[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 46 of about 46
1. Sivendran S, Gruenstein S, Malone AK, Najfeld V: Ring chromosome 18 abnormality in acute myelogenous leukemia: the clinical dilemma. J Hematol Oncol; 2010;3:25
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ring chromosome 18 abnormality in acute myelogenous leukemia: the clinical dilemma.
  • Considering that ring chromosomes are rare in acute myelogenous leukemia (AML), it is difficult to risk stratify patient prognosis, particularly when the ring chromosome occurs as the sole abnormality.
  • Here we report a case of a ring chromosome 18 abnormality in a patient with newly diagnosed AML with monocytic differentiation.
  • Although r(18) chromosomal abnormalities were not classified in the recent updated evidence-and expert opinion-based recommendations for the diagnosis and management of AML (likely due to the small number of reported cases), the patient was treated as high risk with stem cell transplantation.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 18 / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Ring Chromosomes
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Cord Blood Stem Cell Transplantation. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Treatment Outcome


2. Bryant BJ, Alperin JB, Elghetany MT: Paraplegia as the presenting manifestation of extramedullary megakaryoblastic transformation of previously undiagnosed chronic myelogenous leukemia. Am J Hematol; 2007 Feb;82(2):150-4
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Paraplegia as the presenting manifestation of extramedullary megakaryoblastic transformation of previously undiagnosed chronic myelogenous leukemia.
  • Extramedullary tumors, also known as granulocytic sarcomas (GS), occur most frequently in acute myelogenous leukemia (AML).
  • They may signal the onset of the accelerated phase of chronic myelogenous leukemia (CML) or the blastic transformation of a myeloproliferative disorder.
  • Occasionally, a GS may be the presenting sign of undiagnosed AML, and rarely the presenting sign of undiagnosed CML or aleukemic leukemia.
  • Paraplegia due to a spinal cord GS is an extremely rare presentation of undiagnosed leukemia.
  • Further immunohistochemical studies of the tumor were consistent with extramedullary acute megakaryoblastic blast transformation of CML.
  • The combination of acute paraplegia and megakaryoblastic transformation in a previously undiagnosed patient with CML is extremely rare and may pose a diagnostic dilemma.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Lymphocyte Activation. Paraplegia / pathology. Spinal Cord Compression / pathology. Spinal Cord Neoplasms / pathology
  • [MeSH-minor] Combined Modality Therapy. Female. Humans. Middle Aged. Splenic Neoplasms / diagnosis. Splenic Neoplasms / pathology. Splenic Neoplasms / secondary. Splenic Neoplasms / therapy

  • Genetic Alliance. consumer health - Paraplegia.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17019692.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


3. Pidala J, Kim J, Anasetti C, Kharfan-Dabaja MA, Nishihori T, Field T, Perkins J, Perez L, Fernandez HF: Pharmacokinetic targeting of intravenous busulfan reduces conditioning regimen related toxicity following allogeneic hematopoietic cell transplantation for acute myelogenous leukemia. J Hematol Oncol; 2010;3:36
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacokinetic targeting of intravenous busulfan reduces conditioning regimen related toxicity following allogeneic hematopoietic cell transplantation for acute myelogenous leukemia.
  • Optimal conditioning therapy for hematopoietic cell transplantation (HCT) in acute myelogenous leukemia (AML) remains undefined.
  • We retrospectively compared outcomes of a consecutive series of 51 AML patients treated with oral busulfan (1 mg/kg every 6 hours for 4 days) and cyclophosphamide (60 mg/kg IV × 2 days) - (Bu/Cy) with 100 consecutive AML patients treated with pharmacokinetic targeted IV busulfan (AUC < 6000 μM/L*min per day × 4 days) and fludarabine (40 mg/m2 × 4 days) - (t-IV Bu/Flu).
  • Pharmacokinetic targeting of intravenous busulfan in combination with fludarabine is associated with reduced conditioning regimen related toxicity compared to oral busulfan and cyclophosphamide.
  • [MeSH-major] Busulfan / pharmacokinetics. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Transplantation Conditioning

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. BUSULFAN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biol Blood Marrow Transplant. 2002;8(9):468-76 [12374451.001]
  • [Cites] Expert Opin Drug Metab Toxicol. 2009 Aug;5(8):957-69 [19611402.001]
  • [Cites] Bone Marrow Transplant. 2003 Jun;31(12):1089-95 [12796788.001]
  • [Cites] Blood. 2003 Aug 1;102(3):820-6 [12676781.001]
  • [Cites] Blood. 2004 Aug 1;104(3):857-64 [15073038.001]
  • [Cites] Ann Intern Med. 1993 Feb 15;118(4):255-67 [8420443.001]
  • [Cites] Bone Marrow Transplant. 1995 Jun;15(6):825-8 [7581076.001]
  • [Cites] Bone Marrow Transplant. 1996 Feb;17(2):225-30 [8640171.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3599-604 [9808553.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5728-38 [16009946.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5675-87 [16110027.001]
  • [Cites] Cancer. 2005 Nov 1;104(9):1931-8 [16178004.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Dec;11(12):945-56 [16338616.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9387-93 [16314618.001]
  • [Cites] Leukemia. 2006 Feb;20(2):322-8 [16307018.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1092-9 [16551971.001]
  • [Cites] Bone Marrow Transplant. 2007 Sep;40(6):541-7 [17637692.001]
  • [Cites] J Clin Oncol. 2008 Feb 1;26(4):577-84 [18086801.001]
  • [Cites] Bone Marrow Transplant. 2008 Apr;41(8):721-7 [18176613.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Jun;14(6):672-84 [18489993.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Sep;14(9):993-1003 [18721762.001]
  • [Cites] Blood. 2003 Mar 1;101(5):2043-8 [12406916.001]
  • (PMID = 20925957.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ PMC2958877
  •  go-up   go-down


Advertisement
4. Cammenga J: Gatekeeper pathways and cellular background in the pathogenesis and therapy of AML. Leukemia; 2005 Oct;19(10):1719-28
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gatekeeper pathways and cellular background in the pathogenesis and therapy of AML.
  • Acute myelogenous leukemia (AML) is characterized by the accumulation of immature cells due to disturbed differentiation and proliferation of the myeloid lineage.
  • Genetic alterations affecting transcription factors and receptor tyrosine kinases have been identified in AML and causally linked to the disease.
  • The goal of this review is to address the role of the different genetic alterations in self-renewal and proliferation and to discuss the cellular background in which these events occur during the pathogenesis of AML.
  • Data from AML samples, clinical studies and mouse models for AML will be used to support the different theories regarding the leukemogenesis of AML.
  • Finally, this review wants to highlight the implication of these findings for the therapy of AML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / therapy. Signal Transduction / drug effects

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16107893.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 97
  •  go-up   go-down


5. Illmer T, Thiede C, Fredersdorf A, Stadler S, Neubauer A, Ehninger G, Schaich M: Activation of the RAS pathway is predictive for a chemosensitive phenotype of acute myelogenous leukemia blasts. Clin Cancer Res; 2005 May 1;11(9):3217-24
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activation of the RAS pathway is predictive for a chemosensitive phenotype of acute myelogenous leukemia blasts.
  • In acute myeloid leukemia (AML), mutations of the RAS genes cause an intrinsic activation of this pathway.
  • Until now, clinical studies could not find clear association of RAS mutations with the clinical outcome after AML therapy.
  • EXPERIMENTAL DESIGN: In total, 191 AML patients (126 as training population and 65 as test population) were studied for Ras activity with a glutathione S-transferase pull-down assay using Raf binding of activated Ras.
  • RESULTS: AML samples showed a wide range of Ras activity values, which was in contrast to normal bone marrow donors who showed no or very limited Ras activity.
  • Surprisingly, only a minority of RAS mutated AML samples (22.2%) showed strong Ras activity, whereas 25 patients presented strong Ras activity in the absence of RAS mutations.
  • In contrast, Ras activity predicted for a high response rate (P <0.05) and proved to be an independent factor for overall survival rate (P <0.05) in younger AML patients receiving high-dose 1-beta-D-arabinofuranosylcytosine as induction therapy.
  • Intrinsically activated Ras seems to increase sensitivity of the AML blast to high-dose 1-beta-D-arabinofuranosylcytosine therapy.
  • [MeSH-major] Bone Marrow Cells / drug effects. Leukemia, Myeloid, Acute / drug therapy. ras Proteins / metabolism

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15867216.001).
  • [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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 3.6.5.2 / ras Proteins
  •  go-up   go-down


6. Borthakur G, Estey AE: Therapy-related acute myelogenous leukemia and myelodysplastic syndrome. Curr Oncol Rep; 2007 Sep;9(5):373-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related acute myelogenous leukemia and myelodysplastic syndrome.
  • Therapy-related acute myelogenous leukemia and myelodysplastic syndrome (t-AML/MDS) are increasing in prevalence with aging of the population and improved survival of patients treated with chemotherapy or radiotherapy for other malignancies.
  • Research focused on the pathogenesis of t-AML/MDS will provide insight into the pathogenesis of de novo AML/MDS.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced. Neoplasms, Second Primary / chemically induced
  • [MeSH-minor] Humans. Neoplasms / drug therapy. Prognosis


7. Das-Gupta EP, Russell NH, Shaw BE, Pearce RM, Byrne JL: Long-term outcome of unrelated donor transplantation for AML using myeloablative conditioning incorporating pretransplant Alemtuzumab. Biol Blood Marrow Transplant; 2007 Jun;13(6):724-33
Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcome of unrelated donor transplantation for AML using myeloablative conditioning incorporating pretransplant Alemtuzumab.
  • The outcome of 55 patients who underwent matched unrelated donor (MUD) transplantation for acute myelogenous leukemia (AML) following a conditioning regimen of cyclophosphamide and total-body irradiation (TBI) with the addition of Alemtuzumab 10 mg/kg/day on days -5 to -1 is described.
  • Grade II-IV acute GVHD occurred in only 2 patients.
  • In multivariate analysis the receipt of an HLA mismatched transplant was associated with a higher transplant-related mortality (TRM) (55% versus 15%).
  • Twelve of the 14 transplant-related deaths were due to infection.
  • These results support the use of Alemtuzumab for unrelated donor hematopoietic stem cell transplant (HSCT) for poor risk AML in CR1 and for relapsed AML in CR2.
  • The addition of Alemtuzumab is highly effective in preventing both rejection and severe acute and extensive chronic GVHD without an increased relapse risk.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antibodies, Neoplasm / administration & dosage. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antibodies, Monoclonal, Humanized. Cause of Death. Cyclophosphamide / therapeutic use. Female. Graft Rejection / prevention & control. Graft vs Host Disease / prevention & control. Histocompatibility Testing. Humans. Longitudinal Studies. Male. Middle Aged. Myeloablative Agonists / therapeutic use. Survival Analysis. Tissue Donors. Treatment Outcome. Whole-Body Irradiation

  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17531783.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Myeloablative Agonists; 3A189DH42V / alemtuzumab; 8N3DW7272P / Cyclophosphamide
  •  go-up   go-down


8. Podgornik H, Debeljak M, Zontar D, Cernelc P, Prestor VV, Jazbec J: RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia. Cancer Genet Cytogenet; 2007 Oct 1;178(1):77-81
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

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


9. Faller BA, Robu VG, Borghaei H: Therapy-related acute myelogenous leukemia with an 11q23/MLL translocation following adjuvant cisplatin and vinorelbine for non-small-cell lung cancer. Clin Lung Cancer; 2009 Nov;10(6):438-40
Hazardous Substances Data Bank. VINBLASTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related acute myelogenous leukemia with an 11q23/MLL translocation following adjuvant cisplatin and vinorelbine for non-small-cell lung cancer.
  • We present a case of acute myelogenous leukemia with an 11q23/MLL rearrangement diagnosed 1 year after the completion of 4 cycles of cisplatin and vinorelbine for resected NSCLC.
  • To our knowledge, this is the first case of therapy-related acute myelogenous leukemia (t-AML) associated with this chemotherapy combination.
  • The literature on t-AML with the 11q23/MLL rearrangement is reviewed.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Translocation, Genetic / drug effects
  • [MeSH-minor] Aged. Carcinoma, Non-Small-Cell Lung / drug therapy. Chromosomes, Human, Pair 11. Cisplatin / administration & dosage. Follow-Up Studies. Histone-Lysine N-Methyltransferase. Humans. Lung Neoplasms / drug therapy. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Vinblastine / administration & dosage. Vinblastine / analogs & derivatives


10. Krishna G, AbuTarif M, Xuan F, Martinho M, Angulo D, Cornely OA: Pharmacokinetics of oral posaconazole in neutropenic patients receiving chemotherapy for acute myelogenous leukemia or myelodysplastic syndrome. Pharmacotherapy; 2008 Oct;28(10):1223-32
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacokinetics of oral posaconazole in neutropenic patients receiving chemotherapy for acute myelogenous leukemia or myelodysplastic syndrome.
  • STUDY OBJECTIVE: To analyze the pharmacokinetics of posaconazole administered as prophylaxis for invasive fungal infection (IFI) in neutropenic patients receiving chemotherapy for acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS).
  • PATIENTS: One hundred ninety-four patients with AML or MDS who received posaconazole oral suspension 200 mg 3 times/day with meals or a nutritional supplement for a minimum of 7 days to achieve steady state and for a maximum of 12 weeks.
  • [MeSH-major] Antifungal Agents / pharmacokinetics. Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / drug therapy. Mycoses / prevention & control. Myelodysplastic Syndromes / drug therapy. Neutropenia / chemically induced. Triazoles / pharmacokinetics


11. de Lima M, Giralt S: Allogeneic transplantation for the elderly patient with acute myelogenous leukemia or myelodysplastic syndrome. Semin Hematol; 2006 Apr;43(2):107-17
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic transplantation for the elderly patient with acute myelogenous leukemia or myelodysplastic syndrome.
  • Acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS) are diseases of the elderly.
  • Allogeneic hematopoietic stem cell transplantation (HSCT) offers the possibility of cure for these malignancies, but until recently its use was restricted to younger patients due to prohibitive treatment-related mortality.
  • Here we review current results of allogeneic blood and marrow transplantation for AML and MDS in the elderly.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy


12. Perl AE, Carroll M: Exploiting signal transduction pathways in acute myelogenous leukemia. Curr Treat Options Oncol; 2007 Aug;8(4):265-76
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Exploiting signal transduction pathways in acute myelogenous leukemia.
  • Traditional cytotoxic chemotherapy is effective at temporizing AML in the majority of patients but cures a small minority.
  • While signal transduction inhibition is a promising area to advance AML therapy, no agent as monotherapy has demonstrated obvious clinical benefit over traditional cytotoxic chemotherapy.
  • Tipifarnib is perhaps an exception as it is the only signal transduction inhibitor in AML that reproducibly shows clinical benefit using traditional chemotherapy response criteria.
  • Similarly unclear is the benefit of a potent specific kinase inhibitor versus a broad inhibitor of multiple kinases that could prove relevant to leukemia biology.
  • To this end, the extensive measures applied to correlate the biologic activity of FLT3 inhibitors with clinical responses are noteworthy and provide useful lessons for clinical trial design and drug development both in leukemia and other cancers.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Signal Transduction / drug effects


13. Halim TY, Song KW, Barnett MJ, Forrest DL, Hogge DE, Nantel SH, Nevill TJ, Shepherd JD, Smith CA, Sutherland HJ, Toze CL, Lavoie JC: Positive impact of selective outpatient management of high-risk acute myelogenous leukemia on the incidence of septicemia. Ann Oncol; 2007 Jul;18(7):1246-52
MedlinePlus Health Information. consumer health - Sepsis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Positive impact of selective outpatient management of high-risk acute myelogenous leukemia on the incidence of septicemia.
  • BACKGROUND: Curative intent chemotherapy for acute myelogenous leukemia (AML) leads to prolonged severe neutropenia, during which patients are highly susceptible to infection.
  • Our center recently implemented a selective ambulatory management policy for AML patients undergoing chemotherapy.
  • MATERIALS AND METHODS: A retrospective analysis was conducted to assess the occurrence of septicemia in AML patients treated over a 5 years period with curative intent chemotherapy.
  • This review encompasses a change in policy from primarily inpatient care to selective outpatient management coupled with prophylactic antibiotic therapy.
  • No significant emerging resistance and no septicemia-related mortality were noted in the outpatient cohort.
  • CONCLUSION: The observed decrease in the incidence of septicemia in the ambulatory cohort adds supportive evidence to the feasibility of selective outpatient management of AML patients with respect to infectious complications.

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17442662.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


14. Erba HP, Kantarjian HM, Claxton DF, Arellano M, Lyons RM, Kovacsovics TJ, Gabrilove J, Eckert S, Faderl S: Updated remission duration and survival results of single-agent clofarabine in previously untreated older adult patients with acute myelogenous leukemia (AML) unlikely to benefit from standard induction chemotherapy due to unfavorable baseline risk factor(s). J Clin Oncol; 2009 May 20;27(15_suppl):7062

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Updated remission duration and survival results of single-agent clofarabine in previously untreated older adult patients with acute myelogenous leukemia (AML) unlikely to benefit from standard induction chemotherapy due to unfavorable baseline risk factor(s).
  • METHODS: Single arm, multi-center, phase II, open-label, 2-stage study of patients with untreated AML, ≥60 years old, and at least one adverse prognostic factor: age ≥70 years, antecedent hematologic disorder (AHD), PS = 2, and/or intermediate/unfavorable risk karyotype.
  • Median DOR (censored at alternative therapy) for CR/CRp was 56 weeks (95% CI, 33 weeks - not yet estimable [n/e]) and for CR 65 weeks (95% CI, 41 weeks - n/e).
  • Median DFS (not censored at alternative therapy) for CR/CRp was 34 weeks (95% CI, 24 - 65 weeks).
  • CONCLUSIONS: These data expand on the previously reported efficacy and safety data of single agent CLO in adult AML.
  • These results suggest that single agent CLO is an effective and tolerable treatment option for older adult patients with untreated AML and 1 or more unfavorable baseline prognostic factor(s).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27961436.001).
  • [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
  •  go-up   go-down


15. Hatfield KJ, Olsnes AM, Gjertsen BT, Bruserud Ø: Antiangiogenic therapy in acute myelogenous leukemia: targeting of vascular endothelial growth factor and interleukin 8 as possible antileukemic strategies. Curr Cancer Drug Targets; 2005 Jun;5(4):229-48
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antiangiogenic therapy in acute myelogenous leukemia: targeting of vascular endothelial growth factor and interleukin 8 as possible antileukemic strategies.
  • Acute myelogenous leukemia (AML) is an aggressive disorder with an overall disease-free survival of 40-50% even for the younger patients under 60 years of age who can receive the most intensive treatment.
  • The median age at the time of diagnosis is 60-65 years, and the large majority of elderly patients usually receive less intensive chemotherapy or only supportive therapy due to the high treatment-related mortality when using intensive therapy for elderly individuals.
  • Thus, there is a need for new therapeutic approaches to improve the treatment in younger patients and to make AML-directed therapy with acceptable toxicity possible in elderly individuals.
  • Angiogenesis seems to be important both for leukemogenesis and susceptibility to intensive chemotherapy, and antiangiogenic strategies are therefore considered for the treatment of AML.
  • The two proangiogenic mediators vascular endothelial growth factor (VEGF) and interleukin 8, (IL-8, also referred to as CXCL8) seem to be important in human AML: VEGF is released at increased levels due to interactions between AML cells and neighboring nonleukemic cells, whereas IL-8 is released at high levels by native human AML cells.
  • Thus, VEGF as a therapeutic target in AML is suggested both by experimental and clinical observations, whereas IL-8 as a target is mainly suggested by experimental evidence.
  • In the present review we describe and discuss (i) the angioregulatory network of soluble mediators in AML, including both the systemic levels and local release by native human AML cells; and (ii) various therapeutic approaches to target VEGF and IL-8.
  • Although single angioregulatory mediators can be targeted, it should be emphasized that the final effect of soluble mediators on angioregulation is determined by a complex angioregulatory network that varies between AML patients, and the final effect of targeting single mediators may therefore differ between patient subsets.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents / therapeutic use. Interleukin-8 / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Vascular Endothelial Growth Factor A / drug effects. Vascular Endothelial Growth Factor A / therapeutic use

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15975045.001).
  • [ISSN] 1568-0096
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Interleukin-8; 0 / Vascular Endothelial Growth Factor A
  • [Number-of-references] 222
  •  go-up   go-down


16. Dluzniewska A, Balwierz W, Armata J, Balcerska A, Chybicka A, Kowalczyk J, Matysiak M, Ochocka M, Radwanska U, Rokicka-Milewska R, Sonta-Jakimczyk D, Wachowiak J, Wysocki M: Twenty years of Polish experience with three consecutive protocols for treatment of childhood acute myelogenous leukemia. Leukemia; 2005 Dec;19(12):2117-24
Hazardous Substances Data Bank. CYTARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Twenty years of Polish experience with three consecutive protocols for treatment of childhood acute myelogenous leukemia.
  • Until 1983, results of treatment of acute myelogenous leukemia (AML) in Poland with different regimens were very poor.
  • In 1983, the Polish Pediatric Leukemia/Lymphoma Study Group introduced a unified treatment protocol--a modified version of BFM-83 protocol.
  • This led to an increase in the curability of AML from 15% to approximately 32%.
  • In 1994, a modification was made: the high-risk patients (>5% blasts in bone marrow on day 15 of therapy and all M5 cases) received two additional cycles with intermediate-dose cytarabine (ID-ARAC).
  • A new treatment protocol employing idarubicin in place of daunorubicin was introduced in 1998 and produced better initial responses, increase in the number of patients attaining remission after induction therapy and proportional increase of standard-risk patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antineoplastic Protocols / standards. Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Bone Marrow Transplantation. Cause of Death. Child. Child, Preschool. Cytarabine / administration & dosage. Female. Follow-Up Studies. Humans. Idarubicin / therapeutic use. Infant. Infant, Newborn. Male. Poland. Remission Induction / methods. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16107894.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
  •  go-up   go-down


17. Thomas X, Dombret H: Timed-sequential chemotherapy as induction and/or consolidation regimen for younger adults with acute myelogenous leukemia. Hematology; 2007 Feb;12(1):15-28
Hazardous Substances Data Bank. CYTARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Timed-sequential chemotherapy as induction and/or consolidation regimen for younger adults with acute myelogenous leukemia.
  • Increasing the intensity of induction chemotherapy has generated considerable recent interest in the treatment of acute myeloid leukemia.
  • Here we review the results of timed-sequential chemotherapy, used as induction regimen in de novo, relapsed or refractory AML or used as post-remission therapy, and compare them with those from other types of regimens.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Animals. Antimetabolites, Antineoplastic / administration & dosage. Bone Marrow Diseases / chemically induced. Cell Cycle / drug effects. Child. Cytarabine / pharmacology. Disease-Free Survival. Drug Administration Schedule. Drug Resistance, Neoplasm. Flavonoids / administration & dosage. Flavonoids / pharmacology. Granulocyte Colony-Stimulating Factor / administration & dosage. Granulocyte Colony-Stimulating Factor / pharmacology. Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Middle Aged. Piperidines / administration & dosage. Piperidines / pharmacology. Premedication. Prognosis. Rats. Remission Induction / methods. Retrospective Studies. Salvage Therapy. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17364988.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Flavonoids; 0 / Piperidines; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 45AD6X575G / alvocidib; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Number-of-references] 127
  •  go-up   go-down


18. Nemerovski CW, Mackler ER, DePestel DD, Collins CD, Welch KS, Stevenson JG: Drug costs and utilization after implementation of a posaconazole prophylaxis protocol in adults with acute myelogenous leukemia. Am J Health Syst Pharm; 2010 Feb 15;67(4):295-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Drug costs and utilization after implementation of a posaconazole prophylaxis protocol in adults with acute myelogenous leukemia.
  • PURPOSE: Drug costs and utilization after implementation of a posaconazole prophylaxis protocol in adults with acute myelogenous leukemia (AML) were studied.
  • METHODS: Adult patients who initiated induction or reinduction chemotherapy for the treatment of AML between December 1, 2006, and March 31, 2008, at a tertiary care hospital were included in this retrospective cohort study.
  • Prophylactic posaconazole was frequently changed to alternative antifungal therapy due to an adverse drug event, perceived lack of efficacy, avoidance of a drug interaction, or inability to tolerate oral intake.
  • [MeSH-major] Antifungal Agents / administration & dosage. Antifungal Agents / economics. Drug Costs. Leukemia, Myeloid, Acute / drug therapy. Mycoses / prevention & control. Triazoles / administration & dosage

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Fungal Infections.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20133535.001).
  • [ISSN] 1535-2900
  • [Journal-full-title] American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists
  • [ISO-abbreviation] Am J Health Syst Pharm
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antifungal Agents; 0 / Antineoplastic Agents; 0 / Triazoles; 6TK1G07BHZ / posaconazole
  •  go-up   go-down


19. Lancet JE, Gojo I, Gotlib J, Feldman EJ, Greer J, Liesveld JL, Bruzek LM, Morris L, Park Y, Adjei AA, Kaufmann SH, Garrett-Mayer E, Greenberg PL, Wright JJ, Karp JE: A phase 2 study of the farnesyltransferase inhibitor tipifarnib in poor-risk and elderly patients with previously untreated acute myelogenous leukemia. Blood; 2007 Feb 15;109(4):1387-94
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase 2 study of the farnesyltransferase inhibitor tipifarnib in poor-risk and elderly patients with previously untreated acute myelogenous leukemia.
  • Outcomes for older adults with acute myelogenous leukemia (AML) are poor due to both disease and host-related factors.
  • In this phase 2 study, we tested the oral farnesyltransferase inhibitor tipifarnib in 158 older adults with previously untreated, poor-risk AML.
  • Early death in the absence of progressive disease was rare, and drug-related nonhematologic serious adverse events were observed in 74 patients (47%).
  • Tipifarnib is active and well tolerated in older adults with poor-risk AML and may impart a survival advantage in those patients who experience a clinical response.

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1692-7 [12411300.001]
  • [Cites] Blood. 2003 Dec 15;102(13):4527-34 [12947010.001]
  • [Cites] Blood Rev. 2004 Mar;18(1):39-63 [14684148.001]
  • [Cites] J Clin Oncol. 1999 Nov;17(11):3631-52 [10550163.001]
  • [Cites] Oncogene. 1999 Dec 9;18(52):7514-26 [10602510.001]
  • [Cites] Invest New Drugs. 1999;17(3):241-58 [10665477.001]
  • [Cites] J Clin Oncol. 2004 Apr 1;22(7):1287-92 [15051776.001]
  • [Cites] J Clin Oncol. 1989 Sep;7(9):1268-74 [2475589.001]
  • [Cites] Cancer Res. 1992 May 15;52(10):2847-53 [1581898.001]
  • [Cites] Cancer Res. 1994 Jun 15;54(12):3229-32 [8205544.001]
  • [Cites] N Engl J Med. 1995 Jun 22;332(25):1671-7 [7760868.001]
  • [Cites] Blood. 1995 Jul 15;86(2):457-62 [7605984.001]
  • [Cites] Hematol Oncol Clin North Am. 2000 Feb;14(1):251-67 [10680081.001]
  • [Cites] Cancer Res. 2000 Apr 1;60(7):1871-7 [10766174.001]
  • [Cites] Clin Cancer Res. 2000 Jun;6(6):2318-25 [10873082.001]
  • [Cites] Mol Cell Biol. 2000 Aug;20(16):6105-13 [10913192.001]
  • [Cites] J Biol Chem. 2000 Sep 29;275(39):30451-7 [10852915.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4075-83 [11110676.001]
  • [Cites] Exp Cell Res. 2001 Jan 1;262(1):17-27 [11120601.001]
  • [Cites] Cancer Res. 2001 Jan 1;61(1):131-7 [11196150.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3361-9 [11369625.001]
  • [Cites] Blood. 2001 Aug 1;98(3):548-53 [11468148.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1302-11 [11520775.001]
  • [Cites] Cancer Res. 2002 Jan 15;62(2):450-8 [11809695.001]
  • [Cites] Blood. 2002 Jul 1;100(1):29-35 [12070004.001]
  • [Cites] Blood. 2002 Aug 15;100(4):1224-32 [12149202.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2292-302 [12239137.001]
  • [Cites] Cancer Res. 1995 Aug 1;55(15):3295-304 [7614464.001]
  • [Cites] Cancer Res. 1995 Nov 15;55(22):5302-9 [7585592.001]
  • [Cites] Cancer Res. 1997 Feb 15;57(4):708-13 [9044849.001]
  • [Cites] Blood. 1997 May 1;89(9):3323-9 [9129038.001]
  • [Cites] Blood. 1997 Oct 15;90(8):2952-61 [9376575.001]
  • [Cites] Blood. 1997 Oct 15;90(8):2969-77 [9376577.001]
  • [Cites] J Clin Oncol. 1998 Mar;16(3):872-81 [9508168.001]
  • [Cites] Blood. 1998 May 15;91(10):3607-15 [9572995.001]
  • [Cites] Oncogene. 1998 Sep 17;17(11 Reviews):1439-45 [9779989.001]
  • [Cites] N Engl J Med. 1998 Dec 3;339(23):1649-56 [9834301.001]
  • [Cites] Leukemia. 1999 Jun;13(6):843-9 [10360370.001]
  • [Cites] Blood. 1999 Aug 1;94(3):1086-99 [10419902.001]
  • [Cites] Cancer. 2006 Mar 1;106(5):1090-8 [16435386.001]
  • [Cites] Blood. 2006 May 1;107(9):3481-5 [16455952.001]
  • (PMID = 17082323.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA070095; United States / NCI NIH HHS / CA / U01 CA69854; United States / NCI NIH HHS / CA / U01 CA70095
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNAJA1 protein, human; 0 / HSP40 Heat-Shock Proteins; 0 / Quinolones; 192185-72-1 / tipifarnib; EC 2.5.1.29 / Farnesyltranstransferase
  • [Other-IDs] NLM/ PMC1794070
  •  go-up   go-down


20. Pânzaru C, Dan M, Burcoveanu C, Mereuţă A, Buiuc D: Disseminated infection due to Candida guilliermondii in a patient with AML(M4). Case study. Rev Med Chir Soc Med Nat Iasi; 2006 Jul-Sep;110(3):727-30
Hazardous Substances Data Bank. FLUCONAZOLE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disseminated infection due to Candida guilliermondii in a patient with AML(M4). Case study.
  • A 43-year-old patient admitted with acute myelogenous leukemia, developed bronchopneumonia and sepsis during profound neutropenia.
  • Fever and pulmonary infiltrates did not improve by using empiric antibacterial therapy (Cefoperazona-Sulbactam, Trimethoprim-Sulphametoxazol).
  • After a few days of therapy with Voriconazol, fever disappeared and the clinical state of patient was improved.
  • [MeSH-major] Candida / isolation & purification. Candidiasis / complications. Fungemia / microbiology. Immunocompromised Host. Leukemia, Myeloid, Acute / complications
  • [MeSH-minor] Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Bronchopneumonia / microbiology. Drug Therapy, Combination. Fluconazole / therapeutic use. Humans. Male. Middle Aged. Neutropenia / etiology. Pyrimidines / therapeutic use. Treatment Outcome. Triazoles / therapeutic use. Voriconazole

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Yeast Infections.
  • Hazardous Substances Data Bank. AMPHOTERICIN B .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17571574.001).
  • [ISSN] 0048-7848
  • [Journal-full-title] Revista medico-chirurgicală̆ a Societă̆ţ̜ii de Medici ş̧i Naturaliş̧ti din Iaş̧i
  • [ISO-abbreviation] Rev Med Chir Soc Med Nat Iasi
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Pyrimidines; 0 / Triazoles; 7XU7A7DROE / Amphotericin B; 8VZV102JFY / Fluconazole; JFU09I87TR / Voriconazole
  •  go-up   go-down


21. Li H, Lu Y, Piao L, Wu J, Liu S, Marcucci G, Ratnam M, Lee RJ: Targeting human clonogenic acute myelogenous leukemia cells via folate conjugated liposomes combined with receptor modulation by all-trans retinoic acid. Int J Pharm; 2010 Dec 15;402(1-2):57-63
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting human clonogenic acute myelogenous leukemia cells via folate conjugated liposomes combined with receptor modulation by all-trans retinoic acid.
  • Our previous data demonstrated that folate receptor β (FR-β) targeted liposomal doxorubicin (FT-L-DOX) showed enhanced cytotoxicity relative to non-targeted liposomal doxorubicin (CON-L-DOX), and the effect was enhanced by selective FR-β upregulation by all-trans retinoic acid (ATRA) in AML blast cells.
  • In this study, the enhanced cytotoxicity was investigated in the proliferating human AML clonogenic cells by combining FT-L-DOX with ATRA.
  • Colony formation in AML cells was lower due to treatment with FT-L-DOX compared with CON-L-DOX and colony formation further decreased upon pretreatment with ATRA.
  • Moreover, FT-L-DOX was more toxic to AML clonogenic cells than to AML blast cells.
  • The results demonstrate that the efficiency of FR-mediated targeting of FT-L-DOX was preferentially enhanced by ATRA induced FR-β upregulation in AML clonogenic cells.

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.
  • [Cites] Adv Drug Deliv Rev. 2004 Apr 29;56(8):1111-25 [15094210.001]
  • [Cites] Adv Drug Deliv Rev. 2004 Apr 29;56(8):1085-97 [15094208.001]
  • [Cites] Eur J Clin Invest. 2004 Aug;34 Suppl 2:31-40 [15291804.001]
  • [Cites] Oncogene. 2004 Sep 20;23(43):7178-87 [15378078.001]
  • [Cites] Biochim Biophys Acta. 1990 Jun 27;1025(2):143-51 [2364073.001]
  • [Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]
  • [Cites] Drugs. 1994 Feb;47(2):223-58 [7512899.001]
  • [Cites] Biochim Biophys Acta. 1995 Feb 15;1233(2):134-44 [7865538.001]
  • [Cites] Biochemistry. 1995 Nov 7;34(44):14594-600 [7578066.001]
  • [Cites] Leukemia. 1996 Jun;10(6):937-42 [8667648.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] Drugs. 1997;54 Suppl 4:1-7 [9361955.001]
  • [Cites] Antimicrob Agents Chemother. 1998 Sep;42(9):2431-3 [9736577.001]
  • [Cites] Cancer. 1999 Jan 15;85(2):348-57 [10023702.001]
  • [Cites] Med J Aust. 1999 Jan 4;170(1):39-43 [10026673.001]
  • [Cites] Br J Haematol. 1999 Jul;106(1):92-9 [10444168.001]
  • [Cites] Arthritis Rheum. 1999 Aug;42(8):1609-16 [10446858.001]
  • [Cites] Expert Opin Drug Deliv. 2004 Nov;1(1):7-17 [16296717.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4086-92 [16131573.001]
  • [Cites] Cancer Res. 2006 Jun 1;66(11):5875-82 [16740727.001]
  • [Cites] Nat Rev Cancer. 2006 Sep;6(9):688-701 [16900224.001]
  • [Cites] Cancer Metastasis Rev. 2007 Mar;26(1):141-52 [17333345.001]
  • [Cites] J Pharm Sci. 2007 Sep;96(9):2424-35 [17588260.001]
  • [Cites] Leukemia. 2007 Oct;21(10):2233-5 [17554378.001]
  • [Cites] Mol Pharm. 2007 Sep-Oct;4(5):707-12 [17708654.001]
  • [Cites] Pediatr Hematol Oncol. 2008 Mar;25(2):115-8 [18363177.001]
  • [Cites] Int J Pharm. 2008 May 22;356(1-2):29-36 [18258394.001]
  • [Cites] Haematologica. 1999 Dec;84(12):1151-2 [10586216.001]
  • [Cites] Ann N Y Acad Sci. 1999;886:293-6 [10667243.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3529-36 [11071651.001]
  • [Cites] Blood. 2002 Jul 15;100(2):594-602 [12091353.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Oct 11;297(5):1238-44 [12372420.001]
  • [Cites] Pharm Res. 2003 Mar;20(3):417-22 [12669962.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 30;100 Suppl 1:11842-9 [14504387.001]
  • [Cites] Clin Cancer Res. 2003 Dec 15;9(17):6551-9 [14695160.001]
  • [Cites] Adv Drug Deliv Rev. 2004 Apr 29;56(8):1177-92 [15094214.001]
  • (PMID = 20883757.001).
  • [ISSN] 1873-3476
  • [Journal-full-title] International journal of pharmaceutics
  • [ISO-abbreviation] Int J Pharm
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA080183; United States / NCI NIH HHS / CA / P50 CA140158; United States / NCI NIH HHS / CA / R01 CA080183; United States / NCI NIH HHS / CA / R01CA095673; United States / NCRR NIH HHS / RR / UL1 RR025755; United States / NCI NIH HHS / CA / R01 CA095673; United States / NCI NIH HHS / CA / CA095673-05; United States / NCI NIH HHS / CA / R01 CA095673-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Fluoresceins; 0 / Folate Receptor 2; 5688UTC01R / Tretinoin; 80168379AG / Doxorubicin; V0YM2B16TS / fluorexon
  • [Other-IDs] NLM/ NIHMS249454; NLM/ PMC2982872
  •  go-up   go-down


22. Bhatla D, Gerbing RB, Alonzo TA, Mehta PA, Deal K, Elliott J, Meshinchi S, Geiger H, Perentesis JP, Lange BJ, Davies SM, Children's Oncology Group: DNA repair polymorphisms and outcome of chemotherapy for acute myelogenous leukemia: a report from the Children's Oncology Group. Leukemia; 2008 Feb;22(2):265-72
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA repair polymorphisms and outcome of chemotherapy for acute myelogenous leukemia: a report from the Children's Oncology Group.
  • Polymorphisms of DNA repair genes RAD51 and XRCC3 increase susceptibility to acute myeloid leukemia (AML) in adults, an effect enhanced by deletion of the glutathione-S-transferase M1 (GSTM1) gene.
  • In this study, we genotyped 452 children with de novo AML treated on CCG protocols 2941 and 2961 and compared genotype frequencies with those of normal blood donors, and analyzed the impact of genotype on outcome of therapy.
  • XRCC3 Thr241Met, RAD51 G135C and GSTM1 genotypes did not increase susceptibility to AML when assessed singly.
  • In contrast, when XRCC3 and RAD51 genotypes were examined together a significant increase in susceptibility to AML was seen in children with variant alleles.
  • Analysis of outcome of therapy showed that patients heterozygous for the XRCC3 Thr241Met allele had improved post-induction disease-free survival compared to children homozygous for the major or minor allele, each of whom had similar outcomes.
  • Improved survival was due to reduced relapse in the heterozygous children, and this effect was most marked in children randomized to therapy likely to generate DNA double-strand breaks (etoposide, daunomycin), compared with anti-metabolite (fludarabine, cytarabine) based therapy.
  • In contrast, RAD51 G135C and the GSTM1 deletion polymorphism did not influence outcome of AML therapy in our study population.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2001 Sep 1;98(5):1312-20 [11520776.001]
  • [Cites] EMBO J. 2004 Jan 28;23(2):439-49 [14726957.001]
  • [Cites] EMBO J. 2004 Feb 11;23(3):670-80 [14749735.001]
  • [Cites] Clin Cancer Res. 2004 Apr 15;10(8):2675-80 [15102670.001]
  • [Cites] J Biol Chem. 2004 May 28;279(22):23250-4 [15037616.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 May;13(5):801-7 [15159313.001]
  • [Cites] Cancer Res. 2004 Aug 15;64(16):5560-3 [15313891.001]
  • [Cites] Mutat Res. 2004 Nov 22;556(1-2):169-81 [15491645.001]
  • [Cites] Cell. 1996 Nov 15;87(4):757-66 [8929543.001]
  • [Cites] EMBO J. 1998 Jan 15;17(2):598-608 [9430650.001]
  • [Cites] Mol Cell. 1998 May;1(6):783-93 [9660962.001]
  • [Cites] J Biol Chem. 1998 Aug 21;273(34):21482-8 [9705276.001]
  • [Cites] Carcinogenesis. 2004 Dec;25(12):2433-41 [15333465.001]
  • [Cites] Mutat Res. 2005 Feb 15;570(1):105-17 [15680408.001]
  • [Cites] Int J Cancer. 2005 Nov 20;117(4):611-8 [15924337.001]
  • [Cites] Laryngoscope. 2005 Dec;115(12):2221-31 [16369171.001]
  • [Cites] Nat Rev Genet. 2006 Jan;7(1):45-54 [16369571.001]
  • [Cites] Eur J Gynaecol Oncol. 2005;26(6):589-98 [16398215.001]
  • [Cites] World J Gastroenterol. 2005 Nov 14;11(42):6593-600 [16425350.001]
  • [Cites] Hum Mol Genet. 2006 Apr 1;15(7):1217-24 [16505003.001]
  • [Cites] Blood. 2006 Jul 1;108(1):74-80 [16537811.001]
  • [Cites] DNA Cell Biol. 2006 Jul;25(7):406-11 [16848682.001]
  • [Cites] J Clin Oncol. 2006 Aug 10;24(23):3799-808 [16896009.001]
  • [Cites] Eur J Hum Genet. 2006 Oct;14(10):1136-44 [16791138.001]
  • [Cites] Cancer Lett. 2006 Sep 8;241(1):142-9 [16343742.001]
  • [Cites] Mutat Res. 2007 Mar 5;627(2):146-57 [17158087.001]
  • [Cites] J Biol Chem. 2000 Jun 2;275(22):16443-9 [10749867.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2000 Jun;9(6):563-6 [10868689.001]
  • [Cites] Cancer Res. 2000 Oct 15;60(20):5612-6 [11059748.001]
  • [Cites] Nat Genet. 2001 Mar;27(3):247-54 [11242102.001]
  • [Cites] J Clin Oncol. 2001 Mar 1;19(5):1279-87 [11230469.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Mar 13;98(6):3232-6 [11248061.001]
  • [Cites] Int J Cancer. 2001 May 15;92(4):562-7 [11304692.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 May 8;98(10):5538-43 [11331762.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8440-6 [11459987.001]
  • [Cites] Carcinogenesis. 2001 Sep;22(9):1437-45 [11532866.001]
  • [Cites] Hum Mol Genet. 2002 Jun 1;11(12):1399-407 [12023982.001]
  • [Cites] Oncogene. 2002 Jun 13;21(26):4176-80 [12037675.001]
  • [Cites] Nucleic Acids Res. 2002 Jul 1;30(13):2862-70 [12087170.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2002 Dec;11(12):1513-30 [12496039.001]
  • [Cites] Mol Cell. 2003 Apr;11(4):1109-17 [12718895.001]
  • [Cites] Environ Health Perspect. 2003 Nov;111(15):1843-50 [14630517.001]
  • [Cites] J Clin Oncol. 2004 Jan 1;22(1):150-6 [14701777.001]
  • [Cites] Cancer. 2004 Jan 15;100(2):411-7 [14716779.001]
  • (PMID = 18033323.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA10262-01; United States / NCI NIH HHS / CA / R01 CA093552-01; United States / NCI NIH HHS / CA / CA 98543; United States / NCI NIH HHS / CA / R01 CA114563-01; United States / NCI NIH HHS / CA / R01CA93552-01; United States / NCI NIH HHS / CA / R01 CA093552; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA093552-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 3; EC 2.7.7.- / Rad51 Recombinase
  • [Other-IDs] NLM/ NIHMS210453; NLM/ PMC2914507
  •  go-up   go-down


23. Liu Y, Ke XY, Ma J, Shen ZX, Zhang XH, Du X, Zhao YM, Lv JQ, Zhan ZM, Zeng XY, Xu XH, Lu ZS: [Multicenter randomized control trial on safety of domestic idarubicin for acute leukemia]. Zhonghua Zhong Liu Za Zhi; 2006 Sep;28(9):706-8
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Multicenter randomized control trial on safety of domestic idarubicin for acute leukemia].
  • OBJECTIVE: To evaluate the safety of domestically produced idarubicin in the treatment of acute leukemia by a multicenter randomized control trial.
  • METHODS: This trial was carried out in the hemotologica department of five hospitals throughout China, with hospitalized patients who suffered from acute myelogenous leukemia ( AML except M3 type) , acute lymphocytic leukemia ( ALL) , chronic myelogenous leukemia-blast (CML-blast) , totally 155 patients.
  • In this study, 155 leukemia patients were randomly grouped into: 1. test group treated using domestic idarubicin, 2. control group using imported idarubicin.
  • The acute myelogenous leukemia regimen included idarubicin 8 mg/m(2), dl -3 plus cytosine arabinoside 100 mg/m(2), dl - 7 for 1-2 cycles.
  • The regimen for acute lymphocytic leukemia was idarubicin 8 mg/m2, dl - 3; vincristine 2 mg/mr, dl; cyclophosphamide 750 mg/m2, dl ; plus prednisone 60 mg/m(2),dl - 14 for 1-2 cycles.
  • Drug-related death was observed in 3 of 77 patients in the domestic idarubicin group (3.9%) due to cerebral hemorrage or septic infection.
  • CONCLUSION: Domestic idarubicin is comparable to imported counterpart in efficiency and safety for the treatment of acute leukemia.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Idarubicin / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Agranulocytosis / chemically induced. Blast Crisis / drug therapy. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Cytarabine / administration & dosage. Cytarabine / adverse effects. Female. Humans. Male. Middle Aged. Mucositis / chemically induced. Nausea / chemically induced. Prednisone / administration & dosage. Prednisone / adverse effects. Remission Induction. Treatment Outcome. Vincristine / administration & dosage. Vincristine / adverse effects

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17274381.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; ZRP63D75JW / Idarubicin
  •  go-up   go-down


24. Klymenko SV, Bink K, Trott KR, Bebeshko VG, Bazyka DA, Dmytrenko IV, Abramenko IV, Bilous NI, Zitzelsberger H, Misurin AV, Atkinson MJ, Rosemann M: MLL gene alterations in radiation-associated acute myeloid leukemia. Exp Oncol; 2005 Mar;27(1):71-5
Genetic Alliance. consumer health - Leukemia, Myeloid.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MLL gene alterations in radiation-associated acute myeloid leukemia.
  • AIM: Although acute myelogenous leukemia (AML) arising after radiation exposure is considered to be secondary, little is known about the molecular mechanisms by which the radiation induces the leukemogenic phenotype.
  • The aim of the study was to analyze whether the MLL translocations are as frequent in radiation-associated AML as in spontaneous AML cases.
  • METHODS: Sixty one AML samples obtained at diagnosis were analyzed for the presence of MLL abnormalities using fluorescent in situ hybridization and/or reverse transcription polymerase chain reaction.
  • Of these patients, 27 had experienced radiation exposure due to the Chernobyl accident, 32 were non-irradiated (spontaneous AML), and 2 developed therapy-related AML after chemotherapy with topoisomerase II inhibitors.
  • RESULTS: MLL gene translocations were detected in both groups of spontaneous and therapy-related AML (1/32 and 1/2 cases respectively).
  • The sole MLL rearrangement found in the group of radiation-associated AML patients was a duplication of the gene.
  • CONCLUSION: Our data preclude the involvement of MLL gene translocations in radiation-induced leukemogenesis, but support the assumption that loss and gain of chromosomal material could be crucial in the leukemogenesis of AML patients with the history of radiation exposure due to the Chernobyl accident.
  • [MeSH-major] Chernobyl Nuclear Accident. Chromosome Aberrations / radiation effects. DNA, Neoplasm / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein. Reverse Transcriptase Polymerase Chain Reaction

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15812362.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


25. Krug U, Serve H, Müller-Tidow C, Mesters RM, Steffen B, Büchner T, Berdel WE: New molecular therapy targets in acute myeloid leukemia. Recent Results Cancer Res; 2007;176:243-62
The Lens. Cited by Patents in .

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

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17607931.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Proteins; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Number-of-references] 145
  •  go-up   go-down


26. Sato T, Suzuki D, Ichikawa M, Kaneda M, Nakagawa A, Kobayashi R, Ariga T: [Huge brain abscess and invasive pulmonary disease by fungal infection during chemotherapy for infantile acute myeloid leukemia]. Rinsho Ketsueki; 2007 Dec;48(12):1549-54
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Huge brain abscess and invasive pulmonary disease by fungal infection during chemotherapy for infantile acute myeloid leukemia].
  • The authors encountered a 7-year-old girl with a huge brain abscess and invasive pulmonary lesion due to fungus, who had been treated for acute myelogenous leukemia (AML).
  • We discontinued AML treatment because of the severe fungal infection; however, she has remained in continuous remission.
  • [MeSH-major] Brain Abscess / etiology. Leukemia, Myeloid, Acute / drug therapy. Lung Diseases, Fungal / etiology. Zygomycosis / complications

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Pulmonary Disease.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18203515.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


27. Li Y, Li XY, Wang L, Tian Z, Rao Q, Jia HR, Wang HJ, Wang M, Mi YC: [Biological characteristics of Wt1 gene in relation to Ph(+) leukemia cell line K562]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Jun;18(3):564-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Biological characteristics of Wt1 gene in relation to Ph(+) leukemia cell line K562].
  • Wt1 is a dual-function gene involved in hematopoiesis, leukemogenesis and prognosis for leukemia.
  • This gene is highly expressed in acute myeloid leukemia (AML) and the progression of chronic myelogenous leukemia (CML).
  • It was reported elsewhere that high level of wt1 expression indicated worse prognosis for leukemia.
  • Gene wt1 is expected to be further studied as a new therapy target in Ph(+) leukemias.

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. CURCUMIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20561402.001).
  • [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 / RNA, Messenger; 0 / WT1 Proteins; IT942ZTH98 / Curcumin
  •  go-up   go-down


28. Verma D, O'Brien S, Thomas D, Faderl S, Koller C, Pierce S, Kebriaei P, Garcia-Manero G, Cortes J, Kantarjian H, Ravandi F: Therapy-related acute myelogenous leukemia and myelodysplastic syndrome in patients with acute lymphoblastic leukemia treated with the hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone regimens. Cancer; 2009 Jan 1;115(1):101-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related acute myelogenous leukemia and myelodysplastic syndrome in patients with acute lymphoblastic leukemia treated with the hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone regimens.
  • BACKGROUND: Secondary malignancies including myeloid neoplasms occur infrequently in acute lymphoblastic leukemia (ALL) and to the authors' knowledge have not been as well documented in adults as in children.
  • RESULTS: Sixteen patients (2.49%) developed secondary acute myelogenous leukemia (AML) (6 patients) or myelodysplastic syndrome (MDS) (10 patients).
  • At the time of ALL diagnosis, the median age was 53 years; cytogenetics were normal in 11 patients, pseudo-diploidy with del(2) in 1 patient, t(9;22) in 1 patient, and unavailable in 3 patients.
  • Frontline therapy included hyper-CVAD in 7 patients, hyper-CVAD with rituximab in 8 patients, and hyper-CVAD with imatinib in 1 patient.
  • Karyotype at time of AML/MDS diagnosis was -5, -7 in 9 patients, normal in 1 patient, complex in 1 patient, inv(11) in 1 patient, t(4;11) in 1 patient, del(20) in 1 patient, and unavailable in 2 patients.
  • Secondary AML/MDS developed at a median of 32 months after ALL diagnosis.
  • Cytarabine plus anthracycline-based treatment was given to 12 patients with AML and high-risk MDS.
  • Eight patients (1 with AML and 7 with MDS) underwent allogeneic stem cell transplantation, and all but 2 died at a median of 3 months (range, 0.5-11 months) after transplantation.
  • The median overall survival after a diagnosis of secondary AML and MDS was 9.25 months (range, 1+ to 26+ months).
  • CONCLUSIONS: Secondary AML and MDS occur infrequently in adult patients with de novo ALL treated with the hyper-CVAD regimens, and response to therapy is poor.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


29. Penketh PG, Baumann RP, Ishiguro K, Shyam K, Seow HA, Sartorelli AC: Lethality to leukemia cell lines of DNA interstrand cross-links generated by Cloretazine derived alkylating species. Leuk Res; 2008 Oct;32(10):1546-53
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lethality to leukemia cell lines of DNA interstrand cross-links generated by Cloretazine derived alkylating species.
  • Cloretazine [1,2-bis(methylsulfonyl)-1-(2-chloroethyl)-2-[(methylamino)carbonyl]hydrazine; VNP40101M; 101M] is a relatively new prodrug with activity in elderly acute myelogenous leukemia (AML) patients.
  • The numbers of cross-links produced in three experimental leukemia lines (L1210, U937 and HL-60) were fewer than 10 per genome at their respective LC50 concentrations.

  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. GUANINE .
  • Hazardous Substances Data Bank. ETHANE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochem Pharmacol. 2000 Feb 1;59(3):283-91 [10609557.001]
  • [Cites] Annu Rev Biochem. 1967;36:485-518 [18257729.001]
  • [Cites] Genome Res. 2001 May;11(5):645-51 [11337462.001]
  • [Cites] Clin Cancer Res. 2001 Aug;7(8):2309-17 [11489806.001]
  • [Cites] J Clin Oncol. 2002 May 1;20(9):2388-99 [11981013.001]
  • [Cites] Nature. 2002 Dec 5;420(6915):520-62 [12466850.001]
  • [Cites] Nature. 2002 Dec 5;420(6915):563-73 [12466851.001]
  • [Cites] Cancer Chemother Pharmacol. 2004 Apr;53(4):288-95 [14685775.001]
  • [Cites] Cancer Chemother Pharmacol. 2004 Apr;53(4):279-87 [14704831.001]
  • [Cites] J Mol Biol. 1967 Apr 14;25(1):143-60 [5340530.001]
  • [Cites] Nature. 1969 Jul 12;223(5202):206-7 [5791738.001]
  • [Cites] J Mol Biol. 1983 Jun 5;166(4):477-535 [6864790.001]
  • [Cites] Cancer Res. 1984 Sep;44(9):3806-11 [6378375.001]
  • [Cites] Cancer Res. 1988 Mar 15;48(6):1521-7 [3162197.001]
  • [Cites] Cancer Res. 1988 Aug 15;48(16):4489-92 [3396000.001]
  • [Cites] Mutat Res. 1990 Jul;236(1):43-50 [2114540.001]
  • [Cites] J Med Chem. 1990 Aug;33(8):2259-64 [2374151.001]
  • [Cites] Cancer Invest. 1997;15(6):588-98 [9412665.001]
  • [Cites] Mol Pharmacol. 1998 Aug;54(2):334-41 [9687575.001]
  • [Cites] Mol Cancer Ther. 2005 Nov;4(11):1755-63 [16275997.001]
  • [Cites] Clin Cancer Res. 2005 Nov 1;11(21):7817-24 [16278404.001]
  • [Cites] Oncol Res. 2005;15(6):313-25 [16408696.001]
  • [Cites] Am J Physiol. 1991 Dec;261(6 Pt 1):C1154-61 [1767817.001]
  • [Cites] Carcinogenesis. 1993 Apr;14(4):593-8 [8472320.001]
  • [Cites] Mutat Res. 1994 Mar;314(2):99-113 [7510369.001]
  • [Cites] J Med Chem. 1994 Sep 2;37(18):2912-7 [8071939.001]
  • [Cites] Prog Nucleic Acid Res Mol Biol. 1995;51:167-223 [7659775.001]
  • [Cites] Mol Pharmacol. 1997 Aug;52(2):249-58 [9271347.001]
  • [Cites] Anal Biochem. 1997 Oct 1;252(1):210-3 [9324963.001]
  • [Cites] Apoptosis. 2005 Dec;10(6):1317-31 [16215671.001]
  • [Cites] Mol Cancer Ther. 2006 Apr;5(4):969-76 [16648568.001]
  • [Cites] Photochem Photobiol. 1999 Dec;70(6):858-67 [10628299.001]
  • (PMID = 18479747.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA090671-02; United States / NCI NIH HHS / CA / R01 CA122112; United States / NCI NIH HHS / CA / CA090671-03; United States / NCI NIH HHS / CA / R01 CA090671-07; United States / NCI NIH HHS / CA / CA-090671; United States / NCI NIH HHS / CA / R01 CA122112-02; United States / NCI NIH HHS / CA / R01 CA090671-06; United States / NCI NIH HHS / CA / CA090671-04; United States / NCI NIH HHS / CA / CA122112-03; United States / NCI NIH HHS / CA / R01 CA090671-01A1; United States / NCI NIH HHS / CA / CA090671-06; United States / NCI NIH HHS / CA / R01 CA090671-02; United States / NCI NIH HHS / CA / CA122112-02; United States / NCI NIH HHS / CA / R01 CA122112-03; United States / NCI NIH HHS / CA / R01 CA090671-03; United States / NCI NIH HHS / CA / R01 CA122112-01; United States / NCI NIH HHS / CA / R01 CA090671-08; United States / NCI NIH HHS / CA / R01 CA122112-05; United States / NCI NIH HHS / CA / CA122112-04; United States / NCI NIH HHS / CA / CA090671-01A1; United States / NCI NIH HHS / CA / R01 CA090671; United States / NCI NIH HHS / CA / CA090671-05; United States / NCI NIH HHS / CA / CA122112-01; United States / NCI NIH HHS / CA / R01 CA122112-04; United States / NCI NIH HHS / CA / R01 CA090671-04; United States / NCI NIH HHS / CA / CA122112-05; United States / NCI NIH HHS / CA / CA090671-07; United States / NCI NIH HHS / CA / CA-122112; United States / NCI NIH HHS / CA / R01 CA090671-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 1,2-bis(methylsulfonyl)-1-(2-chloroethyl)hydrazine; 0 / Antineoplastic Agents; 0 / Cross-Linking Reagents; 0 / Hydrazines; 0 / Sulfonamides; 14J2G0U3NQ / laromustine; 5Z93L87A1R / Guanine; 8J337D1HZY / Cytosine; 9007-49-2 / DNA; L99N5N533T / Ethane
  • [Other-IDs] NLM/ NIHMS57421; NLM/ PMC2888535
  •  go-up   go-down


30. Bierings M, Nachman JB, Zwaan CM: Stem cell transplantation in pediatric leukemia and myelodysplasia: state of the art and current challenges. Curr Stem Cell Res Ther; 2007 Jan;2(1):53-63
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stem cell transplantation in pediatric leukemia and myelodysplasia: state of the art and current challenges.
  • The role of stem cell transplantation in the treatment of leukemia and myelodysplasia (MDS) in children has changed over the past decade.
  • In pediatric acute lymphoblastic leukemia (ALL), the overall cure-rate is high with conventional chemotherapy.
  • In pediatric acute myeloid leukemia (AML) the role of allo-HSCT in CR1 is declining, due to better outcome with modern multi-agent chemotherapy.
  • In relapsed AML patients, allo-HSCT still seems indispensable.
  • Targeted therapy may change the role of HSCT, in particular in chronic myeloid leukemia, where the role of allografting is changing in the imatinib era.
  • [MeSH-major] Leukemia / therapy. Myelodysplastic Syndromes / therapy. Stem Cell Transplantation / trends
  • [MeSH-minor] Child. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / therapy


31. Oliansky DM, Appelbaum F, Cassileth PA, Keating A, Kerr J, Nieto Y, Stewart S, Stone RM, Tallman MS, McCarthy PL Jr, Hahn T: The role of cytotoxic therapy with hematopoietic stem cell transplantation in the therapy of acute myelogenous leukemia in adults: an evidence-based review. Biol Blood Marrow Transplant; 2008 Feb;14(2):137-80
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of cytotoxic therapy with hematopoietic stem cell transplantation in the therapy of acute myelogenous leukemia in adults: an evidence-based review.
  • Clinical research examining the role of hematopoietic stem cell transplantation (HSCT) in the therapy of acute myelogenous leukemia (AML) in adults is presented and critically evaluated in this systematic evidence-based review.
  • Treatment recommendations based on the evidence are presented in Table 3, entitled Summary of Treatment Recommendations Made by the Expert Panel for Adult Acute Myelogenous Leukemia, and were reached unanimously by a panel of AML experts.
  • The identified priority areas of needed future research in adult AML include:.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Combined Modality Therapy. Evidence-Based Medicine. Humans. PubMed


32. Moore AS, Blagg J, Linardopoulos S, Pearson AD: Aurora kinase inhibitors: novel small molecules with promising activity in acute myeloid and Philadelphia-positive leukemias. Leukemia; 2010 Apr;24(4):671-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aurora kinase inhibitors: novel small molecules with promising activity in acute myeloid and Philadelphia-positive leukemias.
  • It is currently unclear whether the therapeutic activity of these compounds in leukemia is primarily due to selective Aurora or multi-kinase inhibition.
  • The most promising application for Aurora kinase inhibitors to date appears to be in FLT3-mutated acute myeloid leukemia (AML) and imatinib-resistant chronic myeloid leukemia/Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia, particularly when caused by the T315I mutation.
  • Here we review the growing body of evidence supporting the use of Aurora kinase inhibitors as effective agents for AML and Ph+ leukemias.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Serine-Threonine Kinases / antagonists & inhibitors

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20147976.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Number-of-references] 56
  •  go-up   go-down


33. Betancourt-García RD, Castro J, Fernández AC, López-Enríquez A, Fradera J, Pacheco E: Acquired acute myelogenous leukemia after therapy for acute promyelocytic leukemia with t(15;17): a case report and review of the literature. P R Health Sci J; 2009 Jun;28(2):146-50
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acquired acute myelogenous leukemia after therapy for acute promyelocytic leukemia with t(15;17): a case report and review of the literature.
  • Therapy-related myelodysplastic syndrome (t-MDS) and therapy-related acute myelogenous leukemia (t-AML) in patients with acute promyelocytic leukemia (APL) are rare events.
  • The cumulative exposure to chemotherapy with alkylating agents and topoisomerase II inhibitors is associated with t-AML that may develop any time after the completion of the treatment.
  • We report the case of an acquired AML who previously received therapy for APL, after two years of being diagnosed.
  • The diagnosis was established by morphologic findings, membrane markers, cytogenetic studies, and fluorescence in situ hybridization (FISH).
  • To our knowledge this is the first documented case in Puerto Rico of a patient with APL that developed a t-AML without the characteristic chromosomal and morphologic findings of APL.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Leukemia, Promyelocytic, Acute / drug therapy. Neoplasms, Second Primary / etiology. Translocation, Genetic


34. Dirnhofer S, Went P, Tichelli A: Diagnostic problems in follow-up bone marrow biopsies of patients treated for acute and chronic leukaemias and MDS. Pathobiology; 2007;74(2):115-20
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnostic problems in follow-up bone marrow biopsies of patients treated for acute and chronic leukaemias and MDS.
  • Bone marrow biopsy evaluation after therapy for hematolymphoid disorders is complex.
  • In the present paper, we suggest a systematic, integrative and interdisciplinary approach that includes knowledge of the original diagnosis and of the type of prior therapy, considers treatment effects and a use of standardized response criteria for AML and MDS.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myeloid / diagnosis. Myelodysplastic Syndromes / diagnosis. Myeloproliferative Disorders / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Biopsy. Bone Marrow Transplantation. Chronic Disease. Humans. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17587882.001).
  • [ISSN] 1015-2008
  • [Journal-full-title] Pathobiology : journal of immunopathology, molecular and cellular biology
  • [ISO-abbreviation] Pathobiology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 11
  •  go-up   go-down


35. Ryningen A, Apelseth T, Hausken T, Bruserud Ø: Reticulated platelets are increased in chronic myeloproliferative disorders, pure erythrocytosis, reactive thrombocytosis and prior to hematopoietic reconstitution after intensive chemotherapy. Platelets; 2006 Aug;17(5):296-302
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the present study we used flow cytometric analysis to determine the percentage of reticulated platelets in peripheral blood for patients with chronic myeloproliferative disorders (polycythemia vera, essential thrombocytosis) and acute myelogenous leukemia (AML) patients with severe chemotherapy-induced thrombocytopenia.
  • Furthermore, AML patients with severe chemotherapy-induced cytopenia showed low levels that started to increase 1-9 days prior to hematopoietic reconstitution.
  • (ii) patients with pure erythrocytosis often have additional abnormalities in the thrombopoiesis; and (iii) the levels of reticulated platelets seem to predict hematopoietic reconstitution for patients receiving intensive AML therapy.
  • [MeSH-major] Blood Platelets / metabolism. Leukemia, Myeloid, Acute / blood. Myeloproliferative Disorders / blood. Polycythemia / blood. Thrombocytosis / blood. Thrombopoiesis / physiology

  • Genetic Alliance. consumer health - Chronic Myeloproliferative Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16928601.001).
  • [ISSN] 0953-7104
  • [Journal-full-title] Platelets
  • [ISO-abbreviation] Platelets
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


36. Yamamoto M, Kakihana K, Kurosu T, Murakami N, Miura O: Clonal evolution with inv(11)(p15q22) and NUP98/DDX10 fusion gene in imatinib-resistant chronic myelogenous leukemia. Cancer Genet Cytogenet; 2005 Mar;157(2):104-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clonal evolution with inv(11)(p15q22) and NUP98/DDX10 fusion gene in imatinib-resistant chronic myelogenous leukemia.
  • The BCR/ABL tyrosine kinase inhibitor imatinib has shown remarkable efficacy in treating patients with chronic myelogenous leukemia (CML).
  • Leukemic cells from the patient were found to express the fusion transcript of NUP98 and DDX10, which is in accordance with previously reported cases of de novo or therapy-related acute myelogenous leukemia and myelodysplastic syndrome with inv(11)(p15q22).
  • These observations raise a possibility that the NUP98/DDX10 fusion might be involved in imatinib resistance as well as in acute transformation of CML.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 11. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15721630.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / nuclear pore complex protein 98; 8A1O1M485B / Imatinib Mesylate; EC 3.6.1.- / DDX10 protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases; EC 3.6.4.13 / RNA Helicases
  •  go-up   go-down


37. Swiers G, de Bruijn M, Speck NA: Hematopoietic stem cell emergence in the conceptus and the role of Runx1. Int J Dev Biol; 2010;54(6-7):1151-63
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Runx1 is famous for its role in HSC emergence, and notorious for its involvement in leukemia, as chromosomal rearrangements and inactivating mutations in the human RUNX1 gene are some of the most common events in de novo and therapy-related acute myelogenous leukemia, myelodysplastic syndrome and acute lymphocytic leukemia.

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20711992.001).
  • [ISSN] 1696-3547
  • [Journal-full-title] The International journal of developmental biology
  • [ISO-abbreviation] Int. J. Dev. Biol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / U01 HL100405; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit
  • [Other-IDs] NLM/ NIHMS578062; NLM/ PMC4512753
  •  go-up   go-down


38. Carneiro BA, Kaminer L, Eldibany M, Sreekantaiah C, Kaul K, Locker GY: Oxaliplatin-related acute myelogenous leukemia. Oncologist; 2006 Mar;11(3):261-2
Hazardous Substances Data Bank. LEUCOVORIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oxaliplatin-related acute myelogenous leukemia.
  • Bone marrow biopsy was consistent with therapy-related acute myelogenous leukemia.
  • It is likely that the leukemia was related to the oxaliplatin administration.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid, Acute / chemically induced
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Bevacizumab. Cecal Neoplasms / drug therapy. Cecal Neoplasms / pathology. Chromosome Deletion. Female. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Humans. Leucovorin / administration & dosage. Leucovorin / adverse effects. Middle Aged. Omentum / pathology. Organoplatinum Compounds / administration & dosage. Organoplatinum Compounds / adverse effects. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / secondary. Peritoneal Neoplasms / drug therapy. Peritoneal Neoplasms / secondary. Sigmoid Neoplasms / drug therapy. Sigmoid Neoplasms / secondary. Trisomy

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16549810.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Organoplatinum Compounds; 2S9ZZM9Q9V / Bevacizumab; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; Folfox protocol
  •  go-up   go-down


39. Funk RK, Maxwell TJ, Izumi M, Edwin D, Kreisel F, Ley TJ, Cheverud JM, Graubert TA: Quantitative trait loci associated with susceptibility to therapy-related acute murine promyelocytic leukemia in hCG-PML/RARA transgenic mice. Blood; 2008 Aug 15;112(4):1434-42
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitative trait loci associated with susceptibility to therapy-related acute murine promyelocytic leukemia in hCG-PML/RARA transgenic mice.
  • Therapy-related acute myelogenous leukemia (t-AML) is an important late adverse effect of alkylator chemotherapy.
  • Susceptibility to t-AML has a genetic component, yet specific genetic variants that influence susceptibility are poorly understood.
  • We analyzed an F(2) intercross (n = 282 mice) between mouse strains resistant or susceptible to t-AML induced by the alkylator ethyl-N-nitrosourea (ENU) to identify genes that regulate t-AML susceptibility.
  • Each mouse carried the hCG-PML/RARA transgene, a well-characterized initiator of myeloid leukemia.
  • In the absence of ENU treatment, transgenic F(2) mice developed leukemia with higher incidence (79.4% vs 12.5%) and at earlier time points (108 days vs 234 days) than mice in the resistant background.
  • Thirteen QTLs significantly associated with leukemia-free survival, spleen weight, or white blood cell count were identified on 8 chromosomes.
  • These results suggest that susceptibility to ENU-induced leukemia in mice is a complex trait governed by genes at multiple loci.
  • Improved understanding of genetic risk factors should lead to tailored treatment regimens that reduce risk for patients predisposed to t-AML.

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):15103-8 [10611345.001]
  • [Cites] Leukemia. 2005 Nov;19(11):1919-28 [16167058.001]
  • [Cites] Br J Haematol. 2001 Jan;112(1):109-17 [11225603.001]
  • [Cites] Leuk Lymphoma. 2001 Apr;41(3-4):255-76 [11378539.001]
  • [Cites] Cancer Res. 2006 May 15;66(10):5029-38 [16707424.001]
  • [Cites] Heredity (Edinb). 1992 Oct;69(4):315-24 [16718932.001]
  • [Cites] Bone Marrow Transplant. 2007 Jan;39(2):59-70 [17143301.001]
  • [Cites] Br J Haematol. 2007 Feb;136(4):590-6 [17367411.001]
  • [Cites] Br J Haematol. 2007 Jun;137(6):513-29 [17539774.001]
  • [Cites] Br J Radiol. 2007 Sep;80 Spec No 1:S56-62 [17704327.001]
  • [Cites] Oncogene. 2001 Dec 13;20(57):8281-6 [11781843.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1972-6 [12200354.001]
  • [Cites] Pharmacogenetics. 2002 Nov;12(8):605-11 [12439220.001]
  • [Cites] Exp Toxicol Pathol. 2002 Nov;54(3):193-6 [12484555.001]
  • [Cites] Blood. 2003 Mar 1;101(5):2015-23 [12393427.001]
  • [Cites] Bioinformatics. 2003 May 1;19(7):889-90 [12724300.001]
  • [Cites] J Clin Oncol. 2003 Jun 1;21(11):2123-37 [12775738.001]
  • [Cites] Leukemia. 2004 Jan;18(1):120-5 [14586477.001]
  • [Cites] J Clin Oncol. 1986 Mar;4(3):325-45 [3950675.001]
  • [Cites] Genetics. 1989 Jan;121(1):185-99 [2563713.001]
  • [Cites] Blood. 1993 Jun 1;81(11):3091-6 [7684624.001]
  • [Cites] Mutat Res. 1994 Apr 1;306(1):19-34 [7512200.001]
  • [Cites] J Clin Oncol. 1994 May;12(5):1063-73 [8164031.001]
  • [Cites] Leuk Lymphoma. 1996 Feb;20(5-6):365-72 [8833391.001]
  • [Cites] Blood. 1997 Jan 15;89(2):376-87 [9002938.001]
  • [Cites] Cancer. 1997 Apr 1;79(7):1438-46 [9083167.001]
  • [Cites] Cancer. 1997 Dec 1;80(11 Suppl):2199-204 [9395034.001]
  • [Cites] Genet Res. 1997 Oct;70(2):117-24 [9449188.001]
  • [Cites] J Natl Cancer Inst. 1998 Apr 15;90(8):606-11 [9554443.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Oct 27;95(22):13176-81 [9789061.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):166-75 [10508512.001]
  • [Cites] N Engl J Med. 2004 Dec 2;351(23):2403-7 [15575056.001]
  • [Cites] J Clin Oncol. 2005 Jan 20;23(3):482-93 [15534356.001]
  • [Cites] Chem Biol Interact. 2005 May 30;153-154:187-95 [15935816.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 30;102(35):12513-8 [16113082.001]
  • [Cites] J Exp Med. 2001 Feb 19;193(4):531-43 [11181704.001]
  • (PMID = 18552208.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA101937; United States / NCI NIH HHS / CA / P30 CA091842; United States / NIDDK NIH HHS / DK / T35 DK074375; United States / NCI NIH HHS / CA / P30 CA91842
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
  • [Other-IDs] NLM/ PMC2515115
  •  go-up   go-down


40. Bhojwani D, Moskowitz N, Raetz EA, Carroll WL: Potential of gene expression profiling in the management of childhood acute lymphoblastic leukemia. Paediatr Drugs; 2007;9(3):149-56
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potential of gene expression profiling in the management of childhood acute lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) is a heterogeneous disease.
  • Current treatment approaches are tailored according to the clinical features of the host, genotypic features of the leukemic blast, and early response to therapy.
  • Additional promising utilities include prediction of early response to therapy, overall outcome, and adverse effects.
  • Identification of patients who are predicted to have an unfavorable outcome may allow for early intervention such as intensification of therapy or avoidance of drugs that are associated with specific secondary effects such as therapy-related acute myelogenous leukemia.
  • These newer methods of genome analyses complemented by studies involving the proteome as well as host polymorphisms will have a profound impact on the diagnosis and management of childhood ALL.
  • [MeSH-major] Gene Expression Profiling. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17523695.001).
  • [ISSN] 1174-5878
  • [Journal-full-title] Paediatric drugs
  • [ISO-abbreviation] Paediatr Drugs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA114762
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Oncogene Proteins
  • [Number-of-references] 36
  •  go-up   go-down


41. Pyatt DW, Aylward LL, Hays SM: Is age an independent risk factor for chemically induced acute myelogenous leukemia in children? J Toxicol Environ Health B Crit Rev; 2007 Sep-Oct;10(5):379-400
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

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

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17687725.001).
  • [ISSN] 1521-6950
  • [Journal-full-title] Journal of toxicology and environmental health. Part B, Critical reviews
  • [ISO-abbreviation] J Toxicol Environ Health B Crit Rev
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Topoisomerase II Inhibitors
  • [Number-of-references] 92
  •  go-up   go-down


42. Garcia-Manero G, Stoltz ML, Ward MR, Kantarjian H, Sharma S: A pilot pharmacokinetic study of oral azacitidine. Leukemia; 2008 Sep;22(9):1680-4
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Azacitidine has been shown to have survival benefits in patients with high-risk myelodysplastic syndrome (MDS), and has activity in the treatment of acute myelogenous leukemia (AML).
  • In a formulation feasibility pilot study, four subjects with solid malignant tumors, AML or MDS received single oral doses of 60 or 80 mg azacitidine.
  • No severe drug-related toxicities were observed.


43. Rahman MM, Madlambayan GJ, Cogle CR, McFadden G: Oncolytic viral purging of leukemic hematopoietic stem and progenitor cells with Myxoma virus. Cytokine Growth Factor Rev; 2010 Apr-Jun;21(2-3):169-75
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, a major challenge with ABMT for patients with hematologic malignancies is disease relapse, mainly due to either contamination with cancerous hematopoietic stem and progenitor cells (HSPCs) within the autograft or the persistence of residual therapy-resistant disease niches within the patient.
  • MYXV, a novel oncolytic poxvirus with potent anti-cancer properties in a variety of in vivo tumor models, can specifically eliminate cancerous stem and progenitor cells from samples obtained from acute myelogenous leukemia (AML) patients, while sparing normal CD34+ hematopoietic stem and progenitor cells capable of rescuing hematopoiesis following high dose conditioning.
  • We propose that a broader subset of patients with intractable hematologic malignancies who have failed standard therapy could become eligible for ABMT when the treatment schema is coupled with ex vivo oncolytic therapy.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • [Cites] Curr Cancer Drug Targets. 2008 Feb;8(1):27-36 [18288941.001]
  • [Cites] Clin Infect Dis. 2008 May 15;46(10):1555-61 [18419490.001]
  • [Cites] Biochim Biophys Acta. 2008 Apr;1785(2):217-31 [18328829.001]
  • [Cites] Science. 2008 Apr 25;320(5875):531-5 [18436786.001]
  • [Cites] PLoS Pathog. 2008 Jul;4(7):e1000099 [18617992.001]
  • [Cites] Nat Rev Cancer. 2009 Jan;9(1):64-71 [19104515.001]
  • [Cites] J Virol. 2009 Jan;83(2):498-511 [18971273.001]
  • [Cites] J Virol. 2009 Jul;83(13):6883-99 [19386722.001]
  • [Cites] Cancer Immunol Immunother. 2009 Sep;58(9):1355-62 [19266198.001]
  • [Cites] Cytokine. 2009 Sep;47(3):199-205 [19640730.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Blood. 2002 Jul 1;100(1):59-66 [12070009.001]
  • [Cites] Viral Immunol. 2002;15(2):229-46 [12081009.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1957-64 [12200352.001]
  • [Cites] Cancer Res. 2002 Sep 1;62(17):4968-76 [12208748.001]
  • [Cites] Cancer Res. 2002 Sep 1;62(17):5001-7 [12208753.001]
  • [Cites] Cancer Res. 2002 Sep 1;62(17):5013-8 [12208755.001]
  • [Cites] Virus Res. 2002 Sep;88(1-2):17-33 [12297325.001]
  • [Cites] Blood. 2003 Jul 1;102(1):377-87 [12637331.001]
  • [Cites] Leuk Lymphoma. 2003 Nov;44(11):1871-9 [14738138.001]
  • [Cites] Hum Gene Ther. 2004 Sep;15(9):821-31 [15353037.001]
  • [Cites] J Clin Oncol. 1991 Jan;9(1):85-93 [1985173.001]
  • [Cites] Prog Clin Biol Res. 1992;377:181-7 [1438414.001]
  • [Cites] Leuk Lymphoma. 1993;11 Suppl 2:141-8 [8124225.001]
  • [Cites] Blood. 1994 Apr 15;83(8):2345-51 [7512845.001]
  • [Cites] Blood. 1994 Jul 15;84(2):380-3 [8025266.001]
  • [Cites] Ann Med. 1996 Apr;28(2):167-73 [8732646.001]
  • [Cites] J Hematother. 1996 Aug;5(4):427-36 [8877718.001]
  • [Cites] Exp Hematol. 1997 Nov;25(12):1261-9 [9357970.001]
  • [Cites] Blood. 1998 Mar 1;91(5):1820-7 [9473251.001]
  • [Cites] Hum Gene Ther. 1998 Oct 10;9(15):2277-84 [9794211.001]
  • [Cites] Bone Marrow Transplant. 1998 Nov;22(10):957-63 [9849692.001]
  • [Cites] Blood. 1999 Mar 1;93(5):1534-9 [10029581.001]
  • [Cites] Blood. 1999 May 1;93(9):3074-80 [10216104.001]
  • [Cites] Cancer Gene Ther. 1999 Sep-Oct;6(5):409-22 [10505851.001]
  • [Cites] Nat Immunol. 2004 Dec;5(12):1266-74 [15502830.001]
  • [Cites] J Biol Chem. 2004 Dec 10;279(50):52210-7 [15471883.001]
  • [Cites] Mol Ther. 2005 Feb;11(2):180-95 [15668130.001]
  • [Cites] J Clin Invest. 2005 Feb;115(2):379-87 [15690085.001]
  • [Cites] Nat Rev Microbiol. 2005 Mar;3(3):201-13 [15738948.001]
  • [Cites] Bone Marrow Transplant. 2005 Jun;35(11):1055-64 [15821774.001]
  • [Cites] Curr Gene Ther. 2005 Aug;5(4):429-43 [16101516.001]
  • [Cites] Cancer Res. 2005 Nov 1;65(21):9982-90 [16267023.001]
  • [Cites] Virology. 2006 Jan 5;344(1):48-54 [16364735.001]
  • [Cites] J Natl Cancer Inst. 2006 Mar 1;98(5):298-300 [16507823.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 21;103(12):4640-5 [16537421.001]
  • [Cites] Leukemia. 2006 Jun;20(6):911-28 [16642045.001]
  • [Cites] Semin Oncol. 2006 Apr;33(2 Suppl 5):S2-14 [16720198.001]
  • [Cites] Curr Opin Mol Ther. 2006 Aug;8(4):314-21 [16955694.001]
  • [Cites] Nat Med. 2006 Nov;12(11):1310-5 [17086190.001]
  • [Cites] Clin Cancer Res. 2006 Nov 15;12(22):6853-62 [17121907.001]
  • [Cites] J Virol. 2007 Feb;81(3):1251-60 [17108021.001]
  • [Cites] Cancer Res. 2007 Jan 15;67(2):429-32 [17234747.001]
  • [Cites] Nat Clin Pract Oncol. 2007 Feb;4(2):101-17 [17259931.001]
  • [Cites] Vet Res. 2007 Mar-Apr;38(2):299-318 [17296158.001]
  • [Cites] Bone Marrow Transplant. 2007 Jul;40(1):1-12 [17450184.001]
  • [Cites] Expert Opin Biol Ther. 2007 Sep;7(9):1415-25 [17727330.001]
  • [Cites] Cancer Res. 2007 Sep 15;67(18):8818-27 [17875723.001]
  • [Cites] J Neurovirol. 2007 Dec;13(6):549-60 [18097886.001]
  • [Cites] Mol Ther. 2008 Jan;16(1):52-9 [17998900.001]
  • [Cites] Cell Death Differ. 2008 Feb;15(2):332-43 [18034189.001]
  • [Cites] Mol Ther. 2009 Oct;17(10):1677-82 [19672244.001]
  • [Cites] Leukemia. 2009 Dec;23(12):2313-7 [19865109.001]
  • [Cites] FEMS Microbiol Rev. 2000 Apr;24(2):123-33 [10717311.001]
  • [Cites] Nat Med. 2000 Aug;6(8):879-85 [10932224.001]
  • [Cites] Stem Cells. 2000;18(6):422-7 [11072030.001]
  • [Cites] Clin Cancer Res. 2001 Jan;7(1):51-7 [11205918.001]
  • [Cites] Semin Immunol. 2001 Feb;13(1):73-84 [11289802.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):3009-15 [11306480.001]
  • [Cites] J Clin Oncol. 2001 Sep 1;19(17):3771-9 [11533101.001]
  • [Cites] Crit Rev Oncol Hematol. 2002 Feb;41(2):241-50 [11856599.001]
  • [Cites] Biochim Biophys Acta. 2008 Jan;1784(1):228-37 [17905673.001]
  • [Cites] Recent Pat Antiinfect Drug Discov. 2006 Nov;1(3):309-21 [18221156.001]
  • [Cites] Clin Cancer Res. 2008 Feb 15;14(4):1218-27 [18281557.001]
  • (PMID = 20211576.001).
  • [ISSN] 1879-0305
  • [Journal-full-title] Cytokine & growth factor reviews
  • [ISO-abbreviation] Cytokine Growth Factor Rev.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI080607-01A1; United States / NIAID NIH HHS / AI / R01 AI080607; United States / NCI NIH HHS / CA / R01 CA138541; United States / NIAID NIH HHS / AI / R01 AI080607-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 76
  • [Other-IDs] NLM/ NIHMS181384; NLM/ PMC2881168
  •  go-up   go-down


44. Paugam A: [The latest data on posaconazole]. Med Mal Infect; 2007 Feb;37(2):71-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Posaconazole was recently indicated for prophylaxis of invasive fungal infections in the following patients: patients receiving remission-induction chemotherapy for acute myelogenous leukemia (AML) or myelodysplastic syndromes (MDS) expected to result in prolonged neutropenia and hematopoietic stem cell transplant (HSCT) recipients who are undergoing high-dose immunosuppressive therapy for versus host disease.
  • [MeSH-major] Antifungal Agents / therapeutic use. Mycoses / drug therapy. Triazoles / therapeutic use
  • [MeSH-minor] Adult. Animals. Central Nervous System Fungal Infections / drug therapy. Chagas Cardiomyopathy / drug therapy. Clinical Trials as Topic. Drug Evaluation, Preclinical. Drug Resistance, Fungal. Humans. Immunocompromised Host. Mice. Premedication. Trypanocidal Agents / therapeutic use

  • MedlinePlus Health Information. consumer health - Fungal Infections.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17267154.001).
  • [ISSN] 0399-077X
  • [Journal-full-title] Médecine et maladies infectieuses
  • [ISO-abbreviation] Med Mal Infect
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Triazoles; 0 / Trypanocidal Agents; 6TK1G07BHZ / posaconazole
  • [Number-of-references] 65
  •  go-up   go-down


45. Clausen J, Wolf D, Petzer AL, Gunsilius E, Schumacher P, Kircher B, Gastl G, Nachbaur D: Impact of natural killer cell dose and donor killer-cell immunoglobulin-like receptor (KIR) genotype on outcome following human leucocyte antigen-identical haematopoietic stem cell transplantation. Clin Exp Immunol; 2007 Jun;148(3):520-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In patients with acute myelogenous leukaemia or myelodysplastic syndrome (AML/MDS; n = 18), no relapse occurred following transplants meeting both a high (above median) natural killer (NK) cell count and missing HLA-ligand(s) to donor's KIR(s), compared to all other AML/MDS patients (0% versus 44%; P = 0.049).
  • Missing HLA-B and/or HLA-C ligand combined with missing HLA-A3/11 (KIR3DL2 unblocked) predicted for reduced relapse incidence regardless of diagnosis or conditioning type (P = 0.028).
  • Moreover, in AML/MDS patients, this constellation predicted superior overall survival (OS) (P = 0.046).
  • [MeSH-major] Hematologic Neoplasms / therapy. Hematopoietic Stem Cell Transplantation / methods. Killer Cells, Natural / transplantation. Receptors, Immunologic / genetics
  • [MeSH-minor] Acute Disease. Chronic Disease. Cytomegalovirus Infections / immunology. Female. Genotype. Graft vs Host Disease / immunology. Graft vs Host Disease / therapy. Graft vs Tumor Effect / genetics. Histocompatibility Testing. Humans. Ligands. Lymphocyte Count. Male. Opportunistic Infections / immunology. Receptors, KIR. Receptors, KIR3DL2. Recurrence. Retrospective Studies. Survival Analysis. Transplantation Conditioning / methods. Treatment Outcome

  • Genetic Alliance. consumer health - Transplantation.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biol Blood Marrow Transplant. 2005 Feb;11(2):122-8 [15682073.001]
  • [Cites] Leuk Lymphoma. 2005 Feb;46(2):177-83 [15621799.001]
  • [Cites] Exp Hematol. 2005 Mar;33(3):279-85 [15730851.001]
  • [Cites] Blood. 2005 Mar 15;105(6):2594-600 [15536148.001]
  • [Cites] Blood. 2005 Mar 15;105(6):2300-6 [15572597.001]
  • [Cites] Bone Marrow Transplant. 2005 Apr;35(7):637-43 [15654351.001]
  • [Cites] Leukemia. 2005 May;19(5):822-8 [15772701.001]
  • [Cites] Blood. 2005 May 15;105(10):4135-42 [15687235.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4878-84 [15731175.001]
  • [Cites] Eur J Haematol. 2006 May;76(5):414-9 [16480430.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 Aug;12(8):828-36 [16864053.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 Aug;12(8):876-84 [16864058.001]
  • [Cites] Transplantation. 2006 Oct 27;82(8):1024-30 [17060849.001]
  • [Cites] Exp Hematol. 2000 Feb;28(2):119-27 [10706067.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3323-7 [10828011.001]
  • [Cites] Bone Marrow Transplant. 2000 Sep;26(5):489-96 [11019837.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3390-400 [11369628.001]
  • [Cites] Blood. 2001 Dec 1;98(12):3221-7 [11719357.001]
  • [Cites] Biol Blood Marrow Transplant. 2001;7(11):589-95 [11760146.001]
  • [Cites] Science. 2002 Mar 15;295(5562):2097-100 [11896281.001]
  • [Cites] Blood. 2002 Aug 1;100(3):761-7 [12130483.001]
  • [Cites] Bone Marrow Transplant. 2002 Sep;30(5):267-71 [12209347.001]
  • [Cites] J Clin Oncol. 2002 Nov 1;20(21):4324-30 [12409331.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3825-7 [12393440.001]
  • [Cites] Bone Marrow Transplant. 2003 May;31(10):839-45 [12748658.001]
  • [Cites] Leukemia. 2003 May;17(5):869-75 [12750699.001]
  • [Cites] Bone Marrow Transplant. 2003 Jun;31(11):967-72 [12774046.001]
  • [Cites] Br J Haematol. 2003 Jun;121(6):874-85 [12786798.001]
  • [Cites] Blood. 2003 Aug 1;102(3):1108-13 [12649159.001]
  • [Cites] Blood. 2003 Aug 1;102(3):814-9 [12689936.001]
  • [Cites] Bone Marrow Transplant. 2003 Sep;32(5):505-10 [12942097.001]
  • [Cites] Blood. 2003 Oct 15;102(8):3043-51 [12829583.001]
  • [Cites] Blood. 2004 Feb 15;103(4):1521-6 [14504099.001]
  • [Cites] Tissue Antigens. 2004 Mar;63(3):204-11 [14989709.001]
  • [Cites] Leuk Lymphoma. 2004 Jan;45(1):27-34 [15061194.001]
  • [Cites] Curr Opin Immunol. 2004 Oct;16(5):634-43 [15342011.001]
  • [Cites] N Engl J Med. 1986 Mar 20;314(12):729-35 [3513012.001]
  • [Cites] Nature. 1986 Feb 20-26;319(6055):675-8 [3951539.001]
  • [Cites] J Exp Med. 1996 Apr 1;183(4):1817-27 [8666938.001]
  • [Cites] Immunology. 1997 Dec;92(4):567-70 [9497500.001]
  • [Cites] Stat Med. 1999 Mar 30;18(6):695-706 [10204198.001]
  • [Cites] Blood. 1999 Jul 1;94(1):333-9 [10381530.001]
  • [Cites] Bone Marrow Transplant. 2004 Dec;34(11):949-54 [15489870.001]
  • [Cites] Br J Haematol. 2005 Mar;128(5):659-67 [15725088.001]
  • (PMID = 17493020.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / KIR3DL2 protein, human; 0 / Ligands; 0 / Receptors, Immunologic; 0 / Receptors, KIR; 0 / Receptors, KIR3DL2
  • [Other-IDs] NLM/ PMC1941931
  •  go-up   go-down


46. Kobayashi R, Kaneda M, Sato T, Ichikawa M, Suzuki D, Ariga T: The clinical feature of invasive fungal infection in pediatric patients with hematologic and malignant diseases: a 10-year analysis at a single institution at Japan. J Pediatr Hematol Oncol; 2008 Dec;30(12):886-90
MedlinePlus Health Information. consumer health - Fungal Infections.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Univariate analysis showed that age at diagnosis older than 10 years, relapse of original disease, long-term administration of broad-spectrum antibiotics, and acute myelogenous leukemia (AML) were the risk factors for IFI.
  • All patients with IFI received long-term antibiotic therapy.
  • AML was most strongly associated using a multivariate analysis.
  • The prognosis of IFI has been expected poor; therefore, prevention of this condition, especially for older patients with AML, would be important.
  • [MeSH-major] Fungemia / diagnosis. Hematologic Neoplasms / diagnosis. Mycoses / diagnosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19131772.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents
  •  go-up   go-down






Advertisement