183582.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines
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26. Guinan EC: Acquired aplastic anemia in childhood. Hematol Oncol Clin North Am; 2009 Apr;23(2):171-91
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  • In comparison to past decades, children who have acquired aplastic anemia (AA) enjoy excellent overall survival that reflects improvements in supportive care, more accurate exclusion of children who have alternate diagnoses, and advances in transplantation and immunosuppressive therapy (IST).
  • In this latter group, the barriers to overall and complication-free survival include recurrence of AA, clonal evolution with transformation to myelodysplasia/acute myelogenous leukemia, and therapy-related toxicities.
  • Improvements in predicting responses to IST, in alternative-donor HSCT, and in rationalizing therapy by understanding the pathophysiology in individual patients are likely to improve short- and long-term outcomes for these children.
  • [MeSH-major] Anemia, Aplastic / diagnosis. Anemia, Aplastic / therapy. Hematopoietic Stem Cell Transplantation

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  • (PMID = 19327578.001).
  • [ISSN] 1558-1977
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Immunosuppressive Agents; 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 83HN0GTJ6D / Cyclosporine; PVI5M0M1GW / Filgrastim
  • [Number-of-references] 160
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27. Schuster MW, Shore TB, Harpel JG, Greenberg J, Jalilizeinali B, Possley S, Gerwien RW, Hahne W, Halvorsen YD: Safety and tolerability of velafermin (CG53135-05) in patients receiving high-dose chemotherapy and autologous peripheral blood stem cell transplant. Support Care Cancer; 2008 May;16(5):477-83
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  • Patients were diagnosed with multiple myeloma (n = 16), non-Hodgkin's lymphoma (n = 12), acute myelogenous leukemia (n = 1), or desmoplasmic round cell tumor (n = 1).
  • There were no drug-related serious adverse events.
  • [MeSH-major] Fibroblast Growth Factors / adverse effects. Stomatitis / drug therapy
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Hematologic Neoplasms / complications. Hematologic Neoplasms / drug therapy. Hematologic Neoplasms / therapy. Humans. Male. Middle Aged. Peripheral Blood Stem Cell Transplantation. Treatment Outcome

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  • [Cites] Cancer. 2004 May 1;100(9 Suppl):2026-46 [15108223.001]
  • [Cites] Support Cancer Ther. 2005 Jan 1;2(2):122-7 [18628199.001]
  • [Cites] Gastroenterology. 2002 Oct;123(4):1151-62 [12360478.001]
  • [Cites] Cytokine Growth Factor Rev. 2005 Apr;16(2):233-47 [15863038.001]
  • [Cites] Anticancer Res. 2004 Sep-Oct;24(5B):3263-7 [15510621.001]
  • [Cites] Cytokines Cell Mol Ther. 1999 Dec;5(4):187-93 [10850381.001]
  • [Cites] Bone Marrow Transplant. 2005 May;35(10):971-7 [15778725.001]
  • [Cites] Clin Cancer Res. 2003 Aug 15;9(9):3454-61 [12960137.001]
  • [Cites] EMBO J. 2005 Jan 12;24(1):73-84 [15592430.001]
  • [Cites] Semin Oncol. 2004 Jun;31(3 Suppl 8):35-44 [15181607.001]
  • [Cites] Bone Marrow Transplant. 2002 Dec;30(11):769-75 [12439700.001]
  • [Cites] Leuk Res. 2004 Jun;28(6):559-65 [15120931.001]
  • [Cites] Cancer. 2004 May 1;100(9 Suppl):1995-2025 [15108222.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):3131-8 [11306498.001]
  • [Cites] Br J Haematol. 2000 Aug;110(2):292-9 [10971384.001]
  • [Cites] Support Care Cancer. 2004 Apr;12(4):219-26 [14767748.001]
  • [Cites] J Clin Oncol. 2003 Apr 15;21(8):1452-8 [12697866.001]
  • [Cites] N Engl J Med. 2004 Dec 16;351(25):2590-8 [15602019.001]
  • (PMID = 17710442.001).
  • [ISSN] 0941-4355
  • [Journal-full-title] Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer
  • [ISO-abbreviation] Support Care Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / FGF20 protein, human; 62031-54-3 / Fibroblast Growth Factors
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28. McCormack E, Bruserud O, Gjertsen BT: Review: genetic models of acute myeloid leukaemia. Oncogene; 2008 Jun 19;27(27):3765-79
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  • [Title] Review: genetic models of acute myeloid leukaemia.
  • The use of genetically engineered mice (GEM) have been critical in understanding disease states such as cancer, and none more so than acute myelogenous leukaemia (AML), a disease characterized by over 100 distinct chromosomal translocations.
  • A substantial proportion of cases exhibiting recurrent reciprocal translocations at diagnosis, such as t(8;21) or t(15;17) have been exhaustively studied and are currently employed in clinical diagnosis.
  • Furthermore, little emphasis has been paid to the effect of chromosomal translocations other than recurrent genetic abnormalities, with no models reflecting the multiple abnormalities observed in high-risk cases of AML accounting for 8-10% of adult AML.
  • Here we review the differing technologies employed in generation of GEM of AML.
  • We discuss the relevance of GEM AML from embryonic stem cell-mediated (for example retinoic acid receptor-alpha fusions and AML1/ETO) models; through to the valuable retroviral-mediated gene transfer models.
  • The latter have been used to great effect in defining the transforming properties of chromosomal translocation products such as MLL (found in 5-6% of all AML cases) and NUP98 (denoting poor prognosis in therapy-related disease) and particularly when co-transduced with bad prognostic factors such as Flt3 mutations.
  • [MeSH-major] Animals, Genetically Modified / genetics. Leukemia, Myeloid, Acute / genetics. Models, Genetic
  • [MeSH-minor] Animals. Chromosome Aberrations. Disease Models, Animal. Exons. Humans. Leukemia, Promyelocytic, Acute / genetics. Mice. Mice, Transgenic. Prognosis


29. Jabbour E, Cortes J, Kantarjian HM, Giralt S, Jones D, Jones R, Giles F, Andersson BS, Champlin R, de Lima M: Allogeneic stem cell transplantation for patients with chronic myeloid leukemia and acute lymphocytic leukemia after Bcr-Abl kinase mutation-related imatinib failure. Blood; 2006 Aug 15;108(4):1421-3
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  • [Title] Allogeneic stem cell transplantation for patients with chronic myeloid leukemia and acute lymphocytic leukemia after Bcr-Abl kinase mutation-related imatinib failure.
  • Resistance to imatinib mesylate is an emerging problem in the treatment of chronic myeloid leukemia (CML), often associated with point mutations in the Bcr-Abl kinase domain.
  • Ten imatinib-resistant patients with Bcr-Abl kinase mutations received a transplant: 9 had CML (3 in chronic phase, 4 in accelerated phase, and 2 in blast phase) and 1 had Philadelphia-positive acute lymphocytic leukemia (ALL).
  • All patients engrafted; there were no treatment-related deaths.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Point Mutation. Stem Cell Transplantation
  • [MeSH-minor] Adult. Benzamides. Blast Crisis / genetics. Blast Crisis / metabolism. Blast Crisis / mortality. Blast Crisis / therapy. Disease-Free Survival. Female. Graft Survival / drug effects. Graft Survival / genetics. Humans. Imatinib Mesylate. Male. Middle Aged. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Recurrence. Salvage Therapy. Transplantation, Homologous. Treatment Outcome


30. Dalgaard J, Fløisand Y, Stenersen M, Egeland T, Brinch L: [Non-myeloablative allogeneic stem cell transplantation]. Tidsskr Nor Laegeforen; 2007 Mar 15;127(6):721-4
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  • 11 patients suffered from acute graft versus host disease (GVHD), 6 with debut of symptoms after day 100.
  • 14 patients are alive and 7 are dead; 2 due to transplant-related complications and 5 due to disease progression.
  • Acute and chronic GVHD is still a substantial problem.
  • [MeSH-minor] Adult. Female. Graft vs Host Disease / etiology. Graft vs Host Disease / immunology. Graft vs Host Disease / prevention & control. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / therapy. Male. Middle Aged. Remission Induction. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 17363982.001).
  • [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] English Abstract; Journal Article
  • [Publication-country] Norway
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31. Kröger N, Brand R, van Biezen A, Cahn JY, Slavin S, Blaise D, Sierra J, Zander A, Niederwieser D, de Witte T, Myelodysplastic Syndromes Subcommittee of The Chronic Leukaemia Working Party of the European Group for Blood and Marrow Transplantation (EBMT): Autologous stem cell transplantation for therapy-related acute myeloid leukemia and myelodysplastic syndrome. Bone Marrow Transplant; 2006 Jan;37(2):183-9
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  • [Title] Autologous stem cell transplantation for therapy-related acute myeloid leukemia and myelodysplastic syndrome.
  • We report the results of 65 patients with treatment-related myelodysplastic syndrome (MDS)/acute myelogenous leukemia (AML) who were transplanted from an autograft and reported to the EBMT.
  • The primary disease was solid tumors (n = 37), Hodgkin's disease (n = 13), non-Hodgkin's lymphoma (n = 10), acute lymphoblastic leukemia (n = 2) or myeloproliferative syndromes (n = 3).
  • The types of MDS were as follows: RAEB (n = 1; 2%), RAEB-t (n = 3; 5%), or AML (n = 56; 87%).
  • The median time between diagnosis and transplantation was 5 months (range, 3-86).
  • The cumulative incidence of relapse was 58% (95% CI: 44-72%) and of treatment-related mortality 12% (95% CI: 6-38%).
  • Furthermore, age beyond 40 years resulted in a higher treatment-related mortality (47 vs 7%; P = 0.01).
  • Autologous transplantation may cure a substantial number of patients with treatment-related MDS/AML, especially if they are in CR1 and of younger age.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / mortality. Myelodysplastic Syndromes / therapy. Neoplasms, Second Primary / mortality. Neoplasms, Second Primary / therapy. Stem Cell Transplantation


32. Shinder R, Oellers P, Esmaeli B, Schiffman JS: Superior ophthalmic vein thrombosis in a patient with chronic myeloid leukemia receiving antifibrinolytic and thrombopoietin receptor agonist therapy. J Ocul Pharmacol Ther; 2010 Jun;26(3):293-6
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  • [Title] Superior ophthalmic vein thrombosis in a patient with chronic myeloid leukemia receiving antifibrinolytic and thrombopoietin receptor agonist therapy.
  • Isolated superior ophthalmic vein (SOV) thrombosis is a rare condition usually related to inflammation of the orbit or paranasal sinuses.
  • Patients present with acute orbital signs, including proptosis, ophthalmoplegia, globe dystopia, and periorbital edema, and may have diminished vision secondary to optic neuropathy.
  • SOV thrombosis is typically seen in the setting of septic cavernous sinus thrombosis, and antimicrobial therapy is the treatment of choice.
  • We herein report what may be the first case of isolated SOV thrombosis related to hypercoagulability in a patient with cancer who was receiving antifibrinolytic and thrombopoietin receptor agonist medications.
  • [MeSH-minor] Aged. Eye / blood supply. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Male


33. Yamane T, Nakamae H, Hasegawa T, Terada Y, Hagihara K, Ohta K, Hino M: Cord blood transplantation for adult patients with hematological malignancies. Osaka City Med J; 2005 Dec;51(2):83-8
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  • Acute GVHD grade II occurred in 2 cases with engraftment, and chronic GVHD occurred in 1 of 3 evaluable patients.
  • We believe that adult patients without suitable related or unrelated bone marrow donors should be considered as candidates for CBT by the choice of CB including both sufficient nucleated cell dose and CD34+ cell dose.
  • [MeSH-major] Cord Blood Stem Cell Transplantation. Fetal Blood / transplantation. Hematologic Neoplasms / blood. Hematologic Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Antigens, CD34 / blood. Female. Graft vs Host Disease / etiology. Hematopoiesis. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / therapy. Leukemia-Lymphoma, Adult T-Cell / blood. Leukemia-Lymphoma, Adult T-Cell / therapy. Male. Middle Aged. Treatment Outcome

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  • (PMID = 16617685.001).
  • [ISSN] 0030-6096
  • [Journal-full-title] Osaka city medical journal
  • [ISO-abbreviation] Osaka City Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD34
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34. Phan CL, Megat Baharuddin PJ, Chin LP, Zakaria Z, Yegappan S, Sathar J, Tan SM, Purushothaman V, Chang KM: Amplification of BCR-ABL and t(3;21) in a patient with blast crisis of chronic myelogenous leukemia. Cancer Genet Cytogenet; 2008 Jan 1;180(1):60-4
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  • [Title] Amplification of BCR-ABL and t(3;21) in a patient with blast crisis of chronic myelogenous leukemia.
  • The Philadelphia (Ph) chromosome, or t(9;22), is the hallmark of chronic myelogenous leukemia (CML).
  • The t(3;21)(q26;q22) is a recurrent chromosomal abnormality in some cases of CML blast phase and in treatment-related myelodysplastic syndrome and acute myeloid leukemia.
  • Amplification or copy number increase of RUNX1 has been reported in childhood acute lymphoblastic leukemia.
  • Our study indicated that the progenitor of CML was BCR-ABL dependent through the amplification of Ph chromosome as a mechanism of resistance to imatinib therapy.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 3. Fusion Proteins, bcr-abl / genetics. Gene Amplification. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Translocation, Genetic

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  • (PMID = 18068536.001).
  • [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
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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35. Ciurea SO, Rodrigues M, Giralt S, de Lima M: Aging, acute myelogenous leukemia, and allogeneic transplantation: do they belong in the same sentence? Clin Lymphoma Myeloma; 2009 Aug;9(4):289-97
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  • [Title] Aging, acute myelogenous leukemia, and allogeneic transplantation: do they belong in the same sentence?
  • Acute myelogenous leukemia is a disease of the elderly.
  • Disease biology and functional status of this patient population contribute to poorer treatment outcomes with standard therapy.
  • However, transplantation was restricted until recently to younger patients because of prohibitive treatment-related mortality.
  • The development of reduced-intensity preparative regimens and improvements in supportive care now allow older patients with myeloid leukemia a greater opportunity for cure with transplantation.
  • [MeSH-major] Aging / physiology. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy


36. Creutzig U, Reinhardt D, Diekamp S, Dworzak M, Stary J, Zimmermann M: AML patients with Down syndrome have a high cure rate with AML-BFM therapy with reduced dose intensity. Leukemia; 2005 Aug;19(8):1355-60
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  • [Title] AML patients with Down syndrome have a high cure rate with AML-BFM therapy with reduced dose intensity.
  • Despite improved prognosis in acute myelogenous leukaemia (AML) children with Down syndrome (DS), therapy-related toxicity remained a problem.
  • We compared 67 DS patients from study AML-BFM 98 with 51 DS patients of the previous study AML-BFM 93, and the non-DS groups of both studies.
  • AML-DS patients were in median 1.8 years old, and 102/118 (86%) showed the typical morphology of acute megakaryoblastic leukaemia.
  • In study 93, seven DS patients did not receive AML-specific chemotherapy, and treatment modifications were more common.
  • Therapy-related toxicity was generally lower in DS patients treated according to study 98.
  • We conclude that a standardised and dose-reduced treatment schedule including the main components of AML treatment is advisable for AML children with DS.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Down Syndrome / complications. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adolescent. Age Factors. Child. Child, Preschool. Cytarabine / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Idarubicin / administration & dosage. Infant. Leukemia, Megakaryoblastic, Acute / pathology. Male. Survival Rate. Treatment Outcome

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  • [Copyright] Leukemia (2005) 19, 1355-1360.
  • (PMID = 15920490.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZRP63D75JW / Idarubicin; ICE protocol 4
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37. Buckstein R, Kerbel RS, Shaked Y, Nayar R, Foden C, Turner R, Lee CR, Taylor D, Zhang L, Man S, Baruchel S, Stempak D, Bertolini F, Crump M: High-Dose celecoxib and metronomic "low-dose" cyclophosphamide is an effective and safe therapy in patients with relapsed and refractory aggressive histology non-Hodgkin's lymphoma. Clin Cancer Res; 2006 Sep 1;12(17):5190-8
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  • [Title] High-Dose celecoxib and metronomic "low-dose" cyclophosphamide is an effective and safe therapy in patients with relapsed and refractory aggressive histology non-Hodgkin's lymphoma.
  • Three patients developed deep vein thromboses and two heavily pretreated patients developed treatment-related acute myelogenous leukemia or myelodysplasia after 3.7 and 12 months of therapy.
  • [MeSH-major] Cyclophosphamide / administration & dosage. Lymphoma, Non-Hodgkin / drug therapy. Pyrazoles / administration & dosage. Sulfonamides / administration & dosage
  • [MeSH-minor] Administration, Oral. Adult. Aged. Aged, 80 and over. Celecoxib. Disease Progression. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug-Related Side Effects and Adverse Reactions. Female. Follow-Up Studies. Humans. Kaplan-Meier Estimate. Male. Maximum Tolerated Dose. Middle Aged. Prospective Studies. Recurrence. Risk Factors. Survival Rate. Treatment Outcome. Vascular Endothelial Growth Factor A / blood

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  • (PMID = 16951238.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pyrazoles; 0 / Sulfonamides; 0 / Vascular Endothelial Growth Factor A; 8N3DW7272P / Cyclophosphamide; JCX84Q7J1L / Celecoxib
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38. Laport GG, Sandmaier BM, Storer BE, Scott BL, Stuart MJ, Lange T, Maris MB, Agura ED, Chauncey TR, Wong RM, Forman SJ, Petersen FB, Wade JC, Epner E, Bruno B, Bethge WA, Curtin PT, Maloney DG, Blume KG, Storb RF: Reduced-intensity conditioning followed by allogeneic hematopoietic cell transplantation for adult patients with myelodysplastic syndrome and myeloproliferative disorders. Biol Blood Marrow Transplant; 2008 Feb;14(2):246-55
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  • We report the results of 148 patients (median age = 59 years old) with de novo MDS (n = 40), acute myelogenous leukemia (AML) after antecedent MDS/MPD (n = 49), treatment-related MDS (t-MDS) (n = 25), MPD (n = 27), and chronic myelomonocytic leukemia (CMML) (n = 7) who underwent allogeneic HCT using a conditioning regimen of low-dose total body irradiation (TBI) alone (200 cGy) on day 0 (n = 5) or with the addition of fludarabine (Flu) 30 mg/m(2)/day on days -4 to -2 (n = 143).
  • Seventy-five patients (51%) received an allograft from a matched related donor (MRD), and 73 patients (49%) were recipients of unrelated donor (URD) grafts.
  • There was no significant difference in the incidence of acute (gr II-IV) and chronic extensive graft-versus-host disease (aGVHD, cGVHD) between the recipients of related and unrelated donor grafts.
  • The 3-year RFS for the patients with de novo MDS, AML after antecedent MDS/MPD, t-MDS, MPD, and CMML were 22%, 20%, 29%, 37%, and 43%, respectively, and the 3-year OS was 20%, 23%, 27%, 43%, and 43%, respectively.

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  • [Cites] Biol Blood Marrow Transplant. 2007 Apr;13(4):454-62 [17382251.001]
  • [Cites] Blood. 2006 Aug 1;108(3):836-46 [16597592.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2134-41 [11304765.001]
  • [Cites] Blood. 2002 Feb 1;99(3):840-9 [11806985.001]
  • [Cites] Br J Haematol. 2002 Jul;118(1):67-73 [12100129.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1997-2004 [12200358.001]
  • [Cites] Blood. 2002 Sep 15;100(6):2243-5 [12200391.001]
  • [Cites] Ann Hematol. 2003 Jun;82(6):336-42 [12728337.001]
  • [Cites] Bone Marrow Transplant. 2003 Jul;32(1):35-40 [12815476.001]
  • [Cites] J Clin Oncol. 2003 Aug 15;21(16):3060-5 [12915594.001]
  • [Cites] Blood. 2003 Sep 15;102(6):2021-30 [12791654.001]
  • [Cites] Blood. 2003 Oct 15;102(8):3052-9 [12842990.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3912-8 [12920019.001]
  • [Cites] Biol Blood Marrow Transplant. 2003 Dec;9(12):753-9 [14677114.001]
  • [Cites] Blood. 2004 Aug 1;104(3):857-64 [15073038.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1616-23 [15059843.001]
  • [Cites] Bone Marrow Transplant. 2004 Nov;34(9):807-13 [15354205.001]
  • [Cites] Transplantation. 1974 Oct;18(4):295-304 [4153799.001]
  • [Cites] Blood. 1996 Jul 1;88(1):358-65 [8704196.001]
  • [Cites] Blood. 1997 Apr 1;89(7):2578-85 [9116305.001]
  • [Cites] Bone Marrow Transplant. 1997 Nov;20(9):737-43 [9384475.001]
  • [Cites] Bone Marrow Transplant. 1998 Feb;21(3):255-61 [9489648.001]
  • [Cites] Haematologica. 1998 Jun;83(6):543-9 [9676028.001]
  • [Cites] Blood. 1999 May 1;93(9):2831-8 [10216077.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1810-4 [15459007.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1993-2003 [15774790.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Sep;11(9):713-20 [16125642.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4381-8 [16144801.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 Apr;12(4):454-65 [16545729.001]
  • [Cites] Leukemia. 2006 Jan;20(1):128-35 [16270037.001]
  • [Cites] Bone Marrow Transplant. 2006 Jun;37(11):1003-8 [16604096.001]
  • [Cites] Br J Haematol. 2000 Sep;110(3):620-30 [10997974.001]
  • (PMID = 18215785.001).
  • [ISSN] 1523-6536
  • [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
  • [Grant] United States / NCI NIH HHS / CA / P01 CA049605-14; United States / NCI NIH HHS / CA / CA18029; United States / NHLBI NIH HHS / HL / HL036444-27; United States / NCI NIH HHS / CA / K23 CA092058-01; United States / NHLBI NIH HHS / HL / HL36444; United States / NCI NIH HHS / CA / P30 CA015704-31; 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 / CA92058; United States / NCI NIH HHS / CA / CA092058-01; United States / NCI NIH HHS / CA / K23 CA092058; United States / NCI NIH HHS / CA / P01 CA018029-250002; United States / NCI NIH HHS / CA / CA049605-14; United States / NCI NIH HHS / CA / P01 CA018029-270047; United States / NCI NIH HHS / CA / CA15704; United States / NCI NIH HHS / CA / P01 CA078902-09; United States / NCI NIH HHS / CA / CA018029-270047; United States / NCI NIH HHS / CA / CA078902-09; United States / NHLBI NIH HHS / HL / P01 HL036444-27; United States / NCI NIH HHS / CA / CA018029-250002; United States / NHLBI NIH HHS / HL / P01 HL036444; United States / NCI NIH HHS / CA / P01 CA078902; United States / NCI NIH HHS / CA / P01-CA 49605; United States / NCI NIH HHS / CA / CA015704-31; United States / NCI NIH HHS / CA / P01 CA049605
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ NIHMS39955; NLM/ PMC2259225
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39. Parikh SH, Mendizabal A, Martin PL, Prasad VK, Szabolcs P, Driscoll TA, Kurtzberg J: Unrelated donor umbilical cord blood transplantation in pediatric myelodysplastic syndrome: a single-center experience. Biol Blood Marrow Transplant; 2009 Aug;15(8):948-55
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  • The median age was 11.1 years (range: 1.1-19.7), median weight was 38.6 kg (range: 9.6-62.6), 61% of patients were male, and median time from diagnosis to transplant was 6.6 months (range: 2.0-61.4).
  • Patients with acute myelogenous leukemia (AML) were excluded.
  • Three patients developed acute GVHD (aGVHD) grades II-IV with a cumulative incidence at 100 days of 13% (95% CI 0.0%-27.1.0%).
  • UUCB should be actively considered for pediatric MDS patients lacking matched related or unrelated adult donors.
  • [MeSH-major] Cord Blood Stem Cell Transplantation / methods. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Adolescent. Adult. Anemia, Refractory, with Excess of Blasts. Chemoprevention / methods. Child. Female. Graft vs Host Disease / drug therapy. Graft vs Host Disease / prevention & control. Humans. Male. Middle Aged. Retrospective Studies. Survival Analysis. Tissue Donors. Treatment Outcome. Whole-Body Irradiation. Young Adult


40. Schmitt-Graeff A, Hochhaus A: [Hematological side effects of tyrosine kinase inhibition using imatinib]. Pathologe; 2006 Feb;27(1):40-6
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  • Imatinib (STI571, Gleevec/Glivec) and other small-molecule tyrosine kinase inhibitors are highly effective in the treatment of chronic myeloid leukemia (CML), gastrointestinal stromal tumors and, for example, eosinophilia-associated chronic myeloproliferative disorders.
  • This molecularly targeted approach disrupts abnormal tyrosine kinase dependent signalling pathways, thus providing a preferred treatment option for selected neoplastic disorders with activating mutations of Abelson-, Abl-related-, Kit-, and platelet-derived growth factor receptor A and B genes.
  • Therapy is generally well tolerated.
  • Single or multilineage myelodysplasia may be accompanied by an excess of blasts and rarely evolves into acute leukemia in CML patients.
  • [MeSH-minor] Benzamides. Gastrointestinal Diseases / chemically induced. Hematopoiesis / drug effects. Hematopoiesis / genetics. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology

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  • [Cites] Hematology Am Soc Hematol Educ Program. 2003;:132-52 [14633780.001]
  • [Cites] Curr Cancer Drug Targets. 2005 May;5(3):171-93 [15892618.001]
  • [Cites] Pharmacol Rev. 2003 Sep;55(3):401-23 [12869662.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1941-9 [12411298.001]
  • [Cites] Acta Haematol. 2005;114(1):52-60 [15995325.001]
  • [Cites] Stem Cells. 2005 Sep;23(8):1082-8 [16140870.001]
  • [Cites] Leuk Lymphoma. 2005 May;46(5):781-4 [16019519.001]
  • [Cites] Leuk Lymphoma. 2004 Feb;45(2):237-45 [15101707.001]
  • [Cites] N Engl J Med. 2002 Aug 15;347(7):472-80 [12181401.001]
  • [Cites] Lancet. 2004 Sep 25-Oct 1;364(9440):1127-34 [15451219.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):641-56, ix [15271397.001]
  • [Cites] Ann Hematol. 2005 Aug;84(8):487-97 [15931535.001]
  • [Cites] Blood. 2002 Jul 15;100(2):435-41 [12091333.001]
  • [Cites] Nature. 2005 Jun 30;435(7046):1267-70 [15988530.001]
  • [Cites] Expert Opin Drug Saf. 2005 Mar;4(2):183-91 [15794712.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1340-6 [15190256.001]
  • [Cites] Cancer. 2005 Nov 1;104(9):1781-8 [16136600.001]
  • [Cites] Pathologe. 2004 Nov;25(6):428-35 [15179523.001]
  • [Cites] Pathologe. 2004 Mar;25(2):127-34 [15010998.001]
  • [Cites] Dtsch Med Wochenschr. 2004 Oct 1;129(40):2122-7 [15455305.001]
  • [Cites] Cancer. 2005 Apr 15;103(8):1659-69 [15747376.001]
  • [Cites] Blood. 2004 Jan 15;103(2):523-9 [12969987.001]
  • [Cites] Blood. 2002 May 15;99(10):3792-800 [11986238.001]
  • [Cites] Leukemia. 2005 Mar;19(3):460-3 [15625554.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2002;:111-35 [12446421.001]
  • [Cites] Blood. 2002 Jan 1;99(1):381-3 [11756197.001]
  • [Cites] Cell Cycle. 2005 Jul;4(7):851-3 [15917650.001]
  • [Cites] N Engl J Med. 2003 Mar 13;348(11):994-1004 [12637609.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1573-8 [15990860.001]
  • [Cites] Eur J Cancer. 2005 Aug;41(12):1751-7 [16098458.001]
  • [Cites] Ann N Y Acad Sci. 2005 Jun;1044:168-77 [15958710.001]
  • [Cites] Blood. 2004 Oct 1;104(7):1931-9 [15166033.001]
  • [Cites] Histol Histopathol. 2004 Oct;19(4):1277-88 [15375771.001]
  • [Cites] Blood. 2002 May 15;99(10):3530-9 [11986204.001]
  • [Cites] Leuk Res. 2003 Dec;27(12):1163-6 [12921956.001]
  • [Cites] Bone Marrow Transplant. 2005 Sep;36(5):417-24 [16007105.001]
  • (PMID = 16421705.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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41. Drumea K, Yang ZF, Rosmarin A: Retinoic acid signaling in myelopoiesis. Curr Opin Hematol; 2008 Jan;15(1):37-41
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  • Currently, retinoic acid is a front-line agent in the treatment of certain forms of acute myelogenous leukemia.
  • In this review, we focus on recent advances in our understanding of the mechanisms by which retinoids affect growth and proliferation of myeloid cells and contribute to the pathogenesis of leukemia.
  • We have not attempted to summarize the related clinical literature.
  • These findings have resulted in successful rational approaches to the treatment of acute leukemia and provide the promise of improved treatments in the near future.
  • [MeSH-minor] Animals. Cell Differentiation / drug effects. Cell Transformation, Neoplastic. Chromatin / genetics. Chromatin / metabolism. Gene Expression Regulation / physiology. Humans. Leukemia, Myeloid / pathology. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / genetics. Mice. Myeloid Cells / cytology. Myeloid Cells / drug effects. Myeloproliferative Disorders / pathology. Oncogene Proteins, Fusion / metabolism. Protein Processing, Post-Translational. Receptors, Retinoic Acid / drug effects. Receptors, Retinoic Acid / physiology. Retinoids / physiology. Signal Transduction. Transcription Factors / metabolism

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  • (PMID = 18043244.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 1P20 RR 017695; United States / NCRR NIH HHS / RR / 1P20 RR 018757; United States / NHLBI NIH HHS / HL / 1R01 HL 073945; United States / NCRR NIH HHS / RR / P20 RR 15578
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromatin; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Retinoic Acid; 0 / Retinoids; 0 / Transcription Factors; 5688UTC01R / Tretinoin
  • [Number-of-references] 34
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42. 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
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  • Three cases (3%) of secondary acute myelogenous leukemia occurred.
  • It has low morbidity and transplant-related mortality and a low incidence (3%) of posttransplantation malignancy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Lymphoma, Non-Hodgkin / therapy. Peripheral Blood Stem Cell Transplantation / methods
  • [MeSH-minor] Adult. Aged. Carmustine / administration & dosage. Cisplatin / administration & dosage. Drug Resistance, Neoplasm. Etoposide / administration & dosage. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasms, Second Primary / etiology. Radiotherapy, Adjuvant / adverse effects. Radiotherapy, Adjuvant / methods. Radiotherapy, Adjuvant / mortality. Salvage Therapy / methods. Salvage Therapy / mortality. Survival Analysis. Transplantation, Autologous

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  • (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
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43. Karanes C, Nelson GO, Chitphakdithai P, Agura E, Ballen KK, Bolan CD, Porter DL, Uberti JP, King RJ, Confer DL: Twenty years of unrelated donor hematopoietic cell transplantation for adult recipients facilitated by the National Marrow Donor Program. Biol Blood Marrow Transplant; 2008 Sep;14(9 Suppl):8-15
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  • Chronic myelogenous leukemia (CML) was previously the most common diagnosis for unrelated donor transplantation, but it now comprises less than 10% of transplants for adult recipients.
  • Transplants for acute myelogenous leukemia (AML), acute lymphoblastic leukemia (ALL), non-Hodgkin lymphoma (NHL), and myelodysplastic syndromes (MDS) all outnumber CML.
  • Treatment-related mortality (TRM) has declined significantly over the years, particularly in association with myeloablative transplant preparative regimens.
  • [MeSH-minor] Adult. Aged. Hematologic Neoplasms / therapy. History, 20th Century. History, 21st Century. Humans. Middle Aged. Registries. Survival Rate. Tissue Donors. Transplantation, Homologous. United States

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  • (PMID = 18721775.001).
  • [ISSN] 1523-6536
  • [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] Historical Article; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 16
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44. Shackelford D, Kenific C, Blusztajn A, Waxman S, Ren R: Targeted degradation of the AML1/MDS1/EVI1 oncoprotein by arsenic trioxide. Cancer Res; 2006 Dec 1;66(23):11360-9
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  • Arsenic trioxide (ATO) has been found to be an effective treatment for acute promyelocytic leukemia patients and is being tested for treating other hematologic malignancies.
  • We have previously shown that AML1/MDS1/EVI1 (AME), a fusion gene generated by a t(3;21)(q26;q22) translocation found in patients with chronic myelogenous leukemia during blast phase, myelodysplastic syndrome, or acute myelogenous leukemia (AML), impairs hematopoiesis and eventually induces an AML in mice.
  • In this study, we examined whether ATO could target AME and related oncoproteins.
  • Our results suggest that ATO could be used as a part of targeted therapy for AME-, AML1/MDS1-, MDS1/EVI1-, and EVI1-positive human cancers.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Cell Differentiation / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Flow Cytometry. Gene Expression Regulation, Neoplastic / drug effects. Growth Inhibitors / pharmacology. Humans. Leukemia, Experimental / genetics. Leukemia, Experimental / pathology. Leukemia, Experimental / prevention & control. Male. Mice. Mice, Inbred BALB C. NIH 3T3 Cells. Proteasome Endopeptidase Complex / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects. Survival Analysis. Transfection. Ubiquitin / metabolism

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  • (PMID = 17145882.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-MDS1-EVI1 fusion protein, human; 0 / Arsenicals; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Growth Inhibitors; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / Repressor Proteins; 0 / Ubiquitin; EC 3.4.25.1 / Proteasome Endopeptidase Complex; S7V92P67HO / arsenic trioxide
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45. Lichtman MA: Is there an entity of chemically induced BCR-ABL-positive chronic myelogenous leukemia? Oncologist; 2008 Jun;13(6):645-54
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  • [Title] Is there an entity of chemically induced BCR-ABL-positive chronic myelogenous leukemia?
  • Advances in the therapy of malignancy have been accompanied by an increased frequency of cases of secondary acute myelogenous leukemia and related clonal cytopenias and oligoblastic (subacute) myelogenous leukemia (myelodysplastic syndromes).
  • The acute myelogenous leukemia incidence can be increased by high-dose acute ionizing radiation exposure, alkylating agents, topoisomerase II inhibitors, possibly other DNA-damaging therapeutic agents, heavy, prolonged cigarette smoking, and high dose-time exposure to benzene, the latter less frequently seen in industrialized countries with worksite regulations.
  • Acute myelogenous leukemia and myelodysplastic syndromes may result from innumerable primary types of chromosome damage.
  • In the case of chronic myelogenous leukemia, a specific break in chromosome bands 9q34 and 22q11 must occur to result in the causal fusion oncogene (BCR-ABL).
  • A review of 11 studies of the chromosomal abnormalities found in presumptive cases of cytotoxic therapy-induced leukemia and of 40 studies of the subtypes of leukemia that occur following cytotoxic therapy for other cancers has not provided evidence of an increased risk for chemically induced BCR-ABL-positive chronic myelogenous leukemia.
  • Studies of the effects of alkylating agents, topoisomerase inhibitors, and benzene on chromosomes of hematopoietic cells in vitro, coupled with the aforementioned epidemiological studies of secondary leukemia after cytotoxic therapy or of persons exposed to high dose-time concentrations of benzene in the workplace, do not indicate a relationship among chemical exposure, injury to chromosome bands 9q34 and 22q11, and an increased risk for BCR-ABL-positive chronic myelogenous leukemia.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Chromosome Aberrations. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / chemically induced

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  • (PMID = 18586919.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 113
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46. Bylund KC, Giampoli E, Singh D, Doerr T, Sahasrabudhe D, Liesveld J, Constine LS: Soft tissue sarcoma in the setting of chronic cutaneous graft versus host disease after allogenic bone marrow transplantation. Cancer Invest; 2008 Jul;26(6):638-41
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  • This occurred 3.5 years after bone marrow transplant for acute myelogenous leukemia (AML).
  • This suggests that malignant sarcomas may develop in the setting of chronic GVHD, and close surveillance of GVHD-related nodules is warranted.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Graft vs Host Disease / complications. Leukemia, Myeloid, Acute / surgery. Neoplasms, Second Primary. Sarcoma / etiology. Skin Diseases / complications. Soft Tissue Neoplasms / etiology
  • [MeSH-minor] Adult. Biopsy, Fine-Needle. Chemotherapy, Adjuvant. Chronic Disease. Humans. Male. Neoadjuvant Therapy. Radiotherapy, Adjuvant. Time Factors. Tomography, X-Ray Computed. Transplantation, Homologous. Treatment Outcome


47. Matheny CJ, Speck ME, Cushing PR, Zhou Y, Corpora T, Regan M, Newman M, Roudaia L, Speck CL, Gu TL, Griffey SM, Bushweller JH, Speck NA: Disease mutations in RUNX1 and RUNX2 create nonfunctional, dominant-negative, or hypomorphic alleles. EMBO J; 2007 Feb 21;26(4):1163-75
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  • Monoallelic RUNX1 mutations cause familial platelet disorder with predisposition for acute myelogenous leukemia (FPD/AML).
  • Sporadic mono- and biallelic mutations are found at high frequencies in AML M0, in radiation-associated and therapy-related myelodysplastic syndrome and AML, and in isolated cases of AML M2, M5a, M3 relapse, and chronic myelogenous leukemia in blast phase.

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  • [Cites] Nat Biotechnol. 2002 Jan;20(1):87-90 [11753368.001]
  • [Cites] Biochemistry. 2005 Nov 15;44(45):14907-19 [16274238.001]
  • [Cites] Nat Rev Cancer. 2001 Oct;1(1):68-76 [11900253.001]
  • [Cites] Br J Haematol. 2002 Jun;117(4):878-81 [12060124.001]
  • [Cites] Am J Hum Genet. 2002 Oct;71(4):724-38 [12196916.001]
  • [Cites] Blood. 2003 Jan 15;101(2):673-80 [12393679.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1277-83 [12393381.001]
  • [Cites] J Biol Chem. 2003 Aug 29;278(35):33088-96 [12807882.001]
  • [Cites] J Biol Chem. 2003 Aug 29;278(35):33097-104 [12807883.001]
  • [Cites] J Biol Chem. 2004 Feb 13;279(7):5772-80 [14645226.001]
  • [Cites] J Biol Chem. 2004 Mar 5;279(10):9176-89 [14660575.001]
  • [Cites] Mol Cell. 2006 Jun 23;22(6):741-53 [16793544.001]
  • [Cites] Blood. 2007 Jan 1;109(1):11-21 [16940420.001]
  • [Cites] Blood. 2004 Mar 15;103(6):2316-24 [14615365.001]
  • [Cites] Nat Biotechnol. 2004 Apr;22(4):445-9 [14990965.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4284-96 [15156185.001]
  • [Cites] Hum Mol Genet. 1999 Nov;8(12):2311-6 [10545612.001]
  • [Cites] Structure. 1999 Oct 15;7(10):1247-56 [10545320.001]
  • [Cites] Dev Biol. 2000 Apr 1;220(1):27-36 [10720428.001]
  • [Cites] FEBS Lett. 2000 Mar 24;470(2):125-30 [10734220.001]
  • [Cites] FEBS Lett. 2000 Mar 24;470(2):167-72 [10734228.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2862-9 [11023523.001]
  • [Cites] Blood. 2000 Nov 1;96(9):3154-60 [11049997.001]
  • [Cites] J Biol Chem. 2000 Dec 15;275(50):39579-88 [10984496.001]
  • [Cites] Cell. 2001 Mar 9;104(5):755-67 [11257229.001]
  • [Cites] Nat Struct Biol. 2001 Apr;8(4):371-8 [11276260.001]
  • [Cites] J Mol Biol. 2001 Apr 27;308(2):191-203 [11327761.001]
  • [Cites] Blood. 2001 Nov 1;98(9):2856-8 [11675361.001]
  • [Cites] Science. 1990 Oct 5;250(4977):113-6 [2218501.001]
  • [Cites] Cell Growth Differ. 1990 Dec;1(12):571-80 [2288874.001]
  • [Cites] Science. 1995 Mar 10;267(5203):1498-502 [7878469.001]
  • [Cites] Nat Struct Biol. 1994 Dec;1(12):877-90 [7773777.001]
  • [Cites] Cell. 1996 Jan 26;84(2):321-30 [8565077.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3444-9 [8622955.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 29;93(22):12359-63 [8901586.001]
  • [Cites] Cell. 1996 Nov 15;87(4):697-708 [8929538.001]
  • [Cites] Cell. 1997 May 30;89(5):773-9 [9182765.001]
  • [Cites] Nat Genet. 1997 Jul;16(3):307-10 [9207800.001]
  • [Cites] Blood. 1999 Mar 15;93(6):1817-24 [10068652.001]
  • [Cites] J Med Genet. 1999 Mar;36(3):177-82 [10204840.001]
  • [Cites] Nat Struct Biol. 1999 Jul;6(7):615-9 [10404214.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):166-75 [10508512.001]
  • [Cites] Am J Hum Genet. 1999 Nov;65(5):1268-78 [10521292.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3565-72 [15297309.001]
  • [Cites] Cell. 2004 Dec 17;119(6):847-60 [15607980.001]
  • [Cites] J Mol Biol. 2005 Jun 10;349(3):608-20 [15878177.001]
  • [Cites] Blood. 2005 Jul 15;106(2):494-504 [15784726.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1364-72 [11830488.001]
  • (PMID = 17290219.001).
  • [ISSN] 0261-4189
  • [Journal-full-title] The EMBO journal
  • [ISO-abbreviation] EMBO J.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA23108; United States / NCI NIH HHS / CA / P30 CA023108; United States / NCI NIH HHS / CA / R01CA89419; United States / NIGMS NIH HHS / GM / T32 GM008704; United States / NCI NIH HHS / CA / R01 CA089419; United States / NIGMS NIH HHS / GM / T32GM08704
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cbfb protein, mouse; 0 / Core Binding Factor Alpha 1 Subunit; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / DNA Primers; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC1852839
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48. Ramanarayanan J, Dunford LM, Baer MR, Sait SN, Lawrence W, McCarthy PL: Chronic myeloid leukemia after treatment of lymphoid malignancies: response to imatinib mesylate and favorable outcomes in three patients. Leuk Res; 2006 Jun;30(6):701-5
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  • [Title] Chronic myeloid leukemia after treatment of lymphoid malignancies: response to imatinib mesylate and favorable outcomes in three patients.
  • Therapy-related myelodysplasia and acute myeloid leukemia are well described, but secondary chronic myeloid leukemia (CML) has only rarely been reported.
  • We report three patients with CML diagnosed 8, 10 and 2.5 years following Hodgkin's disease, non-Hodgkin's lymphoma and chronic lymphocytic leukemia therapy, respectively.
  • BCR-ABL transcripts were not detected after completion of primary therapy in two cases.
  • All three patients received imatinib therapy, with one patient subsequently undergoing allogeneic hematopoietic stem cell transplantation.
  • All three patients have ongoing favorable responses to CML therapy.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Neoplasms, Second Primary / therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage


49. Kempinska A, Kwak EJ, Angel JB: Reactivation of hepatitis B infection following allogeneic bone marrow transplantation in a hepatitis B-immune patient: case report and review of the literature. Clin Infect Dis; 2005 Nov 1;41(9):1277-82
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  • A review of related cases in the literature was undertaken to identify clinical features associated with this phenomenon.
  • RESULTS: We present a case of reactivation of HBV infection in a 47-year-old man after receipt of an allogeneic bone marrow transplant for acute myelogenous leukemia.
  • Reactivation of HBV infection following bone marrow transplantation appears to occur almost exclusively in patients who have received marrow from an HBsAb-negative donor and have experienced graft-versus-host disease, the onset of which is associated with tapering of immunosuppressive therapy.

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  • [CommentIn] Clin Infect Dis. 2006 Feb 15;42(4):583-4 [16421814.001]
  • (PMID = 16206102.001).
  • [ISSN] 1537-6591
  • [Journal-full-title] Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
  • [ISO-abbreviation] Clin. Infect. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hepatitis B Antibodies
  • [Number-of-references] 24
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50. Chakraborty S, Sun CL, Francisco L, Sabado M, Li L, Chang KL, Forman S, Bhatia S, Bhatia R: Accelerated telomere shortening precedes development of therapy-related myelodysplasia or acute myelogenous leukemia after autologous transplantation for lymphoma. J Clin Oncol; 2009 Feb 10;27(5):791-8
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  • [Title] Accelerated telomere shortening precedes development of therapy-related myelodysplasia or acute myelogenous leukemia after autologous transplantation for lymphoma.
  • PURPOSE: Therapy-related myelodysplasia or acute myelogenous leukemia (t-MDS/AML) is a lethal complication of autologous hematopoietic stem-cell transplantation (aHCT) for Hodgkin's lymphoma (HL) and non-Hodgkin's lymphoma (NHL).
  • Here, we investigated the hypothesis that accelerated telomere shortening after aHCT could contribute to the development of t-MDS/AML.
  • PATIENTS AND METHODS: A prospective longitudinal cohort was constructed to investigate the sequence of cellular and molecular abnormalities leading to development of t-MDS/AML after aHCT for HL/NHL.
  • This cohort formed the sampling frame for a nested case-control study to compare changes in telomere length in serial blood samples from patients who developed t-MDS/AML with matched controls who did not develop t-MDS/AML.
  • RESULTS: An initial increase in telomere length at day 100 after aHCT was followed by an accelerated telomere shortening in t-MDS/AML patients when compared with controls.
  • These telomere alterations preceded the onset of t-MDS and were independent of other known risk factors associated with development of t-MDS/AML on multivariate analysis.
  • Additionally, we observed reduced generation of committed progenitors in patients who developed t-MDS/AML, indicating that these telomere alterations were associated with reduced regenerative capacity of hematopoietic stem cells.
  • CONCLUSION: The development of t-MDS/AML after aHCT is associated with and preceded by markedly altered telomere dynamics in hematopoietic cells.
  • Accelerated telomere loss in patients developing t-MDS/AML may reflect increased clonal proliferation and/or altered telomere regulation in premalignant cells.
  • Genetic instability associated with shortened telomeres may contribute to leukemic transformation in t-MDS/AML.


51. Rizzieri DA, Feldman E, Dipersio JF, Gabrail N, Stock W, Strair R, Rivera VM, Albitar M, Bedrosian CL, Giles FJ: A phase 2 clinical trial of deforolimus (AP23573, MK-8669), a novel mammalian target of rapamycin inhibitor, in patients with relapsed or refractory hematologic malignancies. Clin Cancer Res; 2008 May 1;14(9):2756-62
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  • RESULTS: Fifty-five patients received deforolimus as follows: cohort 1 23 acute myelogenous leukemia, two myelodysplastic syndrome and one chronic myelogenous leukemia in nonlymphoid blast phase; cohort 2, one acute lymphocytic leukemia; cohort 3, nine agnogenic myeloid metaplasia; cohort 4, eight chronic lymphocytic leukemia; cohort 5, nine mantle cell lymphoma and two T-cell leukemia/lymphoma.
  • Common treatment-related adverse events, which were generally mild and reversible, were mouth sores, fatigue, nausea, and thrombocytopenia.
  • Decreased levels of phosphorylated 4E-BP1 in 9 of 11 acute myelogenous leukemia/myelodysplastic syndrome patients after therapy showed mammalian target of rapamycin inhibition by deforolimus.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematologic Neoplasms / drug therapy. Sirolimus / analogs & derivatives. Vascular Endothelial Growth Factor A / blood

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  • (PMID = 18451242.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 48Z35KB15K / ridaforolimus; W36ZG6FT64 / Sirolimus
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52. Khalil F, Cualing H, Cogburn J, Miles L: The criteria for bone marrow recovery post-myelosuppressive therapy for acute myelogenous leukemia: a quantitative study. Arch Pathol Lab Med; 2007 Aug;131(8):1281-9
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  • [Title] The criteria for bone marrow recovery post-myelosuppressive therapy for acute myelogenous leukemia: a quantitative study.
  • OBJECTIVE: To study the rate of recovery of bone marrow in patients given myelosuppressive therapy for acute myelogenous leukemia, establish the histologic criteria of recovered marrow, and correlate the recovery pattern with those patients who received a bone marrow transplant by using histology, peripheral blood, immunophenotyping, and computerized morphometry and mathematical slope equation.
  • These patients were divided into 2 groups: 1 group of 28 cases diagnosed with acute myeloid leukemia, the majority treated with cytarabine (Ara-C) infusion for 7 days and daunorubicin intravenously daily for 3 days (7+3 regimen), and the other control group of 23 cases treated with chemotherapy or allogeneic bone marrow transplantation for a variety of hematologic malignancies.
  • The absolute neutrophil and platelet counts for 28 cases were related to histologic recovery.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow / physiology. Bone Marrow Transplantation. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / physiopathology
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Biopsy. Blood Cell Count. Combined Modality Therapy. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Female. Humans. Image Processing, Computer-Assisted. Immunophenotyping. Male. Middle Aged. Recovery of Function. Remission Induction. Time Factors

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  • (PMID = 17683190.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
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53. Wang Z, Sampath J, Fukuda S, Pelus LM: Disruption of the inhibitor of apoptosis protein survivin sensitizes Bcr-abl-positive cells to STI571-induced apoptosis. Cancer Res; 2005 Sep 15;65(18):8224-32
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  • Although ectopic survivin protected K562 cells from apoptosis induced by STI571, it did not protect cells from apoptosis induced either by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) or the combination of TRAIL plus Hemin.
  • Our results identify a new signal pathway downstream of Bcr-abl, in addition to the Bcl-2 family involved in the antiapoptotic effects of Bcr-abl, and suggest that anti-survivin therapy may have utility in patients with chronic myelogenous leukemia.
  • [MeSH-minor] Animals. Apoptosis Regulatory Proteins / pharmacology. Benzamides. Caspase 9. Caspases / metabolism. Cell Line, Tumor. Cytochromes c / metabolism. Cytochromes c / secretion. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / drug effects. Hematopoietic Stem Cells / physiology. Humans. Imatinib Mesylate. Inhibitor of Apoptosis Proteins. K562 Cells. Leukemia, Megakaryoblastic, Acute / drug therapy. Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Megakaryoblastic, Acute / metabolism. Leukemia, Megakaryoblastic, Acute / pathology. Membrane Glycoproteins / pharmacology. Mice. Oligonucleotides, Antisense / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Signal Transduction. TNF-Related Apoptosis-Inducing Ligand. Transduction, Genetic. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation

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  • (PMID = 16166298.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL079654; United States / NHLBI NIH HHS / HL / HL69669
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / BIRC5 protein, human; 0 / Benzamides; 0 / Inhibitor of Apoptosis Proteins; 0 / Membrane Glycoproteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Oligonucleotides, Antisense; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tnfsf10 protein, mouse; 0 / Tumor Necrosis Factor-alpha; 8A1O1M485B / Imatinib Mesylate; 9007-43-6 / Cytochromes c; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Casp9 protein, mouse; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / Caspases
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54. Huang Q, Wu Y, Snyder DS, Chang KL, Slovak ML, Gaal KK, Palmer JM, Weiss LM: Clinical and pathologic analysis of 16 cases of relapsed chronic myeloid leukemia after stem cell transplantation. Am J Clin Pathol; 2007 Oct;128(4):565-70
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  • [Title] Clinical and pathologic analysis of 16 cases of relapsed chronic myeloid leukemia after stem cell transplantation.
  • Chronic myeloid leukemia (CML) is a myeloproliferative disease that originates in an abnormal pluripotent bone marrow stem cell and is characteristically associated with the Philadelphia chromosome and/or the bcr/abl fusion gene.
  • The results of our analysis showed that relapsed CML after HCT frequently manifested with advanced disease with a more aggressive clinical course and was often refractory to therapy.
  • The frequency of acute leukemic transformation at time of relapse was largely associated with pre-HCT disease status and acquired secondary cytogenetic abnormalities.
  • Disease mortality in patients with relapsed CML after HCT was closely associated with advanced disease and HCT-related complications.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Neoplasm Recurrence, Local / pathology


55. 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
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  • [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

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  • [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
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56. Yang J, Ikezoe T, Nishioka C, Ni L, Koeffler HP, Yokoyama A: Inhibition of mTORC1 by RAD001 (everolimus) potentiates the effects of 1,25-dihydroxyvitamin D(3) to induce growth arrest and differentiation of AML cells in vitro and in vivo. Exp Hematol; 2010 Aug;38(8):666-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of mTORC1 by RAD001 (everolimus) potentiates the effects of 1,25-dihydroxyvitamin D(3) to induce growth arrest and differentiation of AML cells in vitro and in vivo.
  • OBJECTIVE: Differentiation-inducing therapy by agents such as 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) represents a useful approach for the treatment of acute myelogenous leukemia (AML).
  • This study explored the drug interaction of 1,25(OH)(2)D(3) and rapamycin analog RAD001 (everolimus) in AML cells.
  • Effects of RAD001 and 1,25-(OH)(2)D(3) on Akt/mTOR complex-1 (mTORC1) signaling and cell-cycle-related molecules were explored by Western blot analysis.
  • RESULTS: RAD001 potentiated the ability of 1,25(OH)(2)D(3) to induce growth arrest and differentiation of AML cells in parallel with downregulation of the levels of p-S6K and p-4E-BP1, substrates of mTORC1.
  • CONCLUSIONS: Concomitant administration of 1,25(OH)(2)D(3) and the mTORC1 inhibitor may be a promising treatment strategy for individuals with AML.

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  • [Copyright] 2010 ISEH - Society for Hematology and Stem Cells. All rights reserved.
  • (PMID = 20382200.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA026038-31; United States / NCI NIH HHS / CA / R01 CA026038-32; United States / NCI NIH HHS / CA / CA026038-30A2; United States / NCI NIH HHS / CA / R01 CA026038; United States / NCI NIH HHS / CA / R01 CA026038-30A2; United States / NCI NIH HHS / CA / R01 CA026038-30
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Histones; 0 / ITGAM protein, human; 0 / Immunosuppressive Agents; 0 / Multiprotein Complexes; 0 / Proteins; 0 / Receptors, Calcitriol; 0 / Transcription Factors; 0 / Vitamins; 0 / mechanistic target of rapamycin complex 1; 9HW64Q8G6G / Everolimus; EC 2.7.1.1 / TOR Serine-Threonine Kinases; FXC9231JVH / Calcitriol; W36ZG6FT64 / Sirolimus
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57. Liu Y, Ke XY, Ma J, Shen ZX, Zhang XH, Du X, Zhao YM, Lv JQ, Zhan ZM, Zeng XY, Xu XH, Lu ZS: [Multicenter randomized control trial on safety of domestic idarubicin for acute leukemia]. Zhonghua Zhong Liu Za Zhi; 2006 Sep;28(9):706-8
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  • [Title] [Multicenter randomized control trial on safety of domestic idarubicin for acute leukemia].
  • OBJECTIVE: To evaluate the safety of domestically produced idarubicin in the treatment of acute leukemia by a multicenter randomized control trial.
  • METHODS: This trial was carried out in the hemotologica department of five hospitals throughout China, with hospitalized patients who suffered from acute myelogenous leukemia ( AML except M3 type) , acute lymphocytic leukemia ( ALL) , chronic myelogenous leukemia-blast (CML-blast) , totally 155 patients.
  • In this study, 155 leukemia patients were randomly grouped into: 1. test group treated using domestic idarubicin, 2. control group using imported idarubicin.
  • The acute myelogenous leukemia regimen included idarubicin 8 mg/m(2), dl -3 plus cytosine arabinoside 100 mg/m(2), dl - 7 for 1-2 cycles.
  • The regimen for acute lymphocytic leukemia was idarubicin 8 mg/m2, dl - 3; vincristine 2 mg/mr, dl; cyclophosphamide 750 mg/m2, dl ; plus prednisone 60 mg/m(2),dl - 14 for 1-2 cycles.
  • Drug-related death was observed in 3 of 77 patients in the domestic idarubicin group (3.9%) due to cerebral hemorrage or septic infection.
  • CONCLUSION: Domestic idarubicin is comparable to imported counterpart in efficiency and safety for the treatment of acute leukemia.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Idarubicin / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Agranulocytosis / chemically induced. Blast Crisis / drug therapy. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Cytarabine / administration & dosage. Cytarabine / adverse effects. Female. Humans. Male. Middle Aged. Mucositis / chemically induced. Nausea / chemically induced. Prednisone / administration & dosage. Prednisone / adverse effects. Remission Induction. Treatment Outcome. Vincristine / administration & dosage. Vincristine / adverse effects

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  • (PMID = 17274381.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; ZRP63D75JW / Idarubicin
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58. Bryant G: A once-daily dasatinib dosing strategy for chronic myeloid leukemia. Clin J Oncol Nurs; 2009 Jun;13(3):316-23
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  • [Title] A once-daily dasatinib dosing strategy for chronic myeloid leukemia.
  • The BCR-ABL inhibitor imatinib is standard first-line therapy for patients with chronic myeloid leukemia (CML) and has revolutionized treatment of the disease.
  • Food and Drug Administration for the treatment of patients with CML in any phase or Philadelphia chromosome-positive acute lymphoblastic leukemia who are resistant to or intolerant of imatinib.
  • That dosing regimen, combined with appropriate management of dasatinib-related adverse events, may help patients adhere to their prescribed treatment and achieve maximum therapeutic benefit.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Pyrimidines / therapeutic use. Thiazoles / therapeutic use


59. Cohen PR: Sweet's syndrome--a comprehensive review of an acute febrile neutrophilic dermatosis. Orphanet J Rare Dis; 2007;2:34
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  • [Title] Sweet's syndrome--a comprehensive review of an acute febrile neutrophilic dermatosis.
  • Sweet's syndrome (the eponym for acute febrile neutrophilic dermatosis) is characterized by a constellation of clinical symptoms, physical features, and pathologic findings which include fever, neutrophilia, tender erythematous skin lesions (papules, nodules, and plaques), and a diffuse infiltrate consisting predominantly of mature neutrophils that are typically located in the upper dermis.
  • The malignancy-associated Sweet's syndrome (MASS) can occur as a paraneoplastic syndrome in patients with an established cancer or individuals whose Sweet's syndrome-related hematologic dyscrasia or solid tumor was previously undiscovered; MASS is most commonly related to acute myelogenous leukemia.
  • The dermatosis can precede, follow, or appear concurrent with the diagnosis of the patient's cancer.
  • After initiation of treatment with systemic corticosteroids, there is a prompt response consisting of dramatic improvement of both the dermatosis-related symptoms and skin lesions.
  • The symptoms and lesions of Sweet's syndrome may resolved spontaneously, without any therapeutic intervention; however, recurrence may follow either spontaneous remission or therapy-induced clinical resolution.

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  • [Cites] Arch Dermatol. 1971 Jan;103(1):81-4 [5539508.001]
  • [Cites] Dermatologica. 1971;143(3):153-9 [5131096.001]
  • [Cites] Australas J Dermatol. 1971 Dec;12(3):172-7 [5146931.001]
  • [Cites] Arch Dermatol. 1975 Nov;111(11):1461-3 [1239237.001]
  • [Cites] Am J Med. 1976 Sep;61(3):424-32 [961707.001]
  • [Cites] J Rheumatol. 1977 Summer;4(2):201-6 [881698.001]
  • [Cites] S Afr Med J. 1978 Feb 18;53(7):253-6 [653521.001]
  • [Cites] South Med J. 1978 Nov;71(11):1350-2 [280960.001]
  • [Cites] Rev Prat. 1999 Feb 15;49(4):356-8 [10319682.001]
  • [Cites] J Am Acad Dermatol. 1999 May;40(5 Pt 2):838-41 [10321630.001]
  • [Cites] Br J Dermatol. 1999 Jun;140(6):1174-5 [10354095.001]
  • [Cites] Am J Hematol. 1999 Jun;61(2):126-9 [10367792.001]
  • [Cites] Pediatr Cardiol. 1999 Jul-Aug;20(4):295-7 [10368458.001]
  • [Cites] Am J Dermatopathol. 1999 Jun;21(3):247-52 [10380046.001]
  • [Cites] Pediatr Infect Dis J. 1999 Jun;18(6):568-70 [10391198.001]
  • [Cites] Br J Dermatol. 1999 Jul;141(1):169-70 [10417544.001]
  • [Cites] Arch Neurol. 1999 Aug;56(8):1010-3 [10448808.001]
  • [Cites] Br J Dermatol. 1964 Aug-Sep;76:349-56 [14201182.001]
  • [Cites] Br J Dermatol. 2004 Nov;151(5):1096-100 [15541094.001]
  • [Cites] Int J Dermatol. 2004 Dec;43(12):938-41 [15569025.001]
  • [Cites] Ann Rheum Dis. 2005 Jan;64(1):168-9 [15608327.001]
  • [Cites] J Am Acad Dermatol. 2005 Feb;52(2):367-9 [15692491.001]
  • [Cites] Orbit. 2005 Mar;24(1):55-7 [15764119.001]
  • [Cites] Arch Dermatol. 2005 Mar;141(3):368-70 [15781678.001]
  • [Cites] Can J Ophthalmol. 2005 Feb;40(1):90-2 [15825540.001]
  • [Cites] J Am Acad Dermatol. 2005 May;52(5):901-5 [15858487.001]
  • [Cites] J Am Acad Dermatol. 2005 May;52(5):927-8 [15858502.001]
  • [Cites] Neurology. 2005 May 24;64(10):1756-61 [15911805.001]
  • [Cites] Hautarzt. 1988 Oct;39(10):658-61 [3069805.001]
  • [Cites] Am J Dermatopathol. 1989 Apr;11(2):99-111 [2653084.001]
  • [Cites] J Am Acad Dermatol. 1989 Apr;20(4):677-80 [2715414.001]
  • [Cites] J Am Acad Dermatol. 1989 Aug;21(2 Pt 2):339-43 [2526826.001]
  • [Cites] Am J Hematol. 1989 Oct;32(2):134-7 [2667344.001]
  • [Cites] Cutis. 1989 Aug;44(2):125-9 [2758862.001]
  • [Cites] Cutis. 1989 Aug;44(2):157-9 [2758865.001]
  • [Cites] Clin Exp Dermatol. 1988 Sep;13(5):344-6 [3256451.001]
  • [Cites] Br J Dermatol. 2006 Nov;155(5):1103-4 [17034566.001]
  • [Cites] Int J Dermatol. 2006 Oct;45(10):1254-5 [17040460.001]
  • [Cites] Int J Dermatol. 2006 Nov;45(11):1365-8 [17076728.001]
  • [Cites] J Am Acad Dermatol. 2006 Dec;55(6):1066-71 [17097401.001]
  • [Cites] Int J Dermatol. 2007 Jan;46(1):106-11 [17214733.001]
  • [Cites] Australas J Dermatol. 2007 Feb;48(1):50-3 [17222305.001]
  • [Cites] J Am Acad Dermatol. 2007 Feb;56(2 Suppl):S61-2 [17224394.001]
  • [Cites] Br J Dermatol. 2007 Mar;156(3):480-5 [17300237.001]
  • [Cites] Intern Med. 2007;46(4):153-4 [17301507.001]
  • [Cites] Arch Dermatol. 2007 Feb;143(2):275-6 [17310019.001]
  • [Cites] Rev Med Liege. 2006 Dec;61(12):834-6 [17313120.001]
  • [Cites] Presse Med. 2007 Mar;36(3 Pt 1):419-24 [17321363.001]
  • [Cites] J Dermatol. 2007 Apr;34(4):243-7 [17352721.001]
  • [Cites] J Dermatol. 2007 Apr;34(4):258-61 [17352724.001]
  • [Cites] J Am Acad Dermatol. 2007 Apr;56(4):690-3 [17367621.001]
  • [Cites] Ann Dermatol Venereol. 2007 Feb;134(2):151-4 [17375012.001]
  • [Cites] CA Cancer J Clin. 2007 Mar-Apr;57(2):90-104 [17392386.001]
  • [Cites] Actas Dermosifiliogr. 2007 Mar;98(2):102-4 [17397596.001]
  • [Cites] Am J Dermatopathol. 2007 Apr;29(2):125-33 [17414432.001]
  • [Cites] J Neurol. 2003 Jun;250(6):770-1 [12862039.001]
  • [Cites] Actas Dermosifiliogr. 2005 Jun;96(5):315-6 [16476395.001]
  • [Cites] Clin Exp Dermatol. 2006 Mar;31(2):206-7 [16487091.001]
  • [Cites] J Am Acad Dermatol. 2006 Mar;54(3 Suppl 2):S122-6 [16488324.001]
  • [Cites] Arch Dermatol. 2006 Feb;142(2):235-40 [16490855.001]
  • [Cites] Korean J Intern Med. 2005 Dec;20(4):346-8 [16491836.001]
  • [Cites] Clin Rheumatol. 2006 Mar;25(2):268-72 [15902518.001]
  • [Cites] J Otolaryngol. 2006 Apr;35(2):144-7 [16527036.001]
  • [Cites] J Infect. 2006 May;52(5):e155-7 [16213026.001]
  • [Cites] J Eur Acad Dermatol Venereol. 2006 Apr;20(4):401-5 [16643136.001]
  • [Cites] Int J Dermatol. 2006 Jun;45(6):677-80 [16796626.001]
  • [Cites] Int J Dermatol. 2006 Jun;45(6):702-8 [16796632.001]
  • [Cites] Arch Dermatol. 2006 Aug;142(8):1070-1 [16924066.001]
  • [Cites] Arch Dermatol. 2006 Sep;142(9):1170-6 [16983004.001]
  • [Cites] Br J Haematol. 2006 Oct;135(2):148 [16856884.001]
  • [Cites] Br J Dermatol. 2006 Nov;155(5):1089-90 [17034556.001]
  • [Cites] Br J Dermatol. 2006 Nov;155(5):1099-101 [17034564.001]
  • [Cites] J Am Acad Dermatol. 1998 Dec;39(6):940-3 [9843005.001]
  • [Cites] Br J Dermatol. 1998 Sep;139(3):555-6 [9767320.001]
  • [Cites] Eur J Dermatol. 1998 Oct-Nov;8(7):503-5 [9854164.001]
  • [Cites] Br J Dermatol. 1998 Oct;139(4):744-5 [9892926.001]
  • [Cites] Br J Dermatol. 1998 Nov;139(5):930-1 [9892977.001]
  • [Cites] Otolaryngol Head Neck Surg. 1998 Dec;119(6):709-10 [9852556.001]
  • [Cites] Arch Dermatol. 1999 Jan;135(1):62-6 [9923783.001]
  • [Cites] J Rheumatol. 1999 Feb;26(2):440-2 [9972982.001]
  • [Cites] J Am Acad Dermatol. 1999 Feb;40(2 Pt 1):275-9 [10025763.001]
  • [Cites] J Am Acad Dermatol. 1999 Feb;40(2 Pt 2):331-4 [10025862.001]
  • [Cites] Cutis. 1999 Mar;63(3):177-9 [10190073.001]
  • [Cites] Br J Dermatol. 1999 Mar;140(3):565-6 [10233302.001]
  • [Cites] Ann Thorac Surg. 2004 Jul;78(1):341-3 [15223465.001]
  • [Cites] Ann Dermatol Venereol. 2004 Apr;131(4):369-72 [15258512.001]
  • [Cites] J Am Acad Dermatol. 2004 Sep;51(3):474-5 [15337997.001]
  • [Cites] J Eur Acad Dermatol Venereol. 2004 Nov;18(6):716-7 [15482306.001]
  • [Cites] J Eur Acad Dermatol Venereol. 2004 Nov;18(6):745-6 [15482319.001]
  • [Cites] Int J Dermatol. 2004 Oct;43(10):720-2 [15485526.001]
  • [Cites] Int J Dermatol. 2004 Oct;43(10):772-7 [15485540.001]
  • [Cites] Gynecol Oncol. 2004 Nov;95(2):396-9 [15491764.001]
  • [Cites] J Am Acad Dermatol. 1994 Apr;30(4):639-42 [8157792.001]
  • [Cites] Br J Haematol. 1994 Feb;86(2):415-7 [7515269.001]
  • [Cites] Clin Exp Dermatol. 1994 May;19(3):274-7 [8033398.001]
  • [Cites] Br J Haematol. 1994 Mar;86(3):645-8 [7519039.001]
  • [Cites] J Dermatol. 1994 May;21(5):341-6 [8051321.001]
  • [Cites] Int J Dermatol. 1994 Jun;33(6):425-32 [8056477.001]
  • [Cites] Acta Derm Venereol. 1994 May;74(3):229-30 [7915473.001]
  • [Cites] J Am Acad Dermatol. 1994 Oct;31(4):535-56; quiz 557-60 [8089280.001]
  • [Cites] Br J Dermatol. 1979 Jan;100(1):93-9 [427014.001]
  • [Cites] Dermatologica. 1980;160(5):341-7 [7364144.001]
  • [Cites] Br J Dermatol. 1981 Oct;105(4):483 [7295564.001]
  • [Cites] Postgrad Med. 1982 Jan;71(1):55-60 [7054779.001]
  • [Cites] S Afr Med J. 1982 Sep 4;62(11):375-8 [7112306.001]
  • [Cites] Clin Rheum Dis. 1982 Aug;8(2):427-41 [6754235.001]
  • [Cites] Br J Dermatol. 1983 Jan;108(1):99-101 [6821647.001]
  • [Cites] J Pediatr. 1983 Feb;102(2):243-8 [6822929.001]
  • [Cites] Cancer. 1983 Apr 15;51(8):1518-26 [6572088.001]
  • [Cites] Arch Dermatol. 1983 Jul;119(7):610-1 [6574727.001]
  • [Cites] J Am Acad Dermatol. 1983 Jul;9(1):77-81 [6886108.001]
  • [Cites] Cutis. 1983 Aug;32(2):152-4 [6617253.001]
  • [Cites] Arch Intern Med. 1983 Oct;143(10):1993-5 [6625786.001]
  • [Cites] Arch Neurol. 1983 Dec;40(13):829 [6639416.001]
  • [Cites] J Am Acad Dermatol. 1983 Nov;9(5):751-8 [6358279.001]
  • [Cites] Arch Dermatol. 1984 Feb;120(2):245-7 [6696481.001]
  • [Cites] Blut. 1984 May;48(5):297-305 [6722359.001]
  • [Cites] Arch Dermatol. 1985 Jun;121(6):789-91 [4004304.001]
  • [Cites] Dermatologica. 1985;171(2):102-5 [4043468.001]
  • [Cites] Presse Med. 1985 Sep 14;14(30):1599-601 [2995962.001]
  • [Cites] Lupus. 2005;14(5):399-402 [15934441.001]
  • [Cites] South Med J. 2005 May;98(5):570-2 [15954518.001]
  • [Cites] J Am Acad Dermatol. 2005 Aug;53(2 Suppl 1):S135-8 [16021163.001]
  • [Cites] Arch Dermatol. 2005 Jul;141(7):834-42 [16027297.001]
  • [Cites] Arch Dermatol. 2005 Jul;141(7):881-4 [16027305.001]
  • [Cites] Arch Dermatol. 2005 Jul;141(7):887-9 [16027306.001]
  • [Cites] Arch Dermatol. 2005 Jul;141(7):893-5 [16027307.001]
  • [Cites] Clin Dev Immunol. 2005 Jun;12(2):145-9 [16050146.001]
  • [Cites] Int J Dermatol. 2005 Aug;44(8):677-80 [16101872.001]
  • [Cites] Retina. 2005 Sep;25(6):800-2 [16141877.001]
  • [Cites] J Eur Acad Dermatol Venereol. 2005 Sep;19(5):597-9 [16164716.001]
  • [Cites] J Eur Acad Dermatol Venereol. 2005 Sep;19(5):634-7 [16164726.001]
  • [Cites] Br J Haematol. 2005 Oct;131(2):142 [16197442.001]
  • [Cites] Digestion. 2005;72(2-3):195-200 [16179788.001]
  • [Cites] Acta Gastroenterol Belg. 2005 Jul-Sep;68(3):376-9 [16268426.001]
  • [Cites] Ann Dermatol Venereol. 2005 Nov;132(11 Pt 1):883-5 [16327718.001]
  • [Cites] Int J Dermatol. 2005 Nov;44(11):946-7 [16336530.001]
  • [Cites] Pediatr Dermatol. 2005 Nov-Dec;22(6):525-9 [16354254.001]
  • [Cites] Pediatr Dermatol. 2005 Nov-Dec;22(6):530-5 [16354255.001]
  • [Cites] J Indian Med Assoc. 2005 Aug;103(8):433-5 [16363199.001]
  • [Cites] J Assoc Physicians India. 2005 Aug;53:728-30 [16398086.001]
  • [Cites] Leuk Res. 2006 Mar;30(3):364 [16157374.001]
  • [Cites] Int J Dermatol. 2005 Dec;44(12):1051-3 [16409276.001]
  • [Cites] Arch Dermatol. 2006 Jan;142(1):57-63 [16415387.001]
  • [Cites] Int J Dermatol. 2006 Jan;45(1):51-2 [16426377.001]
  • [Cites] Int J Dermatol. 2006 Jan;45(1):70-80 [16426383.001]
  • [Cites] Ann Dermatol Venereol. 2005 Dec;132(12 Pt 1):1003-6 [16446647.001]
  • [Cites] Haematologica. 2005 Dec;90(12 Suppl):ECR43 [16464758.001]
  • [Cites] South Med J. 2007 Oct;100(10):1057-8 [17943059.001]
  • [Cites] Pediatrics. 1999 Nov;104(5 Pt 1):1142-4 [10545563.001]
  • [Cites] Clin Exp Dermatol. 1999 Sep;24(5):368-71 [10564323.001]
  • [Cites] Australas J Dermatol. 1999 Nov;40(4):204-7 [10570557.001]
  • [Cites] J Clin Oncol. 1988 Dec;6(12):1887-97 [3058878.001]
  • [Cites] J Am Acad Dermatol. 1988 Dec;19(6):983-1005 [3060489.001]
  • [Cites] Am Fam Physician. 1989 Mar;39(3):199-204 [2646883.001]
  • [Cites] Ann Intern Med. 1989 Apr 1;110(7):573-4 [2923392.001]
  • [Cites] Semin Oncol. 1997 Jun;24(3):334-59 [9208889.001]
  • [Cites] J Am Acad Dermatol. 1997 Jul;37(1):123-4 [9216537.001]
  • [Cites] Clin Exp Dermatol. 1997 Jan;22(1):54-6 [9330058.001]
  • [Cites] Int J Dermatol. 1997 Sep;36(9):717-8 [9352420.001]
  • [Cites] Br J Dermatol. 1997 Oct;137(4):609-13 [9390341.001]
  • [Cites] Thorac Cardiovasc Surg. 1997 Oct;45(5):247-8 [9402666.001]
  • [Cites] Med Clin (Barc). 1997 Nov 1;109(15):588-91 [9441195.001]
  • [Cites] Int J Dermatol. 1997 Nov;36(11):837-44 [9427076.001]
  • [Cites] Br J Dermatol. 1989 Sep;121(3):413-5 [2803964.001]
  • [Cites] J Pediatr. 1989 Nov;115(5 Pt 1):726-9 [2809903.001]
  • [Cites] J Pediatr. 1989 Nov;115(5 Pt 1):730-4 [2809904.001]
  • [Cites] Vestn Dermatol Venerol. 1989;(11):67-9 [2618175.001]
  • [Cites] Neth J Med. 1990 Feb;36(1-2):62-8 [2278538.001]
  • [Cites] J Rheumatol. 1990 May;17(5):682-4 [2193156.001]
  • [Cites] Rev Clin Esp. 1990 Apr;186(6):264-9 [2203115.001]
  • [Cites] Am J Med. 1990 Sep;89(3):396 [2203266.001]
  • [Cites] J Am Acad Dermatol. 1990 Aug;23(2 Pt 1):247-9 [2212120.001]
  • [Cites] J Am Acad Dermatol. 1990 Sep;23(3 Pt 1):503-7 [2212153.001]
  • [Cites] Int J Dermatol. 1990 Dec;29(10):737 [2269574.001]
  • [Cites] Acta Haematol. 1990;84(4):207-8 [2125789.001]
  • [Cites] Dermatologica. 1991;182(1):43-6 [1826487.001]
  • [Cites] Br J Dermatol. 1991 Apr;124(4):348-53 [2025555.001]
  • [Cites] J R Soc Med. 1991 May;84(5):307-8 [2041012.001]
  • [Cites] Acta Derm Venereol. 1991;71(1):77-9 [1676226.001]
  • [Cites] Ann Dermatol Venereol. 1990;117(11):858-60 [2099706.001]
  • [Cites] Australas J Dermatol. 1991;32(1):55-9 [1834046.001]
  • [Cites] Am J Med. 1991 Nov;91(5):553-4 [1951419.001]
  • [Cites] Dermatologica. 1991;183(3):230-3 [1743390.001]
  • [Cites] Acta Derm Venereol. 2003;83(4):290-1 [12926802.001]
  • [Cites] Br J Dermatol. 2003 Sep;149(3):675-7 [14511020.001]
  • [Cites] Int J Dermatol. 2003 Oct;42(10):761-78 [14521689.001]
  • [Cites] Med Clin (Barc). 2003 Oct 4;121(11):437 [14563281.001]
  • [Cites] J Am Acad Dermatol. 2003 Nov;49(5):907-9 [14576675.001]
  • [Cites] Lancet. 2003 Oct 25;362(9393):1374 [14585639.001]
  • [Cites] Korean J Intern Med. 2003 Sep;18(3):187-90 [14619389.001]
  • [Cites] Br J Dermatol. 2003 Oct;149(4):884 [14616386.001]
  • [Cites] Contact Dermatitis. 2003 Jul;49(1):42 [14641120.001]
  • [Cites] J Cutan Pathol. 2004 Jan;31(1):72-6 [14675289.001]
  • [Cites] J Cutan Pathol. 2004 Feb;31(2):189-94 [14690466.001]
  • [Cites] Int J Dermatol. 2004 Jan;43(1):57-9 [14693024.001]
  • [Cites] QJM. 2004 Jan;97(1):55-6 [14702513.001]
  • [Cites] J Am Acad Dermatol. 2004 Feb;50(2):280-5 [14726888.001]
  • [Cites] Clin Nucl Med. 2004 Feb;29(2):91-2 [14734904.001]
  • [Cites] Eye (Lond). 2004 Feb;18(2):214; discussion 214-6 [14762428.001]
  • [Cites] J Laryngol Otol. 2004 Jan;118(1):48-9 [14979973.001]
  • [Cites] J Eur Acad Dermatol Venereol. 2004 Mar;18(2):233 [15009320.001]
  • [Cites] Leuk Res. 2004 May;28 Suppl 1:S61-3 [15036943.001]
  • [Cites] Dermatology. 2004;208(2):175 [15057014.001]
  • [Cites] J Fam Plann Reprod Health Care. 2004 Apr;30(2):115-6 [15086998.001]
  • [Cites] J Am Acad Dermatol. 2004 May;50(5 Suppl):S90-2 [15097938.001]
  • [Cites] J Am Acad Dermatol. 2004 May;50(5):798-9 [15097971.001]
  • [Cites] Int J Dermatol. 2004 Feb;43(2):95-102 [15125498.001]
  • [Cites] J Pediatr Hematol Oncol. 2004 Mar;26(3):197-9 [15125614.001]
  • [Cites] Arch Dermatol. 2004 May;140(5):570-4 [15148101.001]
  • [Cites] J Med Assoc Thai. 2004 May;87(5):567-72 [15222531.001]
  • [Cites] Am J Hematol. 2004 Jul;76(3):283-5 [15224368.001]
  • [Cites] Br J Haematol. 1993 Sep;85(1):191-2 [7504506.001]
  • [Cites] Dermatology. 1993;187(4):303-5 [8274797.001]
  • [Cites] Acta Derm Venereol. 1993 Oct;73(5):380-1 [7904408.001]
  • [Cites] J Am Acad Dermatol. 1994 Feb;30(2 Pt 2):293-7 [8294584.001]
  • [Cites] J Am Acad Dermatol. 1994 Feb;30(2 Pt 2):297-300 [8294585.001]
  • [Cites] J Cutan Pathol. 1993 Oct;20(5):465-78 [7507948.001]
  • [Cites] Clin Exp Dermatol. 1994 Jan;19(1):51-2 [8313637.001]
  • [Cites] South Med J. 1994 Feb;87(2):193-6 [8115882.001]
  • [Cites] Int J Dermatol. 2001 Dec;40(12):791-3 [11903682.001]
  • [Cites] Ann Hematol. 2002 Feb;81(2):111-4 [11907794.001]
  • [Cites] Acta Orthop Belg. 2002 Feb;68(1):68-71 [11915462.001]
  • [Cites] Gastroenterol Clin Biol. 2002 Mar;26(3):295-7 [11981477.001]
  • [Cites] Int J Dermatol. 2002 Feb;41(2):107-9 [11982648.001]
  • [Cites] Clin Pediatr (Phila). 2002 Apr;41(3):175-7 [11999681.001]
  • [Cites] Br J Dermatol. 2002 Jun;146(6):1087-90 [12072085.001]
  • [Cites] J Occup Environ Med. 2002 Jun;44(6):491-2 [12085472.001]
  • [Cites] Leukemia. 1994 Sep;8(9):1596 [8090038.001]
  • [Cites] Am Fam Physician. 1994 Nov 1;50(6):1273-82 [7942426.001]
  • [Cites] J Am Acad Dermatol. 1994 Dec;31(6):1045-7 [7962753.001]
  • [Cites] Pediatr Dermatol. 1994 Sep;11(3):237-40 [7971558.001]
  • [Cites] J Rheumatol. 1994 Sep;21(9):1766-8 [7799365.001]
  • [Cites] J Am Acad Dermatol. 1995 Feb;32(2 Pt 1):192-8 [7829702.001]
  • [Cites] Mayo Clin Proc. 1995 Mar;70(3):234-40 [7861810.001]
  • [Cites] Leuk Lymphoma. 1994 Oct;15(3-4):261-4 [7532508.001]
  • [Cites] J Am Acad Dermatol. 1995 Mar;32(3):533-5 [7868739.001]
  • [Cites] Int J Dermatol. 1995 Jan;34(1):73-4 [7896497.001]
  • [Cites] Australas J Dermatol. 1994;35(2):91-2 [7702496.001]
  • [Cites] Dermatology. 1995;190(2):160-3 [7727840.001]
  • [Cites] Hum Pathol. 1995 Jun;26(6):687-90 [7774902.001]
  • [Cites] Mayo Clin Proc. 1995 Jun;70(6):605-6 [7632268.001]
  • [Cites] J Am Acad Dermatol. 1995 Jul;33(1):144-5 [7601939.001]
  • [Cites] Int J Dermatol. 1995 May;34(5):323-9 [7607792.001]
  • [Cites] Am J Med. 1995 Aug;99(2):207-16 [7625426.001]
  • [Cites] Semin Dermatol. 1995 Jun;14(2):173-8 [7640199.001]
  • [Cites] Postgrad Med J. 1995 Jun;71(836):383 [7644412.001]
  • [Cites] Acta Derm Venereol. 1995 May;75(3):237-9 [7653187.001]
  • [Cites] Pediatr Dermatol. 1985 Nov;3(1):40-4 [3906610.001]
  • [Cites] Dermatol Clin. 1985 Jan;3(1):153-63 [3912087.001]
  • [Cites] Cutis. 1986 Mar;37(3):167-74 [3514153.001]
  • [Cites] Am J Med. 1986 Sep;81(3):558-60 [2944382.001]
  • [Cites] Dermatologica. 1986;173(2):85-9 [3792603.001]
  • [Cites] Arch Dermatol. 1987 Feb;123(2):251, 254 [2434033.001]
  • [Cites] J Clin Pathol. 1987 Feb;40(2):175-9 [3546396.001]
  • [Cites] Am J Med. 1987 Jun;82(6):1220-6 [3300306.001]
  • [Cites] Cutis. 1987 Aug;40(2):139-42 [3621997.001]
  • [Cites] J Assoc Physicians India. 2002 Oct;50:1322-3 [12568224.001]
  • [Cites] Dermatology. 2003;206(2):81-4 [12592072.001]
  • [Cites] J Cutan Pathol. 2003 Apr;30(4):261-4 [12680958.001]
  • [Cites] Int J Dermatol. 2003 Jun;42(6):438-43 [12786869.001]
  • [Cites] Clin Exp Dermatol. 2003 Jul;28(4):377-9 [12823297.001]
  • [Cites] J Am Acad Dermatol. 2003 Jul;49(1):132-8 [12833027.001]
  • [Cites] Ann Acad Med Singapore. 2003 May;32(3):411-4 [12854387.001]
  • [Cites] Clin Exp Dermatol. 1987 Sep;12(5):345-9 [3446421.001]
  • [Cites] Tunis Med. 2007 Jan;85(1):49-53 [17424710.001]
  • [Cites] South Med J. 2007 Apr;100(4):414-5 [17458409.001]
  • [Cites] Ann Pharmacother. 2007 May;41(5):802-11 [17426076.001]
  • [Cites] Int J Dermatol. 2007 May;46(5):496-9 [17472681.001]
  • [Cites] Clin Rheumatol. 2007 Jul;26(7):1215-6 [17294051.001]
  • [Cites] Australas J Dermatol. 2007 May;48(2):105-9 [17535199.001]
  • [Cites] Int J Dermatol. 2007 Jun;46(6):571-4 [17550553.001]
  • [Cites] Clin Dermatol. 2007 May-Jun;25(3):326-33 [17560310.001]
  • [Cites] J Cutan Pathol. 2007 Jul;34(7):526-34 [17576331.001]
  • [Cites] Ann Hematol. 2007 Aug;86(8):613-4 [17468870.001]
  • [Cites] Med Sci Monit. 2007 Apr;13(4):CS53-5 [17392656.001]
  • [Cites] J Am Acad Dermatol. 1996 Dec;35(6):989-90 [8959963.001]
  • [Cites] J Am Acad Dermatol. 1996 Dec;35(6):995-7 [8959967.001]
  • [Cites] Arch Dermatol. 1996 Dec;132(12):1507, 1510 [8961884.001]
  • [Cites] Br J Dermatol. 1997 Jan;136(1):142-4 [9039324.001]
  • [Cites] Br J Dermatol. 1997 Feb;136(2):296-7 [9068763.001]
  • [Cites] J Am Acad Dermatol. 1997 Mar;36(3 Pt 1):436-9 [9091476.001]
  • [Cites] Dermatology. 1997;194(2):182-4 [9094473.001]
  • [Cites] Int J Dermatol. 1997 Apr;36(4):292-3 [9169331.001]
  • [Cites] Med Pediatr Oncol. 2003 Feb;40(2):135-6 [12461805.001]
  • [Cites] Ann Rheum Dis. 2003 Jan;62(1):81-2 [12480678.001]
  • [Cites] Int J Dermatol. 2002 Dec;41(12):928-30 [12492993.001]
  • [Cites] Arch Dermatol. 2003 Jan;139(1):101-2 [12533182.001]
  • [Cites] Arch Dermatol. 2003 Jan;139(1):102 [12533183.001]
  • [Cites] J Am Acad Dermatol. 1999 Dec;41(6):1033-4 [10570395.001]
  • [Cites] Br J Ophthalmol. 1998 Mar;82(3):328-9 [9602638.001]
  • [Cites] Br J Dermatol. 1998 Feb;138(2):365-6 [9602899.001]
  • [Cites] Clin Exp Dermatol. 1997 Nov;22(6):269-73 [9604452.001]
  • [Cites] Australas J Dermatol. 1998 May;39(2):116-8 [9611384.001]
  • [Cites] Dermatology. 1998;196(3):346-7 [9621146.001]
  • [Cites] Eur Respir J. 1998 Apr;11(4):978-80 [9623707.001]
  • [Cites] Am J Hematol. 1998 Aug;58(4):337-8 [9692401.001]
  • [Cites] Med Pediatr Oncol. 1998 Sep;31(3):178-81 [9722904.001]
  • [Cites] Br J Dermatol. 1998 Jul;139(1):107-10 [9764159.001]
  • [Cites] Ann Hematol. 1998 Sep;77(3):135-8 [9797084.001]
  • [Cites] Dermatology. 1998;197(2):195-6 [9840982.001]
  • [Cites] Intensive Care Med. 1998 Oct;24(10):1106-9 [9840248.001]
  • [Cites] Br J Dermatol. 1999 Oct;141(4):766-7 [10583147.001]
  • [Cites] Br J Dermatol. 1999 Nov;141(5):943-4 [10583195.001]
  • [Cites] J Clin Gastroenterol. 1999 Dec;29(4):349-50 [10599643.001]
  • [Cites] Clin Exp Dermatol. 1999 Nov;24(6):443-5 [10606943.001]
  • [Cites] Leuk Res. 2000 Jan;24(1):83-6 [10634651.001]
  • [Cites] J Am Acad Dermatol. 2000 Feb;42(2 Pt 2):332-4 [10640926.001]
  • [Cites] Am J Med. 2000 Apr 1;108(5):434-5 [10759106.001]
  • [Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000 Apr;89(4):477-9 [10760730.001]
  • [Cites] J Am Acad Dermatol. 2000 May;42(5 Pt 2):932-5 [10767709.001]
  • [Cites] Arch Dermatol. 2000 May;136(5):673-4 [10815868.001]
  • [Cites] Australas J Dermatol. 1991;32(2):61-4 [1781756.001]
  • [Cites] J Am Acad Dermatol. 1991 Oct;25(4):734 [1724249.001]
  • [Cites] Arthritis Rheum. 1992 Apr;35(4):484-6 [1567500.001]
  • [Cites] Dermatologica. 1991;183(4):255-64 [1809587.001]
  • [Cites] Ann Intern Med. 1992 Jun 15;116(12 Pt 1):996-8 [1375012.001]
  • [Cites] J Rheumatol. 1992 May;19(5):814-20 [1613717.001]
  • [Cites] Am Rev Respir Dis. 1992 Jul;146(1):269 [1626811.001]
  • [Cites] Cutis. 1992 Jun;49(6):448-50 [1628515.001]
  • [Cites] Intern Med. 1992 May;31(5):686-9 [1504437.001]
  • [Cites] Aust N Z J Ophthalmol. 1992 Aug;20(3):263-5 [1449782.001]
  • [Cites] Int J Dermatol. 1992 Sep;31(9):670-1 [1459771.001]
  • [Cites] Acta Haematol. 1992;88(2-3):154-7 [1466198.001]
  • [Cites] Br J Dermatol. 1992 Nov;127(5):538-9 [1467297.001]
  • [Cites] J Am Acad Dermatol. 1992 Nov;27(5 Pt 2):801-4 [1469130.001]
  • [Cites] Pediatr Dermatol. 1992 Sep;9(3):288-92 [1488383.001]
  • [Cites] Clin Exp Dermatol. 1993 Jan;18(1):47-9 [8440052.001]
  • [Cites] Cutis. 1993 Mar;51(3):175-9 [8444048.001]
  • [Cites] Cutis. 1993 Feb;51(2):112-4 [8453891.001]
  • [Cites] Int J Dermatol. 1993 Apr;32(4):261-8 [8486457.001]
  • [Cites] Arch Ophthalmol. 1993 May;111(5):587-8 [8489431.001]
  • [Cites] Mayo Clin Proc. 1993 Jun;68(6):620-1 [8497142.001]
  • [Cites] Br J Dermatol. 1993 May;128(5):584-6 [8504055.001]
  • [Cites] Clin Dermatol. 1993 Jan-Mar;11(1):149-57 [8339190.001]
  • [Cites] Arch Dermatol. 1993 Aug;129(8):1062-4 [8352617.001]
  • [Cites] Obstet Gynecol Surv. 1993 Aug;48(8):584-7 [8371901.001]
  • [Cites] Br J Haematol. 1993 Jun;84(2):356-8 [7691149.001]
  • [Cites] Cancer. 1993 Nov 1;72(9):2723-31 [8402496.001]
  • [Cites] Australas J Dermatol. 1993;34(1):31-3 [8240185.001]
  • [Cites] Korean J Intern Med. 2001 Sep;16(3):218-21 [11769583.001]
  • [Cites] Dermatology. 2002;204(1):84 [11834860.001]
  • [Cites] J Dermatol. 2002 Feb;29(2):91-5 [11890302.001]
  • [Cites] Am J Clin Dermatol. 2002;3(2):117-31 [11893223.001]
  • [Cites] Int J Dermatol. 2002 Jan;41(1):28-31 [11895510.001]
  • [Cites] Arch Dermatol. 2002 Mar;138(3):345-9 [11902985.001]
  • [Cites] Arch Dermatol. 2002 Mar;138(3):361-5 [11902987.001]
  • [Cites] Arch Dermatol. 2002 Mar;138(3):400-3 [11902994.001]
  • [Cites] Clin Dermatol. 2000 May-Jun;18(3):265-82 [10856659.001]
  • [Cites] Arch Intern Med. 2000 Jun 26;160(12):1869 [10871983.001]
  • [Cites] Acta Derm Venereol. 2000 Mar-Apr;80(2):145-6 [10877140.001]
  • [Cites] Eur J Haematol. 2000 Jul;65(1):72-3 [10914942.001]
  • [Cites] Br J Dermatol. 2000 Aug;143(2):449-50 [10951165.001]
  • [Cites] J Am Acad Dermatol. 2000 Oct;43(4):691-7 [11004629.001]
  • [Cites] Am J Dermatopathol. 2000 Oct;22(5):429-33 [11048979.001]
  • [Cites] Postgrad Med J. 2000 Nov;76(901):713-4 [11060149.001]
  • [Cites] Br J Dermatol. 2000 Oct;143(4):914-6 [11069494.001]
  • [Cites] Int J Dermatol. 2000 Oct;39(10):795-8 [11095204.001]
  • [Cites] Br J Dermatol. 2000 Dec;143(6):1322-4 [11122045.001]
  • [Cites] J Pediatr Hematol Oncol. 2001 Jan;23(1):59-62 [11196274.001]
  • [Cites] J Am Acad Dermatol. 2000 Nov;43(5 Pt 1):870-4 [11050599.001]
  • [Cites] J Cutan Pathol. 2001 Feb;28(2):90-6 [11168757.001]
  • [Cites] J Am Acad Dermatol. 2001 May;44(5):862-4 [11312438.001]
  • [Cites] Medicine (Baltimore). 2001 May;80(3):173-9 [11388093.001]
  • [Cites] Acta Derm Venereol. 2001 Jan-Feb;81(1):73-4 [11411932.001]
  • [Cites] Am J Med. 2001 Jul;111(1):80-1 [11460854.001]
  • [Cites] J Am Acad Dermatol. 2001 Aug;45(2):300-2 [11464196.001]
  • [Cites] J Neurol Sci. 2001 Jul 15;188(1-2):95-7 [11489291.001]
  • [Cites] Arch Dermatol. 2001 Aug;137(8):1106-8 [11493115.001]
  • [Cites] Yale J Biol Med. 2001 May-Jun;74(3):165-8 [11501712.001]
  • [Cites] J Am Acad Dermatol. 2001 Sep;45(3):325-61; quiz 362-4 [11511831.001]
  • [Cites] J Am Acad Dermatol. 2001 Oct;45(4):590-5 [11568752.001]
  • [Cites] Dis Colon Rectum. 2001 Oct;44(10):1526-9 [11598485.001]
  • [Cites] Clin Exp Dermatol. 2001 Nov;26(8):668-70 [11722452.001]
  • [Cites] Dermatology. 1995;190(4):335-7 [7655121.001]
  • [Cites] J Am Acad Dermatol. 1995 Sep;33(3):393-410; quiz 410-2 [7544812.001]
  • [Cites] Clin Exp Dermatol. 1995 May;20(3):279-80 [7671433.001]
  • [Cites] Arch Dermatol. 1995 Oct;131(10):1175-7 [7574835.001]
  • [Cites] Aust Fam Physician. 1995 Oct;24(10):1867-9 [8546614.001]
  • [Cites] Am J Med. 1995 Dec;99(6):662-71 [7503090.001]
  • [Cites] Br J Dermatol. 1995 Sep;133(3):483-6 [8547011.001]
  • [Cites] Br J Dermatol. 1995 Sep;133(3):490-1 [8547013.001]
  • [Cites] Lancet. 1996 Mar 9;347(9002):690 [8596402.001]
  • [Cites] J Am Acad Dermatol. 1996 Mar;34(3):539 [8609279.001]
  • [Cites] Pediatrics. 1996 Mar;97(3):401-3 [8604280.001]
  • [Cites] Leukemia. 1996 Apr;10(4):731-4 [8618455.001]
  • [Cites] J Am Acad Dermatol. 1996 May;34(5 Pt 2):918-23 [8621829.001]
  • [Cites] Cutis. 1996 Feb;57(2):107-10 [8646854.001]
  • [Cites] Adv Dermatol. 1996;11:215-52; discussion 253 [8718480.001]
  • [Cites] Australas J Dermatol. 1996 May;37(2):99-101 [8687337.001]
  • [Cites] Eur J Cancer B Oral Oncol. 1996 Mar;32B(2):133-6 [8736177.001]
  • [Cites] Br J Dermatol. 1996 Apr;134(4):705-9 [8733376.001]
  • [Cites] J Pediatr Hematol Oncol. 1996 Aug;18(3):282-4 [8689342.001]
  • [Cites] Clin Exp Dermatol. 1996 Mar;21(2):175 [8759219.001]
  • [Cites] Am J Med. 1996 Aug;101(2):231-3 [8757366.001]
  • [Cites] Ann Acad Med Singapore. 1996 Mar;25(2):222-7 [8799010.001]
  • [Cites] J Neurol. 1996 Jul;243(7):556-7 [8836949.001]
  • [Cites] Int J Dermatol. 1996 Jan;35(1):9-15 [8838921.001]
  • [Cites] Respir Med. 1996 Jan;90(1):57-9 [8857328.001]
  • [Cites] J Am Acad Dermatol. 1996 Oct;35(4):629-31 [8859296.001]
  • [Cites] Haematologica. 1996 Jan-Feb;81(1):54-8 [8900854.001]
  • [Cites] J Rheumatol. 1996 Nov;23(11):1995-8 [8923382.001]
  • [Cites] J Cutan Pathol. 2002 May;29(5):301-4 [12100632.001]
  • [Cites] J Am Acad Dermatol. 2002 Aug;47(2):323-4 [12140489.001]
  • [Cites] Ann Hematol. 2002 Jul;81(7):397-8 [12185512.001]
  • [Cites] Br J Dermatol. 2002 Sep;147(3):558-62 [12207601.001]
  • [Cites] Rheumatology (Oxford). 2002 Sep;41(9):1067-9 [12209043.001]
  • [Cites] Acta Derm Venereol. 2002;82(3):221 [12353722.001]
  • [Cites] Am J Psychiatry. 2002 Nov;159(11):1947 [12411238.001]
  • [Cites] Eur J Radiol. 2002 Nov;44(2):139-42 [12413682.001]
  • (PMID = 17655751.001).
  • [ISSN] 1750-1172
  • [Journal-full-title] Orphanet journal of rare diseases
  • [ISO-abbreviation] Orphanet J Rare Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 435
  • [Other-IDs] NLM/ PMC1963326
  •  go-up   go-down


60. Barrera M, Atenafu E, Andrews GS, Saunders F: Factors related to changes in cognitive, educational and visual motor integration in children who undergo hematopoietic stem cell transplant. J Pediatr Psychol; 2008 Jun;33(5):536-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Factors related to changes in cognitive, educational and visual motor integration in children who undergo hematopoietic stem cell transplant.
  • RESULTS: Performance IQ improved over time and was negatively related to maternal depression.
  • Full IQ and educational outcomes were positively related to child's age and mother's age.
  • Poor educational outcomes were related to increased time since diagnosis.
  • Maternal age and depression, child's age, and time since diagnosis are critical factors for these outcomes.
  • [MeSH-major] Achievement. Hematopoietic Stem Cell Transplantation / psychology. Intelligence. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / therapy. Neoplasms / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Psychomotor Performance
  • [MeSH-minor] Age Factors. Child. Combined Modality Therapy. Cranial Irradiation / adverse effects. Depression / psychology. Female. Follow-Up Studies. Humans. Male. Mathematics. Mothers / psychology. Prognosis. Reaction Time / radiation effects. Wechsler Scales


61. Podgornik H, Debeljak M, Zontar D, Cernelc P, Prestor VV, Jazbec J: RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia. Cancer Genet Cytogenet; 2007 Oct 1;178(1):77-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia.
  • Amplification of RUNX1 (alias AML1) is a recurrent karyotypic abnormality in childhood acute lymphoblastic leukemia (ALL) that is generally associated with a poor outcome.
  • It does not occur with other primary chromosomal abnormalities in acute ALL.
  • AML1 amplification in acute myelogenous leukemia (AML) is a rare secondary event described mainly in therapy-related cases.
  • AML1 amplification was found in a 13-year-old patient with AML M4/M5 leukemia that occurred 5 years after she had been diagnosed with common B-cell ALL.
  • Conventional cytogenetic, fluorescent in situ hybridization (FISH), and polymerase chain reaction methods revealed no other chromosomal change expected to occur in a disease that we assumed to be a secondary leukemia.
  • This analysis confirmed that in addition to t(12;21), AML1 amplification and overexpression existed already at the time the diagnosis was made.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Neoplastic. Leukemia, B-Cell / genetics. Leukemia, B-Cell / pathology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


62. Kornblit B, Masmas T, Madsen HO, Ryder LP, Svejgaard A, Jakobsen B, Sengeløv H, Olesen G, Heilmann C, Dickmeiss E, Petersen SL, Vindeløv L: Haematopoietic cell transplantation with non-myeloablative conditioning in Denmark: disease-specific outcome, complications and hospitalization requirements of the first 100 transplants. Bone Marrow Transplant; 2008 May;41(10):851-9
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  • We analysed the outcome and hospitalization requirements of the first 100 patients (Hodgkin's disease (HD), N=13; multiple myeloma (MM), N=14; CLL, N=12; non-Hodgkin's lymphoma (NHL), N=17; myelodysplastic syndrome (MDS), N=18; AML, N=24 and CML, N=2) treated in Denmark with haematopoietic cell transplantation after non-myeloablative conditioning with TBI 2 Gy+/-fludarabine.
  • The cumulative incidence of acute GVHD grade II-IV and extensive chronic GVHD was 67 and 49%.
  • After a median follow-up of 534 days, the overall survival, PFS, relapse-related mortality and treatment-related mortality were 59, 50, 25 and 17%, respectively.
  • Patients with CLL, NHL, AML and MDS with <5% blasts at any time had a favourable outcome with a PFS of 61-71%.
  • [MeSH-minor] Adult. Aged. Denmark / epidemiology. Female. Graft vs Host Disease / epidemiology. Hodgkin Disease / therapy. Hospitalization / statistics & numerical data. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / therapy. Lymphoma, Non-Hodgkin / therapy. Male. Middle Aged. Multiple Myeloma / therapy. Myelodysplastic Syndromes / therapy. Outpatient Clinics, Hospital / utilization. Treatment Outcome. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use. Whole-Body Irradiation

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  • (PMID = 18246114.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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63. Bradley MB, Satwani P, Baldinger L, Morris E, van de Ven C, Del Toro G, Garvin J, George D, Bhatia M, Roman E, Baxter-Lowe LA, Schwartz J, Qualter E, Hawks R, Wolownik K, Foley S, Militano O, Leclere J, Cheung YK, Cairo MS: Reduced intensity allogeneic umbilical cord blood transplantation in children and adolescent recipients with malignant and non-malignant diseases. Bone Marrow Transplant; 2007 Oct;40(7):621-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • There were six primary graft failures (chronic myelogenous leukemia (CML), beta-thalassemia, hemophagocytic lymphohistiocytosis (HLH) and myelodysplastic syndrome (MDS)).
  • The probability of developing grade II to grade IV acute graft-versus-host disease (GVHD) and chronic GVHD was 28.6 and 16.7%, respectively.
  • Incidence of transplant-related mortality (TRM) was 14%.
  • [MeSH-major] Cord Blood Stem Cell Transplantation / methods. Fetal Blood / cytology. Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adult. Antigens, CD34 / analysis. Child. Child, Preschool. Graft vs Host Disease / prevention & control. Granulocyte-Macrophage Colony-Stimulating Factor / therapeutic use. Humans. Immunologic Factors / therapeutic use. Living Donors. Myelodysplastic Syndromes / mortality. Myelodysplastic Syndromes / therapy. Patient Selection. Recombinant Proteins. Survival Analysis. Transplantation Chimera. Transplantation Conditioning. Treatment Failure. Treatment Outcome. beta-Thalassemia / mortality. beta-Thalassemia / therapy

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  • (PMID = 17660841.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5P30CA13697; United States / NIAMS NIH HHS / AR / R21AR49330
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Immunologic Factors; 0 / Recombinant Proteins; 123774-72-1 / sargramostim; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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64. Nivison-Smith I, Bradstock KF, Dodds AJ, Hawkins PA, Szer J: Haemopoietic stem cell transplantation in Australia and New Zealand, 1992-2001: progress report from the Australasian Bone Marrow Transplant Recipient Registry. Intern Med J; 2005 Jan;35(1):18-27
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  • BACKGROUND: Bone marrow and blood stem cell transplantation is now used as curative therapy for a range of haematological malignancies and other conditions.
  • The most common indication for autologous transplantation in 2001 was non-Hodgkin's lymphoma, whereas for allogeneic transplants it was acute myeloid leukaemia.
  • The 9-year actuarial disease-free survival probability for patients aged 16 and above between 1992 and 2000 was 37% for autologous, 39% for allogeneic related donor and 30% for allogeneic unrelated donor transplants.
  • Treatment-related mortality was 16.9% after allogeneic transplantation and 2.1% after autologous transplantation in 2000.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / statistics & numerical data. Leukemia / surgery
  • [MeSH-minor] Acute Disease. Australia. Cause of Death. Disease-Free Survival. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Leukemia, Myeloid / surgery. New Zealand. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery. Registries

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  • (PMID = 15667464.001).
  • [ISSN] 1444-0903
  • [Journal-full-title] Internal medicine journal
  • [ISO-abbreviation] Intern Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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65. Ghoshal K, Bai S: DNA methyltransferases as targets for cancer therapy. Drugs Today (Barc); 2007 Jun;43(6):395-422
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  • [Title] DNA methyltransferases as targets for cancer therapy.
  • Clinical trials have shown that both drugs have therapeutic potential against leukemia such as MDS, acute myeloid leukemia, chronic myelogenous leukemia and chronic myelomonocytic leukemia.
  • Development of related stable drugs that can facilitate gene activation in cancer cells by enhancing degradation of DNA methyltransferases without being incorporated into DNA would be ideal for chemotherapy.
  • [MeSH-minor] Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Azacitidine / therapeutic use. Epigenesis, Genetic. Female. Gene Expression Regulation. Gene Silencing. Hematologic Neoplasms / drug therapy. Hematologic Neoplasms / metabolism. Humans. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Male. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / metabolism. Transcriptional Activation

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  • (PMID = 17612710.001).
  • [ISSN] 1699-3993
  • [Journal-full-title] Drugs of today (Barcelona, Spain : 1998)
  • [ISO-abbreviation] Drugs Today
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA086978; United States / NCI NIH HHS / CA / CA86978
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 776B62CQ27 / decitabine; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; M801H13NRU / Azacitidine
  • [Number-of-references] 252
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66. Shayani S: Dasatinib, a multikinase inhibitor: therapy, safety, and appropriate management of adverse events. Ther Drug Monit; 2010 Dec;32(6):680-7
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  • [Title] Dasatinib, a multikinase inhibitor: therapy, safety, and appropriate management of adverse events.
  • Tyrosine kinase inhibitors are the standard of care for the treatment of chronic myeloid leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia.
  • Dasatinib is a second-generation tyrosine kinase inhibitor that has been shown to be efficacious in treatment of patients with chronic myeloid leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia who are resistant or intolerant to frontline imatinib.
  • In clinical trials of dasatinib, the adverse events that arise during therapy are mostly mild to moderate in severity and are usually reversible and manageable with appropriate intervention.
  • Patients at risk of cardiac abnormalities or bleeding-related events require careful monitoring.
  • Pharmacokinetic analysis of dasatinib indicates interactions with a number of other agents and a complete treatment history should be taken before initiating therapy because mitigating drug-drug interactions are critical for patient safety.
  • [MeSH-minor] Dasatinib. Drug Administration Schedule. Drug Interactions. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukopenia / chemically induced. Leukopenia / therapy. Pleural Effusion / chemically induced. Pleural Effusion / therapy

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  • (PMID = 20864900.001).
  • [ISSN] 1536-3694
  • [Journal-full-title] Therapeutic drug monitoring
  • [ISO-abbreviation] Ther Drug Monit
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
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67. Wang LH, Wang M, Zhou CL, Chen S, Zhang XW, Xing HY, Wang JX: [Detection of point mutation at second tyrosine kinase domain of FLT3 gene in acute myeloid leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2005 Jun;26(6):335-8
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  • [Title] [Detection of point mutation at second tyrosine kinase domain of FLT3 gene in acute myeloid leukemia].
  • OBJECTIVE: To evaluate the prevalence of a novel FLT3 activating mutation in tyrosine kinase domain (TDK) in acute leukemia patients and its clinical implication.
  • METHODS: Genomic DNA from bone marrow mononuclear cells of 143 cases of acute myeloid leukemia (AML), 25 acute lymphocytic leukemia (ALL), 2 acute hybrid leukemia (AHL), 17 myelodysplastic syndromes (MDS) and 7 chronic myelogenous leukemia in blast crisis (CML-BC) was screened by polymerase chain reaction (PCR) and gel electrophoresis for FLT3-TKD point mutations.
  • RESULTS: Among AML patients, FLT3-TKD point mutation (FLT3-TKD(+)) rate was 6.3% (9/143), an incidence significantly lower than that of internal tandem duplication (ITD) mutation (37/143, 25.9%, P < 0.01).
  • The presence of TKD mutations was related neither to age, sex, nor to WBC counts, the marrow blast percentages, and CR rates for induction therapy.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. fms-Like Tyrosine Kinase 3 / genetics


68. Romaguera JE, Fayad L, Rodriguez MA, Broglio KR, Hagemeister FB, Pro B, McLaughlin P, Younes A, Samaniego F, Goy A, Sarris AH, Dang NH, Wang M, Beasley V, Medeiros LJ, Katz RL, Gagneja H, Samuels BI, Smith TL, Cabanillas FF: High rate of durable remissions after treatment of newly diagnosed aggressive mantle-cell lymphoma with rituximab plus hyper-CVAD alternating with rituximab plus high-dose methotrexate and cytarabine. J Clin Oncol; 2005 Oct 1;23(28):7013-23
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  • Five patients died from acute toxicity.
  • Four patients developed treatment-related myelodysplasia/acute myelogenous leukemia, and three patients died while in remission from MCL.
  • A total of eight treatment-related deaths (8%) occurred.
  • Because of the shorter FFS concurrent with significant toxicity in patients more than 65 years of age, this regimen is not recommended as standard therapy for this age subgroup.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Mantle-Cell / drug therapy

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  • [ErratumIn] J Clin Oncol. 2006 Feb 1;24(4):724
  • (PMID = 16145068.001).
  • [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] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; CVAD protocol
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69. Betancourt-García RD, Castro J, Fernández AC, López-Enríquez A, Fradera J, Pacheco E: Acquired acute myelogenous leukemia after therapy for acute promyelocytic leukemia with t(15;17): a case report and review of the literature. P R Health Sci J; 2009 Jun;28(2):146-50
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  • [Title] Acquired acute myelogenous leukemia after therapy for acute promyelocytic leukemia with t(15;17): a case report and review of the literature.
  • Therapy-related myelodysplastic syndrome (t-MDS) and therapy-related acute myelogenous leukemia (t-AML) in patients with acute promyelocytic leukemia (APL) are rare events.
  • The cumulative exposure to chemotherapy with alkylating agents and topoisomerase II inhibitors is associated with t-AML that may develop any time after the completion of the treatment.
  • We report the case of an acquired AML who previously received therapy for APL, after two years of being diagnosed.
  • The diagnosis was established by morphologic findings, membrane markers, cytogenetic studies, and fluorescence in situ hybridization (FISH).
  • To our knowledge this is the first documented case in Puerto Rico of a patient with APL that developed a t-AML without the characteristic chromosomal and morphologic findings of APL.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Leukemia, Promyelocytic, Acute / drug therapy. Neoplasms, Second Primary / etiology. Translocation, Genetic


70. Yamamoto M, Kakihana K, Kurosu T, Murakami N, Miura O: Clonal evolution with inv(11)(p15q22) and NUP98/DDX10 fusion gene in imatinib-resistant chronic myelogenous leukemia. Cancer Genet Cytogenet; 2005 Mar;157(2):104-8
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  • [Title] Clonal evolution with inv(11)(p15q22) and NUP98/DDX10 fusion gene in imatinib-resistant chronic myelogenous leukemia.
  • The BCR/ABL tyrosine kinase inhibitor imatinib has shown remarkable efficacy in treating patients with chronic myelogenous leukemia (CML).
  • Leukemic cells from the patient were found to express the fusion transcript of NUP98 and DDX10, which is in accordance with previously reported cases of de novo or therapy-related acute myelogenous leukemia and myelodysplastic syndrome with inv(11)(p15q22).
  • These observations raise a possibility that the NUP98/DDX10 fusion might be involved in imatinib resistance as well as in acute transformation of CML.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 11. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 15721630.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / nuclear pore complex protein 98; 8A1O1M485B / Imatinib Mesylate; EC 3.6.1.- / DDX10 protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases; EC 3.6.4.13 / RNA Helicases
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71. Luger SM: Treating the elderly patient with acute myelogenous leukemia. Hematology Am Soc Hematol Educ Program; 2010;2010:62-9
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  • [Title] Treating the elderly patient with acute myelogenous leukemia.
  • Decisions regarding the optimal treatment of acute myelogenous leukemia in the elderly patient requires the consideration of multiple factors.
  • Population-based studies have demonstrated that, for all age groups, aggressive therapy results in improved survival and quality of life when compared with palliative care.
  • Furthermore, not all patients are candidates for such therapy.
  • Consideration of patient and disease-related factors can help to determine the appropriateness of intensive therapy in a given patient.
  • For those patients for whom aggressive induction therapy does not seem to be in their best interest, novel agents are being investigated that will hopefully address the issues of induction death and early relapse associated with these patient populations.

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  • (PMID = 21239772.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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72. Chen H, Lu DP, Huang XJ, Liu KY, Xu LP, Han W, Ren HY, Chen YH, Liu DH, Lu J, Jiang Q: [Reduced intensity of BuCy conditioning regimen for transplantation in the treatment of malignant hematologic diseases]. Zhonghua Xue Ye Xue Za Zhi; 2005 May;26(5):273-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Twelve patients with acute lymphoblastic leukemia (ALL, n = 4), acute myelogenous leukemia (AML-M(2), n = 2), chronic myelogenous leukemia (CML, n = 4), and myelodysplastic syndromes-refractory anemia with excess blasts (MDS-RAEB, n = 2) were intolerant of conventional myeloablative therapy because of age (older than 50 years) or having severe concurrent diseases.
  • All patients received cyclosporin A, short-term MTX and mycophenolate mofetil (MMF) for prophylaxis of acute graft-versus-host disease (aGVHD).
  • RESULTS: All the patients were well tolerated the regimen, with no severe regimen related toxicity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Hematologic Neoplasms / drug therapy. Transplantation Conditioning / methods

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  • (PMID = 15949287.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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73. Lashkari A, Lowe T, Collisson E, Paquette R, Emmanouilides C, Territo M, Schiller G: Long-term outcome of autologous transplantation of peripheral blood progenitor cells as postremission management of patients &gt; or =60 years with acute myelogenous leukemia. Biol Blood Marrow Transplant; 2006 Apr;12(4):466-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcome of autologous transplantation of peripheral blood progenitor cells as postremission management of patients > or =60 years with acute myelogenous leukemia.
  • The optimal postremission treatment for elderly patients with acute myelogenous leukemia (AML) is presently unknown, but recent studies report the feasibility of autologous stem cell transplantation in this population.
  • To better understand the long-term outcome of autologous transplantation in AML patients > or =60 years of age, we evaluated high-dose chemoradiotherapy preparative conditioning followed by transplantation of peripheral blood progenitor cells procured after a single cycle of cytarabine-based consolidation chemotherapy as postremission therapy in 27 patients aged 60 to 71 years (median age, 65 years) with newly diagnosed AML in first complete remission (CR).
  • Seven patients are alive in continuous CR, 19 died from relapse, and 1 died as a result of treatment-related infection.
  • Leukemia-free survival and overall survival are 10.3 and 13.4 months, respectively.
  • Actuarial leukemia-free and overall survival at 3 years are 25% +/- 9% and 28% +/- 9%, respectively.
  • Our results demonstrate that autologous transplantation of peripheral blood progenitor cells is well tolerated and feasible for patients > or =60 years of age with AML in first CR.
  • Future investigation should focus on a randomized study evaluating a larger group of elderly patients in first CR comparing autologous stem cell transplantation with conventional cytarabine-based consolidation chemotherapy to identify the optimal postremission therapy.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Peripheral Blood Stem Cell Transplantation. Transplantation Conditioning

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  • (PMID = 16545730.001).
  • [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; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 04079A1RDZ / Cytarabine
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74. Strick R, Zhang Y, Emmanuel N, Strissel PL: Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias. Hum Genet; 2006 Jun;119(5):479-95
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  • [Title] Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias.
  • The t(9;22) BCR/ABL fusion is associated with over 90% of chronic myelogenous and 25% of acute lymphocytic leukemia.
  • Chromosome 11q23 translocations in acute myeloid and lymphoid leukemia cells demonstrate myeloid lymphoid leukemia (MLL) fusions with over 40 gene partners, like AF9 and AF4 on chromosomes 9 and 4, respectively.
  • Therapy-related leukemia is associated with the above gene rearrangements following the treatment with topoisomerase II (topo II) inhibitors.
  • A NHR model presented demonstrates the importance of chromatin structure in chromosome translocations involved with leukemia.
  • [MeSH-major] Chromatin / chemistry. Chromosome Breakage. Chromosomes, Human / genetics. Leukemia / genetics. Leukemia / metabolism. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Cells, Cultured. Chronic Disease. Humans. K562 Cells. Proto-Oncogene Proteins c-bcr / chemistry. Proto-Oncogene Proteins c-bcr / genetics. Recombination, Genetic

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  • [Cites] Biochemistry. 1997 May 20;36(20):5934-9 [9166762.001]
  • [Cites] Cell. 1985 May;41(1):127-32 [2986841.001]
  • [Cites] Gene. 2002 May 29;291(1-2):251-7 [12095698.001]
  • [Cites] EMBO J. 1990 Apr;9(4):1319-27 [2323342.001]
  • [Cites] Science. 1994 Jan 28;263(5146):515-8 [8290959.001]
  • [Cites] Curr Biol. 2000 Jul 27-Aug 10;10(15):923-6 [10959840.001]
  • [Cites] Leukemia. 1996 Feb;10(2):372-7 [8637251.001]
  • [Cites] J Cell Biochem. 2001;82(2):299-309 [11527155.001]
  • [Cites] Genomics. 1995 May 1;27(1):67-82 [7665185.001]
  • [Cites] Annu Rev Biochem. 1989;58:351-75 [2549853.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jun 21;91(13):6236-9 [8016145.001]
  • [Cites] Oncogene. 1989 May;4(5):559-67 [2657572.001]
  • [Cites] Oncogene. 1990 Nov;5(11):1669-73 [2267134.001]
  • [Cites] Oncogene. 2001 May 24;20(23):2900-7 [11420702.001]
  • [Cites] J Cell Biol. 2001 Dec 10;155(6):899-910 [11739403.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Apr;33(4):331-45 [11921269.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4790-5 [10758153.001]
  • [Cites] EMBO J. 2002 Oct 1;21(19):5269-80 [12356743.001]
  • [Cites] Genes Chromosomes Cancer. 2001 Oct;32(2):144-54 [11550282.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Apr;36(4):393-401 [12619163.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2076-80 [2832845.001]
  • [Cites] Nucleic Acids Res. 1997 Feb 1;25(3):511-7 [9016589.001]
  • [Cites] Cancer Res. 1999 Jul 15;59(14 ):3357-62 [10416593.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 14;98 (17 ):9802-7 [11493704.001]
  • [Cites] Oncogene. 1998 Dec 3;17(22):2921-31 [9879998.001]
  • [Cites] J Cell Sci. 2004 Sep 1;117(Pt 19):4583-90 [15331666.001]
  • [Cites] Nucleic Acids Res. 1988 Jun 24;16(12):5533-56 [2838820.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Jul;86(14):5497-501 [2546156.001]
  • [Cites] Cell. 1995 Dec 29;83(7):1137-48 [8548801.001]
  • [Cites] J Cell Biochem Suppl. 2000;Suppl 35:3-22 [11389527.001]
  • [Cites] Hum Mol Genet. 1998 May;7(5):767-76 [9536079.001]
  • [Cites] Hum Mol Genet. 2000 Jul 1;9(11):1671-9 [10861294.001]
  • [Cites] Mol Cell Biol. 1991 Oct;11(10):4973-84 [1656219.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14535-40 [10588740.001]
  • [Cites] Cell Mol Life Sci. 2002 Feb;59(2):373-85 [11915950.001]
  • [Cites] Mol Cell Biol. 1997 Jul;17(7):4070-9 [9199342.001]
  • [Cites] Biochem J. 1994 Nov 1;303 ( Pt 3):681-95 [7980433.001]
  • [Cites] Blood. 1996 Apr 1;87(7):2649-58 [8639880.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 May 15;90(10 ):4631-5 [8506309.001]
  • [Cites] Hum Mol Genet. 2002 Jun 1;11(12):1391-7 [12023981.001]
  • [Cites] J Biol Chem. 2002 Jun 14;277(24):21458-67 [11940566.001]
  • [Cites] Hum Mutat. 2003 Sep;22(3):229-44 [12938088.001]
  • [Cites] Cell. 1992 Nov 13;71(4):701-8 [1423625.001]
  • [Cites] Oncogene. 1998 Dec 10;17 (23 ):3035-44 [9881706.001]
  • [Cites] Genomics. 1999 Jul 15;59(2):187-92 [10409430.001]
  • [Cites] Leuk Res. 2002 Aug;26(8):713-20 [12191565.001]
  • [Cites] Br J Haematol. 1999 Apr;105(1):256-64 [10233389.001]
  • [Cites] Blood. 2000 Feb 1;95(3):738-43 [10648381.001]
  • [Cites] Oncogene. 1999 Dec 23;18(56):7975-84 [10637508.001]
  • [Cites] Cancer Res. 1995 Jan 1;55(1):34-8 [7805037.001]
  • [Cites] Cancer Res. 1996 Apr 15;56(8):1855-62 [8620504.001]
  • [Cites] Blood. 1996 Mar 1;87(5):1912-22 [8634439.001]
  • [Cites] Nature. 2001 Sep 27;413(6854):435-8 [11574892.001]
  • [Cites] Cancer Lett. 2003 Apr 10;193(1):1-9 [12691817.001]
  • [Cites] Leukemia. 1997 Sep;11(9):1571-4 [9305614.001]
  • [Cites] Chromosoma. 1996 Aug;105(2):122-33 [8753702.001]
  • [Cites] Leukemia. 1999 Dec;13(12):2107-13 [10602437.001]
  • [Cites] Cancer Res. 1993 Oct 1;53(19):4489-92 [8402620.001]
  • [Cites] Mol Cell Biol. 1999 Apr;19(4):2986-97 [10082566.001]
  • [Cites] Hum Genet. 2003 Jul;113(1):80-91 [12665971.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3793-803 [9808573.001]
  • [Cites] Genomics. 1998 Jan 15;47(2):217-29 [9479494.001]
  • [Cites] Blood. 2001 Dec 15;98(13):3778-83 [11739186.001]
  • [Cites] Genes Dev. 2001 Dec 15;15(24):3237-42 [11751629.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Sep;35(1):92-6 [12203795.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4550-5 [11389089.001]
  • [Cites] Blood. 1990 Aug 1;76(3):597-601 [2198962.001]
  • [Cites] Genetics. 2002 Apr;160(4):1363-73 [11973293.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):9882-7 [12114534.001]
  • [Cites] Genes Chromosomes Cancer. 2004 Nov;41(3):257-65 [15334549.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4411-3 [10781030.001]
  • [Cites] FASEB J. 2004 Jan;18(1):173-5 [14630694.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Apr;33(4):362-78 [11921271.001]
  • [Cites] Mol Pharmacol. 1998 Jul;54(1):78-85 [9658192.001]
  • [Cites] Cancer Res. 2004 Apr 15;64(8):2656-62 [15087374.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 5;99(5):3070-5 [11867721.001]
  • [Cites] Semin Hematol. 1999 Oct;36(4 Suppl 7):59-72 [10595755.001]
  • [Cites] Chromosoma. 1991 Feb;100(2):97-102 [1849068.001]
  • [Cites] Leukemia. 1998 Mar;12(3):346-52 [9529129.001]
  • [Cites] Leukemia. 1995 Aug;9(8):1305-12 [7643617.001]
  • (PMID = 16572268.001).
  • [ISSN] 0340-6717
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Chromatin; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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75. Kurtz JE, Asmane I, Voegeli AC, Neuville A, Dufresne A, Litique V, Chevreau C, Bergerat JP: A V530I Mutation in c-KIT Exon 10 Is Associated to Imatinib Response in Extraabdominal Aggressive Fibromatosis. Sarcoma; 2010;2010:458156
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  • AF medical therapy includes nonsteroids anti-inflammatory drugs, tamoxifen, with inconsistent results.
  • The previously discovered V530I substitution was characterized in the core binding factor AML, but had never been reported in any other condition, so far.
  • In this paper, we discuss the KIT exon 10 mutations or polymorphisms that have been described in a variety of KIT-related conditions, including acute myelogenous leukemia, mastocytosis, and aggressive fibromatosis.

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  • [Cites] Cancer Chemother Pharmacol. 2009 Aug;64(3):635-40 [19404642.001]
  • [Cites] Br J Haematol. 1999 Jun;105(4):894-900 [10554798.001]
  • [Cites] Target Oncol. 2009 Jan;4(1):45-56 [19343301.001]
  • [Cites] Eur J Surg Oncol. 2009 Feb;35(2):129-34 [18760561.001]
  • [Cites] J Neurosurg. 2007 Aug;107(2):473-5; author reply 475 [17695408.001]
  • [Cites] J Cancer Res Clin Oncol. 2007 Aug;133(8):533-8 [17453242.001]
  • [Cites] Br J Haematol. 2007 Jul;138(1):12-30 [17555444.001]
  • [Cites] J Natl Cancer Inst. 2006 Nov 1;98(21):1583-4 [17077361.001]
  • [Cites] Leukemia. 2006 Jun;20(6):965-70 [16598313.001]
  • [Cites] J Neurosurg. 2006 May;104(5):749-56 [16703880.001]
  • [Cites] J Natl Cancer Inst. 2006 Apr 19;98(8):562-3 [16622127.001]
  • [Cites] J Clin Oncol. 2006 Mar 1;24(7):1195-203 [16505440.001]
  • [Cites] Leukemia. 2006 Feb;20(2):354-5; discussion 356-7 [16307017.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3958-61 [16081693.001]
  • [Cites] Blood. 2005 Jul 15;106(2):721-4 [15790786.001]
  • [Cites] Leuk Res. 2005 Apr;29(4):397-400 [15725473.001]
  • [Cites] Diagn Mol Pathol. 1997 Apr;6(2):98-101 [9098648.001]
  • [Cites] J Mol Diagn. 2004 Nov;6(4):366-70 [15507676.001]
  • [Cites] Cancer. 2003 Jun 1;97(11):2760-6 [12767088.001]
  • [Cites] Cancer. 2002 Dec 1;95(11):2373-9 [12436445.001]
  • [Cites] Arch Dermatol Res. 2009 Jun;301(5):387-9 [19430803.001]
  • (PMID = 20339585.001).
  • [ISSN] 1369-1643
  • [Journal-full-title] Sarcoma
  • [ISO-abbreviation] Sarcoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2841250
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76. Kalaycio M, Rybicki L, Pohlman B, Sobecks R, Andresen S, Kuczkowski E, Bolwell B: Risk factors before autologous stem-cell transplantation for lymphoma predict for secondary myelodysplasia and acute myelogenous leukemia. J Clin Oncol; 2006 Aug 1;24(22):3604-10
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  • [Title] Risk factors before autologous stem-cell transplantation for lymphoma predict for secondary myelodysplasia and acute myelogenous leukemia.
  • PURPOSE: The risk factors for treatment-related myelodysplastic syndrome (t-MDS) and acute myelogenous leukemia (AML) after autologous stem-cell transplantation (ASCT) are similar to those that increase the risk of difficult stem-cell harvests.
  • We reviewed our experience in 526 patients with lymphoma treated by ASCT to determine whether difficult stem-cell harvests predict for an increased risk of t-MDS/AML.
  • RESULTS: With a median follow-up time for surviving patients of 69 months, 20 patients developed t-MDS/AML, for an actuarial incidence of 6.8% at 10 years.
  • Pretransplantation characteristics, including age, diagnosis of non-Hodgkin's lymphoma or Hodgkin's disease, bone marrow involvement, prior radiation therapy, prior exposure to chemotherapy, lactate dehydrogenase at the time of ASCT, disease status, and method of stem-cell mobilization, were then analyzed with respect to the subsequent development of t-MDS/AML.
  • By multivariable analysis, prior exposure to radiation therapy, four or more chemotherapy regimens, and more than 5 days of apheresis needed to harvest enough stem cells were identified as independent risk factors for t-MDS/AML.
  • CONCLUSION: These results suggest that identifiable pretransplantation factors predict for t-MDS/AML after ASCT.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Lymphoma / surgery. Myelodysplastic Syndromes / etiology. Peripheral Blood Stem Cell Transplantation


77. Pyatt DW, Aylward LL, Hays SM: Is age an independent risk factor for chemically induced acute myelogenous leukemia in children? J Toxicol Environ Health B Crit Rev; 2007 Sep-Oct;10(5):379-400
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  • [Title] Is age an independent risk factor for chemically induced acute myelogenous leukemia in children?
  • Secondary or therapy-related acute myelogenous leukemia (t-AML) is a rare but unfortunate consequence of treatment with certain classes of cytotoxic chemotherapeutic agents or chronic exposure to high concentrations of benzene.
  • Drugs known to produce AML following chemotherapy of primary malignancy are usually alkylating agents or topoisomerase II inhibitors.
  • Both children and adults develop AML following treatment with these classes of antineoplastic drugs.
  • In this review, the effect of age at treatment on a child's susceptibility to developing therapy related AML was investigated.
  • As demonstrated in the published literature, the risk of developing AML following chemotherapy is not reliably correlated with the age of the pediatric patient.
  • The age dependency of treatment-related malignancies (all types) in children appears to vary considerably with the type of secondary neoplasm in question.
  • For example, secondary solid tumors such as breast, central nervous system (CNS), bone, and thyroid cancer are highly dependent on the age of the patient at time of diagnosis and treatment; in contrast, an age dependency for t-AML risk was not observed in these same patient populations.
  • Predictably, the induction of t-AML in children follows a rational dose-response relationship, with increasing doses of chemotherapy resulting in greater risk. Recent U.S.
  • Available scientific and medical literature does not support the hypothesis that children necessarily possess an increased risk of developing AML following leukemogenic chemical exposure.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / epidemiology. Neoplasms, Second Primary / epidemiology

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  • (PMID = 17687725.001).
  • [ISSN] 1521-6950
  • [Journal-full-title] Journal of toxicology and environmental health. Part B, Critical reviews
  • [ISO-abbreviation] J Toxicol Environ Health B Crit Rev
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Topoisomerase II Inhibitors
  • [Number-of-references] 92
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78. Klymenko SV, Bink K, Trott KR, Bebeshko VG, Bazyka DA, Dmytrenko IV, Abramenko IV, Bilous NI, Zitzelsberger H, Misurin AV, Atkinson MJ, Rosemann M: MLL gene alterations in radiation-associated acute myeloid leukemia. Exp Oncol; 2005 Mar;27(1):71-5
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  • [Title] MLL gene alterations in radiation-associated acute myeloid leukemia.
  • AIM: Although acute myelogenous leukemia (AML) arising after radiation exposure is considered to be secondary, little is known about the molecular mechanisms by which the radiation induces the leukemogenic phenotype.
  • The aim of the study was to analyze whether the MLL translocations are as frequent in radiation-associated AML as in spontaneous AML cases.
  • METHODS: Sixty one AML samples obtained at diagnosis were analyzed for the presence of MLL abnormalities using fluorescent in situ hybridization and/or reverse transcription polymerase chain reaction.
  • Of these patients, 27 had experienced radiation exposure due to the Chernobyl accident, 32 were non-irradiated (spontaneous AML), and 2 developed therapy-related AML after chemotherapy with topoisomerase II inhibitors.
  • RESULTS: MLL gene translocations were detected in both groups of spontaneous and therapy-related AML (1/32 and 1/2 cases respectively).
  • The sole MLL rearrangement found in the group of radiation-associated AML patients was a duplication of the gene.
  • CONCLUSION: Our data preclude the involvement of MLL gene translocations in radiation-induced leukemogenesis, but support the assumption that loss and gain of chromosomal material could be crucial in the leukemogenesis of AML patients with the history of radiation exposure due to the Chernobyl accident.
  • [MeSH-major] Chernobyl Nuclear Accident. Chromosome Aberrations / radiation effects. DNA, Neoplasm / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15812362.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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79. Slobbe L, Polinder S, Doorduijn JK, Lugtenburg PJ, el Barzouhi A, Steyerberg EW, Rijnders BJ: Outcome and medical costs of patients with invasive aspergillosis and acute myelogenous leukemia-myelodysplastic syndrome treated with intensive chemotherapy: an observational study. Clin Infect Dis; 2008 Dec 15;47(12):1507-12
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  • [Title] Outcome and medical costs of patients with invasive aspergillosis and acute myelogenous leukemia-myelodysplastic syndrome treated with intensive chemotherapy: an observational study.
  • BACKGROUND: Invasive aspergillosis (IA) is a leading cause of mortality in patients with acute leukemia.
  • METHODS: In 269 patients treated for acute myelogenous leukemia-myelodysplastic syndrome (AML-MDS) during 2002-2007, evidence of IA was collected using high-resolution computed tomography and galactomannan measurement in bronchoalveolar lavage fluid specimens.
  • Diagnostic and therapeutic IA-related costs, corrected for neutropenia duration, were comprehensively analyzed from a hospital perspective.
  • In patients with IA, the mortality rate 12 weeks after starting antifungal therapy was 22% (16 of 73 patients).
  • Total IA-related costs increased to euro 8360 and euro 15,280 for patients with possible and probable or proven IA, respectively, compared with patients without IA (P<.001).
  • CONCLUSIONS: Early diagnosis and treatment of IA with oral voriconazole result in acceptable mortality rates.
  • [MeSH-major] Antifungal Agents / therapeutic use. Aspergillosis / drug therapy. Aspergillosis / economics. Drug Therapy / economics. Health Care Costs. Leukemia, Myeloid, Acute / complications


80. Xiao-Jun H, Lan-Ping X, Kai-Yan L, Dai-Hong L, Huan C, Wei H, Yu-Hong C, Jing-Zhi W, Yao C, Xiao-Hui Z, Hong-Xia S, Dao-Pei L: HLA-mismatched/haploidentical hematopoietic stem cell transplantation without in vitro T cell depletion for chronic myeloid leukemia: improved outcomes in patients in accelerated phase and blast crisis phase. Ann Med; 2008;40(6):444-55
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  • [Title] HLA-mismatched/haploidentical hematopoietic stem cell transplantation without in vitro T cell depletion for chronic myeloid leukemia: improved outcomes in patients in accelerated phase and blast crisis phase.
  • BACKGROUND: Allogeneic hematopoietic stem cell transplantation (allo-HSCT) remains the only proven curative therapy for chronic myeloid leukemia (CML), but lack of human leukocyte antigen (HLA)-matched sibling or unrelated donors has restricted its application.
  • RESULTS: Our data showed that the cumulative incidence of acute graft-versus-host disease (GVHD) was 64.52%, and grade III-IV was 26.45%, 61.79% had chronic GVHD, and 28.93% had extensive chronic GVHD.
  • Probability of 1-year and 4-year leukemia-free survival was similar in chronic phase (CP) 1, CP2/CR2, accelerated phase, and blast crisis patients.
  • Multivariate analysis indicated that factors affecting transplantation outcomes were HLA-B+DR mismatches versus others for II-III acute GVHD and III-IV acute GVHD, the stage of disease at transplantation for relapse, and the time from diagnosis to transplantation for leukemia-free survival, overall survival, and transplantation-related mortality.
  • CONCLUSIONS: For patients lacking an HLA-identical related donor, haploidentical relatives are alternative HSCT donors.
  • [MeSH-major] Blast Crisis / therapy. Hematopoietic Stem Cell Transplantation / methods. Histocompatibility Testing. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy


81. Perseghin P, Terruzzi E, Dassi M, Baldini V, Parma M, Coluccia P, Accorsi P, Confalonieri G, Tavecchia L, Verga L, Ravagnani F, Iacone A, Pogliani EM, Pioltelli P: Management of poor peripheral blood stem cell mobilization: incidence, predictive factors, alternative strategies and outcome. A retrospective analysis on 2177 patients from three major Italian institutions. Transfus Apher Sci; 2009 Aug;41(1):33-7
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  • CD34+ peripheral blood hematopoietic stem cells (HSC) are usually collected following mobilization therapy accomplished by using growth factors (GF) such as rHuG-CSF or rHuGM-CSF with or without chemotherapy.
  • In fact, 5-46% of patients who underwent mobilization therapy fail HSC collection due to very low peripheral blood HSC CD34+ count.
  • Patients' characteristics, including age, sex, stage of the underlying disease (complete or partial remission), diagnosis, previously administered radio/chemotherapy regimens, time-lapse from last chemotherapy before mobilization and mobilization schedule (including dose of GF) were considered as possibly predictive of poor or failed mobilization.
  • Therefore, a patient who fails a first mobilization (and when an HLA-compatible related on unrelated donor is not available) could undergo a second attempt either with different mobilization schedule or by using different GF, such as stem cell factor, growth hormone (GH), or more recently newly introduced drugs such as AMD3100, alone or in combination with rHuG- or -rHuGM-CSF.
  • [MeSH-minor] Adult. Antigens, CD34 / blood. Follow-Up Studies. Hematopoiesis. Hematopoietic Stem Cell Mobilization / methods. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / surgery. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Leukemia, Myeloid, Acute / surgery. Lymphoma, Non-Hodgkin / surgery. Multiple Myeloma / surgery. Retrospective Studies. Survival Analysis

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  • (PMID = 19540167.001).
  • [ISSN] 1473-0502
  • [Journal-full-title] Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis
  • [ISO-abbreviation] Transfus. Apher. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34
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82. Kantarjian H, le Coutre P, Cortes J, Pinilla-Ibarz J, Nagler A, Hochhaus A, Kimura S, Ottmann O: Phase 1 study of INNO-406, a dual Abl/Lyn kinase inhibitor, in Philadelphia chromosome-positive leukemias after imatinib resistance or intolerance. Cancer; 2010 Jun 1;116(11):2665-72
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  • BACKGROUND: : INNO-406, a dual v-abl Abelson murine leukemia viral oncogene homolog (Abl)/v-yes-1 Yamaguchi sarcoma viral-related oncogene homolog (Lyn) tyrosine kinase inhibitor (TKI), has demonstrated specific Lyn kinase inhibitory activity with no or limited activity against other sarcoma (Src) family member kinases.
  • In the current study, the authors evaluated the use of INNO-406 in patients with Philadelphia (Ph) chromosome-positive chronic myelogenous leukemia (CML) or acute lymphocytic leukemia (ALL) after imatinib resistance or intolerance.
  • Therapy was allowed to continue for a maximum of 24 months.

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  • [Copyright] (c) 2010 American Cancer Society.
  • [Cites] N Engl J Med. 1999 Jul 15;341(3):164-72 [10403855.001]
  • [Cites] Haematologica. 2008 Sep;93(9):1389-93 [18603549.001]
  • [Cites] Science. 2001 Aug 3;293(5531):876-80 [11423618.001]
  • [Cites] N Engl J Med. 2003 Oct 9;349(15):1451-64 [14534339.001]
  • [Cites] Oncologist. 2004;9(3):259-70 [15169981.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1321-31 [15215876.001]
  • [Cites] Cancer Chemother Rep. 1966 May;50(4):219-44 [4957125.001]
  • [Cites] J Natl Compr Canc Netw. 2005 Nov;3(6):757-68 [16316612.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1061-6 [16642048.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2531-41 [16775234.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2542-51 [16775235.001]
  • [Cites] N Engl J Med. 2006 Dec 7;355(23):2408-17 [17151364.001]
  • [Cites] Ann Intern Med. 2006 Dec 19;145(12):913-23 [17179059.001]
  • [Cites] Blood. 2007 Jan 1;109(1):306-14 [16954504.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2303-9 [17138817.001]
  • [Cites] Cancer. 2007 Jun 1;109(11):2171-81 [17431887.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3540-6 [17715389.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2007;:371-5 [18024653.001]
  • [Cites] Haematologica. 2008 Feb;93(2):186-92 [18223278.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Leuk Res. 2008 Jun;32(6):980-3 [18191450.001]
  • [Cites] Expert Rev Anticancer Ther. 2008 Sep;8(9):1387-98 [18759691.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3948-54 [16105974.001]
  • (PMID = 20310049.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA100632-070007; United States / NCI NIH HHS / CA / CA100632-070007; United States / NCI NIH HHS / CA / P01CA049639; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / P01 CA049639
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 859212-16-1 / bafetinib; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ NIHMS189694; NLM/ PMC2876208
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83. Ubukata H, Katano M, Takemura A, Kasuga T, Motohashi G, Ge L, Tabuchi T: Acute myelogenous leukemia suddenly developing just after surgery for advanced gastric cancer: report of a case. Surg Today; 2005;35(2):153-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myelogenous leukemia suddenly developing just after surgery for advanced gastric cancer: report of a case.
  • We report a case of acute myelogenous leukemia (AML) developing just after surgery for advanced gastric cancer, before adjuvant chemotherapy was started.
  • Acute myelogenous leukemia was diagnosed by an aspiration biopsy of the bone marrow.
  • If the AML had developed later and had become remarkable during or after adjuvant chemotherapy, the differential diagnosis between de novo and therapy-related leukemia would have been very difficult.
  • Most leukemias that develop during the course of chemotherapy or radiotherapy, or both, are indisputably considered to be therapy-related.
  • Thus, we report the clinical course of this patient with reference to the related literature to warn surgeons of the possibility of this unusual manifestation.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Neoplasms, Multiple Primary / diagnosis. Stomach Neoplasms / surgery
  • [MeSH-minor] Aged. Bone Marrow Cells / pathology. Humans. Male. Postoperative Complications / diagnosis


84. Krug U, Serve H, Müller-Tidow C, Mesters RM, Steffen B, Büchner T, Berdel WE: New molecular therapy targets in acute myeloid leukemia. Recent Results Cancer Res; 2007;176:243-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New molecular therapy targets in acute myeloid leukemia.
  • Despite improvements to acute myelogenous leukemia (AML) therapy during the last 25 years, the majority of patients still succumb to the disease.
  • The present chapter focuses on exciting areas of research in the field of AML therapy, including promising results with regards to recent improvements in our understanding of angiogenesis, tyrosine kinase signaling, farnesylation, cell cycling, modulation of gene expression, protein degradation, modulation of intracellular proteins, apoptosis, metabolism, and the possible retargeting of oncogenic proteins.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Leukemia, Myeloid / metabolism. Neovascularization, Pathologic / metabolism
  • [MeSH-minor] Acute Disease. Apoptosis / drug effects. Cell Cycle / drug effects. Gene Expression / drug effects. Humans. Oncogenes / drug effects. Proteins / drug effects. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors

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  • (PMID = 17607931.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Proteins; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Number-of-references] 145
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85. Jung AS, Holman PR, Castro JE, Carrier EK, Bashey A, Lane TA, Nelson CL, Pu M, Messer K, Corringham SM, Ball ED: Autologous hematopoietic stem cell transplantation as an intensive consolidation therapy for adult patients in remission from acute myelogenous leukemia. Biol Blood Marrow Transplant; 2009 Oct;15(10):1306-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autologous hematopoietic stem cell transplantation as an intensive consolidation therapy for adult patients in remission from acute myelogenous leukemia.
  • Autologous peripheral blood stem/progenitor cell transplantation (APBSCT) has been investigated as a potential therapeutic option to improve outcome in patients with acute myelogenous leukemia (AML).
  • We performed a retrospective analysis on 45 patients aged 21 to 73 years (median 51 years) with de novo AML who underwent APBSCT stratified by age, complete remission status, and cytogenetic risk.
  • In addition, there was no treatment-related mortality (TRM).
  • We conclude that APBSCT is a reasonable and safe intensive consolidation for patients with AML who do not have a suitable HLA-matched donor.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy


86. Stone R, Sekeres M, Garcia-Manero G, Lyons RM: Recent advances in low- and intermediate-1-risk myelodysplastic syndrome: developing a consensus for optimal therapy. Clin Adv Hematol Oncol; 2008 Dec;6(12):1-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recent advances in low- and intermediate-1-risk myelodysplastic syndrome: developing a consensus for optimal therapy.
  • MDS patients often develop disease-related anemia requiring chronic blood transfusion; this can lead to complications including iron overload.
  • As MDS progresses and the number of bone marrow blasts increases, the disease transforms into acute myelogenous leukemia (AML).
  • Several agents have been developed or are under investigation for the treatment of MDS, with the therapeutic goal of increasing survival and decreasing the rate of AML transformation.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / analogs & derivatives. Azacitidine / therapeutic use. Myelodysplastic Syndromes / drug therapy. Thalidomide / analogs & derivatives


87. Carneiro BA, Kaminer L, Eldibany M, Sreekantaiah C, Kaul K, Locker GY: Oxaliplatin-related acute myelogenous leukemia. Oncologist; 2006 Mar;11(3):261-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oxaliplatin-related acute myelogenous leukemia.
  • Bone marrow biopsy was consistent with therapy-related acute myelogenous leukemia.
  • It is likely that the leukemia was related to the oxaliplatin administration.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid, Acute / chemically induced
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Bevacizumab. Cecal Neoplasms / drug therapy. Cecal Neoplasms / pathology. Chromosome Deletion. Female. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Humans. Leucovorin / administration & dosage. Leucovorin / adverse effects. Middle Aged. Omentum / pathology. Organoplatinum Compounds / administration & dosage. Organoplatinum Compounds / adverse effects. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / secondary. Peritoneal Neoplasms / drug therapy. Peritoneal Neoplasms / secondary. Sigmoid Neoplasms / drug therapy. Sigmoid Neoplasms / secondary. Trisomy

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  • (PMID = 16549810.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Organoplatinum Compounds; 2S9ZZM9Q9V / Bevacizumab; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; Folfox protocol
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88. Natori K, Izumi H, Kaneko K, Ishihara S, Nagase D, Fujimoto Y, Kato M, Umeda M, Kuraishi Y: [Four cases of therapy-related leukemia in multiple myeloma]. Gan To Kagaku Ryoho; 2007 Jan;34(1):121-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Four cases of therapy-related leukemia in multiple myeloma].
  • We have experienced 4 cases of therapy-related leukemia (TRL) in 119 patients with multiple myeloma (MM) who had received combination chemotherapy including alkylating agents between 1988 and 1998.
  • All 4 cases were acute myelogenous leukemia, 3 were males and 1 was female.
  • Median age at diagnosis of MM was 60 years, and median time to TRL from diagnosis of MM was 5.5 years.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Multiple Myeloma / drug therapy. Neoplasms, Second Primary / etiology