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1. Mashita T, Shimoda T, Yoshioka H, Takahashi Y, Mitsuda M: A cat with acute myeloblastic leukemia without maturation (M1) treated with combination chemotherapy. J Vet Med Sci; 2006 Jan;68(1):97-101
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  • [Title] A cat with acute myeloblastic leukemia without maturation (M1) treated with combination chemotherapy.
  • Acute myeloblastic leukemia without maturation (M1) was diagnosed according to the FAB classification.
  • Chemotherapy was initiated with cyclophosphamide, vincristine, prednisolone, and cytosine arabinoside.

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  • (PMID = 16462128.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; EC 1.11.1.7 / Peroxidase
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2. Dimicoli S, Fohlen-Walter A, Mansuy L, Buisine J, Grégoire MJ, Lecompte T, Bordigoni P, Jonveaux P, Lesesve JF: [Acute myeloblastic leukemia without maturation (AML-M1) with basophilic elements and associated with translocation t(6;9)]. Ann Biol Clin (Paris); 2003 May-Jun;61(3):352-7
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  • [Title] [Acute myeloblastic leukemia without maturation (AML-M1) with basophilic elements and associated with translocation t(6;9)].
  • [Transliterated title] Leucémie aiguë myéloblastique sans maturation (LAM1) avec éléments basophiles associée à la translocation t(6;9).
  • The clinical, hematological, and cytogenetic data from a 4 year-old child with acute myeloid (AML-M1) and basophilia is reported.
  • This abnormality is rare and associated with myelodysplastic syndromes or with subtypes of acute myeloid leukemia (M1, M2, M4, M7), usually with preceding or underlying myelodysplasia.
  • The prognosis is poor, without response to chemotherapy regimen alone.
  • Allogeneic bone marrow transplantation appears likely to be a more appropriate treatment.
  • [MeSH-major] Basophils. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 12805015.001).
  • [ISSN] 0003-3898
  • [Journal-full-title] Annales de biologie clinique
  • [ISO-abbreviation] Ann. Biol. Clin. (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Hemoglobins
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3. Bhatla D, Gerbing RB, Alonzo TA, Mehta PA, Deal K, Elliott J, Meshinchi S, Geiger H, Perentesis JP, Lange BJ, Davies SM, Children's Oncology Group: DNA repair polymorphisms and outcome of chemotherapy for acute myelogenous leukemia: a report from the Children's Oncology Group. Leukemia; 2008 Feb;22(2):265-72
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  • [Title] DNA repair polymorphisms and outcome of chemotherapy for acute myelogenous leukemia: a report from the Children's Oncology Group.
  • Polymorphisms of DNA repair genes RAD51 and XRCC3 increase susceptibility to acute myeloid leukemia (AML) in adults, an effect enhanced by deletion of the glutathione-S-transferase M1 (GSTM1) gene.
  • In this study, we genotyped 452 children with de novo AML treated on CCG protocols 2941 and 2961 and compared genotype frequencies with those of normal blood donors, and analyzed the impact of genotype on outcome of therapy.
  • XRCC3 Thr241Met, RAD51 G135C and GSTM1 genotypes did not increase susceptibility to AML when assessed singly.
  • In contrast, when XRCC3 and RAD51 genotypes were examined together a significant increase in susceptibility to AML was seen in children with variant alleles.
  • Analysis of outcome of therapy showed that patients heterozygous for the XRCC3 Thr241Met allele had improved post-induction disease-free survival compared to children homozygous for the major or minor allele, each of whom had similar outcomes.
  • Improved survival was due to reduced relapse in the heterozygous children, and this effect was most marked in children randomized to therapy likely to generate DNA double-strand breaks (etoposide, daunomycin), compared with anti-metabolite (fludarabine, cytarabine) based therapy.
  • In contrast, RAD51 G135C and the GSTM1 deletion polymorphism did not influence outcome of AML therapy in our study population.

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  • (PMID = 18033323.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA10262-01; United States / NCI NIH HHS / CA / R01 CA093552-01; United States / NCI NIH HHS / CA / CA 98543; United States / NCI NIH HHS / CA / R01 CA114563-01; United States / NCI NIH HHS / CA / R01CA93552-01; United States / NCI NIH HHS / CA / R01 CA093552; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA093552-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 3; EC 2.7.7.- / Rad51 Recombinase
  • [Other-IDs] NLM/ NIHMS210453; NLM/ PMC2914507
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4. Ogasawara T, Yasuyama M, Kawauchi K: Therapy-related myelodysplastic syndrome with monosomy 5 after successful treatment of acute myeloid leukemia (M2). Am J Hematol; 2005 Jun;79(2):136-41
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  • [Title] Therapy-related myelodysplastic syndrome with monosomy 5 after successful treatment of acute myeloid leukemia (M2).
  • We describe a patient who developed myelodysplastic syndrome over 2 years after achieving complete remission of acute myeloid leukemia (AML).
  • The patient was treated in July 1998 with anthracycline, etoposide, and behenoyl cytarabine chemotherapy for AML (French-American-British classification, M2; World Health Organization classification, AML with maturation) and achieved complete remission.
  • The pancytopenia progressed rapidly, and he died 2 months after the diagnosis of MDS.
  • Therapy-related MDS and AML (t-MDS/t-AML) developing after treatment for acute leukemia is unusual; the primary leukemia associated with most cases of t-MDS/t-AML is acute promyelocytic leukemia (APL).
  • This unusual case suggests that AML excluding APL should be considered a primary hematologic malignancy for t-MDS/t-AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosomes, Human, Pair 5. Cytarabine / analogs & derivatives. Leukemia, Myeloid, Acute / chemically induced. Monosomy. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics


5. Sperr WR, Hauswirth AW, Florian S, Ohler L, Geissler K, Valent P: Human leukaemic stem cells: a novel target of therapy. Eur J Clin Invest; 2004 Aug;34 Suppl 2:31-40
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  • [Title] Human leukaemic stem cells: a novel target of therapy.
  • Acute myeloid leukaemia (AML) is a life-threatening haematopoietic disease that is characterized by clonal growth and the accumulation of myelopoietic progenitor cells.
  • Although AML cells only have a limited potential to undergo differentiation and maturation, each AML clone is organized in a hierarchical manner similar to normal haematopoiesis.
  • Recent data have shown that each AML clone consists of leukaemic stem cells and their progeny, and that AML stem cells differ from more mature cells in several aspects, including survival and target antigen profiles.
  • Most importantly, AML stem cells, but not their progeny, have the capacity to repopulate haematopoietic tissues with leukaemias in NOD/SCID mice.
  • Furthermore, AML stem cells are thought to be responsible for the infinite growth of leukaemias in patients with AML.
  • The phenotypic properties of AML stem cells have also been described.
  • In most cases, these cells are detectable within the CD34+, CD38-, Lin-, CD123+ subpopulation of AML cells.
  • Because of their AML-initiating and -renewing capacity and their unique phenotype, which includes several molecular targets of drug therapy, AML stem cells have recently been proposed as novel important target cell populations in the context of curative therapies.
  • The present article gives an overview of our knowledge about AML stem cells, their phenotype, and their role as a 'therapy-target' in new concepts to treat and to cure patients with AML.
  • [MeSH-major] Genetic Therapy / methods. Leukemia, Myeloid / therapy. Neoplastic Stem Cells

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  • (PMID = 15291804.001).
  • [ISSN] 0014-2972
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 108
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6. Hubeek I, Stam RW, Peters GJ, Broekhuizen R, Meijerink JP, van Wering ER, Gibson BE, Creutzig U, Zwaan CM, Cloos J, Kuik DJ, Pieters R, Kaspers GJ: The human equilibrative nucleoside transporter 1 mediates in vitro cytarabine sensitivity in childhood acute myeloid leukaemia. Br J Cancer; 2005 Dec 12;93(12):1388-94
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  • [Title] The human equilibrative nucleoside transporter 1 mediates in vitro cytarabine sensitivity in childhood acute myeloid leukaemia.
  • Cytarabine (ara-C) is the most effective agent for the treatment of acute myeloid leukaemia (AML).
  • Aberrant expression of enzymes involved in the transport/metabolism of ara-C could explain drug resistance.
  • We determined mRNA expression of these factors using quantitative-real-time-PCR in leukemic blasts from children diagnosed with de novo AML.
  • Expression of the inactivating enzyme pyrimidine nucleotidase-I (PN-I) was 1.8-fold lower in FAB-M5 as compared to FAB-M1/2 (P=0.007).
  • In conclusion, decreased expression of hENT1, which transports ara-C across the cell membrane, appears to be a major factor in ara-C resistance in childhood AML.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Cytarabine / pharmacology. Equilibrative Nucleoside Transporter 1 / physiology. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Cell Membrane. Child. Drug Resistance, Neoplasm. Gene Expression Profiling. Humans. RNA, Messenger / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 16333246.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Equilibrative Nucleoside Transporter 1; 0 / RNA, Messenger; 0 / SLC29A1 protein, human; 04079A1RDZ / Cytarabine
  • [Other-IDs] NLM/ PMC2361532
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7. Monteleone PM, Steele DA, King AK, Konefal S, Kelleher JF: Bilateral breast relapse in acute myelogenous leukemia. J Pediatr Hematol Oncol; 2001 Feb;23(2):126-9
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  • [Title] Bilateral breast relapse in acute myelogenous leukemia.
  • We present the case of an 11.5-year-old girl with M1 acute myelogenous leukemia (AML) who had isolated extramedullary relapse develop in both breasts 12 months after diagnosis and 7 months off chemotherapy.
  • She received further chemotherapy, focal radiation therapy, then underwent a matched, unrelated bone marrow transplant and continues in remission 37 months later.
  • Review of the literature revealed 10 cases in other children younger than 21-years-old with AML and breast involvement.
  • Breast involvement in AML is rare in children.
  • However, regular breast examinations should be performed as part of routine follow-up in all girls with AML.
  • [MeSH-major] Breast / pathology. Leukemia, Myeloid, Acute / pathology. Vidarabine / analogs & derivatives
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Bone Marrow Transplantation. Child. Combined Modality Therapy. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Dexamethasone / administration & dosage. Etoposide / administration & dosage. Female. Graft vs Host Disease / etiology. Humans. Idarubicin / administration & dosage. Immunologic Factors / therapeutic use. Interleukin-2 / therapeutic use. Leukemic Infiltration. Radiotherapy, High-Energy. Recurrence. Salvage Therapy. Thioguanine / administration & dosage. Transplantation Conditioning

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  • (PMID = 11216705.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunologic Factors; 0 / Interleukin-2; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; FA2DM6879K / Vidarabine; FTK8U1GZNX / Thioguanine; P2K93U8740 / fludarabine; ZRP63D75JW / Idarubicin; ZS7284E0ZP / Daunorubicin
  • [Number-of-references] 23
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8. Leung J, Pang A, Yuen WH, Kwong YL, Tse EW: Relationship of expression of aquaglyceroporin 9 with arsenic uptake and sensitivity in leukemia cells. Blood; 2007 Jan 15;109(2):740-6
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  • [Title] Relationship of expression of aquaglyceroporin 9 with arsenic uptake and sensitivity in leukemia cells.
  • Arsenic trioxide (As2O3) is highly efficacious in acute promyelocytic leukemia (APL).
  • In 10 of 11 myeloid and lymphoid leukemia lines, quantitative polymerase chain reaction (Q-PCR) and Western blotting showed that AQP9 expression correlated positively with As2O3-induced cytotoxicity.
  • Similarly, the chronic myeloid leukemia line K562 expressed low levels of AQP9 and was As2O3 insensitive.
  • Pretreatment of the myeloid leukemia line HL-60 with all-trans retinoic acid (ATRA) up-regulated AQP9, leading to a significantly increased arsenic uptake and As2O3-induced cytotoxicity on incubation with As2O3, which might explain the synergism between ATRA and As2O3.
  • Q-PCR showed that primary APL cells expressed AQP9 significantly (2-3 logs) higher than other acute myeloid leukemias (AMLs), which might explain their exquisite As2O3 sensitivity.
  • However, APL and AML with maturation expressed comparable AQP9 levels, suggesting that AQP9 expression was related to granulocytic maturation.
  • [MeSH-major] Aquaporins / metabolism. Arsenicals / pharmacology. Leukemia, Myeloid / metabolism. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / metabolism. Oxides / pharmacology
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Cell Proliferation / drug effects. Gene Expression Profiling. Humans. K562 Cells. Point Mutation. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity. Tretinoin / pharmacology. Up-Regulation / drug effects

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  • (PMID = 16968895.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AQP9 protein, human; 0 / Aquaporins; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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9. Kikuchi T, Miyata A, Fujii S, Kikuchi T: [Acute myelogenous leukemia complicated with severe tumor lysis syndrome after a single day of idarubicin/cytarabine chemotherapy]. Rinsho Ketsueki; 2003 Nov;44(11):1113-6
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  • [Title] [Acute myelogenous leukemia complicated with severe tumor lysis syndrome after a single day of idarubicin/cytarabine chemotherapy].
  • We describe a patient with acute myelogenous leukemia (AML) who was complicated with severe tumor lysis syndrome (TLS) after a single day of chemotherapy; a previously unreported occurrence.
  • A 48-year-old man was admitted because of fever and bleeding tendency, and was diagnosed as having AML: M1.
  • Chemotherapy with idarubicin and cytarabine was started.
  • On the second day of the therapy, he developed acute renal failure (ARF) and deterioration of disseminated intravascular coagulation (DIC) with a marked reduction in his WBC (8500/microliter).
  • Immediately after a diagnosis of tumor lysis syndrome (TLS), the following chemotherapy was discontinued.
  • Hemodiafiltration and hemofiltration were initiated to treat the ARF, concomitant with anticoagulant and antifibrinolysis therapy for the DIC.
  • Chemotherapy with daunorubicin and cytarabine was resumed on the 12th day, recognizing a regrowth of leukemic cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Tumor Lysis Syndrome / etiology

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  • (PMID = 14689878.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
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10. Ressel A, Trümper L, Bäsecke J: [Occlusion of the femoral arteries in de novo AML]. Med Klin (Munich); 2007 May 15;102(5):388-92
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  • [Title] [Occlusion of the femoral arteries in de novo AML].
  • [Transliterated title] Femoralarterienverschluss bei De-novo-AML.
  • BACKGROUND: Leukemic emboli in acute (AML) and chronic myelocytic leukemia (CML) are associated with hyperleukocytosis (>100,000/microl leukocytes) and most frequently detected at autopsy.
  • CASE REPORT: A 53-year-old woman was admitted with hyperleukocytosis and acute pain in her right leg.
  • An occlusion of the right femoral arteries as the presenting symptom of a de novo AML (FAB M1/WHO: AML without maturation) with hyperleukocytosis was diagnosed.
  • CONCLUSION: Leukemic emboli of large vessels are uncommon in leukemia with hyperleukocytosis.
  • Leukemic emboli mainly occur in AML and CML in blast crisis and are rare in acute (ALL) and chronic lymphocytic leukemia (CLL).
  • Therapeutic options, apart from the immediate start of chemotherapy, are leukapheresis and embolectomy.
  • [MeSH-major] Arterial Occlusive Diseases / etiology. Femoral Artery. Leukemia, Myeloid, Acute / diagnosis. Neoplastic Cells, Circulating
  • [MeSH-minor] Angiography. Blood Coagulation Tests. Diagnosis, Differential. Female. Granulocyte Precursor Cells / pathology. Humans. Leukocyte Count. Leukocytosis / diagnosis. Leukocytosis / pathology. Middle Aged

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  • (PMID = 17497090.001).
  • [ISSN] 0723-5003
  • [Journal-full-title] Medizinische Klinik (Munich, Germany : 1983)
  • [ISO-abbreviation] Med. Klin. (Munich)
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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11. Jelić-Puskarić B, Ostojić-Kolonić S, Planinc-Peraica A, Obad-Kovacević D, Kardum-Skelin I, Jaksić B: Myeloid sarcoma involving the breast. Coll Antropol; 2010 Jun;34(2):641-4
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  • [Title] Myeloid sarcoma involving the breast.
  • Myeloid sarcoma is a tumor mass with extramedullary growth pattern, composed of myeloblasts or immature myeloid cells.
  • The development of myeloid sarcoma may precede or concur with acute or chronic myeloid leukemia (AML or CML) or other myeloproliferative diseases or myelodysplastic syndromes (MDS).
  • Isolated myeloid sarcoma of the breast is very rare.
  • Based on the morphology, cytochemical characteristics and immature cell immunophenotype, it was considered a case of acute myeloid leukemia without maturation.
  • In spite of intensive chemotherapy, the patient died within a year of diagnosis.
  • In cases of isolated breast myeloid sarcoma, the diagnosis can be missed if the possibility of myeloid sarcoma is not remembered on differential diagnosis of a breast neoplasm.
  • [MeSH-major] Breast Neoplasms / pathology. Sarcoma, Myeloid / pathology
  • [MeSH-minor] Adult. Anemia / etiology. Anemia / pathology. Biopsy, Fine-Needle. Bone Marrow / pathology. Fatal Outcome. Female. Humans. Leukemia, Myeloid, Acute / pathology. Leukocytosis / etiology. Leukocytosis / pathology. Recurrence. Thrombocytopenia / etiology. Thrombocytopenia / pathology

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  • (PMID = 20698144.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Croatia
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12. Li S, Zhang L, Kern WF, Andrade D, Forsberg JE, Bates FR, Mulvihill JJ: Identification of t(15;17) and a segmental duplication of chromosome 11q23 in a patient with acute myeloblastic leukemia M2. Cancer Genet Cytogenet; 2002 Oct 15;138(2):149-52
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  • [Title] Identification of t(15;17) and a segmental duplication of chromosome 11q23 in a patient with acute myeloblastic leukemia M2.
  • A 32-year-old man was newly diagnosed with acute myelocytic leukemia, classified as acute myeloblastic leukemia with maturation (AML-M2) according to the French-American-British classification system.
  • Conventional chromosome analysis before chemotherapy treatment revealed an abnormal karyotype: a possible segmental duplication of 11q23, plus a translocation between chromosomes 15 and 17 [t(15;17) (q22;q21.1)] in the majority of cells analyzed.
  • To our knowledge, this is the first report of a combination of t(15;17) and a segmental duplication of 11q23 in a patient with AML-M2.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics. Gene Duplication. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 12505261.001).
  • [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
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13. Guo C, Inghirami G, Ibrahim S, Sen F: Epistaxis and severe weakness in a patient with multiple myeloma. Therapy-related acute myeloid leukemia, pure erythroid leukemia. Arch Pathol Lab Med; 2006 Jul;130(7):1075-6
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  • [Title] Epistaxis and severe weakness in a patient with multiple myeloma. Therapy-related acute myeloid leukemia, pure erythroid leukemia.
  • Therapy-related acute myeloid leukemias arise as a result of cytotoxic chemotherapy and/or radiation therapy.
  • The most common types of acute myeloid leukemia arising in this setting are acute myeloid leukemia with maturation, and lesser numbers of acute myelomonocytic leukemia, acute monocytic leukemia, acute erythroleukemia, or acute megakaryocytic leukemia.
  • We present a patient with multiple myeloma who was treated with melphalan and 4 years later developed acute erythroid leukemia.
  • The morphologic diagnosis of pure erythroid leukemia developing in the setting of multiple myeloma may be challenging.
  • [MeSH-major] Epistaxis / complications. Leukemia, Erythroblastic, Acute / complications. Multiple Myeloma / complications. Muscle Weakness / complications
  • [MeSH-minor] Acute Disease. Aged, 80 and over. Antineoplastic Agents, Alkylating / adverse effects. Humans. Leukemia, Myeloid. Male. Melphalan / adverse effects

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  • (PMID = 16831041.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; Q41OR9510P / Melphalan
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14. Wong KF, Yuen HL, Siu LL, Pang A, Kwong YL: t(8;16)(p11;p13) predisposes to a transient but potentially recurring neonatal leukemia. Hum Pathol; 2008 Nov;39(11):1702-7
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  • [Title] t(8;16)(p11;p13) predisposes to a transient but potentially recurring neonatal leukemia.
  • A Chinese girl presented with generalized papular rash and monocytic leukemia 19 days after birth.
  • Cytogenetic analysis showed t(8;16)(p11.2;p13.3) as the sole chromosomal abnormality.
  • Spontaneous regression of the leukemia was observed after 2 months, although the t(8;16) translocation persisted cytogenetically.
  • This was followed 7 months later by the development of acute myeloid leukemia with maturation and cytogenetic evolution with extra chromosomes 4 and 8.
  • Molecular study showed that the reciprocal MYST3 and CREBBP gene fusion characteristic of t(8;16) translocation persisted throughout the clinical course, even during spontaneous regression of the neonatal leukemia, and after chemotherapy-induced remission of the subsequent acute myeloid leukemia.
  • The possible role of MYST3 and CREBBP gene fusion in the pathogenesis of the leukemia is discussed.
  • [MeSH-major] Leukemia, Monocytic, Acute / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 18657848.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CREBBP protein, human; EC 2.3.1.48 / CREB-Binding Protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human
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15. McGrattan P, Alexander HD, Humphreys MW, Kettle PJ: Tetrasomy 13 as the sole cytogenetic abnormality in acute myeloid leukemia M1 without maturation. Cancer Genet Cytogenet; 2002 Jun;135(2):192-5
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  • [Title] Tetrasomy 13 as the sole cytogenetic abnormality in acute myeloid leukemia M1 without maturation.
  • We report a case of acute myeloid leukemia (AML) M1 showing a 48,XY,+13,+13 karyotype.
  • Treatment was according to the Medical Research Council AML14 trial protocol with two courses of DAT chemotherapy.
  • Tetrasomy 13 as the sole cytogenetic abnormality has not been reported previously in M1 AML and has only been reported in three other AML cases, all with an immature phenotype and poor outcome.
  • [MeSH-major] Aneuploidy. Chromosomes, Human, Pair 13. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Drug Resistance, Neoplasm. Fatal Outcome. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Male. Middle Aged. Thioguanine / administration & dosage. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 12127406.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; FTK8U1GZNX / Thioguanine; ZS7284E0ZP / Daunorubicin; DAT protocol 1; FLAG protocol
  • [Number-of-references] 10
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16. Yan ZQ, Bolognesi MP, Steeber DA, Tedder TF, Chen LE, Seaber AV, Urbaniak JR: Blockade of L-selectin attenuates reperfusion injury in a rat model. J Reconstr Microsurg; 2000 Apr;16(3):227-33
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  • Using a rat extensor digitorum longus (EDL) muscle model, the present study tested the hypothesis that in vivo administration of the function-blocking monoclonal antibody (mAb) LAM1-116 which recognizes L-selectin, a cell-surface adhesion receptor, could decrease I/R injury.
  • In 46 rats, one EDL served as a normal control and the opposite EDL underwent 3 hr of ischemia followed by 3 hr of reperfusion after pretreatment with LAM1-116 mAb, control IgG, or saline.
  • Myeloperoxidase (MPO) activity showed only a two-fold increase from normal in LAM1-116-treated I/R EDL while a 27-fold increase occurred in the IgG2a and saline groups, with a statistically significant (p < 0.001) difference.
  • A significantly (p < 0.05) lower wet weight ratio, improved fatigue contractile force, and less neutrophil infiltration were found in LAM1-116-treated EDL, when compared to those in control IgG- or saline-treated EDL.
  • The results indicate that blockade of L-selectin by LAM1-116 mAb can effectively reduce neutrophil infiltration in reperfused skeletal muscle, thereby decreasing tissue edema and improving muscle fatigue contractile force.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. L-Selectin / drug effects. Peroxidase / metabolism. Reperfusion Injury / drug therapy
  • [MeSH-minor] Animals. Disease Models, Animal. Dose-Response Relationship, Drug. Female. Immunoglobulin G / metabolism. Immunoglobulin G / pharmacology. Leukocyte Count / drug effects. Muscle Contraction / drug effects. Muscle, Skeletal / pathology. Organ Size / drug effects. Rats. Rats, Sprague-Dawley. Reference Values. Sensitivity and Specificity

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  • (PMID = 10803628.001).
  • [ISSN] 0743-684X
  • [Journal-full-title] Journal of reconstructive microsurgery
  • [ISO-abbreviation] J Reconstr Microsurg
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI-26872; United States / NHLBI NIH HHS / HL / HL 36046; United States / NHLBI NIH HHS / HL / HL-50985; etc
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoglobulin G; 126880-86-2 / L-Selectin; EC 1.11.1.7 / Peroxidase
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17. Graf M, Hecht K, Reif S, Pelka-Fleischer R, Pfister K, Schmetzer H: Expression and prognostic value of hemopoietic cytokine receptors in acute myeloid leukemia (AML): implications for future therapeutical strategies. Eur J Haematol; 2004 Feb;72(2):89-106
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  • [Title] Expression and prognostic value of hemopoietic cytokine receptors in acute myeloid leukemia (AML): implications for future therapeutical strategies.
  • There is evidence to suggest, that those receptors (R) could play a role in leukemia with respect to cell differentiations and its regulation, prognosis, and pathobiology.
  • Knowledge of individual cytokine receptor (CKR) profiles could provide new discoveries about CKR-supported therapeutic considerations.
  • METHODS: We have studied the expression of CKR on mononuclear bone marrow (BM) cells of 89 patients with acute myeloid leukemia (AML) at first diagnosis, three patients at relapse or with persisting AML and eight healthy probands by fluorescence-activated cell sorting (FACS) analysis using directly fluorescein-conjugated antibodies: CD114 (hG-CSF-R), CD116 (hGM-CSF-R), CD117 (hSCF-R), CD123 (hIL-3-R), CD130 (gp130subunit), CD135 (hFL-R).
  • RESULTS: All investigated CKR were more frequently expressed in AML-samples than in healthy BM-samples, except CD130, which was only expressed on 5-6% of AML-blasts in all and with only one healthy BM-sample being CD130(+).
  • Within the French-American-British (FAB) types we observed a maturation- and lineage (granulocytic/monocytic)-committed expression profile.
  • Monocytic subtypes (FAB-type M4/M5) showed significantly more GM-CSF-R(+) (P = 0.001) and FL-R(+) (P = 0.001) and significantly less stem cell factor-R (SCF-R(+)) (P = 0.02) cases.
  • Highest proportions of G-CSF-R(+) blasts were observed in FAB-type M3.
  • In undifferentiated leukemias (FAB-type M1, M2) high amounts of SCF-R(+), IL-3-R(+), and FL-R(+) blasts could be detected.
  • FL-R was the only CKR, which was positive in FAB-type M0 (n = 2).
  • For clinical evaluation only patients treated by the AML-CG-protocol, were included (n = 53).
  • CONCLUSION: We can conclude, that CKR-expression in AML is maturation- and lineage-committed and the proportions of especially early acting CKR have influence on relapse-free survival probability of AML-patients, independently of the karyotype.
  • With respect to the individual CKR status the benefit of cytokines as priming agents, as agents to treat neutropenia or to influence the metabolism of chemotherapy can be discussed under new points of view.
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology. Receptors, Cytokine / blood
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Bone Marrow Cells / immunology. Bone Marrow Cells / pathology. Female. Humans. Male. Middle Aged. Predictive Value of Tests. Prognosis. Recurrence. Time Factors


18. Watanabe A, Koike K, Fukushima T, Izumi I, Ohba K, Tsuchida M: [Complex translocation (8;15;21) (q22;p12;q22) in a child with AML-M2 showing de novo appearance of the short form of AML1-MTG8 chimeric mRNA during the course]. Rinsho Ketsueki; 2001 Feb;42(2):110-4
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  • [Title] [Complex translocation (8;15;21) (q22;p12;q22) in a child with AML-M2 showing de novo appearance of the short form of AML1-MTG8 chimeric mRNA during the course].
  • A 4-year-old boy admitted with exophthalmos was diagnosed as having acute myeloblastic leukemia with maturation (AML-M2).
  • During chemotherapy, RT-PCR demonstrated the short form of AML1-MTG8 mRNA, in addition to chimeric mRNA of the usual length.
  • A literature search failed to reveal any similar cases of t(8;21) AML-M2 associated with this deletion of chimeric mRNA.
  • [MeSH-major] Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. RNA, Messenger / genetics. Translocation, Genetic

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  • (PMID = 11280916.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / RNA, Messenger
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19. Baines P, Fisher J, Truran L, Davies E, Hallett M, Hoy T, Burnett AK: The MEK inhibitor, PD98059, reduces survival but does not block acute myeloid leukemia blast maturation in vitro. Eur J Haematol; 2000 Apr;64(4):211-8
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  • [Title] The MEK inhibitor, PD98059, reduces survival but does not block acute myeloid leukemia blast maturation in vitro.
  • The appearance of blasts in acute myeloid leukemia (AML) reflects a shift from cellular processes inducing maturation and cell death to those favouring survival and accumulation.
  • We have monitored changes in the growth factor signalling molecule MAPKinase, in the cytoprotective protein Bcl-2 and in the cell death protein Bax, during maturation of proliferating and non-proliferating AML blasts in vitro.
  • Eighteen AML samples were cultured for 7 d in serum-free medium with or without a supplement of recombinant cytokines comprising c-kit ligand, IL3 and GMCSF.
  • Maturation of AML blasts, as assessed by morphology on Romanowsky-stained slides of 7/18 samples and by changes in surface CD markers on all 18 leukemias, occurred in both the absence and presence of cytokines.
  • Immunoblotting demonstrated that ERK was briefly phosphorylated after seeding AML blasts into culture.
  • PD98059, an inhibitor of MAPKinase kinase (MEK) which activates MAPKinase, inhibited this transient ERK phosphorylation but was unable to block maturation as measured by acquisition of CD15 in samples from 12 patients with low starting numbers of CD15-positive cells.
  • PD98059, however, reduced cell numbers in 7-d liquid culture and, in cytokine-supplemented cultures, this was associated with a 1.3-fold increase in Bcl-2 (p = 0.012) and a 1.4-fold increase in Bax (p = 0.02).
  • The MAPKinase pathway is not required for this maturation, but it does maintain cell viability in the absence or presence of cytokines.
  • A rise in Bcl-2 may not protect AML blasts in the face of elevated Bax.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Flavonoids / pharmacology. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Adult. Aged. Calcium-Calmodulin-Dependent Protein Kinases / antagonists & inhibitors. Cell Differentiation / drug effects. Cell Survival / drug effects. Female. Humans. Male. Middle Aged. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Signal Transduction / drug effects. Tumor Cells, Cultured. bcl-2-Associated X Protein

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  • (PMID = 10776691.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] DENMARK
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / BAX protein, human; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
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20. Inuzuka M, Tokura Y: Sterile suppurative folliculitis associated with acute myeloblastic leukaemia. Br J Dermatol; 2002 May;146(5):904-7
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  • [Title] Sterile suppurative folliculitis associated with acute myeloblastic leukaemia.
  • A 20-year-old woman presented with a 4-month history of follicular papules distributed over the trunk and extremities.
  • One month later, routine blood tests were abnormal, showing acute myeloblastic leukaemia (M1 in the French-American-British classification).
  • The follicular eruption improved promptly in response to chemotherapy for the leukaemia.
  • We suggest that this case may represent a rare, follicular variant of neutrophilic dermatosis associated with myelogenous leukaemia.
  • [MeSH-major] Folliculitis / etiology. Leukemia, Myeloid, Acute / complications. Sweet Syndrome / etiology
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Follow-Up Studies. Humans

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  • (PMID = 12000394.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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21. Drabkin HA, Parsy C, Ferguson K, Guilhot F, Lacotte L, Roy L, Zeng C, Baron A, Hunger SP, Varella-Garcia M, Gemmill R, Brizard F, Brizard A, Roche J: Quantitative HOX expression in chromosomally defined subsets of acute myelogenous leukemia. Leukemia; 2002 Feb;16(2):186-95
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  • [Title] Quantitative HOX expression in chromosomally defined subsets of acute myelogenous leukemia.
  • We used a degenerate RT-PCR screen and subsequent real-time quantitative RT-PCR assays to examine the expression of HOX and TALE-family genes in 34 cases of chromosomally defined AML for which outcome data were available.
  • Higher levels of expression were also observed in the FAB subtype, AML-M1.
  • While we did not detect any significant correlations between HOX expression and complete response rates or age in this limited set of patients, there was a significant correlation between event-free survival and HOXA7 with a trend toward significance for HoxA9, HoxA4 and HoxA5.
  • Thus, although HOX overexpression and clinical resistance to chemotherapy often coincide, they are not inextricably linked.
  • Our results indicate that quantitative HOX analysis has the potential to add new information to the management of patients with AML, especially where characteristic chromosomal alterations are lacking.
  • [MeSH-major] Gene Expression Profiling / methods. Gene Expression Regulation, Leukemic. Genes, Homeobox. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Chromosome Aberrations. Chromosomes, Human / genetics. Computer Systems. DNA Primers. Female. Follow-Up Studies. Gene Amplification. Homeodomain Proteins / biosynthesis. Humans. Male. Middle Aged. Multigene Family. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. ROC Curve. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Treatment Outcome

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  • (PMID = 11840284.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Homeodomain Proteins; 0 / Neoplasm Proteins
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22. Fujii S, Miyata A, Kikuchi T, Kibata M: [An elderly case of acute myelocytic leukemia complicated with bleeding gastric angiodysplasia, successfully treated with topical endoscopic polidocanol injection]. Nihon Ronen Igakkai Zasshi; 2004 May;41(3):334-8
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  • [Title] [An elderly case of acute myelocytic leukemia complicated with bleeding gastric angiodysplasia, successfully treated with topical endoscopic polidocanol injection].
  • A 72-year-old man with acute myelocytic leukemia (AML) suffered relapsing massive bleeding from gastric angiodysplasia.
  • He had hypercellular (nucleated cell count 42 x 10(4)/microl) bone marrow with 90% myeloblasts, and AML (FAB: M1) was diagnosed.
  • Remission induction therapy by BHAC/DM regimen failed.
  • While considering subsequent regimens, massive hematemesis from a solitary gastric angiodysplasia developed.
  • After achievement of complete remission by CAG therapy, he was treated on an outpatient basis.
  • In July, his AML relapsed and he was treated mainly by transfusion therapy.
  • In September, hematemesis recurred resulting in hemostasis with the same procedure.
  • In this case, topical injection of polidocanol was an effective procedure for the massive bleeding from it even in an elderly patient with the complication of thrombocytopenia due to AML.
  • [MeSH-major] Angiodysplasia / complications. Gastrointestinal Hemorrhage / drug therapy. Leukemia, Myeloid, Acute / complications. Polyethylene Glycols / administration & dosage. Stomach Diseases / complications


23. Srivastava MD, Ambrus JL: Effect of 1,25(OH)2 Vitamin D3 analogs on differentiation induction and cytokine modulation in blasts from acute myeloid leukemia patients. Leuk Lymphoma; 2004 Oct;45(10):2119-26
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  • [Title] Effect of 1,25(OH)2 Vitamin D3 analogs on differentiation induction and cytokine modulation in blasts from acute myeloid leukemia patients.
  • In acute myeloid leukemia (AML), cell proliferation and differentiation are uncoupled, causing a maturation block.
  • Induction of terminal differentiation is a potential therapeutic strategy.
  • We investigated 1alpha, 25(OH)2 Vitamin D3 and 5 of its more potent analogs with reduced calcium resorbing activity for differentiation of blast cells from AML (FAB M1) patients, compared to TPA.
  • Vitamin D3 and its analogs can induce differentiation of primary cells from AML patients in vitro, but may need to be combined with other agents for terminal differentiation of blasts and effective therapy in vivo.
  • [MeSH-major] Calcitriol / analogs & derivatives. Cell Differentiation / drug effects. Cytokines / antagonists & inhibitors. Granulocyte Precursor Cells / drug effects. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Acute Disease. Cell Adhesion. Cells, Cultured. Dose-Response Relationship, Drug. Humans. Interleukin-6 / antagonists & inhibitors. Interleukin-8 / antagonists & inhibitors. Structure-Activity Relationship

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  • (PMID = 15370259.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-6; 0 / Interleukin-8; FXC9231JVH / Calcitriol
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24. Makita K, Ohta K, Mugitani A, Hagihara K, Ohta T, Yamane T, Hino M: Acute myelogenous leukemia in a donor after granulocyte colony-stimulating factor-primed peripheral blood stem cell harvest. Bone Marrow Transplant; 2004 Mar;33(6):661-5
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  • [Title] Acute myelogenous leukemia in a donor after granulocyte colony-stimulating factor-primed peripheral blood stem cell harvest.
  • This article describes the first case of acute myeloid leukemia (AML) in a healthy donor at 14 months after granulocyte colony-stimulating factor (G-CSF)-primed peripheral blood stem cell (PBSC) harvest.
  • In November 2002, the donor, admitted with high fever and leukocytosis with 98.5% blastoid cells, was diagnosed as having AML (M1).
  • Her leukemia cells were positive for CD13, CD33, and G-CSF receptor without chromosomal abnormality and responded to G-CSF in vitro.
  • During chemotherapy, she died of progressive pneumonia.
  • If our case is truly the first, the incidence of leukemia in donors may not be higher than that of naturally occurring leukemia.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / therapeutic use. Hematopoietic Stem Cell Mobilization / adverse effects. Leukemia, Myeloid, Acute / diagnosis. Tissue Donors
  • [MeSH-minor] Female. Humans. Male. Middle Aged. Multiple Myeloma / therapy. Recombinant Proteins. Tissue and Organ Harvesting

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  • (PMID = 14716337.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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25. Øyan AM, Bø TH, Jonassen I, Gjertsen BT, Bruserud Ø, Kalland KH: cDNA microarray analysis of non-selected cases of acute myeloid leukemia demonstrates distinct clustering independent of cytogenetic aberrations and consistent with morphological signs of differentiation. Int J Oncol; 2006 May;28(5):1065-80
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  • [Title] cDNA microarray analysis of non-selected cases of acute myeloid leukemia demonstrates distinct clustering independent of cytogenetic aberrations and consistent with morphological signs of differentiation.
  • Acute myeloid leukemia (AML) is a heterogeneous disease with respect to biology and clinical course.
  • Until now the basis for prognostic evaluation and therapeutic decision has been the karyotype, genetic FLT3 abnormalities and the initial chemotherapy response.
  • In an attempt to address this question, we performed cDNA microarray analysis on peripheral blood samples of 25 patients with newly diagnosed AML with high blast counts.
  • Leave-one-out crossvalidation (LOOCV) showed with high accuracy that gene expression classifiers could predict if leukaemia samples belonged to the FAB AML-M1 or to the FAB AML-M2 groups.
  • Except for an accumulation of samples classified as FAB M1 and M2 in cluster 3, there was no evident relationship between the clusters and the FAB classification.
  • Each subgroup displayed clearly distinguished gene expression patterns validated using real-time quantitative PCR analysis.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Oligonucleotide Array Sequence Analysis


26. Nishikawa M, Yamamoto M, Watanabe Y, Kita K, Shiku H: Clinical significance of low protein phosphatase-1 activity of blasts in acute myelogenous leukemia with high white cell counts. Int J Oncol; 2001 Mar;18(3):559-65
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  • [Title] Clinical significance of low protein phosphatase-1 activity of blasts in acute myelogenous leukemia with high white cell counts.
  • To determine the clinical importance of PP1 expression, we compared PP1 activity of leukemic blasts with other putative prognostic factors in 46 patients with acute myelogenous leukemia (AML) who were treated with remission induction chemotherapy.
  • PP1 was ubiquitously but differently expressed in various FAB subtypes (M1-M5), although PP1 activity was significantly higher in blasts of AML-M4 than in AML-M2.
  • PP1 activity was significantly lower in elderly patients > or =55 years (P=0.005), and in those with high white cell counts > or =100,000/microl (P=0.039) at initial diagnosis.
  • Correlation was observed between PP1 activity (<0.15 vs > or =0.15 nmol/min/10(8) cells) and prognosis of AML patients.
  • The median overall survival was 8 months for patients with low PP1 activity compared to 27 months for those with high PP1 activity in their AML cells.
  • This preliminary study suggests that low PP1 activity may be associated with shortened survival time for AML patients with high white cell counts.
  • [MeSH-major] Leukemia, Myeloid, Acute / enzymology. Leukocytosis / enzymology. Phosphoprotein Phosphatases / metabolism
  • [MeSH-minor] Antigens, CD34 / metabolism. Antineoplastic Agents / therapeutic use. Cytosol / physiology. Female. Humans. Leukocyte Count. Male. Middle Aged. Prognosis. Protein Phosphatase 1. Remission Induction. Survival Analysis. Treatment Outcome

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  • (PMID = 11179487.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 1
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27. Suzuki A, Kimura Y, Ohyashiki K, Kitano K, Kageyama S, Kasai M, Miyawaki S, Ohno R: Trisomy 10 in acute myeloid leukemia. Three additional cases from the database of the Japan Adult Leukemia Study Group (JALSG) AML-92 and AML-95. Cancer Genet Cytogenet; 2000 Jul 15;120(2):141-3
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  • [Title] Trisomy 10 in acute myeloid leukemia. Three additional cases from the database of the Japan Adult Leukemia Study Group (JALSG) AML-92 and AML-95.
  • To clarify the clinical and hematologic features of a rare numerical chromosome abnormality, we searched for trisomy 10 in acute myelogenous leukemias (AMLs) using the database of the Japan Adult Leukemia Study Group (JALSG) AML 92 and 95.
  • Among the sequentially registered patients of JALSG-AML 92 (655 patients) and JALSG-AML 95 (531 patients), chromosome results were obtained in 1,074 patients (90.6%), and we found 3 patients with trisomy 10 as a sole abnormality.
  • The first patient had an AML-M1 morphology with CD7 antigen; the patient obtained complete remission (CR) with the first course of chemotherapy.
  • The second patient had an AML-M1 morphology without expressing CD7 antigen; this patient obtained CR, but relapsed 3 months later, and underwent allogeneic bone marrow transplantation.
  • He suffered from chronic graft-versus-host disease and expired 38 months after the AML diagnosis.
  • The third patient had AML-M0 with CD7 positivity.
  • In the literature, the mean age of patients with trisomy 10 AML is 57.8 years, the gender ratio is M/F = 1.5, and the frequency of M0/M1/M2 is 85.7%.
  • 8%) of CD7 expression of leukemia cells is notable.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Leukemia, Myeloid, Acute / genetics. Trisomy


28. Lesesve JF, Dugué F, Grégoire MJ, Witz F, Dror Y: Shwachman-Diamond syndrome with late-onset neutropenia and fatal acute myeloid leukaemia without maturation: a case report. Eur J Haematol; 2003 Nov;71(5):393-5
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  • [Title] Shwachman-Diamond syndrome with late-onset neutropenia and fatal acute myeloid leukaemia without maturation: a case report.
  • We report on a male patient affected by Shwachman Diamond syndrome (SDS) who presented an unusual delayed neutropenia and then developed a poorly differentiated acute myeloid leukaemia (M0-AML) with trilineage myelodysplasia in adulthood.
  • The patient was treated with conventional chemotherapy but never reached complete remission of leukaemia and died 18 months after diagnosis.
  • SDS is an inherited bone marrow failure syndrome with a high propensity to leukaemic transformation.
  • [MeSH-major] Exocrine Pancreatic Insufficiency / complications. Leukemia, Myeloid / etiology. Neutropenia / etiology
  • [MeSH-minor] Acute Disease. Cell Differentiation. Child. Fatal Outcome. Genetic Predisposition to Disease. Humans. Male. Pancytopenia / etiology. Sepsis / etiology. Syndrome

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  • (PMID = 14667205.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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29. Murohashi I, Yoshida K, Kishimoto K, Takahashi T, Wakao D, Jinnai I, Yagasaki F, Kawai N, Suzuki T, Matsuda A, Hirashima K, Bessho M: Differential response to stem cell factor and Flt3 ligand by the FAB subtype in acute myeloid leukemia clonogenic cells. J Interferon Cytokine Res; 2002 Mar;22(3):335-41
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  • [Title] Differential response to stem cell factor and Flt3 ligand by the FAB subtype in acute myeloid leukemia clonogenic cells.
  • Proliferative response of blast clonogenic cells to various hematopoietic growth factors (HGF), including stem cell factor (SCF) and flt3 ligand (FL) was investigated in 100 patients with acute myeloid leukemia (AML) and chronic myelogenous leukemia (CML) in myeloid crisis (MC).
  • The frequency of spontaneous colony formation was significantly high in CML in MC (55%) and AML French-American-British (FAB) subtype M4 (48%) compared with M2 (16%).
  • No spontaneous colony was formed in any of the patients with M1 and M3.
  • The frequency of proliferative response to various HGF alone and in combination according to FAB subtype and CML in MC was as follows: that to granulocyte colony-stimulating factor (G-CSF) was lowest in M1 and CML in MC (50%) compared with other FAB subtypes (>or=86%), that to granulocyte-macrophage CSF (GM-CSF) was lowest in CML in MC (44%) compared with FAB subtypes (>or=74%), and that to interleukin-3 (IL-3) was lowest in CML in MC (30%) compared with FAB subtypes (>or=78%).
  • The frequency of proliferative response to both SCF and FL increased in the order of M1 (33%), M2 (63%), M4-5 (95%), and M6 (100%).
  • M1 and M2 were intermediate between CML in MC and M4-6.
  • The relation between in vitro growth pattern of blast clonogenic cells and prognosis in AML FAB subtype and CML in MC is discussed.
  • [MeSH-major] Leukemia, Myeloid / drug therapy. Leukemia, Myelomonocytic, Acute / drug therapy. Membrane Proteins / pharmacology. Stem Cell Factor / pharmacology
  • [MeSH-minor] Acute Disease. Blast Crisis / drug therapy. Blast Crisis / pathology. Cell Division / drug effects. Clone Cells. Granulocyte Colony-Stimulating Factor / pharmacology. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Interleukin-3 / pharmacology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Recombinant Proteins / pharmacology. Retrospective Studies. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 12034041.001).
  • [ISSN] 1079-9907
  • [Journal-full-title] Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
  • [ISO-abbreviation] J. Interferon Cytokine Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-3; 0 / Membrane Proteins; 0 / Recombinant Proteins; 0 / Stem Cell Factor; 0 / Tumor Necrosis Factor-alpha; 0 / flt3 ligand protein; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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30. Suzuki A, Ohyashiki K, Kimura Y, Yamada H, Sano F, Miyawaki S, Kuriyama K, Ohno R, Japan Adult Leukemia Study Group: Trisomy 11 acute myeloid leukemia: 5 additional cases from the Japan Adult Leukemia Study Group AML-92 and AML-95 databases. Int J Hematol; 2000 Dec;72(4):466-9
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  • [Title] Trisomy 11 acute myeloid leukemia: 5 additional cases from the Japan Adult Leukemia Study Group AML-92 and AML-95 databases.
  • We searched for trisomy 11 in acute myelogenous leukemia (AML) patients using the Japan Adult Leukemia Study Group (JALSG) AML-92 and -95 databases to clarify the clinical and hematologic features of a rare numerical chromosome abnormality.
  • Among the sequentially registered patients of JALSG AML-92 (655 patients) and JALSG AML-95 (531 patients), chromosome findings were obtained for 1074 patients (90.6%); we found 5 patients with trisomy 11 as the sole abnormality.
  • The patients were 4 women and 1 man with trisomy 11 AML, all aged more than 45 years (median, 52 years), with 4 M1 morphologies and 1 M2.
  • No patients manifested hepatosplenomegaly or lymph node enlargement, and no central nervous system leukemia or extramedullary lesions were detectable.
  • Except for 1 patient, all achieved complete remission after 1 course of induction chemotherapy, but 2 relapsed after discontinuation of chemotherapy.
  • A third case of relapse occurred during intensification of chemotherapy, and the patient underwent allogenic bone marrow transplantation but died from interstitial pneumonia.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid / genetics. Trisomy / pathology
  • [MeSH-minor] Acute Disease. Aged. Databases, Factual. Female. Humans. Immunophenotyping. Japan. Male. Middle Aged


31. Thiébaut A, Thomas X, Belhabri A, Anglaret B, Archimbaud E: Impact of pre-induction therapy leukapheresis on treatment outcome in adult acute myelogenous leukemia presenting with hyperleukocytosis. Ann Hematol; 2000 Sep;79(9):501-6
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  • [Title] Impact of pre-induction therapy leukapheresis on treatment outcome in adult acute myelogenous leukemia presenting with hyperleukocytosis.
  • Acute myeloid leukemia (AML) presenting with hyperleukocytosis is generally of poor prognosis due to an increased early death rate and a lower response to initial chemotherapy.
  • Between April 1985 and December 1995, all patients with newly diagnosed AML admitted to our institution with an initial white blood cell (WBC) count greater than 100 x 10(9)/l were scheduled to undergo leukapheresis.
  • Morphologic subtypes, according to the French-American-British classification, showed 3 M0, 16 M1, 6 M2, 10 M4, 16 M5, and 2 unclassified cases of AML.
  • The median WBC count at the time of starting chemotherapy was 85 x 10(9)/l (range 23-264 x 10(9)/l).
  • In this study, early death rate is lower than data previously published in the literature and almost all patients could receive chemotherapy.
  • This might suggest a benefit of initial leukapheresis in the treatment of AML presenting with hyperleukocytosis.
  • [MeSH-major] Leukapheresis. Leukemia, Myeloid, Acute / therapy. Leukocytosis / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Treatment Outcome

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  • (PMID = 11043421.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] GERMANY
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32. Reisch N, Roehnisch T, Sadeghi M, Greiner L, Regenbogen C, Rieger J, Emmerich B, Oduncu F: AML M1 presenting with recurrent acute large arterial vessel thromboembolism. Leuk Res; 2007 Jun;31(6):869-71
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  • [Title] AML M1 presenting with recurrent acute large arterial vessel thromboembolism.
  • Acute leukemia may be associated with coagulopathy, predominantly severe bleeding diathesis caused by disseminated intravascular coagulation (DIC) and/or hyperfibrinolysis.
  • Disordered hemostasis is characteristic for acute promyelocytic leukemia (APL, FAB M3).
  • We report a case of severe recurrent acute arterial thromboembolism at presentation in AML FAB M1.
  • Most likely, the ischemic events in our patient resulted from leukemia as the thrombus material included many leukemic blasts.
  • Despite leg amputation just a couple of hours before and extremely high infectious risk of the patient, chemotherapy was administered.
  • The clinical course of cessation of the ischemic events and a fast reduction of the blasts in the peripheral blood smear after chemotherapeutic treatment of the patient outlines the importance and life saving role of early chemotherapy even under adverse circumstances.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Thromboembolism / etiology
  • [MeSH-minor] Adult. Amputation. Disseminated Intravascular Coagulation / etiology. Female. Hemorrhagic Disorders / etiology. Humans. Iliac Artery / pathology. Iliac Artery / radiography. Ischemia / etiology. Ischemia / pathology. Ischemia / radiography. Ischemia / surgery. Leg / blood supply. Leg / pathology. Leg / radiography. Leg / surgery. Leukemia, Promyelocytic, Acute / complications

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  • (PMID = 17011031.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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33. Chelghoum Y, Danaïla C, Belhabri A, Charrin C, Le QH, Michallet M, Fiere D, Thomas X: Influence of cigarette smoking on the presentation and course of acute myeloid leukemia. Ann Oncol; 2002 Oct;13(10):1621-7
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  • [Title] Influence of cigarette smoking on the presentation and course of acute myeloid leukemia.
  • BACKGROUND: It is known that cigarette smoking is associated with an approximately 50% increase in leukemia risk.
  • In order to detect a possible influence of cigarette smoking on initial characteristics at the time of presentation and on the course of the disease, we conducted a retrospective study in 643 patients with newly diagnosed acute myeloid leukemia.
  • RESULTS: Cigarette smoking was significantly related to male gender (P <0.0001), professional occupancy (P = 0.002), presence of organomegaly (P = 0.01), and lower peripheral blood and bone marrow leukemic cell involvement (P = 0.007 and P = 0.0001, respectively).
  • Leukemia of French-American-British (FAB) M1 subtype was more frequent in non-smokers (P = 0.005).
  • However, a higher rate of severe pulmonary infection was observed in smokers during induction chemotherapy (P = 0.02).
  • Other characteristics associated with poor prognosis included mainly older age, unfavorable karyotype, secondary acute myeloid leukemia (AML) and elevated World Health Organization (WHO) performance status.
  • CONCLUSIONS: Cigarette smoking has a deleterious effect on survival in AML by shortening complete remission duration and subsequent survival.

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  • (PMID = 12377652.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
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34. Skladanowski A, Bozko P, Sabisz M, Larsen AK: Dual inhibition of PI3K/Akt signaling and the DNA damage checkpoint in p53-deficient cells with strong survival signaling: implications for cancer therapy. Cell Cycle; 2007 Sep 15;6(18):2268-75
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  • [Title] Dual inhibition of PI3K/Akt signaling and the DNA damage checkpoint in p53-deficient cells with strong survival signaling: implications for cancer therapy.
  • Natural (intrinsic) resistance of many tumor types to DNA damaging agents is closely associated with their capacity to undergo robust cell cycle arrest in G(2)/M.
  • G(2) arrest is regulated by the DNA damage checkpoint and by survival signaling, with a potential role of PI3K/Akt in checkpoint function.
  • We compared the influence of UCN-01, which affects both the DNA damage checkpoint and PI3K/Akt-mediated survival signaling, with the PI3K inhibitors wortmannin and LY294002 in p53-deficient M1 acute myeloid leukemia cells treated with the DNA damaging agent cisplatin.
  • Unexpectedly, dual inhibition of both survival and checkpoint signaling by UCN-01, also increased the cytotoxicity of cisplatin, but to a lesser degree than wortmannin or LY294002.
  • Our results elucidate a novel function for PI3K/Akt as a survival factor during DNA damage-induced G(2) arrest and could have important pharmacological consequences for the application of response modulators in p53-deficient tumors with strong survival signaling.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. DNA Damage / physiology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Signal Transduction / physiology. Tumor Suppressor Protein p53 / deficiency
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / genetics. Cell Survival / physiology. Mice. Neoplasms / drug therapy. Neoplasms / enzymology

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  • (PMID = 17890906.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tumor Suppressor Protein p53; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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35. Herry A, Douet-Guilbert N, Guéganic N, Morel F, Le Bris MJ, Berthou C, De Braekeleer M: Del(5q) and MLL amplification in homogeneously staining region in acute myeloblastic leukemia: a recurrent cytogenetic association. Ann Hematol; 2006 Apr;85(4):244-9
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  • [Title] Del(5q) and MLL amplification in homogeneously staining region in acute myeloblastic leukemia: a recurrent cytogenetic association.
  • We report here a 71 year-old female presenting with acute myeloblastic leukemia (FAB-M1) after treatment of essential thrombocythemia with Vercyte.
  • Twenty-one cases, including ours, of myelodysplastic syndromes and acute myelogenous leukemia with MLL amplification present in hsr or dmin were found in the literature.
  • Most of these patients shared some characteristics: they were old, they had de novo acute myeloid leukemia (AML) with a complex karyotype and a short survival, 90% of them having also a del(5q).
  • Therefore, the simultaneous presence of MLL amplification and del(5q) appears to be a nonrandom association that could be the signature of AML in elderly patients with a poor prognosis.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 7 / genetics. Gene Amplification. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] 6-Mercaptopurine / therapeutic use. Aged. Cytogenetic Analysis. Fatal Outcome. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence / methods. Karyotyping. Pipobroman / therapeutic use. Prognosis. Sensitivity and Specificity. Thrombocytosis / diagnosis. Thrombocytosis / drug therapy

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  • (PMID = 16425025.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6Q99RDT97R / Pipobroman; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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36. Okoshi Y, Shimizu S, Kojima H, Obara N, Mukai HY, Komeno T, Hasegawa Y, Mori N, Nagasawa T: Detection of minimal residual disease in a patient having acute myelogenous leukemia with t(16;21)(p11;q22) treated by allogeneic bone marrow transplantation. Acta Haematol; 2001;105(1):45-8
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  • [Title] Detection of minimal residual disease in a patient having acute myelogenous leukemia with t(16;21)(p11;q22) treated by allogeneic bone marrow transplantation.
  • A 29-year-old woman having acute myelogeneous leukemia-M1 subtype with the chromosomal abnormality t(16;21)(p11;q22) is presented.
  • Complete blood count at onset showed a hemoglobin level of 7.2 g/dl, a platelet count of 48 x 10(9)/l, and a white blood cell count of 161.2 x 10(9)/l with 99% blasts and 1% lymphocytes.
  • After achieving complete remission following conventional chemotherapy, she received an HLA-matched bone marrow transplantation (BMT) from her sibling after conditioning with busulfan, etoposide and cyclophosphamide.
  • However, 9 months later, the leukemia relapsed as a painful extramedullary mass in her left femur.
  • In spite of intensive re-induction chemotherapy, she died of progressive disease and sepsis.
  • We consider that even high-dose chemotherapy with BMT may not be effective in the eradication of this type of leukemia, and that the detection of minimal residual disease possibly contributes to the better planning of the therapeutic strategy.
  • [MeSH-major] Bone Marrow Transplantation. Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Leukemia, Myeloid, Acute / genetics. Neoplasm, Residual / diagnosis. Translocation, Genetic
  • [MeSH-minor] Adult. Antigens, CD / analysis. Antigens, CD13 / analysis. Antigens, CD34 / analysis. Antigens, CD56 / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow / pathology. Fatal Outcome. Female. Hemoglobins / analysis. Humans. Karyotyping. Leukocyte Count. Peroxidase / analysis. Platelet Count. Radiotherapy. Recurrence. Remission Induction. Reverse Transcriptase Polymerase Chain Reaction. Sialic Acid Binding Ig-like Lectin 3. Transplantation, Homologous. Treatment Failure

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  • [Copyright] Copyright 2001 S. Karger AG, Basel
  • (PMID = 11340253.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, CD56; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Hemoglobins; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 1.11.1.7 / Peroxidase; EC 3.4.11.2 / Antigens, CD13
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37. Gianni' M, Boldetti A, Guarnaccia V, Rambaldi A, Parrella E, Raska I Jr, Rochette-Egly C, Del Sal G, Rustighi A, Terao M, Garattini E: Inhibition of the peptidyl-prolyl-isomerase Pin1 enhances the responses of acute myeloid leukemia cells to retinoic acid via stabilization of RARalpha and PML-RARalpha. Cancer Res; 2009 Feb 1;69(3):1016-26
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  • [Title] Inhibition of the peptidyl-prolyl-isomerase Pin1 enhances the responses of acute myeloid leukemia cells to retinoic acid via stabilization of RARalpha and PML-RARalpha.
  • The retinoic acid receptor RARalpha and the acute-promyelocytic-leukemia-specific counterpart PML-RARalpha directly interact with Pin1.
  • Inhibition is relieved by Pin1-targeted short interfering RNAs and by pharmacologic inhibition of the catalytic activity of the protein.
  • In the acute myelogenous leukemia cell lines HL-60 and NB4, Pin1 interacts with RARalpha in a constitutive fashion.
  • Treatment of the two cell lines and freshly isolated acute myelogenous leukemia blasts (M1 to M4) with ATRA and a pharmacologic inhibitor of Pin1 causes similar effects.
  • Our results add a further layer of complexity to the regulation of nuclear retinoic acid receptors and suggest that Pin1 represents an important target for strategies aimed at increasing the therapeutic index of retinoids.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Oncogene Proteins, Fusion / metabolism. Peptidylprolyl Isomerase / antagonists & inhibitors. Receptors, Retinoic Acid / metabolism. Tretinoin / pharmacology
  • [MeSH-minor] Acute Disease. Animals. COS Cells. Cercopithecus aethiops. HL-60 Cells. Humans. Transcriptional Activation. Transfection

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  • (PMID = 19155306.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NIMA-interacting peptidylprolyl isomerase; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Retinoic Acid; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 0 / retinoic acid receptor alpha; 5688UTC01R / Tretinoin; EC 5.2.1.8 / Peptidylprolyl Isomerase
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38. Zhang XJ, Zheng GG, Ma XT, Yang YH, Li G, Rao Q, Nie K, Wu KF: Expression of P2X7 in human hematopoietic cell lines and leukemia patients. Leuk Res; 2004 Dec;28(12):1313-22
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  • [Title] Expression of P2X7 in human hematopoietic cell lines and leukemia patients.
  • Here, we investigated P2X7 expression in 11 human hematopoietic cell lines, representing different lineages, as well as bone marrow mononuclear cells (BMMC) samples from 87 leukemia and 10 myelodysplastic syndrome (MDS) patients.
  • Semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) and flow cytometry results showed that both P2X7 mRNA and protein were detected in eight cell lines with a non-lineage-specific manner.
  • Samples from 69 leukemia and 9 MDS patients were P2X7 positive at mRNA level.
  • Moreover, both positive rates and relative expression levels were significantly higher in acute myelogenous leukemia (AML), acute lymphoblastic leukemia (ALL), chronic myelogenous leukemia (CML), and MDS groups than that in normal donor group.
  • The expression levels varied among AML subtypes with higher levels being observed in M4, M5, and M6 groups but not in M1 or M2 group.
  • Furthermore, after one course of standard induction therapies, the remission rate in high P2X7 expression group was lower than that in either P2X7 negative group or low P2X7 expression group.
  • [MeSH-major] Leukemia / genetics. Receptors, Purinergic P2 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Blood Cells / chemistry. Bone Marrow Cells / chemistry. Calcium Signaling. Case-Control Studies. Cell Line. Child. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. RNA, Messenger / analysis. Receptors, Purinergic P2X7. Treatment Outcome. Tumor Cells, Cultured


39. Lo Nigro L, Schiliro G: Occurrence of a FAB-M1 AML in a child during treatment of APL: emergence of an immature clone or a therapy related-AML? Haematologica; 2002 May;87(5):ELT26
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  • [Title] Occurrence of a FAB-M1 AML in a child during treatment of APL: emergence of an immature clone or a therapy related-AML?
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Leukemia, Promyelocytic, Acute / drug therapy. Neoplasms, Second Primary / etiology
  • [MeSH-minor] Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Child. Fatal Outcome. Humans. Male

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  • (PMID = 12010686.001).
  • [ISSN] 0390-6078
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating
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40. Takahashi T, Maruyama Y, Satoh Y, Yoshimoto M, Tsujisaki M: Complex t(8;14;21)(q22;q13;q22), a variant of t(8;21), with t(15;21)(q15;p11) in a patient with acute myelogenous leukemia (M1). Cancer Genet Cytogenet; 2004 Dec;155(2):152-3
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  • [Title] Complex t(8;14;21)(q22;q13;q22), a variant of t(8;21), with t(15;21)(q15;p11) in a patient with acute myelogenous leukemia (M1).
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Genetic Variation. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / prevention & control. Translocation, Genetic
  • [MeSH-minor] Antimetabolites, Antineoplastic / therapeutic use. Core Binding Factor Alpha 2 Subunit. Cytarabine / therapeutic use. Drug Therapy, Combination. Female. Humans. Idarubicin / therapeutic use. Karyotyping. Leukocytes, Mononuclear / chemistry. Middle Aged. Oncogene Proteins, Fusion / genetics. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Secondary Prevention. Transcription Factors / genetics

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  • (PMID = 15571802.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Antimetabolites, Antineoplastic; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / Transcription Factors; 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
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