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1. Falini B, Mecucci C, Saglio G, Lo Coco F, Diverio D, Brown P, Pane F, Mancini M, Martelli MP, Pileri S, Haferlach T, Haferlach C, Schnittger S: NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities: a comparative analysis of 2562 patients with acute myeloid leukemia. Haematologica; 2008 Mar;93(3):439-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities: a comparative analysis of 2562 patients with acute myeloid leukemia.
  • Acute myeloid leukemia carrying NPM1 mutations and cytoplasmic nucleophosmin (NPMc(+) acute myeloid leukemia) represents one-third of adult AML (50-60% of all acute myeloid leukemia with normal karyotype) and shows distinct biological, pathological and clinical features.
  • We confirm in 2562 patients with acute myeloid leukemia our previous observation that NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities.
  • Taken together, these findings make NPMc+ acute myeloid leukemia a good candidate for inclusion in the upcoming World Health Organization classification.
  • [MeSH-major] Cytoplasm / chemistry. Leukemia, Myeloid / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Acute Disease. Bone Marrow / pathology. Cell Nucleus / chemistry. Chromosome Aberrations. Chromosome Inversion. Cohort Studies. DNA Mutational Analysis. Germany / epidemiology. Humans. In Situ Hybridization, Fluorescence. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic

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  • (PMID = 18268276.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin
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2. Raffoux E, Chaibi P, Dombret H, Degos L: Valproic acid and all-trans retinoic acid for the treatment of elderly patients with acute myeloid leukemia. Haematologica; 2005 Jul;90(7):986-8
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  • [Title] Valproic acid and all-trans retinoic acid for the treatment of elderly patients with acute myeloid leukemia.
  • Valproic acid (VPA) has been demonstrated to be able to inhibit histone deacetylase activity and to synergize with all-trans retinoic acid (ATRA) in inducing the differentiation of acute myeloid leukemia (AML) cells.
  • A pilot study of the VPA/ATRA combination was performed in 11 elderly patients with de novo AML (median age, 82 years).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Tretinoin / administration & dosage. Valproic Acid / administration & dosage

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  • (PMID = 15996941.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] Italy
  • [Chemical-registry-number] 5688UTC01R / Tretinoin; 614OI1Z5WI / Valproic Acid
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3. Jordheim LP, Nguyen-Dumont T, Thomas X, Dumontet C, Tavtigian SV: Differential allelic expression in leukoblast from patients with acute myeloid leukemia suggests genetic regulation of CDA, DCK, NT5C2, NT5C3, and TP53. Drug Metab Dispos; 2008 Dec;36(12):2419-23
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  • [Title] Differential allelic expression in leukoblast from patients with acute myeloid leukemia suggests genetic regulation of CDA, DCK, NT5C2, NT5C3, and TP53.
  • mRNA expression levels of certain genes have shown predictive value for the outcome of cytarabine-treated AML-patients.
  • We studied leukoblasts from 82 patients with acute myeloid leukemia and observed various extent and frequency of differential allelic expression in the CDA, DCK, NT5C2, NT5C3, and TP53 genes.
  • Our attempts to identify the causative regulatory single nucleotide polymorphisms by a bioinformatics approach did not succeed.
  • [MeSH-major] 5'-Nucleotidase / genetics. Alleles. Cytidine Deaminase / genetics. Deoxycytidine Kinase / genetics. Gene Expression Regulation, Neoplastic / genetics. Leukemia, Myeloid, Acute / metabolism. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 18775979.001).
  • [ISSN] 1521-009X
  • [Journal-full-title] Drug metabolism and disposition: the biological fate of chemicals
  • [ISO-abbreviation] Drug Metab. Dispos.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Equilibrative Nucleoside Transporter 1; 0 / Glycoproteins; 0 / SLC29A1 protein, human; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 04079A1RDZ / Cytarabine; EC 2.7.1.74 / Deoxycytidine Kinase; EC 3.1.3.5 / 5'-Nucleotidase; EC 3.1.3.5 / NT5C2 protein, human; EC 3.1.3.5 / NT5C3 protein, human; EC 3.5.4.5 / Cytidine Deaminase
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4. Satoh C, Ogata K: Hypothesis: myeloid-restricted hematopoietic stem cells with self-renewal capacity may be the transformation site in acute myeloid leukemia. Leuk Res; 2006 Apr;30(4):491-5
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  • [Title] Hypothesis: myeloid-restricted hematopoietic stem cells with self-renewal capacity may be the transformation site in acute myeloid leukemia.
  • The transformation site in acute myeloid leukemia (AML) has been proposed to be pluripotent hematopoietic stem cells (PHSCs), and the lymphoid development of leukemic PHSCs may be suppressed by leukemogenic events.
  • Recent data from multiple laboratories have contradicted the current hierarchical model of hematopoiesis and indicated the presence of myeloid HSCs with minimal lymphopoietic potential (MyHSCs) in mice.
  • Based on these findings and re-evaluating the published data on AML stem cells, we hypothesize that MyHSCs may be the transformation site in AML.
  • [MeSH-major] Hematopoietic Stem Cells / pathology. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Animals. Humans. Mice

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  • (PMID = 16183117.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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5. Perz JB, Ho AD: Histamine dihydrochloride for the treatment of acute myeloid leukemia, malignant melanoma and renal cell carcinoma. Future Oncol; 2008 Apr;4(2):169-77
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  • [Title] Histamine dihydrochloride for the treatment of acute myeloid leukemia, malignant melanoma and renal cell carcinoma.
  • Clinical trials in solid tumors and in acute myeloid leukemia have demonstrated the potential to improve treatment outcome when histamine dihydrochloride is combined with immunotherapy.
  • On the other hand, less promising results were reported for histamine dihydrochloride added to cytokines in patients with other solid tumors, especially in advanced renal cell carcinoma.
  • A recent international Phase III trial performed in 320 patients showed that maintenance therapy with histamine dihydrochloride and IL-2 was able to improve leukemia-free survival in patients with acute myeloid leukemia, without an effect on overall survival.
  • The combination of histamine dihydrochloride with IL-2 potentially offers an efficacious and tolerable maintenance strategy for patients with acute myeloid leukemia; however, its impact on survival remains to be explored.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Renal Cell / drug therapy. Histamine / therapeutic use. Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antioxidants / therapeutic use. Dose-Response Relationship, Drug. Humans. Kidney Neoplasms / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Melanoma / drug therapy. Receptors, Histamine H2 / physiology. Skin Neoplasms / drug therapy. Treatment Outcome

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  • (PMID = 18407731.001).
  • [ISSN] 1744-8301
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antioxidants; 0 / Receptors, Histamine H2; 820484N8I3 / Histamine
  • [Number-of-references] 22
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6. Goyal R, Vaiphei K, Vankalakunti M, Marwaha RK: Pathology teach and tell disseminated candidiasis in an infant with acute myeloid leukemia without prior chemotherapy. Fetal Pediatr Pathol; 2006 Nov-Dec;25(6):333-8
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  • [Title] Pathology teach and tell disseminated candidiasis in an infant with acute myeloid leukemia without prior chemotherapy.
  • Opportunistic fungal infections are significant problems for neutropenic patients who are undergoing cytotoxic therapy for acute leukemia.
  • Systemic and hepatosplenic candidiasis have been reported in acute leukemic patients who are on chemotherapy.
  • Gastrointestinal tract involvement is a rare phenomenon in disseminated candidiasis, especially in acute leukemia.
  • We report one such rare case of acute myeloid leukemia in an infant who died of disseminated candidiasis with gastrointestinal tract involvement prior to the institution of chemotherapy.
  • [MeSH-major] Candidiasis / complications. Gastrointestinal Diseases / microbiology. Leukemia, Myeloid / complications. Opportunistic Infections / complications
  • [MeSH-minor] Acute Disease. Fatal Outcome. Female. Humans. Infant. Intestinal Mucosa / microbiology. Intestinal Mucosa / pathology

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  • (PMID = 17696044.001).
  • [ISSN] 1551-3815
  • [Journal-full-title] Fetal and pediatric pathology
  • [ISO-abbreviation] Fetal Pediatr Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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7. Rangan A, Arora B, Rangan P, Dadu T: Florid plasmacytosis in a case of acute myeloid leukemia: A diagnostic dilemma. Indian J Med Paediatr Oncol; 2010 Jan;31(1):36-8
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  • [Title] Florid plasmacytosis in a case of acute myeloid leukemia: A diagnostic dilemma.
  • The association of acute myeloid leukemia (AML) with plasmacytosis is a known, although rare event.
  • There are very few case reports documenting an increase in the number of plasma cells at the time of AML diagnosis.
  • Here, we present the case of a 65-year-old male diagnosed as acute myelomonocytic leukemia with exuberant plasmacytosis, which posed a difficulty in diagnosis.
  • Paracrine interleukin-6 production by leukemic blast cells is thought to contribute to this associated reactive plasma cell proliferation.

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  • (PMID = 20931021.001).
  • [ISSN] 0975-2129
  • [Journal-full-title] Indian journal of medical and paediatric oncology : official journal of Indian Society of Medical & Paediatric Oncology
  • [ISO-abbreviation] Indian J Med Paediatr Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2941603
  • [Keywords] NOTNLM ; Acute myeloid leukemia / myeloma / plasmacytosis
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8. Colado E, Alvarez-Fernández S, Maiso P, Martín-Sánchez J, Vidriales MB, Garayoa M, Ocio EM, Montero JC, Pandiella A, San Miguel JF: The effect of the proteasome inhibitor bortezomib on acute myeloid leukemia cells and drug resistance associated with the CD34+ immature phenotype. Haematologica; 2008 Jan;93(1):57-66
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  • [Title] The effect of the proteasome inhibitor bortezomib on acute myeloid leukemia cells and drug resistance associated with the CD34+ immature phenotype.
  • Acute myeloid leukemia (AML) is an immnunophenotypically heterogeneous group of diseases, with CD34(+) cases being associated with drug resistance and poor outcome.
  • We investigated the effects of bortezomib on the growth and survival of AML cells.
  • DESIGN AND METHODS: We studied the in vitro activity and mechanism of action of bortezomib on both cell lines and fresh cells from 28 AML patients including CD34(+) and CD34(-) cases.
  • RESULTS: Bortezomib showed potent anti-AML activity (IC(50) < 50 nM), which was greater than that of conventional agents (doxorubicin, cytarabine and fludarabine).
  • Mechanistically, bortezomib induced accumulation of cells in the G(2)/M phase, with up-regulation of p27, together with cell death through an increase in the mitochondrial outer membrane permeability involving caspase-dependent and -independent pathways.
  • CONCLUSIONS: Bortezomib induces apoptosis in acute myeloid leukemia cells in vitro.
  • Whether this drug might be useful in the treatment of patients with acute myeloid leukemia can be established only in ad hoc clinical trials.
  • [MeSH-major] Antigens, CD34 / biosynthesis. Boronic Acids / pharmacology. Drug Resistance, Neoplasm. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / pathology. Protease Inhibitors / pharmacology. Pyrazines / pharmacology
  • [MeSH-minor] Aged. Antineoplastic Agents / pharmacology. Apoptosis. Bortezomib. Cell Line, Tumor. Humans. Inhibitory Concentration 50. Middle Aged. Phenotype. Proteasome Endopeptidase Complex / metabolism

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  • (PMID = 18166786.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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9. Maalouf T, Angioi K, Ssi-Yan-Kai I, Vernerey F, Witz B, George J: Dacryoadenitis associated with subcutaneous Sweet's syndrome in a patient with acute myeloid leukemia. Orbit; 2005 Mar;24(1):55-7
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  • [Title] Dacryoadenitis associated with subcutaneous Sweet's syndrome in a patient with acute myeloid leukemia.
  • A 26-year-old woman presented with a painful skin eruption which led to the diagnosis of acute myeloid leukemia.
  • Careful observation of the clinical course, computed tomography, and orbital biopsy were necessary to establish the diagnosis of dacryoadenitis associated with subcutaneous Sweet's syndrome.
  • [MeSH-major] Dacryocystitis / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Sweet Syndrome / diagnosis

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  • (PMID = 15764119.001).
  • [ISSN] 0167-6830
  • [Journal-full-title] Orbit (Amsterdam, Netherlands)
  • [ISO-abbreviation] Orbit
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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10. Kemta Lekpa F, Zahra K, Pautas C, Maury S, Chevalier X, Claudepierre P: Acute myeloid leukemia after infliximab: a case report. Clin Exp Rheumatol; 2009 Nov-Dec;27(6):999-1000
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  • [Title] Acute myeloid leukemia after infliximab: a case report.
  • Concern has arisen regarding a possible increase in the risk of malignant diseases such as lymphoproliferative disorders in a patient taking TNF-alpha antagonists for the treatment of chronic inflammatory diseases.
  • The evidence of a causal link remains unclear.
  • We report a case of 60-year-old male patient who developed acute myeloid leukemia during infliximab therapy for ankylo-sing spondylitis.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Spondylitis, Ankylosing / therapy

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  • (PMID = 20149321.001).
  • [ISSN] 0392-856X
  • [Journal-full-title] Clinical and experimental rheumatology
  • [ISO-abbreviation] Clin. Exp. Rheumatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antirheumatic Agents; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab
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11. J B, A N, A D, G L: Pseudomonas aeruginosa endocarditis in acute myeloid leukemia: a rare complication. Int J Biomed Sci; 2008 Dec;4(4):330-2

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  • [Title] Pseudomonas aeruginosa endocarditis in acute myeloid leukemia: a rare complication.
  • Infectious endocarditis is a rarely encountered complication among leukemia patient during induction therapy.
  • We describe a young patient who developed prolonged high fever after aggressive chemotherapy for Acute Myeloid Leukemia.
  • Our purpose is to emphasize the need for an early diagnosis of this rare, albeit treatable complication.

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  • (PMID = 23675106.001).
  • [ISSN] 1550-9702
  • [Journal-full-title] International journal of biomedical science : IJBS
  • [ISO-abbreviation] Int J Biomed Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3614722
  • [Keywords] NOTNLM ; endocarditis / leukemia / platelets
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12. Sung KW, Choi J, Hwang YK, Lee SJ, Kim HJ, Lee SH, Yoo KH, Jung HL, Koo HH: Overexpression of Apollon, an antiapoptotic protein, is associated with poor prognosis in childhood de novo acute myeloid leukemia. Clin Cancer Res; 2007 Sep 1;13(17):5109-14
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  • [Title] Overexpression of Apollon, an antiapoptotic protein, is associated with poor prognosis in childhood de novo acute myeloid leukemia.
  • The overexpression of Apollon, a member of inhibitor of apoptosis proteins, is intuitively expected to be associated with unfavorable clinical features in malignant diseases; however, there have been no clinical studies reporting the prognostic relevance of Apollon expression in human malignancies.
  • This study was done to investigate the clinical relevance of the expression of Apollon in childhood de novo acute myeloid leukemia.
  • EXPERIMENTAL DESIGN: In 55 pediatric patients with de novo acute myeloid leukemia, the level of Apollon expression was determined by using quantitative reverse transcriptase-PCR and was analyzed with respect to the patients' clinical features and treatment outcomes.
  • RESULTS: Apollon expression was found to be higher in patients with a leukocyte number of >or=10,000/microL, patients with extramedullary disease, and patients with the French-American-British classification subtype M7.
  • CONCLUSION: This is the first study demonstrating the prognostic implication of the Apollon expression in human cancers, indicating that Apollon overexpression may be used as a poor prognostic marker in childhood acute myeloid leukemia through validation by further studies.
  • [MeSH-major] Inhibitor of Apoptosis Proteins / analysis. Leukemia, Myeloid, Acute / metabolism

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  • (PMID = 17785565.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC6 protein, human; 0 / Inhibitor of Apoptosis Proteins
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13. Craddock C, Nagra S, Peniket A, Brookes C, Buckley L, Nikolousis E, Duncan N, Tauro S, Yin J, Liakopoulou E, Kottaridis P, Snowden J, Milligan D, Cook G, Tholouli E, Littlewood T, Peggs K, Vyas P, Clark F, Cook M, Mackinnon S, Russell N: Factors predicting long-term survival after T-cell depleted reduced intensity allogeneic stem cell transplantation for acute myeloid leukemia. Haematologica; 2010 Jun;95(6):989-95
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  • [Title] Factors predicting long-term survival after T-cell depleted reduced intensity allogeneic stem cell transplantation for acute myeloid leukemia.
  • BACKGROUND: Reduced intensity conditioning regimens permit the delivery of a potentially curative graft-versus-leukemia effect in older patients with acute myeloid leukemia.
  • Although T-cell depletion is increasingly used to reduce the risk of graft-versus-host disease its impact on the graft-versus-leukemia effect and long-term outcome post-transplant is unknown.
  • DESIGN AND METHODS: We have characterized pre- and post-transplant factors determining overall survival in 168 patients with acute myeloid leukemia transplanted using an alemtuzumab based reduced intensity conditioning regimen with a median duration of follow-up of 37 months.
  • RESULTS: The 3-year overall survival for patients transplanted in CR1 or CR2/CR3 was 50% (95% CI, 38% to 62%) and 44% (95% CI, 31% to 56%), respectively compared to 15% (95% CI, 2% to 36%) for patients with relapsed/refractory disease.
  • Multivariate analysis demonstrated that both survival and disease relapse were influenced by status at transplant (P=0.008) and presentation cytogenetics (P=0.01).
  • CONCLUSIONS: Disease stage, presentation karyotype and post-transplant CsA exposure are important predictors of outcome in patients undergoing a T-cell depleted reduced intensity conditioning allograft for acute myeloid leukemia.
  • These data confirm the presence of a potent graft-versus-leukemia effect after a T-cell depleted reduced intensity conditioning allograft in acute myeloid leukemia and identify CsA exposure as a manipulable determinant of outcome in this setting.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / surgery. T-Lymphocytes. Transplantation Conditioning / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Disease-Free Survival. Female. Follow-Up Studies. Graft vs Host Disease / immunology. Graft vs Host Disease / mortality. Graft vs Host Disease / prevention & control. Humans. Male. Middle Aged. Predictive Value of Tests. Time Factors. Transplantation, Homologous. Treatment Outcome. Young Adult

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  • (PMID = 19951968.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab
  • [Other-IDs] NLM/ PMC2878799
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14. Sato K, Izumi T, Toshima M, Nagai T, Muroi K, Komatsu N, Ozawa K: Retropharyngeal abscess due to methicillin-resistant Staphylococcus aureus in a case of acute myeloid leukemia. Intern Med; 2005 Apr;44(4):346-9
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  • [Title] Retropharyngeal abscess due to methicillin-resistant Staphylococcus aureus in a case of acute myeloid leukemia.
  • We describe a case of acute myeloid leukemia (AML) complicated with retropharyngeal abscess (RPA) due to methicillin-resistant Staphylococcus aureus (MRSA) in a 56-year-old man.
  • [MeSH-major] Leukemia, Myeloid / complications. Methicillin Resistance. Retropharyngeal Abscess / complications. Staphylococcal Infections / complications. Staphylococcus aureus / isolation & purification
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Diagnosis, Differential. Drug Therapy, Combination. Follow-Up Studies. Humans. Injections, Intravenous. Male. Middle Aged. Tomography, X-Ray Computed. Vancomycin / administration & dosage. Vancomycin / therapeutic use

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  • (PMID = 15897650.001).
  • [ISSN] 0918-2918
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 6Q205EH1VU / Vancomycin
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15. Pea F, Viale P, Damiani D, Pavan F, Cristini F, Fanin R, Furlanut M: Ceftazidime in acute myeloid leukemia patients with febrile neutropenia: helpfulness of continuous intravenous infusion in maximizing pharmacodynamic exposure. Antimicrob Agents Chemother; 2005 Aug;49(8):3550-3
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  • [Title] Ceftazidime in acute myeloid leukemia patients with febrile neutropenia: helpfulness of continuous intravenous infusion in maximizing pharmacodynamic exposure.
  • The pharmacokinetic-pharmacodynamic profile of a fixed 6-g daily continuous intravenous infusion of ceftazidime was assessed in 20 febrile neutropenic patients with acute myeloid leukemia.
  • [MeSH-major] Anti-Bacterial Agents. Ceftazidime. Fever / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Neutropenia / drug therapy. Pseudomonas Infections / drug therapy

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  • (PMID = 16048982.001).
  • [ISSN] 0066-4804
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 9M416Z9QNR / Ceftazidime
  • [Other-IDs] NLM/ PMC1196227
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16. Suzushima H, Wada N, Yamasaki H, Eto K, Shimomura T, Kugimiya MH, Horikawa K, Nishimura S, Tsuda H, Mitsuya H, Asou N: Low-dose cytarabine and aclarubicin in combination with granulocyte colony-stimulating factor for elderly patients with previously untreated acute myeloid leukemia. Leuk Res; 2010 May;34(5):610-4
Hazardous Substances Data Bank. CYTARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low-dose cytarabine and aclarubicin in combination with granulocyte colony-stimulating factor for elderly patients with previously untreated acute myeloid leukemia.
  • We evaluated the efficacy of low-dose cytarabine and aclarubicin combined with granulocyte colony-stimulating factor (CAG) in elderly patients with previously untreated acute myeloid leukemia.
  • Patients aged between 60 and 70 years who were not eligible for standard chemotherapy protocols and patients aged over 70 years were all registered.
  • Median disease-free survival was 10 months and overall survival was nine months.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Aclarubicin / administration & dosage. Age Factors. Aged. Aged, 80 and over. Cytarabine / administration & dosage. Disease-Free Survival. Dose-Response Relationship, Drug. Female. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Kaplan-Meier Estimate. Male. Middle Aged

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19744710.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 74KXF8I502 / Aclarubicin
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17. Han TJ, Xu XP: [Advances of study on prognostic factors of molecular biology in acute myeloid leukemia with normal cytogenetics]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Aug;18(4):1063-8
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  • [Title] [Advances of study on prognostic factors of molecular biology in acute myeloid leukemia with normal cytogenetics].
  • Acute myeloid leukemia (AML) is a group of diseases with a conspicuous heterogeneity.
  • Following the development of cytogenetics, multiple reproducible chromosome aberrations have been discovered in AML, many of which not only are diagnostic markers for specific AML subtypes but also significant prognostic factors for determining complete remission (CR), relapse risk, and overall survival (OS).
  • However, with the foundation of available chromosome analysis, a large group of acute myeloid leukemia (AML) patients, 40% to 49% of adults and 25% of children had not been found abnormality of chromosome karyotype under microscope.
  • These so-called cytogenetically normal acute myeloid leukemia (CN-AML) patients have usually been classified in an intermediate-risk prognostic category.
  • Nevertheless, the outcome of the CN-AML patients are varied in clinical studies, likely because there exist diverse gene mutations in these patients according to recent researches.
  • Those mutations at the molecular level, on basis of which AML could be further classified, are significantly associated with CN-AML patients and offer potential targets for specific therapeutic studies.
  • The review focuses on research advances abroad in this field including gene mutations suggesting bad prognosis such as FMS-related tyrosine kinase 3 gene mutation, Baalc gene and ETS-related gene hyperexpression, Wilms' tumor gene mutation and other gene mutations as well as gene mutations suggesting good prognosis such as nucleophosmin gene mutation, mixed lineage leukemia-partial tandem duplication, CCAAT/enhancer-binding protein α gene mutation.

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  • (PMID = 20723330.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
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18. Klammer M, Roddie PH: Current progress in the development of a cell-based vaccine for the immunotherapy of acute myeloid leukemia. Expert Rev Vaccines; 2006 Apr;5(2):211-22
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  • [Title] Current progress in the development of a cell-based vaccine for the immunotherapy of acute myeloid leukemia.
  • Evidence that immunological control contributes to the elimination of residual leukemia has emerged from allogeneic hematopoietic stem cell transplantation.
  • This review assesses the current understanding of immunobiology of acute myeloid leukemia and how dendritic cells and T cells may be harnessed using in vitro and in vivo priming techniques.
  • Preclinical and clinical dendritic cell vaccine trials reported to date are considered and the prospects for immunotherapy with dendritic cell-based vaccine constructs evaluated.
  • [MeSH-major] Cancer Vaccines / immunology. Cancer Vaccines / therapeutic use. Dendritic Cells / immunology. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / therapy. T-Lymphocytes / immunology

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  • (PMID = 16608421.001).
  • [ISSN] 1744-8395
  • [Journal-full-title] Expert review of vaccines
  • [ISO-abbreviation] Expert Rev Vaccines
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines
  • [Number-of-references] 110
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19. Niemann CU, Kjeldsen L, Ralfkiaer E, Jensen MK, Borregaard N: Serglycin proteoglycan in hematologic malignancies: a marker of acute myeloid leukemia. Leukemia; 2007 Dec;21(12):2406-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serglycin proteoglycan in hematologic malignancies: a marker of acute myeloid leukemia.
  • Serglycin is the major cell-associated proteoglycan of hematopoietic cells.
  • Serglycin expression was found to distinguish acute myeloid leukemia (AML) from acute lymphoblastic leukemia.
  • In contrast to myeloperoxidase, serglycin was found to be a selective marker for immature myeloid cells, distinguishing AML from Philadelphia chromosome-negative chronic myeloproliferative disorders.
  • [MeSH-major] Biomarkers, Tumor / analysis. Granulocyte Precursor Cells / chemistry. Hematologic Neoplasms / metabolism. Leukemia, Myeloid, Acute / diagnosis. Neoplasm Proteins / analysis. Proteoglycans / analysis. Vesicular Transport Proteins / analysis
  • [MeSH-minor] Blood Cells / chemistry. Bone Marrow Cells / chemistry. Cell Differentiation. Cytoplasmic Granules / chemistry. Diagnosis, Differential. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / metabolism. Lymphoma, Non-Hodgkin / metabolism. Myeloproliferative Disorders / metabolism. Peroxidase / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Predictive Value of Tests

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  • (PMID = 17928883.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Proteoglycans; 0 / Vesicular Transport Proteins; 0 / serglycin; EC 1.11.1.7 / Peroxidase
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20. Park S, Park CH, Hahm ER, Kim K, Kimler BF, Lee SJ, Park HK, Lee SH, Kim WS, Jung CW, Park K, Riordan HD, Lee JH: Activation of Raf1 and the ERK pathway in response to l-ascorbic acid in acute myeloid leukemia cells. Cell Signal; 2005 Jan;17(1):111-9
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  • [Title] Activation of Raf1 and the ERK pathway in response to l-ascorbic acid in acute myeloid leukemia cells.
  • L-ascorbic acid (LAA) shows cytotoxicity and induces apoptosis of malignant cells in vitro, but the mechanisms by which such effects occur have not been elucidated.
  • In the present study, we provide evidence that the ERK MAP kinase pathway is activated in response to LAA (< 1 mM) in acute myeloid leukemia cell lines.
  • Although the ERK pathway has been known to activate cell proliferation, pharmacologic inhibition of ERK reduces LAA-dependent apoptosis and growth inhibitory response of acute myeloid leukemia cell lines, suggesting that this signaling cascade positively regulates induction of apoptotic response by LAA.
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Cell Survival / drug effects. HL-60 Cells. Humans. Leukemia, Myeloid, Acute. Phosphorylation

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  • [Copyright] Copyright 2004 Elsevier Inc.
  • (PMID = 15451031.001).
  • [ISSN] 0898-6568
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.11.1 / Proto-Oncogene Proteins c-raf; PQ6CK8PD0R / Ascorbic Acid
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21. Grier DD, Eskew A, White T, McLean TW: An unusual case of acute myeloid leukemia: late isolated testicular relapse followed by isolated central nervous system relapse. Pediatr Blood Cancer; 2010 Dec 1;55(6):1231-3
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  • [Title] An unusual case of acute myeloid leukemia: late isolated testicular relapse followed by isolated central nervous system relapse.
  • Testicular relapse of acute myeloid leukemia without bone marrow involvement is a rare event.
  • We describe a case of an 18-year-old male who had an isolated testicular relapse 86 months (7.2 years) from original diagnosis.
  • Fluorescence in situ hybridization and immunohistochemistry were used to establish the diagnosis of a relapse rather than a new leukemic process.
  • He was treated with intrathecal chemotherapy and systemic reinduction, followed by a stem cell transplant.
  • This patient had a 7.2-year period between original diagnosis and the testicular relapse of acute myeloid leukemia.
  • [MeSH-major] Central Nervous System Neoplasms / drug therapy. Leukemia, Myeloid, Acute / surgery. Neoplasm Recurrence, Local / diagnosis. Testicular Neoplasms / drug therapy

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  • (PMID = 20589624.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; FTK8U1GZNX / Thioguanine; ZS7284E0ZP / Daunorubicin
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22. Garzon R, Liu S, Fabbri M, Liu Z, Heaphy CE, Callegari E, Schwind S, Pang J, Yu J, Muthusamy N, Havelange V, Volinia S, Blum W, Rush LJ, Perrotti D, Andreeff M, Bloomfield CD, Byrd JC, Chan K, Wu LC, Croce CM, Marcucci G: MicroRNA-29b induces global DNA hypomethylation and tumor suppressor gene reexpression in acute myeloid leukemia by targeting directly DNMT3A and 3B and indirectly DNMT1. Blood; 2009 Jun 18;113(25):6411-8
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  • [Title] MicroRNA-29b induces global DNA hypomethylation and tumor suppressor gene reexpression in acute myeloid leukemia by targeting directly DNMT3A and 3B and indirectly DNMT1.
  • Aberrant DNA hypermethylation contributes to myeloid leukemogenesis by silencing structurally normal genes involved in hematopoiesis.
  • In the current study, we showed that enforced expression of miR-29b in acute myeloid leukemia cells resulted in marked reduction of the expression of DNA methyltransferases DNMT1, DNMT3A, and DNMT3B at both RNA and protein levels.
  • Although down-regulation of DNMT3A and DNMT3B was the result of a direct interaction of miR-29b with the 3' untranslated regions of these genes, no predicted miR-29b interaction sites were found in the DNMT1 3' untranslated regions.
  • Altogether, these data provide novel functional links between miRNAs and aberrant DNA hypermethylation in acute myeloid leukemia and suggest a potentially therapeutic use of synthetic miR-29b oligonucleotides as effective hypomethylating compounds.

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  • (PMID = 19211935.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01-CA81534; United States / NCI NIH HHS / CA / R01 CA102031; United States / NCI NIH HHS / CA / R01-CA102031; United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / P01 CA076259; United States / NCI NIH HHS / CA / P01-CA76259
  • [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 / 3' Untranslated Regions; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Estrogen Receptor alpha; 0 / MicroRNAs; 0 / Neoplasm Proteins; 0 / RNA, Neoplasm; 0 / Sp1 Transcription Factor; 0 / estrogen receptor alpha, human; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA (cytosine-5-)-methyltransferase 1; EC 2.1.1.37 / DNA methyltransferase 3A; EC 2.1.1.37 / DNA methyltransferase 3B
  • [Other-IDs] NLM/ PMC2710934
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23. Patroglu T, Torun YA, Karakukcu M, Gorozen F: A case of Turner syndrome associated with acute myeloid leukemia (M2). J Pediatr Hematol Oncol; 2006 Oct;28(10):682-3
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  • [Title] A case of Turner syndrome associated with acute myeloid leukemia (M2).
  • A 9-year-old girl was diagnosed as acute myeloid leukemia-M2 according to the French-American-British classification.
  • In addition, a diagnosis of Turner syndrome (TS) was made, on the basis of the presence of the chromosomal abnormality, ovarian failure, and abnormal physical features.
  • In particular, children with Down syndrome have increased risk of developing acute myeloblastic leukemia especially M7.
  • On the other hand, cases of myeloid leukemia that are complicated with TS are extremely rare.
  • This is the first report of TS with acute myeloid leukemia of M2 subtype and t (8;.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Turner Syndrome / genetics


24. McCormack E, Skavland J, Mujic M, Bruserud Ø, Gjertsen BT: Lentinan: hematopoietic, immunological, and efficacy studies in a syngeneic model of acute myeloid leukemia. Nutr Cancer; 2010;62(5):574-83
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  • [Title] Lentinan: hematopoietic, immunological, and efficacy studies in a syngeneic model of acute myeloid leukemia.
  • We investigated the effects of nutritional grade lentinan upon BN rats and in a preclinical syngeneic model of acute myeloid leukemia.
  • Lentinan treatment of BN rats with BNML leukemia resulted in improved cage-side health and reduced cachexia in the terminal stage of this aggressive disease.
  • Combination of lentinan with standards of care in acute myeloid leukemia, idarubicin, and cytarabine increased average survival compared with monotherapy and reduced cachexia.
  • [MeSH-major] Adjuvants, Immunologic / therapeutic use. Hematopoiesis / drug effects. Lentinan / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Animals. Blood Cell Count. Cytokines / blood. Disease Models, Animal. Male. Rats. Rats, Inbred BN

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  • (PMID = 20574918.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Cytokines; 37339-90-5 / Lentinan
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25. Ramamoorthy K, Ramesh P, Al Bahar S: Primary treatment of acute myeloid leukemia (non M3) in elderly: a review. Gulf J Oncolog; 2008 Jul;(4):19-26
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  • [Title] Primary treatment of acute myeloid leukemia (non M3) in elderly: a review.
  • Treatment of acute myeloid leukemia (AML) in the elderly has always been a challenging task.
  • Acute myeloid leukemia in older adults is a biologically and clinically distinct entity.
  • Due to comorbid disease and impaired bone marrow stem cell reserve, older adults tolerate myelosuppressive chemotherapy poorly, with a treatment-related mortality rate of 25%.
  • In spite of various available targeted therapies, the overall survival has not improved dramatically in the past decade.
  • Standard allogeneic bone marrow transplantation is too dangerous to be considered as a mean to eradicate minimal residual disease after remission is obtained and myelointensive chemotherapy is not a beneficial post-remission strategy in this age cohort.
  • The advent of non-myeloablative regimens has shown some prospects in select group of patients with good performance status.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 20084771.001).
  • [ISSN] 2078-2101
  • [Journal-full-title] The Gulf journal of oncology
  • [ISO-abbreviation] Gulf J Oncolog
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Kuwait
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 39
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26. Pardee TS, Zuber J, Lowe SW: Effects of the Flt3 ITD on response to chemotherapy in a murine model of acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7060

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of the Flt3 ITD on response to chemotherapy in a murine model of acute myeloid leukemia.
  • : 7060 Background: Acute myeloid leukemia (AML) is an aggressive, genetically heterogeneous malignancy.
  • The Flt3 receptor tyrosine kinase containing an internal tandem duplication (Flt3 ITD) is a common mutation in AML and associated with a poor prognosis; however, its effect on chemotherapy response is currently unknown.
  • METHODS: Murine AML was generated by retroviral transduction of an MLL-ENL fusion protein into fetal liver cells and subsequent transplantation into syngeneic mice.
  • Blasts were harvested from moribund animals and myeloid lineage confirmed by immunophenotyping.
  • In contrast there was no difference in leukemic burden between Ara-C treated, dox treated or control animals in AML without Flt3 ITD (p = 0.2833).
  • These results suggest AML patients with Flt3 ITD may benefit more from high-dose cytarabine regimens then anthracyclines.

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  • (PMID = 27961434.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Bommer M, von Harsdorf S, Döhner H, Bunjes D, Ringhoffer M: Neoplastic meningitis in patients with acute myeloid leukemia scheduled for allogeneic hematopoietic stem cell transplantation. Haematologica; 2010 Nov;95(11):1969-72
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  • [Title] Neoplastic meningitis in patients with acute myeloid leukemia scheduled for allogeneic hematopoietic stem cell transplantation.
  • We analyzed the frequency of neoplastic meningitis in patients with acute myeloid leukemia prior to allogeneic hematopoietic stem cell transplantation at our institution.
  • Between 1996 and 2009, cerebrospinal fluid samples of 204 adult patients were examined during pre-transplant work-up for cell counts and, if abnormal, morphologically.
  • The proportion of patients with central nervous system involvement was significantly higher in patients with refractory disease at the time of transplantation compared with patients responding to prior systemic therapy (19% vs. 4.6%; P=0.003).
  • Since most of the patients with central nervous system involvement were asymptomatic, cerebrospinal fluid evaluation should be considered at least in patients with refractory acute myeloid leukemia.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Meningeal Neoplasms / mortality. Meningeal Neoplasms / therapy
  • [MeSH-minor] Adult. Disease-Free Survival. Female. Humans. Male. Meningitis / cerebrospinal fluid. Meningitis / mortality. Meningitis / pathology. Meningitis / therapy. Middle Aged. Retrospective Studies. Survival Rate. Transplantation, Homologous

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  • (PMID = 20663946.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2966922
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28. van den Ancker W, van Luijn MM, Westers TM, Bontkes HJ, Ruben JM, de Gruijl TD, Ossenkoppele GJ, van de Loosdrecht AA: Recent advances in antigen-loaded dendritic cell-based strategies for treatment of minimal residual disease in acute myeloid leukemia. Immunotherapy; 2010 Jan;2(1):69-83
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  • [Title] Recent advances in antigen-loaded dendritic cell-based strategies for treatment of minimal residual disease in acute myeloid leukemia.
  • Therapeutic vaccination with dendritic cells (DCs) is recognized as an important experimental therapy for the treatment of minimal residual disease in acute myeloid leukemia.
  • Many sources of leukemia-associated antigens and different methods for antigen loading of DCs have been used in an attempt to optimize anti-tumor responses.
  • For instance, monocyte-derived DCs have been loaded with apoptotic whole-cell suspensions, necrotic cell lysates, tumor-associated peptides, eluted peptides and cellular DNA or RNA.
  • This review discusses recent advances in DC research and the application of this knowledge towards new strategies for antigen loading of DCs in the treatment of minimal residual disease in acute myeloid leukemia.
  • [MeSH-major] Antigens / immunology. Dendritic Cells / immunology. Leukemia, Myeloid / immunology. Neoplasm, Residual / immunology
  • [MeSH-minor] Acute Disease. Humans. Immunotherapy / methods. Immunotherapy / trends. Killer Cells, Natural / immunology. Models, Immunological. T-Lymphocytes / immunology

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  • (PMID = 20635890.001).
  • [ISSN] 1750-7448
  • [Journal-full-title] Immunotherapy
  • [ISO-abbreviation] Immunotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens
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29. Wang SH, Yu L, Wang QS, Li HH, Zhao Y, Li F: [Effects of FLAG protocol in treatment of the first time induced non-remission acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Dec;15(6):1297-9
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  • [Title] [Effects of FLAG protocol in treatment of the first time induced non-remission acute myeloid leukemia].
  • In order to evaluate the efficacy of FLAG protocol (fludarabine, cytosine arabinoside and granulocyte colony-stimulating factor) in treatment of the first time induced non-remission acute myeloid leukemia (AML), 19 patients with first time induced non-remission acute myeloid leukemia were treated with FLAG protocol.
  • Among the patients in CR 5 patients had been received allogeneic stem cell transplantation, 3 patients from them survived without disease, including 1 patient has survived 26 months and still remains in CR.
  • Main toxicities of this protocol were gastrointestinal side effects, myelosuppression and neutropenia, slight abnormality of liver function and so on.
  • It is concluded that the FLAG protocol should be employed for the the first time induced non-remission patients as early as possible, and provides conditions for the hematopoietic stem cell transplantation.

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  • (PMID = 18088488.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine
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30. Schaefer EW, Loaiza-Bonilla A, Juckett M, DiPersio JF, Roy V, Slack J, Wu W, Laumann K, Espinoza-Delgado I, Gore SD, Mayo P2C Phase II Consortium: A phase 2 study of vorinostat in acute myeloid leukemia. Haematologica; 2009 Oct;94(10):1375-82
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  • [Title] A phase 2 study of vorinostat in acute myeloid leukemia.
  • SAHA) in patients with relapsed acute myeloid leukemia and in selected untreated patients with high-risk acute myeloid leukemia.
  • DESIGN AND METHODS: Patients with relapsed or untreated acute myeloid leukemia who were not candidates for chemotherapy entered one of the two treatment arms.
  • CONCLUSIONS: Vorinostat monotherapy demonstrated minimal activity in this group of patients with acute myeloid leukemia.
  • Future studies of vorinostat in acute myeloid leukemia should focus on combinations with other drugs with which it might interact pharmacodynamically.
  • [MeSH-major] Hydroxamic Acids / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 19794082.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00305773
  • [Grant] United States / NCI NIH HHS / CA / K24 CA111717; United States / NCI NIH HHS / CA / K24 CA111717-05; United States / NCI NIH HHS / CM / N01 CM17104
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Hydroxamic Acids; 58IFB293JI / vorinostat
  • [Other-IDs] NLM/ PMC2754953
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31. Chai JY, Zheng WQ, Wei N: [Clinical research of modified CAG regimen for the treatment of relapsed acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Aug;17(4):1061-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical research of modified CAG regimen for the treatment of relapsed acute myeloid leukemia].
  • The objective of study was to observe the efficacy and adverse events of modified CAG regimen in treating patients with relapsed acute myeloid leukemia.
  • CAG regimen with prolongation of aclarubicin up to 7 days were used to treat 17 cases of relapsed acute myeloid.
  • After 1 course of chemotherapy, the efficacy and adverse events were evaluated, patients who did not achieve remission were excluded from this regimen, patients who achieved remission were continuously given 1 course of CAG regimen.
  • In conclusion, treatment for relapsed acute myeloid leukemia with modified CAG regiment is safe and effective, and can provide conditions for allo-hematopoietic stem cell transplantation, but its long term efficacy needs to further study.

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  • (PMID = 19698260.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 74KXF8I502 / Aclarubicin
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32. Chionh F, Herbert KE, Seymour JF, Prince HM, Wolf M, Zimet A, Tam C, Kennedy GA: Ante-mortem diagnosis of localized invasive esophageal aspergillosis in a patient with acute myeloid leukemia. Leuk Lymphoma; 2005 Apr;46(4):603-5
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  • [Title] Ante-mortem diagnosis of localized invasive esophageal aspergillosis in a patient with acute myeloid leukemia.
  • We report a case of localized gastrointestinal IA complicating induction chemotherapy for acute myeloid leukemia (AML).
  • A review of the literature suggests that although localized gastrointestinal IA is rare, involvement of the gastrointestinal tract is not uncommon in disseminated infection.
  • [MeSH-major] Aspergillosis / complications. Aspergillosis / diagnosis. Esophageal Diseases / complications. Esophageal Diseases / diagnosis. Leukemia, Myeloid / complications. Opportunistic Infections / complications
  • [MeSH-minor] Acute Disease. Aged. Gastroscopy. Humans. Male. Neoplasm Invasiveness. Remission Induction


33. Ural AU, Avcu F, Yilmaz MI, Guden M, Ozturk B, Ozcan A, Guran S, Bahce M, Yalcin A: Development of squamous cell carcinoma of the tongue during induction chemotherapy for acute myeloid leukemia. Tumori; 2005 Jan-Feb;91(1):81-3
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  • [Title] Development of squamous cell carcinoma of the tongue during induction chemotherapy for acute myeloid leukemia.
  • Immunosuppression is a well-recognized cause of skin tumors, in particular squamous cell carcinomas (SCC).
  • In patients with hematological malignancies undergoing chemotherapy, SCC has been reported late in the course of the disease or many years after completion of treatment.
  • Here we report a patient with acute myeloid leukemia who developed a SCC of the tongue while receiving the third course of induction chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Carcinoma, Squamous Cell / chemically induced. Immunosuppression / adverse effects. Leukemia, Myeloid, Acute / drug therapy. Neoplasms, Second Primary / chemically induced. Tongue Neoplasms / chemically induced


34. Tagliafico E, Tenedini E, Manfredini R, Grande A, Ferrari F, Roncaglia E, Bicciato S, Zini R, Salati S, Bianchi E, Gemelli C, Montanari M, Vignudelli T, Zanocco-Marani T, Parenti S, Paolucci P, Martinelli G, Piccaluga PP, Baccarani M, Specchia G, Torelli U, Ferrari S: Identification of a molecular signature predictive of sensitivity to differentiation induction in acute myeloid leukemia. Leukemia; 2006 Oct;20(10):1751-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of a molecular signature predictive of sensitivity to differentiation induction in acute myeloid leukemia.
  • Acute myeloid leukemia (AML) blasts are immature committed myeloid cells unable to spontaneously undergo terminal maturation, and characterized by heterogeneous sensitivity to natural differentiation inducers.
  • Here, we show a molecular signature predicting the resistance or sensitivity of six myeloid cell lines to differentiation induced in vitro with retinoic acid or vitamin D.
  • The identified signature was further validated by TaqMan assay for the prediction of response to an in vitro differentiation assay performed on 28 freshly isolated AML blast populations.
  • The TaqMan assay successfully predicts the in vitro resistance or responsiveness of AML blasts to differentiation inducers.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm / genetics. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics. Tretinoin / pharmacology
  • [MeSH-minor] Acute Disease. Cell Differentiation / drug effects. Cell Line, Tumor. Cluster Analysis. Databases, Factual. Gene Expression Regulation, Leukemic / drug effects. Humans. Meta-Analysis as Topic. Oligonucleotide Array Sequence Analysis. Predictive Value of Tests. Reverse Transcriptase Polymerase Chain Reaction. Vitamin D / pharmacology. Vitamins / pharmacology

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  • (PMID = 16932344.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Vitamins; 1406-16-2 / Vitamin D; 5688UTC01R / Tretinoin
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35. He GS, Zhou L, Wu DP, Xue YQ, Zhu MQ, Liu DD, Sun AN, Jin ZM, Qiu HY, Miao M, Tang XW, Fu ZZ, Ma X, Wang XL: [Abnormal expression of cCD79a/cCD22 in acute myeloid leukemia with t (8;21)]. Zhonghua Xue Ye Xue Za Zhi; 2006 Mar;27(3):187-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Abnormal expression of cCD79a/cCD22 in acute myeloid leukemia with t (8;21)].
  • OBJECTIVE: To report abnormal expression of cCD79a/cCD22 in four cases of acute myeloid leukemia (AML) with t (8;21).
  • METHODS: The characteristics of morphology, immunophenotype, chromosome karyotype (MIC) and clinical manifestations of 4 AML patients with t (8;21) expressing cCD79a/cCD22 were analyzed.
  • (5) morphology showed acute myeloid leukemia with high percentage of blast cells;.
  • (6) B-lymphoid and myeloid immunophenotype, and high expression of CD34;.
  • (9) response well to chemotherapy regimen which simultaneously treated myeloid and lymphocytic leukemia.
  • CONCLUSION: Abnormal expression of cCD79a/cCD22 in AML with t (8;21) (q22;q22) suggested that this kind of leukemia might be related with abnormal expression gene of B cell.
  • [MeSH-major] Antigens, CD79 / metabolism. Leukemia, Myeloid, Acute / genetics. Sialic Acid Binding Ig-like Lectin 2 / metabolism

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  • (PMID = 16792922.001).
  • [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
  • [Chemical-registry-number] 0 / Antigens, CD79; 0 / Sialic Acid Binding Ig-like Lectin 2
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36. Zhang SJ, Shi JY, Zhu YM, Shi ZZ, Yan-Sheng, Gu BW, Bai XT, Shen ZX, Li JY: The investigation of mutation and single nucleotide polymorphism of receptor tyrosine kinases and downstream scaffold molecules in acute myeloid leukemia. Leuk Lymphoma; 2006 Dec;47(12):2610-6
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  • [Title] The investigation of mutation and single nucleotide polymorphism of receptor tyrosine kinases and downstream scaffold molecules in acute myeloid leukemia.
  • We investigate the role of mutations of receptor tyrosine kinases as well as their downstream scaffold molecules in leukemogenesis of acute myeloid leukemia (AML) in Chinese patients.
  • In addition, FLT3 mutations were seen in three of five patients with AML following myelodysplastic syndrome (60%) and 39 of 268 (14.6%) de novo AML patients (P < 0.05).
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Polymorphism, Single Nucleotide. Receptor Protein-Tyrosine Kinases / genetics

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  • (PMID = 17169806.001).
  • [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 / DNA Primers; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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37. Batty G, Kantarjian H, Issa JJ, Garcia-Manero G, Pierce S, O'Brien S, Jabbour E, Cortes J, Ravandi F: Feasibility of hypomethylating therapy in patients with renal insufficiency. J Clin Oncol; 2009 May 20;27(15_suppl):7089

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: We investigated the outcomes of pts with RI and MDS, chronic myelomonocytic leukemia (CMML), or acute myeloid leukemia (AML) receiving therapy with HA.
  • We used the International Working Group criteria to evaluate the response rates.
  • RESULTS: Forty-two pts with sCr ≥ 1.5 mg/dL (including 17 with MDS, 16 with AML, and 9 with CMML) were treated with DAC or 5AZA alone or in combination with other agents (primarily histone deacetylase inhibitors).
  • The incidence of complications, DA, and the response rate were not significantly different for pts with sCr > 2.0 mg/dL.
  • CONCLUSIONS: The use of HA is well tolerated in pts with MDS and AML and RI who achieved comparable OR rates to those without RI.

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  • (PMID = 27961273.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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38. Ritchie DS, McBean M, Westerman DA, Kovalenko S, Seymour JF, Dobrovic A: Complete molecular response of e6a2 BCR-ABL-positive acute myeloid leukemia to imatinib then dasatinib. Blood; 2008 Mar 1;111(5):2896-8
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  • [Title] Complete molecular response of e6a2 BCR-ABL-positive acute myeloid leukemia to imatinib then dasatinib.
  • De novo presentation of acute myeloid leukemia (AML) expressing the Philadelphia (Ph) chromosomal abnormality is rare and is associated with a dismal prognosis.
  • To date, reported cases of Ph(+) AML have expressed either the e13a2 or e14a2 BCR-ABL fusion transcripts.
  • We report a unique case of de novo AML expressing the e6a2 fusion transcript and describe disease sensitivity to both imatinib before allogeneic stem-cell transplantation and dasatinib for AML relapse after allogeneic stem-cell transplantation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use

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  • (PMID = 18073350.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
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39. Cornelissen JJ, Löwenberg B: Role of allogeneic stem cell transplantation in current treatment of acute myeloid leukemia. Hematology Am Soc Hematol Educ Program; 2005;:151-5
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  • [Title] Role of allogeneic stem cell transplantation in current treatment of acute myeloid leukemia.
  • Allogeneic hematopoietic stem cell transplantation (alloSCT) has been established as an effective consolidation therapy in acute myeloid leukemia (AML) in first or subsequent remission.
  • Here, we review studies that identify categories of AML patients who may specifically benefit from alloSCT.
  • In addition, we discuss recent developments with respect to alternative donors, stem cell sources, and supportive care.
  • Finally, we highlight recent results obtained with reduced-intensity alloSCT, which already significantly influence our therapeutic strategy in elderly patients with AML.

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  • (PMID = 16304373.001).
  • [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; Review
  • [Publication-country] United States
  • [Number-of-references] 34
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40. Tadmor T, Vadazs Z, Dar H, Laor R, Attias D: Hemophagocytic syndrome preceding acute myeloid leukemia with der t [7:17][q12; q11], monosomy, 17 and 5p-. J Pediatr Hematol Oncol; 2006 Aug;28(8):544-6
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  • [Title] Hemophagocytic syndrome preceding acute myeloid leukemia with der t [7:17][q12; q11], monosomy, 17 and 5p-.
  • Hemophagocytic syndrome (HS) is a severe and acute proliferative process of histiocytes, often associated with infection or malignancy.
  • No consistent clonal abnormality has been reported in HS.
  • We report a case of a child presented with HS, who progressed later to acute myeloid leukemia (AML)-M4, associated with a clonal evolution, from normal to a complex karyotype consisting of t [7:17] and deletions in chromosomes 7, 17, and 5.
  • This is the second report of involvement of 7q rearrangement in a child with HS that has progressed to AML.
  • Additional studies are required to establish the association reported here, between HS with progression to AML and chromosome rearrangements that involve chromosome 7q.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 17 / genetics. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 7 / genetics. Leukemia, Myeloid / genetics. Lymphohistiocytosis, Hemophagocytic / genetics
  • [MeSH-minor] Acute Disease. Child, Preschool. Fatal Outcome. Humans. Male. Remission Induction. Treatment Outcome

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  • (PMID = 16912598.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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41. Hayden JT, Wood KM, Pedler S, Lawson A, Skinner R: Invasive aspergillosis of the small bowel in an infant with acute myeloid leukemia and intestinal obstruction. Pediatr Hematol Oncol; 2009 Jan;26(1):84-91
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  • [Title] Invasive aspergillosis of the small bowel in an infant with acute myeloid leukemia and intestinal obstruction.
  • Acute myeloid leukemia was diagnosed in an infant with fever and pancytopenia.
  • Intestinal obstruction was present at diagnosis and laparotomy performed after failure of conservative management demonstrated leukemic infiltration of the resected terminal ileum.
  • Invasive aspergillosis may unusually present at nonpulmonary sites at initial presentation of acute leukemia.
  • Microbiological or histological diagnosis is needed to guide aggressive appropriate management.
  • [MeSH-major] Aspergillosis / pathology. Ileal Diseases / microbiology. Intestinal Obstruction / etiology. Leukemia, Myeloid, Acute / complications


42. Fehniger TA, Byrd JC, Marcucci G, Abboud CN, Kefauver C, Payton JE, Vij R, Blum W: Single-agent lenalidomide induces complete remission of acute myeloid leukemia in patients with isolated trisomy 13. Blood; 2009 Jan 29;113(5):1002-5
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  • [Title] Single-agent lenalidomide induces complete remission of acute myeloid leukemia in patients with isolated trisomy 13.
  • Patients with acute myeloid leukemia (AML) frequently fail chemotherapy due to refractory disease, relapse, or toxicity.
  • Among older AML patients (age > 60 years), there are few long-term survivors.
  • Lenalidomide is a candidate for study in AML based on its clinical activity in a related disorder, myelodysplastic syndrome (MDS), with the 5q- chromosomal abnormality.
  • We report induction of sustained morphologic and cytogenetic complete remission in 2 older AML patients treated with high-dose, single-agent lenalidomide; each patient had trisomy 13 as the sole cytogenetic abnormality.
  • We show for the first time that lenalidomide has clinical activity in this poor-risk cytogenetic subset of AML.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Chromosomes, Human, Pair 13 / genetics. Leukemia, Myeloid, Acute / drug therapy. Thalidomide / analogs & derivatives. Trisomy / genetics

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  • (PMID = 18824593.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00466895/ NCT00546897
  • [Grant] United States / NCI NIH HHS / CA / K23 CA120708; United States / NCI NIH HHS / CA / K23CA120708
  • [Publication-type] Case Reports; Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide
  • [Other-IDs] NLM/ PMC2947363
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43. Bernasconi P: Molecular pathways in myelodysplastic syndromes and acute myeloid leukemia: relationships and distinctions-a review. Br J Haematol; 2008 Sep;142(5):695-708
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  • [Title] Molecular pathways in myelodysplastic syndromes and acute myeloid leukemia: relationships and distinctions-a review.
  • The myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are both hematopoietic stem cell disorders.
  • These engraftment difficulties may be due to the unique nature of MDS genetic lesions that are truly able to recapitulate the disease phenotype.
  • MDS and AML of younger patients harbour clonal yet different chromosomal markers, whereas MDS and AML of the elderly present similar defects.
  • Potential involvement of tumor suppressor genes in MDS has been hypothesized but never confirmed, while cooperation between class I and class II mutations has been identified in AML.
  • The reciprocal interactions between stromal cells and neoplastic clones are disrupted in both MDS and AML.
  • In early MDS, stromal and neoplastic cells produce high levels of inhibitory cytokines, whereas in advanced MDS and AML they produce high levels of anti-apoptotic molecules.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


44. Pluta A, Wrzesien-Kus A, Cebula-Obrzut B, Wolska A, Szmigielska-Kaplon A, Czemerska M, Pluta P, Robak T, Smolewski P, Wierzbowska A: Influence of high expression of Smac/DIABLO protein on the clinical outcome in acute myeloid leukemia patients. Leuk Res; 2010 Oct;34(10):1308-13
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  • [Title] Influence of high expression of Smac/DIABLO protein on the clinical outcome in acute myeloid leukemia patients.
  • The role of the Smac/DIABLO protein, a novel apoptosis agonist, in acute myeloid leukemia (AML) is not clearly determined.
  • The expression of Smac/DIABLO protein in AML leukemic cells and its relationship with clinical outcome was evaluated in this study.
  • The intracellular expression of Smac/DIABLO protein was assessed using multi-color flow cytometry in 71 newly diagnosed AML patients treated with conventional chemotherapy.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / analysis. Leukemia, Myeloid, Acute / mortality. Mitochondrial Proteins / analysis

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20061022.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DIABLO protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Mitochondrial Proteins
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45. Gronda M, Brandwein J, Minden MD, Pond GR, Schuh AC, Wells RA, Messner H, Chun K, Schimmer AD: Assessment of the downstream portion of the mitochondrial pathway of caspase activation in patients with acute myeloid leukemia. Apoptosis; 2005 Dec;10(6):1285-94
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  • [Title] Assessment of the downstream portion of the mitochondrial pathway of caspase activation in patients with acute myeloid leukemia.
  • Most chemotherapeutic agents used in the treatment of acute myeloid leukemia (AML) induce apoptosis by triggering the mitochondrial pathway of caspase activation.
  • To investigate the downstream portion of the mitochondrial pathway of caspase activation in patients with AML, cytosolic lysates were stimulated with cytochrome c and dATP and hydrolysis of Ac-DEVD-AFC by effector caspases was measured.
  • Defects in the distal mitochondrial pathway were more common in samples from patients with AML that relapsed rapidly after induction chemotherapy compared to samples from treatment naïve patients.
  • The incidence of blocked pathways did not differ based on response to induction chemotherapy, as even nonresponders generally had an intact pathway.
  • When the distal mitochondrial pathway was blocked, defects were usually at the level of the effector caspases.
  • Thus, functional defects in the distal portion of the mitochondrial pathway of caspase activation may help explain the nature of response and relapse after treatment.
  • [MeSH-major] Caspases / metabolism. Leukemia, Myeloid, Acute / enzymology. Mitochondria / enzymology

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  • (PMID = 16215669.001).
  • [ISSN] 1360-8185
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Caspase Inhibitors; 0 / Enzyme Inhibitors; 0 / Inhibitor of Apoptosis Proteins; 8L70Q75FXE / Adenosine Triphosphate; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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46. Sárová I, Brezinová J, Zemanová Z, Lizcová L, Berková A, Izáková S, Malinová E, Fuchs O, Kostecka A, Provazníková D, Filkuková J, Maaloufová J, Starý J, Michalová K: A partial nontandem duplication of the MLL gene in four patients with acute myeloid leukemia. Cancer Genet Cytogenet; 2009 Dec;195(2):150-6
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  • [Title] A partial nontandem duplication of the MLL gene in four patients with acute myeloid leukemia.
  • Unusual MLL gene rearrangements were found in bone marrow cells of four patients with acute myeloid leukemia.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 19963115.001).
  • [ISSN] 1873-4456
  • [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 / DNA Primers; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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47. Ikawa Y, Sugimoto N, Koizumi S, Yachie A, Saikawa Y: Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene. J Clin Oncol; 2009 May 20;27(15_suppl):10045

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene.
  • While CD10 negativity reflects an earlier stage of B-cell development, complete IgH gene rearrangements (VDJ<sub>H</sub>) show more mature IgH status.
  • METHODS: CD10-negative infant ALL with MLL/AF4, CD10-positive infant ALL with germ-line MLL, CD10-positive pre-B ALL cell line, infant AML (M5) with MLL/AF9 and pediatric AML (M2) with AML1/ETO were analyzed for VDJ<sub>H</sub> status and methylation of CD10 gene promoters.
  • RESULTS: Three of 4 cases with infant ALL revealed complete rearrangements of VDJ<sub>H</sub> gene with productive joints.
  • In contrast, none or a few of the CpG dinucleotides were methylated in the CD10-positive ALL, AML (M5) with MLL/AF9 or AML (M2) with AML1/ETO.

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  • (PMID = 27962471.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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48. Impera L, Albano F, Mancini M, Aventin A, Rocchi M, Storlazzi CT: Similar mechanisms formed ring markers containing chromosome 12 pericentromeric region in two patients with therapy-related acute myeloid leukemia. Cancer Genet Cytogenet; 2008 Mar;181(2):131-7
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  • [Title] Similar mechanisms formed ring markers containing chromosome 12 pericentromeric region in two patients with therapy-related acute myeloid leukemia.
  • Two cases of therapy-related acute myeloid leukemia showed complex karyotypes, including a small ring and a larger D-chromosome.
  • The deleted segment of 12 was found fused to the short arm of a D-group chromosome.
  • A fusion at the short arms of chromosome 12 and a D-group chromosome was accompanied by excision and ligation of the chromosome 12 pericentromeric region to form a small ring chromosome.
  • [MeSH-major] Chromosomes, Human, Pair 12. Leukemia, Myeloid, Acute / genetics. Ring Chromosomes


49. Benites BD, Fattori A, Hackel C, Lorand-Metze I, De Souza CA, Schulz E, Costa FF, Saad ST: Low expression of APAF-1XL in acute myeloid leukemia may be associated with the failure of remission induction therapy. Braz J Med Biol Res; 2008 Jul;41(7):571-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low expression of APAF-1XL in acute myeloid leukemia may be associated with the failure of remission induction therapy.
  • In the present study, the mRNA expression analysis of different APAF-1 transcripts (APAF-1S, APAF-1LC, APAF-1LN, and APAF-1XL) was analyzed in bone marrow samples from 37 patients with acute myeloid leukemia (newly diagnosed, with no previous treatment).
  • Only 46% of the patients presented complete remission in response to remission induction therapy (represented by less than 5% marrow blasts and hematological recovery), all but 2 cases being from group 1, 21.6% did not attain complete remission (only 1 case from group 1), and 32.4% of the patients died early.
  • Both groups showed similar characteristics regarding white blood cell counts, cytogenetic data or presence of gene rearrangements associated with good prognosis as AML1-ETO, CBFB-MYH11 and PML/RARA.
  • Since it has been shown that only the isoforms with the extra WD-40 repeat region activate procaspase-9, we suggest that low procaspase-9 activation may also be involved in the deregulation of apoptosis and chemotherapy resistance in acute myeloid leukemia.

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  • (PMID = 18719738.001).
  • [ISSN] 1414-431X
  • [Journal-full-title] Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
  • [ISO-abbreviation] Braz. J. Med. Biol. Res.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Apoptotic Protease-Activating Factor 1; 0 / Biomarkers, Tumor; 0 / DNA, Complementary; 0 / RNA, Messenger; 0 / Transcription Factors
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50. Dai G, Chan KK, Liu S, Hoyt D, Whitman S, Klisovic M, Shen T, Caligiuri MA, Byrd J, Grever M, Marcucci G: Cellular uptake and intracellular levels of the bcl-2 antisense g3139 in cultured cells and treated patients with acute myeloid leukemia. Clin Cancer Res; 2005 Apr 15;11(8):2998-3008
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  • [Title] Cellular uptake and intracellular levels of the bcl-2 antisense g3139 in cultured cells and treated patients with acute myeloid leukemia.
  • PURPOSE: Down-regulation of Bcl-2 by the antisense G3139, currently under clinical evaluations, could restore chemosensitivity in otherwise resistant malignant cells.
  • EXPERIMENTAL DESIGN: Cellular uptake of G3139 was studied in leukemia myeloid cell lines and blasts collected from treated patients using a newly developed, novel, and highly sensitive ELISA-based assay.
  • Robust intracellular concentrations of G3139 were achieved in vivo in bone marrow (range, 3.4-40.6 pmol/mg protein) and peripheral blood mononuclear cells (range, 0.47-19.4 pmol/mg protein) from acute myeloid leukemia patients treated with G3139.
  • CONCLUSIONS: This is the first evidence that measurable intracellular levels of G3139 are achievable in vivo in acute myeloid leukemia patients and that Bcl-2 down-regulation is likely to depend on the achievable intracellular concentrations rather than on plasma concentrations.
  • [MeSH-major] Leukemia, Myeloid / metabolism. Oligonucleotides, Antisense / pharmacokinetics. Proto-Oncogene Proteins c-bcl-2 / genetics. Thionucleotides / pharmacokinetics
  • [MeSH-minor] Acute Disease. Base Sequence. Cell Line, Tumor. Chromatography, High Pressure Liquid / methods. Enzyme-Linked Immunosorbent Assay / methods. Humans. K562 Cells. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reproducibility of Results. Reverse Transcriptase Polymerase Chain Reaction. Time Factors

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  • (PMID = 15837754.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30CA16058; United States / NCI NIH HHS / CA / R21 CA 94552; United States / NCI NIH HHS / CA / UO1-CA 76576
  • [Publication-type] Comparative Study; 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 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Thionucleotides; 85J5ZP6YSL / oblimersen
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51. Pulsoni A, Iacobelli S, Bernardi M, Borgia M, Camera A, Cantore N, Di Raimondo F, Fazi P, Ferrara F, Leoni F, Liso V, Mancini M, Marmont F, Matturro A, Maurillo L, Melillo L, Meloni G, Mirto S, Specchia G, Valentini CG, Venditti A, Leone G, Foà R, Mandelli F, Pagano L: M4 acute myeloid leukemia: the role of eosinophilia and cytogenetics in treatment response and survival. The GIMEMA experience. Haematologica; 2008 Jul;93(7):1025-32
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  • [Title] M4 acute myeloid leukemia: the role of eosinophilia and cytogenetics in treatment response and survival. The GIMEMA experience.
  • BACKGROUND: Myelomonocytic acute myeloid leukemia (M4-AML) is frequently associated with the cytogenetic marker inv(16) and/or the presence of eosinophilia.
  • DESIGN AND METHODS: Adult patients with acute myeloid leukemia consecutively enrolled in the GIMEMA trials AML10 and LAM99p were retrospectively analyzed.
  • RESULTS: Among 1686 patients, 400 cases of M4-AML were identified; of these, 78% had neither eosinophilia nor inv(16), 6% had eosinophilia only, 8% had inv(16) only and 8% had both.
  • The presence of only one of the two factors also increased the probabilities of complete remission and overall survival, but not to a statistically significant extent.
  • The relapse-free survival of the responding patients was not influenced by the two factors.
  • CONCLUSIONS: In a large series of patients with M4-AML we confirmed the favorable role of inv(16), but the weight of this factor among the whole M4 population was of limited relevance.
  • Based on the results of this large case population, overall and relapse-free survival rates of patients with M4-AML are not significantly better than those of patients with non-M4 AML, while the concomitant presence of both inv(16) and eosinophilia was associated with a significantly improved prognosis.
  • [MeSH-major] Cytogenetics / methods. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / therapy
  • [MeSH-minor] Adolescent. Adult. Age Factors. Chromosome Inversion. Combined Modality Therapy. Disease-Free Survival. Eosinophilia / diagnosis. Eosinophilia / genetics. Humans. Middle Aged. Prognosis. Remission Induction. Retrospective Studies. Treatment Outcome

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  • (PMID = 18508801.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial
  • [Publication-country] Italy
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52. Zhao JM, Wang HW, Xu ZF, Zhu L, Bai B, Ge XY: [Detection of CCAAT/enhancer binding protein alpha gene mutations in acute myeloid leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2005 May;26(5):299-302
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  • [Title] [Detection of CCAAT/enhancer binding protein alpha gene mutations in acute myeloid leukemia].
  • OBJECTIVE: To explore the relationship between CCAAT/enhancer binding protein alpha (C/EBPalpha) gene mutations and the development of acute myeloid leukemia (AML).
  • METHODS: The whole coding region of C/EBPalpha gene were screened in 48 cases of AML and 11 normal subjects by PCR-single strand conformation polymorphism (PCR-SSCP) and sequencing.
  • RESULTS: C/EBPalpha mutations were detected in 5 of 48 AML patients.
  • CONCLUSIONS: Different mutation types of C/EBPalpha gene exist in a small number of patients with AML and might be related to the pathogenesis of some leukemias.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 15949295.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha
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53. Khalid S, Adil SN, Vaziri IA: Granulocytic sarcoma in the absence of acute myeloid leukemia: a case report. Indian J Pathol Microbiol; 2007 Jan;50(1):88-90
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  • [Title] Granulocytic sarcoma in the absence of acute myeloid leukemia: a case report.
  • Granulocytic sarcoma is an extramedullary tumor composed of immature granulocytic precursor cells.
  • The tumor may develop during the course of acute myeloid leukemia, chronic myeloid leukemia or other myelodysplastic disorders.
  • It can occur without blood or bone marrow manifestations of leukemia and in this case, the diagnosis is difficult.
  • Our patient was initially diagnosed as a case of T-cell non Hodgkin's lymphoma and received one cycle of CHOP with only transient improvement in his symptoms.
  • Subsequently, his biopsy slides were reviewed at our centre and were reported as granulocytic sarcoma.
  • [MeSH-major] Sarcoma, Myeloid / diagnosis
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Biopsy. Bone Marrow / pathology. Cyclophosphamide / administration & dosage. Diagnosis, Differential. Doxorubicin / administration & dosage. Histocytochemistry. Humans. Leukemia, Myeloid, Acute / complications. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / drug therapy. Male. Neoplasms. Prednisolone / administration & dosage. Vincristine / administration & dosage

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  • (PMID = 17474271.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; VAP-cyclo protocol
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54. de Oliveira FM, Tone LG, Simões BP, Falcão RP, Brassesco MS, Sakamoto-Hojo ET, dos Santos GA, Marinato AF, Jácomo RH, Rego EM: Acute myeloid leukemia (AML-M2) with t(5;11)(q35;q13) and normal expression of cyclin D1. Cancer Genet Cytogenet; 2007 Jan 15;172(2):154-7
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  • [Title] Acute myeloid leukemia (AML-M2) with t(5;11)(q35;q13) and normal expression of cyclin D1.
  • We report a case of acute myeloid leukemia (AML) subtype M2, with t(5;11)(q35;q13), in a 30-year-old man.
  • Conventional cytogenetic, spectral karyotyping, and fluorescence in situ hybridization (FISH) studies on bone marrow sample obtained at diagnosis revealed an abnormal karyotype in all cells examined.
  • Similar to the 11q23 region, 11q13 changes can be found in both myeloid and lymphoid neoplasias with different chromosomes serving as donors in translocations.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 5 / genetics. Cyclin D1 / biosynthesis. Cyclin D1 / genetics. Gene Expression Regulation, Neoplastic / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Humans. Leukemia, Myelomonocytic, Acute. Male


55. Pawarode A, Sait SN, Nganga A, Coignet LJ, Barcos M, Baer MR: Acute myeloid leukemia developing during imatinib mesylate therapy for chronic myeloid leukemia in the absence of new cytogenetic abnormalities. Leuk Res; 2007 Nov;31(11):1589-92
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  • [Title] Acute myeloid leukemia developing during imatinib mesylate therapy for chronic myeloid leukemia in the absence of new cytogenetic abnormalities.
  • The BCR/ABL tyrosine kinase inhibitor imatinib mesylate produces a high rate of cytogenetic responses in patients with Philadelphia (Ph)-positive chronic myeloid leukemia (CML), but secondary clonal chromosome abnormalities may develop in Ph-negative cells, and acute myeloid leukemia (AML) has been reported in patients with secondary chromosome abnormalities.
  • We report a patient who developed AML during imatinib treatment of Ph-positive CML despite a cytogenetic response and absence of secondary chromosome abnormalities.
  • Thus, development of AML as a rare event in CML patients with cytogenetic responses to imatinib therapy does not depend on the development of secondary cytogenetic abnormalities.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Acute / chemically induced. Piperazines / therapeutic use. Pyrimidines / therapeutic use


56. Al-Mawali A, Gillis D, Lewis I: The role of multiparameter flow cytometry for detection of minimal residual disease in acute myeloid leukemia. Am J Clin Pathol; 2009 Jan;131(1):16-26
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  • [Title] The role of multiparameter flow cytometry for detection of minimal residual disease in acute myeloid leukemia.
  • The presence of minimal residual disease (MRD) in the bone marrow (BM) of patients with acute myeloid leukemia (AML) following chemotherapy has been established by many studies to be strongly associated with relapse of leukemia.
  • This review is not an overview of all MRD studies, but rather discusses the possibilities for optimizing MRD detection, the use of multiparameter flow cytometry (MFC) techniques in MRD detection, and the implications for future patient treatment.
  • This review focuses on MRD detection in AML using MFC and discusses the reported correlations of MRD, clinical and biologic features of the disease, and outcome.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis

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  • (PMID = 19095561.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34
  • [Number-of-references] 65
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57. Koçoğlu E, Karabay O: [Catheter associated Staphylococcus sciuri sepsis in a patient with acute myeloid leukemia]. Mikrobiyol Bul; 2006 Oct;40(4):397-400
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  • [Title] [Catheter associated Staphylococcus sciuri sepsis in a patient with acute myeloid leukemia].
  • [Transliterated title] Akut myelositik lösemili bir olguda kateter ile ilişkili Staphylococcus sciuri sepsisi.
  • In this paper, S. sciuri bacteremia which was associated with an indwelling catheter of a patient with acute myeloid leukemia (AML) and neutropenia was presented.
  • An empirical intravenous antibiotic therapy (meropenem, vancomycin) was initiated with the preliminary diagnosis of febrile neutropenia and catheter infection.
  • [MeSH-major] Bacteremia / microbiology. Catheters, Indwelling / microbiology. Leukemia, Myeloid, Acute / complications. Neutropenia / complications. Staphylococcal Infections / microbiology. Staphylococcus / isolation & purification

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  • (PMID = 17205699.001).
  • [ISSN] 0374-9096
  • [Journal-full-title] Mikrobiyoloji bülteni
  • [ISO-abbreviation] Mikrobiyol Bul
  • [Language] tur
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Thienamycins; 6Q205EH1VU / Vancomycin; FV9J3JU8B1 / meropenem; UH95VD7V76 / Oxacillin
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58. Leymarie V, Flandrin G, Noguera ME, Leymarie F, Lioure B, Daliphard S, Groupe Ouest-Est des Leucémies Aiguës et Autres Maladies du Sang cytologists: Telehematology: a pilot experience of cytological diagnosis of acute myeloid leukemia via the Internet. A GOELAMS study. Haematologica; 2006 Sep;91(9):1285-6
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  • [Title] Telehematology: a pilot experience of cytological diagnosis of acute myeloid leukemia via the Internet. A GOELAMS study.
  • Although modern communication technology is well developed, telehematology does not readily lend itself to practical laboratory use.
  • The cytologists of the AML-2001 protocol established an innovative organization to demonstrate the reliability of the diagnostic assessment of acute myeloid leukemia through a rapid and decentralized exchange of information via the internet and to define the conditions optimizing expert diagnosis.
  • [MeSH-major] Internet. Leukemia, Myeloid / diagnosis. Telemedicine
  • [MeSH-minor] Acute Disease. Cytological Techniques. Hematology / methods. Humans. Pilot Projects

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  • (PMID = 16956838.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] Italy
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59. Maslak PG, Dao T, Krug LM, Chanel S, Korontsvit T, Zakhaleva V, Zhang R, Wolchok JD, Yuan J, Pinilla-Ibarz J, Berman E, Weiss M, Jurcic J, Frattini MG, Scheinberg DA: Vaccination with synthetic analog peptides derived from WT1 oncoprotein induces T-cell responses in patients with complete remission from acute myeloid leukemia. Blood; 2010 Jul 15;116(2):171-9
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  • [Title] Vaccination with synthetic analog peptides derived from WT1 oncoprotein induces T-cell responses in patients with complete remission from acute myeloid leukemia.
  • A pilot study was undertaken to assess the safety, activity, and immunogenicity of a polyvalent Wilms tumor gene 1 (WT1) peptide vaccine in patients with acute myeloid leukemia in complete remission but with molecular evidence of WT1 transcript.
  • Immune responses were evaluated by delayed-type hypersensitivity, CD4+ T-cell proliferation, CD3+ T-cell interferon-gamma release, and WT1 peptide tetramer staining.
  • Of the 9 evaluable patients, 7 completed 6 vaccinations and WT1-specific T-cell responses were noted in 7 of 8 patients.
  • With a mean follow-up of 30 plus or minus 8 months after diagnosis, median disease-free survival has not been reached.
  • Further studies are needed to establish the role of vaccination as viable postremission therapy for acute myeloid leukemia.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Leukemia, Myeloid, Acute / therapy. Oncogene Proteins / therapeutic use. Vaccination / methods. WT1 Proteins / therapeutic use
  • [MeSH-minor] Adult. Aged. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Cytotoxicity, Immunologic. Disease-Free Survival. Female. HLA-A Antigens / genetics. HLA-A Antigens / immunology. HLA-A2 Antigen. Humans. Hypersensitivity, Delayed / immunology. Interferon-gamma / biosynthesis. Interferon-gamma / immunology. Kaplan-Meier Estimate. Male. Middle Aged. Pilot Projects. Remission Induction. Reverse Transcriptase Polymerase Chain Reaction. Vaccines, Subunit / genetics. Vaccines, Subunit / immunology. Young Adult

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  • (PMID = 20400682.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00398138
  • [Grant] United States / NCI NIH HHS / CA / P01 CA023766; United States / PHS HHS / / P01 23766
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / Oncogene Proteins; 0 / Vaccines, Subunit; 0 / WT1 Proteins; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2910606
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60. Yoo SJ, Chi HS, Jang S, Seo EJ, Seo JJ, Lee JH, Park HS, Park CJ: Quantification of AML1-ETO fusion transcript as a prognostic indicator in acute myeloid leukemia. Haematologica; 2005 Nov;90(11):1493-501
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  • [Title] Quantification of AML1-ETO fusion transcript as a prognostic indicator in acute myeloid leukemia.
  • BACKGROUND AND OBJECTIVES: In spite of the high complete remission rate that chemotherapy achieves in acute myeloid leukemia with AML1-ETO gene rearrangement, relapse is a major cause of treatment failure in this condition.
  • DESIGN AND METHODS: We serially monitored AML1-ETO fusion transcripts using RQ-PCR in 113 bone marrow or peripheral blood samples from 21 patients with AML1-ETO-positive acute myeloid leukemia and analyzed the prognostic relevance of the results.
  • RESULTS: Higher transcript levels at diagnosis were associated with a higher probability of relapse (p=0.038 in all patients and p=0.001 in adult patients).
  • A decrease of less than 3-log at the time of achieving complete remission was also associated with a higher risk of relapse (p=0.035 in all patients and p=0.011 in adult patients).
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 16266896.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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61. Gupta V, Daly A, Lipton JH, Hasegawa W, Chun K, Kamel-Reid S, Tsang R, Yi QL, Minden M, Messner H, Kiss T: Nonmyeloablative stem cell transplantation for myelodysplastic syndrome or acute myeloid leukemia in patients 60 years or older. Biol Blood Marrow Transplant; 2005 Oct;11(10):764-72
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  • [Title] Nonmyeloablative stem cell transplantation for myelodysplastic syndrome or acute myeloid leukemia in patients 60 years or older.
  • We analyzed the outcomes of 24 consecutive patients aged >or=60 years with poor-prognosis myelodysplastic syndrome or acute myeloid leukemia undergoing transplantation with nonmyeloablative conditioning using fludarabine (125 mg/m2) and low-dose total body irradiation (2 Gy) followed by allogeneic peripheral blood stem cell grafts from HLA-identical sibling donors.
  • Graft-versus-host disease (GVHD) prophylaxis consisted of cyclosporine and mycophenolate mofetil.
  • In addition to age, 88% of patients had 1 or more adverse biological features of the disease.
  • With a median follow-up of 21 months, 12 patients are alive, 11 of whom are disease free.
  • The cumulative probabilities of relapse and of acute and chronic GVHD were 27%, 45%, and 74%, respectively.
  • These data suggest that nonmyeloablative stem cell transplantation is a feasible treatment option in patients aged >or=60 years with poor-prognosis myelodysplastic syndrome or acute myeloid leukemia.
  • The reasonable disease control with nonmyeloablative transplantation in this high-risk group of patients merits further investigation.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Acute Disease. Aged. Female. Graft Survival. Graft vs Host Disease. Histocompatibility Testing. Humans. Male. Middle Aged. Opportunistic Infections. Siblings. Survival Analysis. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Whole-Body Irradiation


62. Chang H, Yi QL: Acute myeloid leukemia with pseudo-Chèdiak-Higashi anomaly exhibits a specific immunophenotype with CD2 expression. Am J Clin Pathol; 2006 May;125(5):791-4
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  • [Title] Acute myeloid leukemia with pseudo-Chèdiak-Higashi anomaly exhibits a specific immunophenotype with CD2 expression.
  • Acute myeloid leukemia (AML) with pseudo-Chèdiak-Higashi (PCH) anomaly is a rare morphologic entity.
  • We characterized 5 cases by multiparameter flow cytometry and found that in all cases, the blasts aberrantly expressed CD2, a pan-T cell-associated marker, in addition to their myeloid-associated markers.
  • In contrast, CD2 was expressed in only 25 (17.9%) of 140 cases of newly diagnosed AML without PCH anomaly.
  • CD2 expression correlated strongly with AML with PCH anomaly (P < .01), suggesting a link between a specific immunophenotypic marker, CD2, and AML with PCH anomaly.
  • [MeSH-major] Antigens, CD2 / metabolism. Chediak-Higashi Syndrome / pathology. Immunophenotyping. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / metabolism. Female. Flow Cytometry. Humans. Karyotyping. Male. Middle Aged. Treatment Outcome

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  • (PMID = 16707384.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD2; 0 / Biomarkers, Tumor
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63. Chang H, Lin TL, Ho WJ, Hsu LA: Acute myeloid leukemia associated with acute myocardial infarction and dural sinus thrombosis: the possible role of leukemia-related hyperhomocysteinemia. J Chin Med Assoc; 2008 Aug;71(8):416-20
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  • [Title] Acute myeloid leukemia associated with acute myocardial infarction and dural sinus thrombosis: the possible role of leukemia-related hyperhomocysteinemia.
  • The association of acute myeloid leukemia (AML) and acute myocardial infarction (AMI) is rare.
  • We encountered a 40-year-old female with inferior wall myocardial infarction that occurred simultaneously with the diagnosis of AML.
  • She developed subsequent dural sinus thrombosis during chemotherapy for AML.
  • Remission induction was not affected by the occurrence of AMI, although anthracyclines were avoided in all cases.
  • In the absence of conventional risk factors for coronary artery disease, AMI can be related to leukemia per se and the role of homocysteine is worth further investigation.
  • [MeSH-major] Hyperhomocysteinemia / complications. Leukemia, Myeloid, Acute / complications. Myocardial Infarction / etiology. Sinus Thrombosis, Intracranial / etiology

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  • (PMID = 18772122.001).
  • [ISSN] 1726-4901
  • [Journal-full-title] Journal of the Chinese Medical Association : JCMA
  • [ISO-abbreviation] J Chin Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] China (Republic : 1949- )
  • [Number-of-references] 14
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64. Voso MT, Hohaus S, Guidi F, Fabiani E, D'Alò F, Groner S, Späth D, Doehner K, Leone G, Doehner H, Schlenk RF: Prognostic role of glutathione S-transferase polymorphisms in acute myeloid leukemia. Leukemia; 2008 Sep;22(9):1685-91
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  • [Title] Prognostic role of glutathione S-transferase polymorphisms in acute myeloid leukemia.
  • We were interested whether their polymorphic variants may account for differences in outcome of patients with acute myeloid leukemia (AML) following chemotherapy.
  • We studied the prognostic role of polymorphisms in three GST genes (GSTP1/M1/T1) in a large patient cohort of the German Austrian Acute Myeloid Leukemia Study Group, treated according to prospective multicenter clinical trials (AML HD98A: 254 patients; AML HD98-B: 100 patients), with a median follow-up of 46 months.
  • Looking at short-term adverse drug reactions, homozygous carriers of the GSTP1*105 Val allele had a faster neutrophil and platelet recovery (P=0.002 and 0.02, respectively) and a reduced need of red cell and platelet transfusions (P=0.01 and 0.03, respectively).
  • Response to induction chemotherapy did not vary according to GST polymorphisms.
  • [MeSH-major] Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics. Polymorphism, Genetic

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  • (PMID = 18580952.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 2.5.1.18 / Glutathione Transferase
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65. Tsavaris N, Kopterides P, Kosmas C, Siakantaris M, Patsouris E, Pangalis G: Spontaneous remission of acute myeloid leukemia associated with GnRH agonist treatment. Leuk Lymphoma; 2006 Mar;47(3):557-60
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  • [Title] Spontaneous remission of acute myeloid leukemia associated with GnRH agonist treatment.
  • Spontaneous remission of acute myeloid leukemia (AML) in adults is a rare but well documented phenomenon.
  • This study reports on a 64-year-old male patient with acute myelogenous leukemia (AML-M4, according to the French-American-British classification) that was developed on a background of chronic myelomonocytic leukemia (CMML) and then underwent remission after treatment with the gonadotropin-releasing hormone agonist (GnRH agonist) triptorelin for presumed prostate cancer.
  • To the author' knowledge, this is the first report of remission in an AML-M4 case associated with hormone manipulation.
  • [MeSH-major] Gonadotropin-Releasing Hormone / agonists. Leukemia, Myelomonocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / pathology. Leukemia, Myelomonocytic, Chronic / drug therapy. Triptorelin Pamoate / therapeutic use

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  • (PMID = 16396781.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 33515-09-2 / Gonadotropin-Releasing Hormone; 57773-63-4 / Triptorelin Pamoate
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66. Al-Bahar S, Adriana Z, Pandita R: Acute myeloid leukemia as a genetic disease. Review article. Gulf J Oncolog; 2008 Jan;(3):9-15
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  • [Title] Acute myeloid leukemia as a genetic disease. Review article.
  • The number of recurring genetic abnormalities recognized in acute myeloid leukemia (AML) has increased rapidly in recent years and at present, acute leukemia is probably the most extensively analyzed human cancer.
  • Combined cytogenetic and molecular genetic studies have revealed that clonal chromosome abnormalities are present in the majority of patients with AML that are very closely, and sometimes uniquely, associated with distinct subsets of leukemia.
  • Continued identification and characterization of genes involved in the development of leukemia has a major impact on our understanding of the molecular biology of cancer and in formulating of biologically based therapies.
  • [MeSH-major] Genetic Diseases, Inborn. Genetic Predisposition to Disease. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 20084792.001).
  • [ISSN] 2078-2101
  • [Journal-full-title] The Gulf journal of oncology
  • [ISO-abbreviation] Gulf J Oncolog
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Kuwait
  • [Number-of-references] 18
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67. Ghoshal Gupta S, Baumann H, Wetzler M: Epigenetic regulation of signal transducer and activator of transcription 3 in acute myeloid leukemia. Leuk Res; 2008 Jul;32(7):1005-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epigenetic regulation of signal transducer and activator of transcription 3 in acute myeloid leukemia.
  • We have demonstrated that constitutive signal transducer and activator of transcription (STAT) 3 activity, observed in approximately 50% of acute myeloid leukemia (AML) cases, is associated with adverse treatment outcome.
  • Here we review the literature addressing epigenetic regulation as a mechanism controlling STAT3 signaling in AML.
  • A better understanding of mechanisms of dysregulation of STAT signaling pathways may serve as a basis for designing novel therapeutic strategies that target these pathways in leukemia cells.

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  • (PMID = 18192010.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016056; United States / NCI NIH HHS / CA / CA16056; United States / NCI NIH HHS / CA / CA85580; United States / NCI NIH HHS / CA / CA99238; United States / NCI NIH HHS / CA / R01 CA085580; United States / NCI NIH HHS / CA / R21 CA099238; United States / NCI NIH HHS / CA / R21 CA099238-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / STAT3 Transcription Factor
  • [Number-of-references] 90
  • [Other-IDs] NLM/ NIHMS49243; NLM/ PMC4629448
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68. Long JK, Choueiri TK, Hall GS, Avery RK, Sekeres MA: Daptomycin-resistant Enterococcus faecium in a patient with acute myeloid leukemia. Mayo Clin Proc; 2005 Sep;80(9):1215-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Daptomycin-resistant Enterococcus faecium in a patient with acute myeloid leukemia.
  • We describe a patient with acute myeloid leukemia whose febrile neutropenia was treated with daptomycin and who later developed daptomycin-resistant Enterococcus faecium infection.
  • [MeSH-major] Anti-Bacterial Agents. Daptomycin. Drug Resistance, Bacterial. Enterococcus faecium. Gram-Positive Bacterial Infections / etiology. Leukemia, Myeloid / complications
  • [MeSH-minor] Acute Disease. Adult. Antineoplastic Agents / therapeutic use. Female. Humans

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  • [CommentIn] Mayo Clin Proc. 2005 Sep;80(9):1122-5 [16178491.001]
  • (PMID = 16178502.001).
  • [ISSN] 0025-6196
  • [Journal-full-title] Mayo Clinic proceedings
  • [ISO-abbreviation] Mayo Clin. Proc.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antineoplastic Agents; NWQ5N31VKK / Daptomycin
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69. Qian J, Yao DM, Lin J, Chen Q, Li Y, Ji RB, Yang J, Qian Z, Xiao GF, Wang YL: [Alteration of methylation status of death-associated protein kinase (dapk) gene promoter in patients with acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Dec;18(6):1390-4
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  • [Title] [Alteration of methylation status of death-associated protein kinase (dapk) gene promoter in patients with acute myeloid leukemia].
  • This study was purposed to analyze the methylation status of death-associated protein kinase (dapk) gene promoter in Chinese patients with acute myeloid leukemia (AML) and its relationship with clinical features.
  • The methylation-specific PCR (MSP) technique was used to detect dapk promoter methylation in bone marrow samples from 112 cases of AML.
  • The results indicated that gene dapk promoter hypermethylation was detected in 82 cases (73.2%), but not in 13 control group.
  • There was no correlation of dapk gene hypermethylation with sex, age, WBC counts, platelet counts, hematologic parameters, chromosomal abnormalities and different subtypes of AML patients.
  • It is concluded that dapk gene hypermethylation may be a common molecular event in AML.

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  • (PMID = 21176336.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
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70. Qian Z, Lin J, Qian J, Yao DM, Wang YL, Han LX, Zhu ZH, Xiao GF: [Quantification of GRAF gene expression in patients with acute myeloid leukemia using EvaGreen real time quantitative PCR]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2010 Jun;27(3):290-3
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  • [Title] [Quantification of GRAF gene expression in patients with acute myeloid leukemia using EvaGreen real time quantitative PCR].
  • OBJECTIVE: To quantify the expression level of GRAF gene in acute myeloid leukemia (AML) and analyze its clinical significance.
  • METHODS: The EvaGreen real-time quantitative polymerase chain reaction (RQ-PCR) assay was established and performed to measure the GRAF gene transcripts in 71 cases with AML and 21 with nonmalignant hematological diseases.
  • The GRAF expression level was significantly lower in AML (0.01%-169.75%, median 3.82%) than that in controls (14.49%-126.85%, median 56.04%) (P<0.05).
  • CONCLUSION: The GRAF gene was down-regulated in AML, which might play a role in the leukemogenesis.
  • [MeSH-major] GTPase-Activating Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Polymerase Chain Reaction / methods

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  • (PMID = 20533268.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ARHGAP26 protein, human; 0 / GTPase-Activating Proteins
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71. Tobal K, Liu Yin JA: Diagnosis and monitoring of AML1-MTG8 (ETO)-positive acute myeloid leukemia by qualitative and real-time quantitative RT-PCR. Methods Mol Med; 2006;125:149-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis and monitoring of AML1-MTG8 (ETO)-positive acute myeloid leukemia by qualitative and real-time quantitative RT-PCR.
  • Assessing the level of residual disease in leukemia is vital for evaluating patients' response to treatment and for identifying those at high risk of relapse.
  • One of the most common translocations in acute myeloid leukemia (AML) is the t(8;21).
  • t(8;21) AML is characterized by a relatively good prognosis.
  • This chapter discusses both qualitative and quantitative (real-time quantitative reverse-transcription polymerase chain reaction [RQ-PCR]) protocols for the diagnosis and minimal residual disease (MRD) monitoring in t(8;21) AML.
  • The chapter provides a simple equation for assessing the sensitivity/reliability of RQ-PCR assays, which enables scientists to assess the accuracy and reliability of their data.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Computer Systems. DNA Primers. Humans. Monitoring, Physiologic / methods. Neoplasm, Residual / diagnosis. Neoplasm, Residual / genetics. Transcription, Genetic. Translocation, Genetic

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  • (PMID = 16502583.001).
  • [ISSN] 1543-1894
  • [Journal-full-title] Methods in molecular medicine
  • [ISO-abbreviation] Methods Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA Primers; 0 / Oncogene Proteins, Fusion
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72. Pereira GH, Pádua SS, Park MV, Muller RP, Passos RM, Menezes Y: Chronic meningitis by histoplasmosis: report of a child with acute myeloid leukemia. Braz J Infect Dis; 2008 Dec;12(6):555-7
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  • [Title] Chronic meningitis by histoplasmosis: report of a child with acute myeloid leukemia.
  • In leukemia, the impaired of the T cells function can predispose to the disseminated form.
  • We have described a child with acute myeloid leukemia (AML), that developed skin lesions and asymptomatic chronic meningitis, with a good evolution after prolonged treatment with amphotericin B deoxycholate followed by fluconazole.
  • [MeSH-major] Histoplasmosis / diagnosis. Leukemia, Myeloid / immunology. Meningitis, Fungal / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Chronic Disease. Deoxycholic Acid / therapeutic use. Drug Combinations. Drug Therapy, Combination. Fluconazole / therapeutic use. Humans. Immunocompromised Host. Male. Treatment Outcome

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  • (PMID = 19287853.001).
  • [ISSN] 1678-4391
  • [Journal-full-title] The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases
  • [ISO-abbreviation] Braz J Infect Dis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Drug Combinations; 005990WHZZ / Deoxycholic Acid; 7XU7A7DROE / Amphotericin B; 87687-70-5 / amphotericin B, deoxycholate drug combination; 8VZV102JFY / Fluconazole
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73. Wang TF, Horsley SW, Lee KF, Chu SC, Li CC, Kao RH: Translocation between chromosome 5q35 and chromosome 11q13-- an unusual cytogenetic finding in a primary refractory acute myeloid leukemia. Clin Lab Haematol; 2006 Jun;28(3):160-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translocation between chromosome 5q35 and chromosome 11q13-- an unusual cytogenetic finding in a primary refractory acute myeloid leukemia.
  • Cytogenetic abnormalities are observed in approximately two-thirds of patients with acute myeloid leukemia (AML).
  • Chromosome rearrangements are associated with specific subtypes of AML and associated prognosis.
  • We report a patient with AML, M2, who was primarily refractory to standard induction chemotherapy with idarubicin and cytarabine.
  • Flow cytometry of a bone marrow aspirate showed aberrant expression of B-cell markers including CD19.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 5 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 16706931.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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74. Lam CC, Ma ES, Kwong YL: Therapy-related acute myeloid leukemia after single-agent treatment with fludarabine for chronic lymphocytic leukemia. Am J Hematol; 2005 Aug;79(4):288-90
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  • [Title] Therapy-related acute myeloid leukemia after single-agent treatment with fludarabine for chronic lymphocytic leukemia.
  • A 70-year-old man with B-cell chronic lymphocytic leukemia (CLL) received single-agent treatment with the purine analogue fludarabine, which led to complete remission.
  • Marrow examination showed acute myeloid leukemia (AML) with trilineage myelodysplasia (MDS).
  • Cytogenetic analysis showed an unbalanced der(1;7)(p10;q10) that resulted effectively in deletion 7q; confirming the diagnosis of therapy-related AML (t-AML).
  • Together with previous reports of secondary cancers after fludarabine treatment and the association of monosomy 7/7q- with another purine analogue azathioprine, results suggest that t-AML might develop after fludarabine therapy.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid / chemically induced. Neoplasms, Second Primary / chemically induced. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Aged. Bone Marrow / pathology. Chromosomes, Human, Pair 7. Humans. Male. Monosomy


75. Preston R, Däbritz J, Hänfler J, Oettle H: Mutational analysis of K-ras codon 12 in blood samples of patients with acute myeloid leukemia. Leuk Res; 2010 Jul;34(7):883-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutational analysis of K-ras codon 12 in blood samples of patients with acute myeloid leukemia.
  • Mutations in K-ras are frequent in acute myeloid leukemia (AML).
  • We used quantitative PCR with peptide nucleic acid mediated PCR clamping to specifically analyze 257 blood samples of 31 AML patients for K-ras codon 12 alterations.
  • A total of 20 samples of nine patients harbored a K-ras mutation.
  • [MeSH-major] Genes, ras. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Amino Acid Substitution. Biomarkers, Tumor / blood. Biomarkers, Tumor / genetics. Codon / genetics. DNA Mutational Analysis. DNA, Neoplasm / blood. DNA, Neoplasm / genetics. Female. Humans. Male. Middle Aged. Mutation, Missense. Point Mutation. Polymerase Chain Reaction. Prognosis

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20304488.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Codon; 0 / DNA, Neoplasm
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76. Henschler R, Göttig S, Junghahn I, Bug G, Seifried E, Müller AM, Fichtner I: Transplantation of human acute myeloid leukemia (AML) cells in immunodeficient mice reveals altered cell surface phenotypes and expression of human endothelial markers. Leuk Res; 2005 Oct;29(10):1191-9
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  • [Title] Transplantation of human acute myeloid leukemia (AML) cells in immunodeficient mice reveals altered cell surface phenotypes and expression of human endothelial markers.
  • To better characterize acute myeloid leukemia (AML) development in non-obese diabetic (NOD)/severe combined immunodeficiency (SCID) mice, we transplanted samples from patients with AML or KG-1 and EOL-1 cell lines.
  • We found 9/12 primary AML samples and both cell lines to engraft within 2-8 weeks, with 5-80% human cells in bone marrow.
  • Compared with freshly isolated AML cells, percentages of human CD33+, CD38+, CD31+ CD13+ or CD15+ subpopulations increased after transplantation, whereas percentages of CD34+ cells decreased.
  • Engrafted mice frequently showed expression of human endothelial cell markers.
  • Thus, transplantation of human AML into NOD/SCID mice reveals expression of hematopoietic and endothelial differentiation markers.
  • [MeSH-major] Antigens, Surface / metabolism. Biomarkers, Tumor / metabolism. Leukemia, Myeloid / pathology. Transplantation, Heterologous / pathology
  • [MeSH-minor] Acute Disease. Adult. Aged. Animals. Endothelium, Vascular / cytology. Endothelium, Vascular / embryology. Endothelium, Vascular / pathology. Flow Cytometry. Humans. Mice. Mice, Inbred NOD. Mice, SCID. Middle Aged. Phenotype. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 15941586.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Surface; 0 / Biomarkers, Tumor
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77. Barragan E, Collado M, Cervera J, Martin G, Bolufer P, Roman J, Sanz MA: The GST deletions and NQO1*2 polymorphism confers interindividual variability of response to treatment in patients with acute myeloid leukemia. Leuk Res; 2007 Jul;31(7):947-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The GST deletions and NQO1*2 polymorphism confers interindividual variability of response to treatment in patients with acute myeloid leukemia.
  • Functional polymorphisms in the genes encoding detoxification enzymes could modify the response to treatment in acute myeloid leukemia and therefore affect the final clinical outcome.
  • In the present study, we genotyped 153 patients diagnosed with de novo acute myeloid leukemia (AML) to clarify the influence of the genetic polymorphisms CYP1A1*2A, CYP3A4*1B, CYP2E1*5B, del{GSTT1}, del{GSTM1}, and NQO1*2 on disease outcome.
  • The presence of GST deletions was associated with a lower probability of disease-free survival (DFS) and this effect was more relevant in male patients.
  • [MeSH-major] Gene Deletion. Glutathione Transferase / genetics. Leukemia, Myeloid / genetics. NAD(P)H Dehydrogenase (Quinone) / genetics. Polymorphism, Genetic / genetics
  • [MeSH-minor] Acute Disease. Cytochrome P-450 CYP1A1 / genetics. Cytochrome P-450 CYP2E1 / genetics. Cytochrome P-450 CYP3A. Cytochrome P-450 Enzyme System / genetics. Disease-Free Survival. Female. Genotype. Humans. Male. Middle Aged. Survival Rate. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 17118447.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.13.- / Cytochrome P-450 CYP2E1; EC 1.14.13.67 / CYP3A4 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 1.14.14.1 / Cytochrome P-450 CYP3A; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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78. Majeti R, Chao MP, Alizadeh AA, Pang WW, Jaiswal S, Gibbs KD Jr, van Rooijen N, Weissman IL: CD47 is an adverse prognostic factor and therapeutic antibody target on human acute myeloid leukemia stem cells. Cell; 2009 Jul 23;138(2):286-99
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  • [Title] CD47 is an adverse prognostic factor and therapeutic antibody target on human acute myeloid leukemia stem cells.
  • Acute myeloid leukemia (AML) is organized as a cellular hierarchy initiated and maintained by a subset of self-renewing leukemia stem cells (LSC).
  • We hypothesized that increased CD47 expression on human AML LSC contributes to pathogenesis by inhibiting their phagocytosis through the interaction of CD47 with an inhibitory receptor on phagocytes.
  • We found that CD47 was more highly expressed on AML LSC than their normal counterparts, and that increased CD47 expression predicted worse overall survival in three independent cohorts of adult AML patients.
  • Furthermore, blocking monoclonal antibodies directed against CD47 preferentially enabled phagocytosis of AML LSC and inhibited their engraftment in vivo.
  • Finally, treatment of human AML LSC-engrafted mice with anti-CD47 antibody depleted AML and targeted AML LSC.
  • In summary, increased CD47 expression is an independent, poor prognostic factor that can be targeted on human AML stem cells with blocking monoclonal antibodies capable of enabling phagocytosis of LSC.
  • [MeSH-major] Antigens, CD47 / immunology. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology. Phagocytosis

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  • (PMID = 19632179.001).
  • [ISSN] 1097-4172
  • [Journal-full-title] Cell
  • [ISO-abbreviation] Cell
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009302; United States / NIAID NIH HHS / AI / T32 AI007290; United States / NCI NIH HHS / CA / R01 CA086017-07; United States / NCI NIH HHS / CA / R01 CA086017-06; United States / NCI NIH HHS / CA / R01 CA086017; United States / NCI NIH HHS / CA / R01CA86017; United States / NCI NIH HHS / CA / R01 CA086017-08; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / R01 CA086017-09; United States / NCI NIH HHS / CA / R01 CA086017-10
  • [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 / Antibodies, Monoclonal; 0 / Antigens, CD47; 0 / Ptpns1 protein, mouse; 0 / Receptors, Immunologic
  • [Other-IDs] NLM/ NIHMS122682; NLM/ PMC2726837
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79. Zhang Y, Askenazi M, Jiang J, Luckey CJ, Griffin JD, Marto JA: A robust error model for iTRAQ quantification reveals divergent signaling between oncogenic FLT3 mutants in acute myeloid leukemia. Mol Cell Proteomics; 2010 May;9(5):780-90
The Lens. Cited by Patents in .

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  • [Title] A robust error model for iTRAQ quantification reveals divergent signaling between oncogenic FLT3 mutants in acute myeloid leukemia.
  • Point mutations within the activation loop and in-frame tandem duplications of the juxtamembrane domain represent the most frequent molecular abnormalities observed in acute myeloid leukemia.
  • Application of our error model to quantitative proteomics data for FLT3 signaling provides evidence that phosphorylation of tyrosine phosphatase SHP1 abrogates the transformative potential, but not overall kinase activity, of FLT3-D835Y in acute myeloid leukemia.

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  • (PMID = 20019052.001).
  • [ISSN] 1535-9484
  • [Journal-full-title] Molecular & cellular proteomics : MCP
  • [ISO-abbreviation] Mol. Cell Proteomics
  • [Language] ENG
  • [Grant] United States / NHGRI NIH HHS / HG / P50 HG004233; United States / NHGRI NIH HHS / HG / P50HG004233
  • [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 / Ligands; 0 / Mutant Proteins; 0 / Peptides; 0 / STAT5 Transcription Factor; 21820-51-9 / Phosphotyrosine; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / Janus Kinases; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6
  • [Other-IDs] NLM/ PMC2871413
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80. Hess CJ, Feller N, Denkers F, Kelder A, Merle PA, Heinrich MC, Harlow A, Berkhof J, Ossenkoppele GJ, Waisfisz Q, Schuurhuis GJ: Correlation of minimal residual disease cell frequency with molecular genotype in patients with acute myeloid leukemia. Haematologica; 2009 Jan;94(1):46-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Correlation of minimal residual disease cell frequency with molecular genotype in patients with acute myeloid leukemia.
  • BACKGROUND: About 70-80 percent of patients with acute myeloid leukemia enter complete remission, but at least half of these patients who achieve remission go on to relapse.
  • Minimal residual disease assessment may offer such an end-point since it is a strong independent prognostic factor.
  • As proof of principle we examined this concept for FLT3-ITD status at diagnosis.
  • DESIGN AND METHODS: We determined FLT3-ITD status in bone marrow samples from 196 patients with newly diagnosed acute myeloid leukemia.
  • The frequencies of residual leukemic cells of these 196 patients were assessed in 267 follow-up bone marrow samples using immunophenotypic assessment of minimal residual disease.
  • CONCLUSIONS: This study shows that it could be possible to study the efficacy of FLT3 inhibitors using the level of minimal residual disease as a short-term end-point.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology

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  • (PMID = 19042917.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Recombinant Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC2625416
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81. Damiani D, Tiribelli M, Michelutti A, Geromin A, Cavallin M, Fabbro D, Pianta A, Malagola M, Damante G, Russo D, Fanin R: Fludarabine-based induction therapy does not overcome the negative effect of ABCG2 (BCRP) over-expression in adult acute myeloid leukemia patients. Leuk Res; 2010 Jul;34(7):942-5
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fludarabine-based induction therapy does not overcome the negative effect of ABCG2 (BCRP) over-expression in adult acute myeloid leukemia patients.
  • Over-expression of multidrug resistance (MDR) proteins PGP and BCRP has a negative prognostic impact in acute myeloid leukemia (AML) patients.
  • We investigated the role of BCRP in 138 adult AML patients receiving induction therapy with fludarabine.
  • Conversely, high levels of BCRP significantly affected disease-free survival, as higher relapse rates (48.5% vs 28.5%) and earlier relapse occurred in BCRP+ patients.
  • [MeSH-major] ATP-Binding Cassette Transporters / physiology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Neoplasm / drug effects. Gene Expression Regulation, Leukemic. Leukemia, Myeloid / drug therapy. Neoplasm Proteins / physiology. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Male. Middle Aged. Multidrug Resistance-Associated Proteins / physiology. P-Glycoprotein / physiology. Remission Induction. Young Adult

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20122734.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / Multidrug Resistance-Associated Proteins; 0 / Neoplasm Proteins; 0 / P-Glycoprotein; 0 / multidrug resistance-associated protein 1; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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82. Mihailov G, Ganeva P, Vassileva N, Guenova M, Balacenko G, Toshkov S, Hodjadjik D: Secondary acute myeloid leukemia early after therapy for Hodgkin's disease--a case report. J BUON; 2007 Jul-Sep;12(3):403-6
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  • [Title] Secondary acute myeloid leukemia early after therapy for Hodgkin's disease--a case report.
  • A case of acute myeloid leukemia (AML) after successful therapy for Hodgkin's disease (HD) is reported.
  • Seven months after the CR was obtained the patient developed AML.
  • Knowing that the prognosis of patients with secondary AML (sAML) after primary HD is poor we decided to perform autologous peripheral stem cells' transplantation.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / surgery. Neoplasms, Second Primary / diagnosis. Neoplasms, Second Primary / surgery
  • [MeSH-minor] Adult. Female. Hodgkin Disease / drug therapy. Hodgkin Disease / radiotherapy. Hodgkin Disease / therapy. Humans. Treatment Outcome

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  • (PMID = 17918297.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
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83. DiNardo CD, Ky B, Vogl DT, Forfia P, Loren A, Luger S, Mato A, Tsai DE: Differentiation syndrome in non-M3 acute myeloid leukemia treated with the retinoid X receptor agonist bexarotene. Med Oncol; 2008;25(3):299-302
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  • [Title] Differentiation syndrome in non-M3 acute myeloid leukemia treated with the retinoid X receptor agonist bexarotene.
  • Differentiation Syndrome, also known as all-trans retinoic acid (ATRA) syndrome, is a well-described clinical phenomenon occurring in patients with the M3 subtype of acute myeloid leukemia receiving ATRA chemotherapy.
  • Bexarotene is a novel synthetic compound that selectively binds and activates retinoic X receptors, a subclass of retinoid receptors not targeted by ATRA.
  • We report a patient with refractory non-M3 acute promyelocytic leukemia (AML) who developed differentiation syndrome during bexarotene monotherapy.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / pathology. Retinoid X Receptors / agonists. Tetrahydronaphthalenes / adverse effects
  • [MeSH-minor] Cell Differentiation. Humans. Male. Middle Aged. Pericardial Effusion / chemically induced. Syndrome

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  • (PMID = 18181037.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [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 / Retinoid X Receptors; 0 / Tetrahydronaphthalenes; A61RXM4375 / bexarotene
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84. Fianchi L, Pagano L, Leoni F, Storti S, Voso MT, Valentini CG, Rutella S, Scardocci A, Caira M, Gianfaldoni G, Leone G: Gemtuzumab ozogamicin, cytosine arabinoside, G-CSF combination (G-AraMy) in the treatment of elderly patients with poor-prognosis acute myeloid leukemia. Ann Oncol; 2008 Jan;19(1):128-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gemtuzumab ozogamicin, cytosine arabinoside, G-CSF combination (G-AraMy) in the treatment of elderly patients with poor-prognosis acute myeloid leukemia.
  • BACKGROUND: Gemtuzumab ozogamicin (GO) is effective as single agent in the treatment of acute myeloid leukemia (AML).
  • We evaluated efficacy and safety of a chemotherapy including growth factors, cytarabine, and GO (G-AraMy) in the treatment of poor-prognosis AML in elderly patients.
  • PATIENTS AND METHODS: In three Italian hematology departments from September 2003 to September 2006, 53 elderly patients [median age 69 years (range 65-77)] with untreated or primary refractory/relapsed AML were enrolled on the combination G-AraMy administered according to two consecutive schedules (G-AraMy1 and G-AraMy2), with intensified consolidation in the second.
  • Twenty-three of 53 patients had a secondary acute myeloid leukemia (sAML).
  • No differences for response rate and toxicity profile were observed between untreated and primary resistant/relapsed patients, de novo AML and sAML, and in the two treatment trials.
  • Median disease-free survival and overall survival were 8 months (range 2-23+) and 9 months (range 2-24+).
  • CONCLUSIONS: G-AraMy therapy may be considered an useful treatment approach for poor-risk elderly AML patients, with a complete remission rate comparable to literature data with reduced side-effects, also in a poor-prognosis population.

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  • (PMID = 17906298.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / gemtuzumab; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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85. Ceric-Dehdari P, Houcinat Y, Berger TG: [Disseminated papules in a patient with acute myeloid leukemia]. Hautarzt; 2010 Nov;61(11):980-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Disseminated papules in a patient with acute myeloid leukemia].
  • This article reports on the case of a 20-year-old female patient with acute myeloid leukemia who suddenly developed disseminated livid red papules and papulovesicles.
  • The clinical picture and in particular the histopathology findings led to the diagnosis of cutaneous cryptococcosis, which was successfully treated with amphotericin B.
  • For the differential diagnosis generalized herpes zoster, erythema exudativum multiforme and disseminated molluscum contagiosum must be considered.
  • To confirm the diagnosis attempts can also be made to culture the pathogen from skin biopsy preparations.
  • [MeSH-major] Cryptococcosis / diagnosis. Cryptococcosis / etiology. Dermatomycoses / diagnosis. Dermatomycoses / etiology. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / diagnosis

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  • (PMID = 20927503.001).
  • [ISSN] 1432-1173
  • [Journal-full-title] Der Hautarzt; Zeitschrift für Dermatologie, Venerologie, und verwandte Gebiete
  • [ISO-abbreviation] Hautarzt
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 7XU7A7DROE / Amphotericin B
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86. Zarrinkar PP, Gunawardane RN, Cramer MD, Gardner MF, Brigham D, Belli B, Karaman MW, Pratz KW, Pallares G, Chao Q, Sprankle KG, Patel HK, Levis M, Armstrong RC, James J, Bhagwat SS: AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML). Blood; 2009 Oct 1;114(14):2984-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML).
  • Activating mutations in the receptor tyrosine kinase FLT3 are present in up to approximately 30% of acute myeloid leukemia (AML) patients, implicating FLT3 as a driver of the disease and therefore as a target for therapy.
  • The data reveal that the combination of excellent potency, selectivity, and pharmacokinetic properties is unique to AC220, which therefore is the first drug candidate with a profile that matches the characteristics desirable for a clinical FLT3 inhibitor.


87. Fiedler W, Mesters R, Heuser M, Ehninger G, Berdel WE, Zirrgiebel U, Robertson JD, Puchalski TA, Collins B, Jürgensmeier JM, Serve H: An open-label, Phase I study of cediranib (RECENTIN) in patients with acute myeloid leukemia. Leuk Res; 2010 Feb;34(2):196-202
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An open-label, Phase I study of cediranib (RECENTIN) in patients with acute myeloid leukemia.
  • VEGFR and c-Kit signaling pathways may contribute to the pathophysiology of acute myeloid leukemia (AML).
  • Thirty-five patients with AML received cediranib (RECENTIN), an oral, highly potent VEGF signaling inhibitor with c-Kit activity, at doses of < or =30 mg/day.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Quinazolines / administration & dosage

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19674789.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Quinazolines; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; NQU9IPY4K9 / cediranib
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88. Trivedi PJ, Patel PS, Brahmbhatt MM, Patel BP, Gajjar SB, Iyer RR, Parikh EH, Shukla SN, Shah PM, Bakshi SR: A case of acute myeloid leukemia-M2 with trisomy 4 in addition to t(8;21). Indian J Hum Genet; 2008 Jan;14(1):20-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of acute myeloid leukemia-M2 with trisomy 4 in addition to t(8;21).
  • t(8;21)(q22;q22) is the most frequently observed karyotypic abnormality associated with acute myeloid leukemia (AML), specifically in FAB-M2.
  • Short-term unstimulated bone marrow (BM) and peripheral blood lymphocyte culture showed 47,XX, +4,t(8;21) in all metaphase plates; and interphase and metaphase results of AML-ETO fusion was positive and trisomy of 4 was confirmed with WCP probes.
  • Trisomy 4 in AML with t(8;21) is a rare numerical abnormality.
  • Here we present such case of patient which may constitute a distinctive subtype.

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  • [Cites] Blood. 1986 May;67(5):1328-32 [3697508.001]
  • [Cites] Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2007 Aug;24(4):369-72 [17680522.001]
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  • [Cites] Leuk Res. 1998 Oct;22(10):899-903 [9766750.001]
  • (PMID = 20300287.001).
  • [ISSN] 0971-6866
  • [Journal-full-title] Indian journal of human genetics
  • [ISO-abbreviation] Indian J Hum Genet
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2840780
  • [Keywords] NOTNLM ; Acute myeloid leukemia / cytogenetics / fluorescence in situ hybridization
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89. Xiao Z, Xue H, Li R, Zhang L, Yu M, Hao Y: The prognostic significance of leukemic cells clearance kinetics evaluation during the initial course of induction therapy with HAD (homoharringtonine, cytosine arabinoside, daunorubicin) in patients with de novo acute myeloid leukemia. Am J Hematol; 2008 Mar;83(3):203-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The prognostic significance of leukemic cells clearance kinetics evaluation during the initial course of induction therapy with HAD (homoharringtonine, cytosine arabinoside, daunorubicin) in patients with de novo acute myeloid leukemia.
  • The impact of the percentage of residual leukemic cells (RLCs) at the end of first course of induction chemotherapy (T1) or during aplasia (T2) on complete remission (CR) rate, disease-free survival (DFS), and overall survival (OS) were retrospectively analyzed in 72 cases of de novo acute myeloid leukemia (AML) treated with HAD (homoharringtonine, cytosine arabinoside, and daunorubicin) regimen.
  • We further confirmed that the percentage of RLCs at T1 or T2 is an independent prognostic factor of AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacokinetics. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adolescent. Adult. Cytarabine / administration & dosage. Daunorubicin / pharmacokinetics. Disease-Free Survival. Female. Harringtonines / administration & dosage. Humans. Male. Metabolic Clearance Rate. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17874451.001).
  • [ISSN] 0361-8609
  • [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 / Harringtonines; 04079A1RDZ / Cytarabine; 6FG8041S5B / homoharringtonine; ZS7284E0ZP / Daunorubicin
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90. Stasevich I, Utskevich R, Kustanovich A, Litvinko N, Savitskaya T, Chernyavskaya S, Saharova O, Aleinikova O: Translocation (10;11)(p12;q23) in childhood acute myeloid leukemia: incidence and complex mechanism. Cancer Genet Cytogenet; 2006 Sep;169(2):114-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translocation (10;11)(p12;q23) in childhood acute myeloid leukemia: incidence and complex mechanism.
  • This translocation represented 28% of all cases of childhood AML treated at our center in 2004, and 63% of AML with rearrangements of 11q23.
  • The median event-free survival of patients was 8.1 months, and we conclude that the t(10;11)(p12;q23) is associated with unfavorable prognosis in childhood acute myeloid leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 11. Leukemia, Myeloid / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Chromosome Banding. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Karyotyping. Male. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16938568.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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91. Benz R, Goede JS, Parlier V, Mühlematter D, Jotterand M, Fehr J: G-CSF-induced remission in two cases of acute myeloid leukemia. Leuk Res; 2008 Jul;32(7):1148-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] G-CSF-induced remission in two cases of acute myeloid leukemia.
  • We report on two elderly patients with newly diagnosed acute myeloid leukemia (AML) who were treated in palliative intention because of comorbidities and intermediate or poor risk cytogenetics.
  • Although a direct therapeutic effect of myeloid growth factors seems to be unusual in AML, the use of G-CSF or GM-CSF may be recommended in patients such as elderly patients who are not suited for intensive chemotherapy.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 18166225.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
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92. Riccio B, Mato A, Olson EM, Berns JS, Luger S: Spontaneous tumor lysis syndrome in acute myeloid leukemia: two cases and a review of the literature. Cancer Biol Ther; 2006 Dec;5(12):1614-7
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  • [Title] Spontaneous tumor lysis syndrome in acute myeloid leukemia: two cases and a review of the literature.
  • Spontaneous tumor lysis syndrome (TLS) is a constellation of electrolyte abnormalities and acute renal failure, which occurs in the setting of rapid cell turnover prior to the administration of cytotoxic chemotherapy.
  • We present two cases of spontaneous TLS in patients with newly diagnosed acute myeloid leukemia (AML) followed by a review of the literature in this field.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Tumor Lysis Syndrome / complications

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  • (PMID = 17204864.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] AYI8EX34EU / Creatinine
  • [Number-of-references] 45
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93. Rulina AV, Spirin PV, Prassolov VS: Activated leukemic oncogenes AML1-ETO and c-kit: role in development of acute myeloid leukemia and current approaches for their inhibition. Biochemistry (Mosc); 2010 Dec;75(13):1650-66
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  • [Title] Activated leukemic oncogenes AML1-ETO and c-kit: role in development of acute myeloid leukemia and current approaches for their inhibition.
  • Acute myeloid leukemia (AML) is a malignant blood disease caused by different mutations that enhance the proliferative activity and survival of blood cells and affect their differentiation and apoptosis.
  • The most frequent disorders in AML are translocations between chromosomes 21 and 8 leading to production of a chimeric oncogene, AML1-ETO, and hyperexpression of the receptor tyrosine kinase KIT.
  • The current approaches for treatment of oncologic diseases (bone marrow transplantation, radiotherapy, and chemotherapy) have significant shortcomings, and thus many laboratories are intensively developing new approaches against leukemias.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / antagonists & inhibitors. Core Binding Factor Alpha 2 Subunit / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / therapy. Oncogene Proteins, Fusion / antagonists & inhibitors. Oncogene Proteins, Fusion / metabolism. Proto-Oncogene Proteins c-kit / antagonists & inhibitors. Proto-Oncogene Proteins c-kit / metabolism

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  • (PMID = 21417999.001).
  • [ISSN] 1608-3040
  • [Journal-full-title] Biochemistry. Biokhimii︠a︡
  • [ISO-abbreviation] Biochemistry Mosc.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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94. Gesundheit B, Shapira MY, Resnick IB, Amar A, Kristt D, Dray L, Budowski E, Or R: Successful cell-mediated cytokine-activated immunotherapy for relapsed acute myeloid leukemia after hematopoietic stem cell transplantation. Am J Hematol; 2009 Mar;84(3):188-90
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  • [Title] Successful cell-mediated cytokine-activated immunotherapy for relapsed acute myeloid leukemia after hematopoietic stem cell transplantation.
  • Acute myeloid leukemia (AML) is an extremely aggressive disease with a high relapse rate even after allogeneic hematopoietic stem cell transplantation (HSCT).
  • We report the successful outcome of cell-mediated cytokine-activated immunotherapy in a high-risk pediatric AML patient who relapsed shortly after allogeneic HSCT.
  • Donor lymphocyte infusion along with interferon induced a graft-versus-leukemia effect, presenting as a reversible episode of graft-versus-host disease, which led to stable complete donor chimerism and total eradication of AML for over 24 months, at the time of this report.
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / therapy. Lymphocyte Transfusion. Neoplasm Recurrence, Local / immunology. Neoplasm Recurrence, Local / therapy
  • [MeSH-minor] Child. Graft vs Host Disease. Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation. Humans. Immunologic Factors / administration & dosage. Immunotherapy. Interferon-alpha / administration & dosage. Male. Recombinant Proteins

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  • (PMID = 19105234.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunologic Factors; 0 / Interferon-alpha; 0 / Recombinant Proteins; 76543-88-9 / interferon alfa-2a
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95. Yeh C, Ma W, Kantarjian H, Zhang ZJ, Cortes J, Albitar M: BCR-ABL truncation due to premature translation termination as a mechanism of resistance to kinase inhibitors. J Clin Oncol; 2009 May 20;27(15_suppl):7028

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 7028 Background: The major mechanism underlying imatinib resistance in patients with chronic myeloid leukemia (CML) is clonal expansion of leukemic cells with point mutations in the BCR-ABL tyrosine kinase.
  • We describe three novel ABL premature termination mutations leading to BCR-ABL truncation in leukemia patients with multidrug (imatinib/nilotinib/dasatinib) resistance.
  • Total nucleic acids were purified and subjected to two rounds of PCR analysis, with the first PCR designed to eliminate amplification of the wild-type, non-translocated ABL gene.
  • HL60 cells (a Ph-negative myeloid leukemia cell line) and peripheral blood of healthy subjects were used as negative controls; a human CML cell line (K562) was used as a positive control.
  • RESULTS: We identified an exon 7 deletion in three CML patients, a 4-nt insertion (908insCAGG) near the exon 5/6 junction in one CML case, and an exon 6 point mutation (997C>T) in one patient with acute lymphoblastic leukemia (ALL).

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  • (PMID = 27961401.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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96. Blum WG, Klisovic R, Liu S, Kefauver C, Grever MR, Schaaf L, Chan K, Byrd JC, Villalona-Calero M, Marcucci G: Efficacy of a novel schedule of decitabine in previously untreated AML, age 60 or older. J Clin Oncol; 2009 May 20;27(15_suppl):7010

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy of a novel schedule of decitabine in previously untreated AML, age 60 or older.
  • : 7010 Background: We established an optimal daily dose of decitabine in AML at 20mg/m<sup>2</sup>/day based on re-expression of epigenetically silenced genes, with promising clinical activity seen in poor risk older patients (pts) (Blum, J Clin Oncol. 2007).
  • METHODS: We designed a phase II study of decitabine for untreated AML pts of age≥60 who were not candidates for intensive chemotherapy (or who refused it).
  • Pts with persistent AML at the end of a cycle received a repeat of the 10 day course, but responding pts received maintenance with abbreviated courses of 3-5 days depending on degree and duration of neutropenia.
  • 15 pts had either secondary or t-AML.
  • 31/33 pts had at least 2 poor-risk factors of age ≥70, antecedent hematologic disorder, unfavorable karyotype, or ECOG 2, and 28/33 had HCT-CI scores of ≥2.
  • CR occurred in all subsets of disease and cytogenetic risk groups.
  • Median OS has not been reached; median f/u of 19 surviving pts is 8 months.
  • Though non-hematologic toxicities were infrequent, infection and/or febrile neutropenia were common (in 24/33 pts).

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  • (PMID = 27961371.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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97. Schiller GJ, O'Brien SM, Vey N, Pigneux A, DeAngelo DJ, Karp JE, Hudak D, Kell J, Stuart RK, Giles FJ: Comorbidity description using the hematopoietic cell transplantation-specific comorbidity index (HCT-CI) in elderly de novo poor-risk AML patients (pts) treated with laromustine. J Clin Oncol; 2009 May 20;27(15_suppl):7050

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comorbidity description using the hematopoietic cell transplantation-specific comorbidity index (HCT-CI) in elderly de novo poor-risk AML patients (pts) treated with laromustine.
  • : 7050 Background: Treatment of older pts with AML is often complicated by comorbidities and pts with comorbidities are often underrepresented in clinical trials.
  • The HCT-CI, which was developed in pts receiving allogeneic SCT, has been applied to pts receiving induction therapy for AML in an effort to assist in therapeutic and investigational decisions (Kantarjian 2006; Etienne 2007; Giles 2007).
  • HCT-CI scores have been shown to be predictive of early death and survival in pts ≥ 60 years receiving induction therapy for AML, with early death rates of 3%, 11%, and 29% for pts with HCT-CI scores of 0, 1-2, and ≥ 3, respectively (Giles 2007).
  • METHODS: 140 pts age ≥ 60 with poor risk de novo AML from two phase II studies were scored for comorbidity by HCT-CI.
  • CONCLUSIONS: The majority (81%) of these older poor risk AML pts treated with laromustine had a HCT-CI score ≥ 3, confirming the poor risk nature of this patient group.
  • The induction death rate for pts treated with laromustine and with HCT-CI score ≥ 3 was lower than that reported for a group of pts with HCT-CI score ≥ 3 treated with standard induction chemotherapy (14% vs 29%; Giles 2007).

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  • (PMID = 27961414.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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98. Falini B, Martelli MP, Mecucci C, Liso A, Bolli N, Bigerna B, Pucciarini A, Pileri S, Meloni G, Martelli MF, Haferlach T, Schnittger S: Cytoplasmic mutated nucleophosmin is stable in primary leukemic cells and in a xenotransplant model of NPMc+ acute myeloid leukemia in SCID mice. Haematologica; 2008 May;93(5):775-9
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  • [Title] Cytoplasmic mutated nucleophosmin is stable in primary leukemic cells and in a xenotransplant model of NPMc+ acute myeloid leukemia in SCID mice.
  • We investigated the NPM1 mutation status or subcellular expression of NPM protein (nuclear vs. aberrant cytoplasmic) at diagnosis and relapse in 125 patients with acute myeloid leukemia from Italy and Germany.
  • All 52 patients with acute myeloidleukemia carrying at diagnosis mutated or cytoplasmic NPM (NPMc(+) acute myeloid leukemia) retained this feature at relapse.
  • Notably, cytoplasmic mutated NPM has now been retained for eight years in a xenotransplant model of NPMc(+) acute myeloid leukemia in immunodeficient mice.
  • None of 73 acute myeloid leukemia patients carrying at diagnosis wild-type NPM1 gene or showing at immunohistochemistry nucleus-restricted expression of nucleophosmin (NPMc(-) acute myeloid leukemia), which is predictive of NPM1 gene in germline configuration, acquired cytoplasmic mutated NPM at relapse.
  • This finding further confirms that NPMc(+) acute myeloid leukemia represents a primary event rather than a transformation stage of NPMc(-) acute myeloid leukemia.
  • The stability of cytoplasmic mutated NPM in patients with acute myeloid leukemia, even at relapse in extramedullary sites, and in a xenotransplant model, suggest this event is crucial for leukemogenesis and represents the rationale for monitoring minimal residual disease and molecular targeted therapy in NPMc(+) acute myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Mutation. Nuclear Proteins / genetics

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  • (PMID = 18367491.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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99. Niedermeier DM, Frei-Lahr DA, Hall PD: Treatment of acute myeloid leukemia during the second and third trimesters of pregnancy. Pharmacotherapy; 2005 Aug;25(8):1134-40
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  • [Title] Treatment of acute myeloid leukemia during the second and third trimesters of pregnancy.
  • Fortunately, the occurrence of acute myeloid leukemia (AML) during pregnancy is rare.
  • A 37-year-old woman in her second trimester (21 wks) of pregnancy was found to have acute myeloid leukemia.
  • Her hospital course was complicated by Pseudomonas vesicularis and gram-positive bacilli (not Bacillus anthracis) septicemia, but she obtained complete remission.
  • On day 14 of consolidation, filgrastim 16 mug/kg was added to improve stem cell mobilization.
  • Approximately 4 weeks after delivery, the mother underwent autologous peripheral stem cell transplantation.
  • Unfortunately, 100 days after transplantation, she had a relapse of AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Pregnancy Complications, Neoplastic / drug therapy

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  • (PMID = 16207105.001).
  • [ISSN] 0277-0008
  • [Journal-full-title] Pharmacotherapy
  • [ISO-abbreviation] Pharmacotherapy
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; PVI5M0M1GW / Filgrastim
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100. Balwierz W, Pietrzyk JJ, Wator G, Stozek K, Klekawka T, Kwiecińska K, Dłuzniewska A, Matysiak M, Malinowska I, Sikorska-Fic B, Balcerska A, Maciejka-Kapuścińska L, Sońta-Jakimczyk D, Tomaszewska R, Chybicka A, Krawczuk-Rybak M, Muszyńska-Rosłan K, Młynarski W, Stolarska M, Urasiński T, Kamieńska E, Sobol G, Wieczorek M, Karolczyk G, Wysocki M, Kołtan S, Kowalczyk JR, Wójcik B, Ksiazek T, Szewczyk K: [Genotyping and minimal residual disease study in children with acute myeloid leukemia: preliminary results]. Przegl Lek; 2010;67(6):371-4
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  • [Title] [Genotyping and minimal residual disease study in children with acute myeloid leukemia: preliminary results].
  • [Transliterated title] Genotypowanie i oznaczania choroby resztkowej u dzieci z ostra białaczka mieloblastycznq: wstepne wyniki.
  • The aim of the paper is to present the initial results of molecular examination which was started in 2006 for children with acute myeloid leukemia.
  • Better knowledge of biology of this disease, can result in establishing of new risk factors what allows more precise patient stratification to different therapeutic groups.
  • Study was obtained patients until to 18 years of age treated according to AML-BFM 2004 INTERIM protocol in 14 centers of the Polish Pediatric Leukemia/Lymphoma Study Group.
  • Mononuclear cells were collected from bone marrow on time points established according to the AML-BFM 2004 INTERIM protocol.
  • To perform quantitative RT-PCR and RQ-PCR reactions 4 fusion gene transcripts (AML1-ETO, CBFb-MYH11, PML-RARA /subtype bcrl and bcr3/) were used according to the protocol established by Europe Against Cancer Program.
  • Genotyping was performed in 75 patients with acute myeloid leukemia so far.
  • PML-RARA (subtype bcr3) and CBFB-MYH11 gene transcripts were detected in 3 (4%) and 3 (4%) patients, respectively.
  • To establish the rate of molecular marker presence in AML in children and the influence of the presence of MRD on the treatment results as well, the study has to be conducted on a larger group of patients with longer follow-up.
  • [MeSH-major] Genes, Wilms Tumor. Genetic Markers / genetics. Genotype. Neoplasm, Residual / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 21344764.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Genetic Markers
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