[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 331
1. Quintás-Cardama A, Cortes J: Omacetaxine mepesuccinate--a semisynthetic formulation of the natural antitumoral alkaloid homoharringtonine, for chronic myelocytic leukemia and other myeloid malignancies. IDrugs; 2008 May;11(5):356-72
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Omacetaxine mepesuccinate--a semisynthetic formulation of the natural antitumoral alkaloid homoharringtonine, for chronic myelocytic leukemia and other myeloid malignancies.
  • ChemGenex Pharmaceuticals Ltd, in collaboration with Stragen Group, is developing omacetaxine mepesuccinate, a semisynthetic formulation of HHT, as a potential treatment for chronic myelocytic leukemia (CML), myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML).
  • In preclinical studies, omacetaxine mepesuccinate induced apoptosis in leukemia cell lines.
  • Phase I and II clinical trials for omacetaxine mepesuccinate in the treatment of AML and MDS are also ongoing; intravenous, subcutaneous and oral formulations of the drug are being developed.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Harringtonines / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy



2. Klymenko S, Trott K, Atkinson M, Bink K, Bebeshko V, Bazyka D, Dmytrenko I, Abramenko I, Bilous N, Misurin A, Zitzelsberger H, Rosemann M: Aml1 gene rearrangements and mutations in radiation-associated acute myeloid leukemia and myelodysplastic syndromes. J Radiat Res; 2005 Jun;46(2):249-55
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aml1 gene rearrangements and mutations in radiation-associated acute myeloid leukemia and myelodysplastic syndromes.
  • Several studies suggested a causal link between AML1 gene rearrangements and both radiation-induced acute myeloid leukaemia (AML) and myelodysplastic syndromes (MDS).
  • Fifty-three AML samples were analyzed for the presence of AML1 abnormalities using fluorescent in-situ hybridization (FISH) and reverse transcription polymerase chain reaction (RT-PCR).
  • Of these patients, 24 had experienced radiation exposure due to the Chernobyl accident, and 29 were non-irradiated spontaneous AML cases and served as controls.
  • AML1/ETO translocations were found in 9 of 29 spontaneous AML but only in 1 of 24 radiation-associated AML cases.
  • Following age stratification, the difference becomes less pronounced but remains on borderline significance (p=0.053).
  • AML1 mutation status was assessed in 5 clean-up workers at Chernobyl NPP with MDS, or AML following MDS, by direct sequencing of genomic DNA from the coding region (exon 3 through 8).
  • In one patient who developed MDS following an acute radiation syndrome, a hexanucleotide duplication of CGGCAT in exon 8 was found, inserted after base position 1502.
  • Our results suggest that AML1 gene translocations are infrequent in radiation-induced leukemogenesis but are consistent with the idea that radiation may contribute to the development of MDS through AML1 gene mutation.
  • [MeSH-major] Chernobyl Nuclear Accident. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / epidemiology. Myelodysplastic Syndromes / metabolism. Neoplasms, Radiation-Induced / epidemiology. Neoplasms, Radiation-Induced / metabolism. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics



3. Tanaka-Harada Y, Kawakami M, Oka Y, Tsuboi A, Katagiri T, Elisseeva OA, Nishida S, Shirakata T, Hosen N, Fujiki F, Murao A, Nakajima H, Oji Y, Kanda Y, Kawase I, Sugiyama H: Biased usage of BV gene families of T-cell receptors of WT1 (Wilms' tumor gene)-specific CD8+ T cells in patients with myeloid malignancies. Cancer Sci; 2010 Mar;101(3):594-600
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biased usage of BV gene families of T-cell receptors of WT1 (Wilms' tumor gene)-specific CD8+ T cells in patients with myeloid malignancies.
  • WT1 (Wilms' tumor gene 1) protein is a potent pan-tumor-associated antigen (TAA) and WT1-specific cytotoxic T lymphocytes (WT1 tetramer(+) CD8(+) T cells) are spontaneously induced in patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
  • We conducted a single-cell level comparative analysis of T-cell receptor beta-chain variable region (TCR-BV) gene families of a total of 1242 spontaneously induced WT1 tetramer(+) CD8(+) T cells in HLA-A*2402(+) patients with AML or MDS and those in healthy donors (HDs).
  • (ii) that BV4 was commonly biased in HDs and MDS patients;.
  • (iii) that BV19 was commonly biased in the patients; and (iv) that BVs 7 and 28, BVs 9 and 15, and BVs 12 and 29 were specifically biased in HDs, AML, and MDS patients, respectively.
  • However, statistical analysis of similarity among HD, AML, and MDS of individual usage frequencies of 24 kinds of TCR-BV gene families indicated that the usage frequencies of TCR-BV gene families in AML and MDS patients reflect those in HDs.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. Genes, T-Cell Receptor beta. Leukemia, Myeloid, Acute / immunology. Myelodysplastic Syndromes / immunology. WT1 Proteins / immunology



Advertisement
4. Watanabe-Okochi N, Oki T, Komeno Y, Kato N, Yuji K, Ono R, Harada Y, Harada H, Hayashi Y, Nakajima H, Nosaka T, Kitaura J, Kitamura T: Possible involvement of RasGRP4 in leukemogenesis. Int J Hematol; 2009 May;89(4):470-81
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To understand the molecular mechanism of leukemogenesis, particularly progression of myelodysplastic syndrome (MDS) to acute leukemia, we made cDNA libraries from the samples of patients and screened them by expression-cloning to detect class I mutations that render HF6 cells factor-independent.
  • We identified RasGRP4, an activator of Ras, as a candidate for class I mutation from three of six patients (MDS/MPD = 1, MDS-RA = 1, MDS/AML = 2, CMMoL/AML = 1 and AML-M2 = 1).
  • C57BL/6J mice transplanted with RasGRP4-transduced primary bone marrow cells died of T cell leukemia, myeloid leukemia, or myeloid leukemia with T cell leukemia.
  • The double transduction led to early onset of T cell leukemia but not of AML in the transplanted mice when compared to transduction of RasGRP4 alone.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Leukemia / metabolism. Leukemia / pathology. ras Guanine Nucleotide Exchange Factors / metabolism

  • MedlinePlus Health Information. consumer health - Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2003 Feb 15;101(4):1277-83 [12393381.001]
  • [Cites] J Biol Chem. 2002 Aug 23;277(34):30508-14 [11880369.001]
  • [Cites] J Clin Invest. 2005 Apr;115(4):919-29 [15761502.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2776-84 [17957027.001]
  • [Cites] Leukemia. 2006 Apr;20(4):635-44 [16467864.001]
  • [Cites] Leukemia. 2006 Jun;20(6):965-70 [16598313.001]
  • [Cites] Blood. 2006 Mar 1;107(5):1806-9 [16291592.001]
  • [Cites] Blood. 1999 May 1;93(9):3074-80 [10216104.001]
  • [Cites] Hematol J. 2002;3(6):283-9 [12522450.001]
  • [Cites] Cancer. 2006 Feb 15;106(4):950-6 [16404744.001]
  • [Cites] Br J Haematol. 2003 Jun;121(5):775-7 [12780793.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3768-76 [16105978.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8283-8 [12060771.001]
  • [Cites] Oncogene. 2008 Apr 3;27(15):2249-56 [17968322.001]
  • [Cites] Br J Haematol. 2005 Nov;131(4):495-507 [16281942.001]
  • [Cites] Int J Hematol. 1998 Jun;67(4):351-9 [9695408.001]
  • [Cites] Leukemia. 1994 Feb;8(2):258-63 [7508533.001]
  • [Cites] Br J Haematol. 2003 Jan;120(1):89-92 [12492581.001]
  • [Cites] Blood. 2000 Jan 15;95(2):726-7 [10660321.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Sep 26;92(20):9146-50 [7568090.001]
  • [Cites] Exp Hematol. 2003 Nov;31(11):1007-14 [14585362.001]
  • [Cites] Blood. 2008 Apr 15;111(8):4297-308 [18192504.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3589-95 [11369655.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 25;102(4):1104-9 [15650049.001]
  • [Cites] Leukemia. 2002 Nov;16(11):2185-9 [12399960.001]
  • [Cites] Leukemia. 2005 Oct;19(10 ):1794-805 [16094415.001]
  • [Cites] Curr Opin Hematol. 2002 Jul;9(4):274-81 [12042700.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1708-15 [16675706.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2232-40 [16281072.001]
  • [Cites] Blood. 2004 Mar 15;103(6):2316-24 [14615365.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2492-9 [14562119.001]
  • [Cites] Blood. 2004 Feb 1;103(3):1085-8 [14504097.001]
  • [Cites] Oncogene. 2001 Dec 13;20(57):8236-48 [11781838.001]
  • [Cites] Genes Chromosomes Cancer. 2004 Feb;39(2):110-8 [14695990.001]
  • [Cites] Leukemia. 2005 Jul;19(7):1153-60 [15889156.001]
  • [Cites] Haematologica. 2004 Aug;89(8):920-5 [15339674.001]
  • [Cites] J Biol Chem. 2007 Jun 22;282(25):17997-8008 [17438331.001]
  • [Cites] J Biol Chem. 2002 Jul 12;277(28):25756-74 [11956218.001]
  • [Cites] J Clin Invest. 2005 Aug;115(8):2159-68 [16025155.001]
  • (PMID = 19350351.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / RASGRP4 protein, human; 0 / Rasgrp4 protein, mouse; 0 / ras Guanine Nucleotide Exchange Factors
  •  go-up   go-down



5. Fabre C, Grosjean J, Tailler M, Boehrer S, Adès L, Perfettini JL, de Botton S, Fenaux P, Kroemer G: A novel effect of DNA methyltransferase and histone deacetylase inhibitors: NFkappaB inhibition in malignant myeloblasts. Cell Cycle; 2008 Jul 15;7(14):2139-45
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Malignant myeloblasts arising in high-risk myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) are characterized by the constitutive activation of the anti-apoptotic transcription factor NFkappaB.
  • We found that DNA methyltransferase (DNMT) inhibitors (such as azacytidine and 5-aza-2'-deoxycytidine) and histone deacetylase (HDAC) inhibitors (such as trichostatin and valproic acid) efficiently induced apoptosis in the P39 MDS/AML cell line, correlating with an inhibition of NFkappaB (which translocated from the nucleus to the cytoplasm).
  • Finally, circulating myeloblasts from AML patients treated with the DNMT inhibitor 5-aza-2'-deoxycytidine manifested a rapid (2 hours post-treatment) inhibition of NFkappaB and IKKalpha/beta.
  • [MeSH-minor] Azacitidine / pharmacology. Cell Line, Tumor. Female. Humans. Hydroxamic Acids / pharmacology. I-kappa B Kinase / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. Male. Middle Aged. Valproic Acid / pharmacology

  • Hazardous Substances Data Bank. AZACITIDINE .
  • Hazardous Substances Data Bank. VALPROIC ACID .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18641459.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / NF-kappa B; 3X2S926L3Z / trichostatin A; 614OI1Z5WI / Valproic Acid; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.7.11.10 / I-kappa B Kinase; M801H13NRU / Azacitidine
  •  go-up   go-down



6. Cataldo VD, Cortes J, Quintás-Cardama A: Azacitidine for the treatment of myelodysplastic syndrome. Expert Rev Anticancer Ther; 2009 Jul;9(7):875-84
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Azacitidine for the treatment of myelodysplastic syndrome.
  • The myelodysplastic syndromes (MDS) encompass a heterogeneous group of malignant hematologic disorders characterized by ineffective hematopoiesis, peripheral cytopenias, frequent karyotypic abnormalities and significant risk for transformation to acute myeloid leukemia (AML).
  • The prognosis of patients with intermediate- or high-risk MDS is very poor.
  • Neither autologous stem cell transplantation (SCT) nor chemotherapeutic regimens have been shown to prolong survival in patients with MDS.
  • Allogeneic SCT, while potentially curative, is only available to a selected group of patients and is associated with high morbidity and mortality in elderly patients, which constitute the majority of patients with MDS.
  • Hypermethylation of tumor-suppressor genes has been invoked as an important pathogenetic mechanism in MDS.
  • The pyrimidine nucleoside analog azacitidine, which inhibits DNA methyltransferases, has recently become the first therapeutic to prolong survival in patients with MDS, thus changing the natural history of these malignancies.
  • The activity of azacitidine in MDS has spurred the development of combinations of this agent with other epigenetic modifiers for the treatment of MDS and AML.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Myelodysplastic Syndromes / drug therapy



7. Bruserud Ø, Reikvam H: Therapeutic targeting of NF-κB in myelodysplastic syndromes and acute myeloid leukaemia - the biological heterogeneity. Expert Opin Ther Targets; 2010 Nov;14(11):1139-42
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic targeting of NF-κB in myelodysplastic syndromes and acute myeloid leukaemia - the biological heterogeneity.
  • This is also true for the malignant cells in acute myeloid leukaemia (AML) and myelodysplastic syndromes (MDS), including the malignant stem cells.
  • However, both AML and MDS patients are heterogeneous with regard to the effect of pharmacological NF-κB inhibition, and the final effect will probably also depend on the pharmacological agent used for the inhibition, e.g. proteasomal inhibitiors versus specific inhibitors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Design. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. NF-kappa B / antagonists & inhibitors



8. Hake CR, Graubert TA, Fenske TS: Does autologous transplantation directly increase the risk of secondary leukemia in lymphoma patients? Bone Marrow Transplant; 2007 Jan;39(2):59-70
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does autologous transplantation directly increase the risk of secondary leukemia in lymphoma patients?
  • Patients who undergo autologous stem cell transplantation (ASCT) for lymphoma have a significant risk of therapy-related acute myeloid leukemia and myelodysplasia (t-AML/MDS).
  • Compared to that seen in other indications such as breast cancer, multiple myeloma or germ cell tumors, there is a substantially increased risk for t-AML/MDS following ASCT for lymphoma.
  • In many of the larger series to date, it has not been possible to directly implicate autologous transplantation itself as a risk factor for t-AML/MDS.
  • Although pre-transplant therapy is certainly an important factor in the development of t-AML/MDS, specific components of the autologous transplantation procedure itself may also contribute to the risk of t-AML/MDS.
  • Specifically, priming chemotherapy, total body irradiation, and the extensive cellular proliferation which occurs during engraftment may all play a role in the development of t-AML/MDS.
  • Furthermore, there is an increasing body of evidence that certain inherited polymorphisms in genes governing drug metabolism, DNA repair and leukemogenesis may influence susceptibility to t-AML/MDS.
  • In this paper, we review the evidence implicating the above risk factors for t-AML/MDS, present a potential mechanism for t-AML/MDS and propose interventions to reduce the rate of t-AML/MDS in lymphoma patients.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Leukemia, Myeloid / etiology. Lymphoma / surgery. Transplantation, Autologous / adverse effects
  • [MeSH-minor] Humans. Incidence. Myelodysplastic Syndromes / epidemiology. Myelodysplastic Syndromes / etiology



9. Asou H, Matsui H, Ozaki Y, Nagamachi A, Nakamura M, Aki D, Inaba T: Identification of a common microdeletion cluster in 7q21.3 subband among patients with myeloid leukemia and myelodysplastic syndrome. Biochem Biophys Res Commun; 2009 May 29;383(2):245-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of a common microdeletion cluster in 7q21.3 subband among patients with myeloid leukemia and myelodysplastic syndrome.
  • Monosomy 7 and interstitial deletions in the long arm of chromosome 7 (-7/7q-) is a common nonrandom chromosomal abnormality found frequently in myeloid disorders including acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and juvenile myelomonocytic leukemia (JMML).
  • Gene copy number assessment of three genes by real-time PCR revealed heterozygous deletion of these three genes in adult patients with AML and MDS at high frequency, in addition to JMML patients.
  • The three genes located to 7q21.3 would be candidates for myeloid tumor-suppressor genes on 7q.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 7 / genetics. Genes, Tumor Suppressor. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Sequence Deletion



10. Swolin B, Rödjer S, Westin J: Therapy-related patterns of cytogenetic abnormalities in acute myeloid leukemia and myelodysplastic syndrome post polycythemia vera: single center experience and review of literature. Ann Hematol; 2008 Jun;87(6):467-74
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related patterns of cytogenetic abnormalities in acute myeloid leukemia and myelodysplastic syndrome post polycythemia vera: single center experience and review of literature.
  • A minor fraction of patients with polycythemia vera (PV) develop a terminal acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
  • Analysis of the cytogenetic abnormalities during AML or MDS may help in understanding if this development is part of the natural course of the disease or induced by myelosuppressive therapy.
  • Thirty-six cases with AML or MDS post PV, collected in a single Swedish institution during a 33-year period, are described with special regard to time to development of AML or MDS, therapy given during active PV, and cytogenetic findings during AML or MDS.
  • A further 118 cases of AML or MDS post PV, in whom type of therapy during active PV and cytogenetic findings during AML or MDS were reported, were collected from the literature.
  • AML or MDS developed in our own series after 1-30 years with a fairly constant rate (two cases per year).
  • The type of therapy given during active PV influences the type of chromosome abnormalities present during terminal AML or MDS and can also be instrumental in the development of leukemia.
  • [MeSH-major] Abnormalities, Drug-Induced / genetics. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Polycythemia Vera / complications



11. Zharlyganova D, Harada H, Harada Y, Shinkarev S, Zhumadilov Z, Zhunusova A, Tchaizhunusova NJ, Apsalikov KN, Kemaikin V, Zhumadilov K, Kawano N, Kimura A, Hoshi M: High frequency of AML1/RUNX1 point mutations in radiation-associated myelodysplastic syndrome around Semipalatinsk nuclear test site. J Radiat Res; 2008 Sep;49(5):549-55
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High frequency of AML1/RUNX1 point mutations in radiation-associated myelodysplastic syndrome around Semipalatinsk nuclear test site.
  • It is known that bone marrow is a sensitive organ to ionizing radiation, and many patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) have been diagnosed in radiation-treated cases and atomic bomb survivors in Hiroshima and Nagasaki.
  • The AML1/RUNX1 gene has been known to be frequently mutated in MDS/AML patients among atomic bomb survivors and radiation therapy-related MDS/AML patients.
  • In this study, we investigated the AML1 mutations in radiation-exposed patients with MDS/AML among the residents near the Semipalatinsk Nuclear Test Site (SNTS), where the risk of solid cancers and leukemias was increased due to the radiation effects.
  • AML1 mutations were identified in 7 (39%) of 18 radiation-exposed MDS/AML patients.
  • In contrast, no AML1 mutation was found in 13 unexposed MDS/AML cases.
  • The frequency of AML1 mutations in radiation-exposed patients with MDS/AML was significantly higher compared with unexposed patients (p < 0.05).We also found a significant correlation between individual estimated doses and AML1 mutations (p < 0.05).
  • Considering these results, AML1 point mutations might be a useful biomarker that differentiates radio-induced MDS/AML from spontaneous MDS/AML.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Environmental Exposure / analysis. Environmental Exposure / statistics & numerical data. Myelodysplastic Syndromes / epidemiology. Myelodysplastic Syndromes / genetics. Nuclear Warfare. Radiation Injuries / epidemiology. Radiation Injuries / genetics



12. Padmanabhan A, Baker JA, Zirpoli G, Sait SN, Ford LA, Moysich KB, Baer MR: Acute myeloid leukemia and myelodysplastic syndrome following breast cancer: increased frequency of other cancers and of cancers in multiple family members. Leuk Res; 2008 Dec;32(12):1820-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia and myelodysplastic syndrome following breast cancer: increased frequency of other cancers and of cancers in multiple family members.
  • Adjuvant chemotherapy and radiation therapy for breast cancer are associated with therapy-related acute myeloid leukemia (AML)/myelodysplastic syndromes (MDS), but little is known about additional risk factors.
  • Thirty-four patients with AML (n=26)/MDS (n=8) following breast cancer (cases) were compared with 2029 breast cancer patients without AML/MDS (controls).
  • Thus risk factors for AML/MDS following breast cancer include older age, other cancers and multiple first-degree relatives with cancer.
  • [MeSH-major] Breast Neoplasms / complications. Leukemia, Myeloid, Acute / epidemiology. Myelodysplastic Syndromes / epidemiology. Neoplasms / complications. Neoplasms, Second Primary / epidemiology



13. Slobbe L, Polinder S, Doorduijn JK, Lugtenburg PJ, el Barzouhi A, Steyerberg EW, Rijnders BJ: Outcome and medical costs of patients with invasive aspergillosis and acute myelogenous leukemia-myelodysplastic syndrome treated with intensive chemotherapy: an observational study. Clin Infect Dis; 2008 Dec 15;47(12):1507-12
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcome and medical costs of patients with invasive aspergillosis and acute myelogenous leukemia-myelodysplastic syndrome treated with intensive chemotherapy: an observational study.
  • BACKGROUND: Invasive aspergillosis (IA) is a leading cause of mortality in patients with acute leukemia.
  • METHODS: In 269 patients treated for acute myelogenous leukemia-myelodysplastic syndrome (AML-MDS) during 2002-2007, evidence of IA was collected using high-resolution computed tomography and galactomannan measurement in bronchoalveolar lavage fluid specimens.
  • [MeSH-major] Antifungal Agents / therapeutic use. Aspergillosis / drug therapy. Aspergillosis / economics. Drug Therapy / economics. Health Care Costs. Leukemia, Myeloid, Acute / complications



14. Rassool FV, Gaymes TJ, Omidvar N, Brady N, Beurlet S, Pla M, Reboul M, Lea N, Chomienne C, Thomas NS, Mufti GJ, Padua RA: Reactive oxygen species, DNA damage, and error-prone repair: a model for genomic instability with progression in myeloid leukemia? Cancer Res; 2007 Sep 15;67(18):8762-71
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reactive oxygen species, DNA damage, and error-prone repair: a model for genomic instability with progression in myeloid leukemia?
  • Myelodysplastic syndromes (MDS) comprise a heterogeneous group of disorders characterized by ineffective hematopoiesis, with an increased propensity to develop acute myelogenous leukemia (AML).
  • The molecular basis for MDS progression is unknown, but a key element in MDS disease progression is loss of chromosomal material (genomic instability).
  • Using our two-step mouse model for myeloid leukemic disease progression involving overexpression of human mutant NRAS and BCL2 genes, we show that there is a stepwise increase in the frequency of DNA damage leading to an increased frequency of error-prone repair of double-strand breaks (DSB) by nonhomologous end-joining.
  • Our data link gene abnormalities to constitutive DNA damage and increased DSB repair errors in vivo and provide a mechanism for an increase in the error rate of DNA repair with MDS disease progression.
  • These data suggest treatment strategies that target RAS/RAC pathways and ROS production in human MDS/AML.
  • [MeSH-major] DNA Damage. DNA Repair. Genomic Instability. Leukemia, Myeloid / genetics. Reactive Oxygen Species / metabolism



15. Rund D, Krichevsky S, Bar-Cohen S, Goldschmidt N, Kedmi M, Malik E, Gural A, Shafran-Tikva S, Ben-Neriah S, Ben-Yehuda D: Therapy-related leukemia: clinical characteristics and analysis of new molecular risk factors in 96 adult patients. Leukemia; 2005 Nov;19(11):1919-28
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related leukemia: clinical characteristics and analysis of new molecular risk factors in 96 adult patients.
  • Therapy-related leukemia or myelodysplasia (t-leuk/MDS) is a serious problem that is increasing in frequency.
  • We studied the clinical characteristics of 96 patients (pts) with a mean age of 48 years, and analyzed the molecular parameters that could predispose to t-leuk/MDS.
  • The mean latency until the development of t-AML was 45.5 months.
  • Analysis of drug metabolism and disposition genes showed a protective effect of the CYP3A4 1*B genotype against the development of t-leuk/MDS, whereas the CC genotype of MDR1 C3435T and the NAD(P)H:quinone oxidoreductase1 codon 187 polymorphism were both noncontributory.
  • In conclusion, genetic predisposition as well as epigenetic events contribute to the etiology of t-AML/MDS.
  • [MeSH-major] Genetic Predisposition to Disease. Leukemia / chemically induced. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics. Neoplasms, Second Primary / chemically induced. Neoplasms, Second Primary / genetics

  • MedlinePlus Health Information. consumer health - Leukemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16167058.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / MLH1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.13.67 / CYP3A4 protein, human; EC 1.14.14.1 / CYP3A protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP3A; EC 2.7.11.1 / RPS6KA4 protein, human; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 90-kDa
  •  go-up   go-down



16. Martin MG, Uy GL, Procknow E, Stockerl-Goldstein K, Cashen A, Westervelt P, Abboud CN, Augustin K, Luo J, DiPersio JF, Vij R: Allo-SCT conditioning for myelodysplastic syndrome and acute myeloid leukemia with clofarabine, cytarabine and ATG. Bone Marrow Transplant; 2009 Jul;44(1):13-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allo-SCT conditioning for myelodysplastic syndrome and acute myeloid leukemia with clofarabine, cytarabine and ATG.
  • Given the evidence of activity of clofarabine and cytarabine in myelodysplastic syndrome/acute myeloid leukemia (MDS/AML), we explored a novel reduced-intensity conditioning regimen based on this backbone.
  • Their median age was 54 years; three were with MDS and four with AML.
  • Toxicities included hand-foot syndrome (57% grade 2), elevated alanine aminotransferase (ALT) (57% grade 3), elevated aspartate aminotransferase (AST) (86% grade 3) and hyperbilirubinemia (29% grade 3-5).
  • No acute GVHD was observed.
  • [MeSH-major] Adenine Nucleotides / administration & dosage. Antilymphocyte Serum / administration & dosage. Antimetabolites, Antineoplastic / administration & dosage. Arabinonucleosides / administration & dosage. Cytarabine / administration & dosage. Immunosuppressive Agents / administration & dosage. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Stem Cell Transplantation. Transplantation Conditioning / methods



17. Majeed F, Jadko S, Freedman MH, Dror Y: Mutation analysis of SBDS in pediatric acute myeloblastic leukemia. Pediatr Blood Cancer; 2005 Dec;45(7):920-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutation analysis of SBDS in pediatric acute myeloblastic leukemia.
  • BACKGROUND: Shwachman-Diamond syndrome (SDS) is associated with a high risk of myelodysplasia, acute myeloid leukemia (AML), and chromosome 7 abnormalities.
  • Herein, we studied the role of genetic alterations in SBDS in AML.
  • PROCEDURE: DNA was extracted from marrows of SDS patients with AML, as well as from children with de novo AML.
  • To study whether SBDS heterozygosity confers a risk for MDS/AML, data on family members of SDS patients on the Canadian Inherited Marrow Failure Registry (CIMFR) was analyzed.
  • RESULTS: Of two SDS patients with SDS/AML one was homozygous 258 + 2T > C, and one was compound heterozygous 183-184TA > CT/258 + 2T > C.
  • To determine whether a subset of patients with SDS can present with AML, we analyzed 48 AML samples at remission, but no mutations were identified.
  • To address whether acquired mutated SBDS gene is associated with leukemic transformation in de novo AML, we analyzed 77 AML samples at diagnosis or relapse (4 with -7 and 7q-) for SBDS mutations; no alterations were detected.
  • Also, among the relatives of an SDS patient cohort on the registry no cases of MDS/AML were reported.
  • CONCLUSIONS: Common mutations occurred in our SDS patients who develop AML, and thus, AML is not confined to a rare genetic subgroup of SDS.
  • Newly diagnosed patients with AML are unlikely to have an underlying undiagnosed SDS.
  • Acquired SBDS gene mutations also would appear unlikely to play a mechanistic role in de novo AML, and might not be involved in the pathogenesis of chromosome 7 abnormalities as well.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 7 / genetics. Exons. Leukemia, Myeloid, Acute / genetics. Point Mutation. Proteins / genetics
  • [MeSH-minor] Bone Marrow Diseases / complications. Bone Marrow Diseases / genetics. Case-Control Studies. Child. Child, Preschool. Cohort Studies. DNA Mutational Analysis. Exocrine Pancreatic Insufficiency / complications. Exocrine Pancreatic Insufficiency / genetics. Heterozygote. Humans. Male. Osteochondrodysplasias / complications. Osteochondrodysplasias / genetics. Syndrome

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2005 Wiley-Liss, Inc.
  • (PMID = 16007594.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proteins; 0 / SBDS protein, human
  •  go-up   go-down



18. Barouk-Simonet E, Soenen-Cornu V, Roumier C, Cosson A, Laï JL, Fenaux P, Preudhomme C: Role of multiplex FISH in identifying chromosome involvement in myelodysplastic syndromes and acute myeloid leukemias with complex karyotypes: a report on 28 cases. Cancer Genet Cytogenet; 2005 Mar;157(2):118-26
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of multiplex FISH in identifying chromosome involvement in myelodysplastic syndromes and acute myeloid leukemias with complex karyotypes: a report on 28 cases.
  • Chromosomal abnormalities are found by conventional cytogenetic (CC) analysis in about 50% of myelodysplastic syndromes (MDS) and 70% of acute myeloid leukemias (AML).
  • We studied by M-FISH 28 cases of MDS and AML with complex chromosomal abnormalities, 10 of them were therapy-related.
  • [MeSH-major] Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Female. Humans. Karyotyping. Male. Middle Aged



19. Armand P, Kim HT, DeAngelo DJ, Ho VT, Cutler CS, Stone RM, Ritz J, Alyea EP, Antin JH, Soiffer RJ: Impact of cytogenetics on outcome of de novo and therapy-related AML and MDS after allogeneic transplantation. Biol Blood Marrow Transplant; 2007 Jun;13(6):655-64
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of cytogenetics on outcome of de novo and therapy-related AML and MDS after allogeneic transplantation.
  • Cytogenetics has an important impact on the prognosis of patients undergoing allogeneic hematopoietic stem cell transplantation (HSCT) for acute myelogenous leukemia (AML) or myelodysplastic syndromes (MDS).
  • In this study, we retrospectively analyzed data on 556 patients with AML or MDS transplanted at our institution.
  • After accounting for cytogenetics, patients with therapy-related AML or MDS had an equivalent outcome to those with de novo disease.

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Haematologica. 1999 Dec;84(12):1085-7 [10586209.001]
  • [Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4075-83 [11110676.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2134-41 [11304765.001]
  • [Cites] J Clin Oncol. 2001 May 1;19(9):2482-92 [11331327.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Leukemia. 2002 Dec;16(12):2366-78 [12454741.001]
  • [Cites] Blood. 2003 Jul 1;102(1):43-52 [12623843.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1232-40 [12714526.001]
  • [Cites] J Clin Oncol. 2003 Sep 15;21(18):3440-6 [12668650.001]
  • [Cites] Ann Hematol. 2004;83 Suppl 1:S45-8 [15124668.001]
  • [Cites] J Clin Oncol. 2004 Jun 15;22(12):2510-1 [15197216.001]
  • [Cites] Int J Hematol. 2004 Jun;79(5):495-500 [15239403.001]
  • [Cites] Blood. 1981 Oct;58(4):759-67 [7272506.001]
  • [Cites] Cancer Genet Cytogenet. 1984 Mar;11(3):332-50 [6704938.001]
  • [Cites] Blood. 1985 Jun;65(6):1364-72 [3857944.001]
  • [Cites] J Clin Oncol. 1986 Dec;4(12):1748-57 [3783201.001]
  • [Cites] Br J Haematol. 1989 May;72(1):45-53 [2736242.001]
  • [Cites] Blood. 1990 Sep 15;76(6):1083-91 [2400804.001]
  • [Cites] Leuk Res. 1992;16(1):43-6 [1732669.001]
  • [Cites] J Clin Oncol. 1993 Dec;11(12):2370-9 [8246025.001]
  • [Cites] Blood Rev. 1994 Mar;8(1):30-6 [8205008.001]
  • [Cites] Bone Marrow Transplant. 1995 Aug;16(2):203-8 [7581137.001]
  • [Cites] Br J Haematol. 1995 Sep;91(1):104-8 [7577615.001]
  • [Cites] Blood. 1997 Mar 15;89(6):2079-88 [9058730.001]
  • [Cites] Blood. 1997 Apr 1;89(7):2578-85 [9116305.001]
  • [Cites] Blood. 1997 Oct 15;90(8):2931-8 [9376573.001]
  • [Cites] Bone Marrow Transplant. 1997 Nov;20(9):737-43 [9384475.001]
  • [Cites] Blood. 1998 Sep 15;92(6):1910-7 [9731047.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] J Clin Oncol. 1999 Oct;17(10):3128-35 [10506609.001]
  • [Cites] Ann Hematol. 2005 Jan;84(1):25-32 [15349754.001]
  • [Cites] J Clin Oncol. 2006 Feb 10;24(5):790-7 [16418499.001]
  • [Cites] Blood. 2006 Mar 1;107(5):1791-9 [16254134.001]
  • [Cites] J Clin Oncol. 2000 Mar;18(5):963-71 [10694545.001]
  • (PMID = 17531775.001).
  • [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
  • [Grant] United States / NIAID NIH HHS / AI / U19 AI029530-14; United States / NIAID NIH HHS / AI / U19 AI 29530; United States / NHLBI NIH HHS / HL / P01 HL070149; United States / NCI NIH HHS / CA / T32 CA009172; United States / NIAID NIH HHS / AI / AI029530-14; United States / NHLBI NIH HHS / HL / P01 HL 070149; United States / NIAID NIH HHS / AI / U19 AI029530
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS25237; NLM/ PMC2743535
  •  go-up   go-down



20. Fischer T, Stone RM, Deangelo DJ, Galinsky I, Estey E, Lanza C, Fox E, Ehninger G, Feldman EJ, Schiller GJ, Klimek VM, Nimer SD, Gilliland DG, Dutreix C, Huntsman-Labed A, Virkus J, Giles FJ: Phase IIB trial of oral Midostaurin (PKC412), the FMS-like tyrosine kinase 3 receptor (FLT3) and multi-targeted kinase inhibitor, in patients with acute myeloid leukemia and high-risk myelodysplastic syndrome with either wild-type or mutated FLT3. J Clin Oncol; 2010 Oct 01;28(28):4339-45
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase IIB trial of oral Midostaurin (PKC412), the FMS-like tyrosine kinase 3 receptor (FLT3) and multi-targeted kinase inhibitor, in patients with acute myeloid leukemia and high-risk myelodysplastic syndrome with either wild-type or mutated FLT3.
  • PURPOSE: Mutations leading to constitutive activation of the FMS-like tyrosine kinase 3 receptor (FLT3) occur in blasts of 30% of patients with acute myeloid leukemia (AML).
  • Midostaurin (PKC412; N-benzoylstaurosporin) is a multitargeted tyrosine kinase inhibitor, with demonstrated activity in patients with AML/myelodysplastic syndrome (MDS) with FLT3 mutations.
  • PATIENTS AND METHODS: Ninety-five patients with AML or MDS with either wild-type (n = 60) or mutated (n = 35) FLT3 were randomly assigned to receive oral midostaurin at 50 or 100 mg twice daily.
  • The degree of clinical activity observed supports additional studies that combine midostaurin and other agents such as chemotherapy especially in FLT3-mutant AML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / genetics. Staurosporine / analogs & derivatives. fms-Like Tyrosine Kinase 3 / genetics



21. Paulsson K, Heidenblad M, Strömbeck B, Staaf J, Jönsson G, Borg A, Fioretos T, Johansson B: High-resolution genome-wide array-based comparative genome hybridization reveals cryptic chromosome changes in AML and MDS cases with trisomy 8 as the sole cytogenetic aberration. Leukemia; 2006 May;20(5):840-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-resolution genome-wide array-based comparative genome hybridization reveals cryptic chromosome changes in AML and MDS cases with trisomy 8 as the sole cytogenetic aberration.
  • Although trisomy 8 as the sole chromosome aberration is the most common numerical abnormality in acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS), little is known about its pathogenetic effects.
  • Considering that +8 is a frequent secondary change in AML/MDS, cryptic--possibly primary--genetic aberrations may occur in cases with trisomy 8 as the apparently single anomaly.
  • We performed a high-resolution genome-wide array-based comparative genome hybridization (array CGH) analysis of 10 AML/MDS cases with isolated +8, utilizing a 32K bacterial artificial chromosome array set, providing >98% coverage of the genome with a resolution of 100 kb.
  • A 1.8 Mb deletion at 7p14.1, which had occurred prior to the +8, was identified in MDS transforming to AML.
  • The present results show that cryptic genetic abnormalities are frequent in trisomy 8-positive AML/MDS cases and that +8 as the sole cytogenetic aberration is not always the primary genetic event.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 8 / genetics. Genome. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Nucleic Acid Hybridization / methods. Trisomy / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged



22. Tong FK, Chow S, Hedley D: Pharmacodynamic monitoring of BAY 43-9006 (Sorafenib) in phase I clinical trials involving solid tumor and AML/MDS patients, using flow cytometry to monitor activation of the ERK pathway in peripheral blood cells. Cytometry B Clin Cytom; 2006 May;70(3):107-14
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacodynamic monitoring of BAY 43-9006 (Sorafenib) in phase I clinical trials involving solid tumor and AML/MDS patients, using flow cytometry to monitor activation of the ERK pathway in peripheral blood cells.
  • In this article, we describe its application to phase I trials of BAY 43-9006 in solid tumor and AML/MDS patients.
  • A modified whole blood fixation protocol was developed for the AML/MDS trial, using the c-kit ligand stem cell factor (SCF) to activate ERK as an alternative to PMA, and incorporating immunophenotypic markers to identify leukemic blasts.
  • A similar effect was seen in the lymphocytes of AML/MDS patients during treatment with BAY 43-9006.
  • [MeSH-major] Benzenesulfonates / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukocytes, Mononuclear / drug effects. MAP Kinase Signaling System / drug effects. Myelodysplastic Syndromes / drug therapy. Neoplasms / drug therapy. Pyridines / therapeutic use



23. de Melo Campos P, Traina F, da Silva Santos Duarte A, Lorand-Metze I, Costa FF, Saad ST: Reduced expression of FLIP SHORT in bone marrow of low risk myelodysplastic syndrome. Leuk Res; 2007 Jun;31(6):853-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reduced expression of FLIP SHORT in bone marrow of low risk myelodysplastic syndrome.
  • Apoptosis is dysregulated in patients with myelodysplastic syndrome (MDS) and acute myelogenous leukaemia (AML).
  • Here, we characterize the expression level of FLIP(LONG) and FLIP(SHORT) mRNA in bone marrow aspirates from 61 patients diagnosed with MDS or AML.
  • FLIP(SHORT) mRNA expression was significantly lower in low risk MDS, compared to high risk MDS, according to FAB classification (RA/RARS versus RAEB/RAEBt, P=0.0127) and IPSS (low risk/intermediate-1 versus intermediate-2/high risk, P=0.0345).
  • Furthermore, FLIP(SHORT) mRNA expression was significantly lower in low risk MDS, compared to MDS-AML/AML de novo (P=0.0006), according to FAB classification.
  • Increased levels of FLIP(SHORT) in RAEB and AML may be related to apoptosis resistance in these diseases and to MDS progression.
  • [MeSH-major] Apoptosis. Apoptosis Regulatory Proteins / biosynthesis. CASP8 and FADD-Like Apoptosis Regulating Protein / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism



24. Björk J, Johansson B, Broberg K, Albin M: Smoking as a risk factor for myelodysplastic syndromes and acute myeloid leukemia and its relation to cytogenetic findings: a case-control study. Leuk Res; 2009 Jun;33(6):788-91
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Smoking as a risk factor for myelodysplastic syndromes and acute myeloid leukemia and its relation to cytogenetic findings: a case-control study.
  • In this case-control study, interview data on smoking habits were available for 179 de novo cases (116 with cytogenetic data) of acute myeloid leukemia (AML) or myelodysplastic syndromes (MDS).
  • Each pack-year of smoking increased the risk of MDS with 1.3% (95% CI 0.1-2.6%), corresponding to an estimated excess risk of 71% (95% CI 3-180%) for 40 pack-years.
  • Associations between smoking and the specific aberrations -5/5q-, -7/7q-, and +8 in AML and MDS were indicated but the estimates were imprecise.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / etiology. Smoking / adverse effects



25. Alencar C, Abramowtiz M, Parekh S, Braunshweig I, Jacobson M, Silverman L, Verma A: Atypical presentations of Sweet's syndrome in patients with MDS/AML receiving combinations of hypomethylating agents with histone deacetylase inhibitors. Am J Hematol; 2009 Oct;84(10):688-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical presentations of Sweet's syndrome in patients with MDS/AML receiving combinations of hypomethylating agents with histone deacetylase inhibitors.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Sweet Syndrome / chemically induced

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19722261.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Histone Deacetylase Inhibitors; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
  •  go-up   go-down



26. See HT, Thomas DA, Bueso-Ramos C, Kavanagh J: Secondary leukemia after treatment with paclitaxel and carboplatin in a patient with recurrent ovarian cancer. Int J Gynecol Cancer; 2006 Jan-Feb;16 Suppl 1:236-40
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary leukemia after treatment with paclitaxel and carboplatin in a patient with recurrent ovarian cancer.
  • The occurrence of myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML) has been reported after treatment with cytotoxic alkylating agent-based chemotherapy for solid tumors.
  • We report a patient with metastatic ovarian carcinoma treated with carboplatin and paclitaxel, who developed secondary acute erythroid leukemia.
  • Monitoring of the long-term outcome of paclitaxel- and platinum-based regimens is warranted, particularly with regard to monitoring the development of secondary MDS and/or AML.
  • The incidence and outcome of secondary leukemia in the setting of active ovarian carcinoma is reviewed.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Erythroblastic, Acute / chemically induced. Liver Neoplasms / therapy. Neoplasms, Glandular and Epithelial / therapy. Ovarian Neoplasms / therapy

  • Genetic Alliance. consumer health - Ovarian cancer.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. TAXOL .
  • Hazardous Substances Data Bank. CARBOPLATIN .
  • Hazardous Substances Data Bank. BUSULFAN .
  • Hazardous Substances Data Bank. VIDARABINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16515597.001).
  • [ISSN] 1048-891X
  • [Journal-full-title] International journal of gynecological cancer : official journal of the International Gynecological Cancer Society
  • [ISO-abbreviation] Int. J. Gynecol. Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; BG3F62OND5 / Carboplatin; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine; P88XT4IS4D / Paclitaxel; ZRP63D75JW / Idarubicin
  •  go-up   go-down



27. Kufner S, Fleischer RP, Kroell T, Schmid C, Zitzelsberger H, Salih H, de Valle F, Treder W, Schmetzer HM: Serum-free generation and quantification of functionally active Leukemia-derived DC is possible from malignant blasts in acute myeloid leukemia and myelodysplastic syndromes. Cancer Immunol Immunother; 2005 Oct;54(10):953-70
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum-free generation and quantification of functionally active Leukemia-derived DC is possible from malignant blasts in acute myeloid leukemia and myelodysplastic syndromes.
  • Functional dendritic cells (DC) are professional antigen presenting cells (APC) and can be generated in vitro from leukemic cells from acute myeloid leukemia AML patients, giving rise to APC of leukemic origin presenting leukemic antigens (DC(leu)).
  • We have already shown that DC can be successfully generated from AML and myeloplastic syndromes (MDS) cells in serum-free 'standard' medium (X-vivo + GM-CSF + IL-4 +TNFalpha + FL) in 10-14 days.
  • In this study, we present that DC counts generated from mononuclear cells (MNC) varied between 20% (from 55 MDS samples), 34% (from 100 AML samples) and 25% (from 38 healthy MNC samples) medium.
  • DC harvests were highest in monocytoid FAB types (AML-M4/M5, MDS-CMML) and independent from cytogenetic risk groups, demonstrating that DC-based strategies can be applied for patients with all cytogenetic risk groups.
  • Proof of the clonal derivation of DC generated was obtained in five AML and four MDS cases with a combined FISH/immunophenotype analysis (FISH-IPA): The clonal numerical chromosome aberrations of the diseases were regularly codetectable with DC markers; however, not with all clonal cells being convertible to leukemia-derived DC(leu) (on average, 53% of blasts in AML or MDS).
  • In 41 AML and 13 MDS cases with a suitable antigen expression, we could confirm FISH-IPA data by Flow cytometry: although DC(leu) are regularly detectable, on average only 57% of blasts in AML and 64% of blasts in MDS were converted to DC(leu).
  • After coculture with DC in mixed lymphocyte reactions (MLR), autologous T cells from AML and MDS patients proliferate and upregulate costimulatory receptors.
  • The specific lysis of leukemic cells by autologous T cells could be demonstrated in three cases with AML in a Fluorolysis assay.
  • (1) the generation of DC is regularly possible in AML and also in MDS under serum-free conditions. (2) Clonal/leukemia-derived DC(leu) can be regularly generated from MDS and AML-MNC; however, not with all blasts being converted to DC(leu) and not all DC generated carrying leukemic markers.
  • We recommend to select DC(leu) for vaccinations or ex vivo T-cell activations to avoid contaminations with non-converted blasts and non-leukemia-derived DC and to improve the harvest of specific, anti-leukemic T cells.
  • DC and DC-primed T cells could provide a practical strategy for the immunotherapy of AML and MDS.
  • [MeSH-major] Dendritic Cells / immunology. Leukemia, Myeloid / immunology. Leukocytes, Mononuclear / immunology. Myelodysplastic Syndromes / immunology
  • [MeSH-minor] Acute Disease. Adult. Aged. Antigen-Presenting Cells. Antigens, CD. Antigens, CD80 / immunology. Antigens, CD80 / metabolism. Blast Crisis. Cell Culture Techniques. Culture Media, Serum-Free. Female. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Immunoglobulins / immunology. Immunoglobulins / metabolism. Interleukin-4 / pharmacology. Lymphocyte Activation. Male. Membrane Glycoproteins / immunology. Membrane Glycoproteins / metabolism. Middle Aged. T-Lymphocytes / immunology. T-Lymphocytes, Cytotoxic. Tumor Necrosis Factor-alpha / pharmacology

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15789235.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD80; 0 / CD83 antigen; 0 / Culture Media, Serum-Free; 0 / Immunoglobulins; 0 / Membrane Glycoproteins; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  •  go-up   go-down



28. Watanabe-Okochi N, Kitaura J, Ono R, Harada H, Harada Y, Komeno Y, Nakajima H, Nosaka T, Inaba T, Kitamura T: AML1 mutations induced MDS and MDS/AML in a mouse BMT model. Blood; 2008 Apr 15;111(8):4297-308
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AML1 mutations induced MDS and MDS/AML in a mouse BMT model.
  • Myelodysplastic syndrome (MDS) is a hematopoietic stem-cell disorder characterized by trilineage dysplasia and susceptibility to acute myelogenous leukemia (AML).
  • Analysis of molecular basis of MDS has been hampered by the heterogeneity of the disease.
  • Recently, mutations of the transcription factor AML1/RUNX1 have been identified in 15% to 40% of MDS-refractory anemia with excess of blasts (RAEB) and MDS/AML.
  • Most mice developed MDS and MDS/AML-like symptoms within 4 to 13 months after BMT.
  • Interestingly, among integration sites identified, Evi1 seemed to collaborate with an AML1 mutant harboring a point mutation in the Runt homology domain (D171N) to induce MDS/AML with an identical phenotype characterized by marked hepatosplenomegaly, myeloid dysplasia, leukocytosis, and biphenotypic surface markers.
  • Collaboration between AML1-D171N and Evi1 was confirmed by a BMT model where coexpression of AML1-D171N and Evi1 induced acute leukemia of the same phenotype with much shorter latencies.
  • On the other hand, a C-terminal truncated AML1 mutant (S291fsX300) induced pancytopenia with erythroid dysplasia in transplanted mice, followed by progression to MDS-RAEB or MDS/AML.
  • Thus, we have developed a useful mouse model of MDS/AML that should help in the understanding of the molecular basis of MDS and the progression of MDS to overt leukemia.
  • [MeSH-major] Bone Marrow Transplantation. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Myelodysplastic Syndromes / genetics



29. Zatkova A, Schoch C, Speleman F, Poppe B, Mannhalter C, Fonatsch C, Wimmer K: GAB2 is a novel target of 11q amplification in AML/MDS. Genes Chromosomes Cancer; 2006 Sep;45(9):798-807
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GAB2 is a novel target of 11q amplification in AML/MDS.
  • Chromosome arm 11q amplifications involving the mixed lineage leukemia gene (MLL) locus are rare but recurrent aberrations in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
  • Thus, the adaptor molecule GAB2 that has already been shown to enhance oncogenic signaling in other neoplasias appears as a novel target of 11q amplification in AML/MDS.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Chromosomes, Human, Pair 11. Gene Amplification / physiology. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics



30. Leleu X, Tamburini J, Roccaro A, Morel P, Soumerai J, Lévy V, Wemeau M, Balkaran S, Poulain S, Hunter ZR, Ghobrial IM, Treon SP, Leblond V: Balancing risk versus benefit in the treatment of Waldenström's Macroglobulinemia patients with nucleoside analogue-based therapy. Clin Lymphoma Myeloma; 2009 Mar;9(1):71-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • There are sporadic reports on increased incidence of transformation to high grade non-Hodgkin lymphoma (transformation to NHL) and development of therapy related-myelodysplasia/acute leukemia (t-MDS/AML) among WM patients treated with NA.
  • The incidences of transformation to NHL and t-MDS/AML ranged from 4.7% to 8%, and from 1.4% to 8.9%, respectively, and demonstrated an increased incidence of these late events among WM patients treated with NA.
  • [MeSH-minor] Disease Progression. Humans. Leukemia, Myeloid, Acute / pathology. Lymphoma, Non-Hodgkin / pathology

  • COS Scholar Universe. author profiles.
  • 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 = 19362978.001).
  • [ISSN] 1557-9190
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nucleosides
  •  go-up   go-down



31. Liu TX, Becker MW, Jelinek J, Wu WS, Deng M, Mikhalkevich N, Hsu K, Bloomfield CD, Stone RM, DeAngelo DJ, Galinsky IA, Issa JP, Clarke MF, Look AT: Chromosome 5q deletion and epigenetic suppression of the gene encoding alpha-catenin (CTNNA1) in myeloid cell transformation. Nat Med; 2007 Jan;13(1):78-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromosome 5q deletion and epigenetic suppression of the gene encoding alpha-catenin (CTNNA1) in myeloid cell transformation.
  • Interstitial loss of all or part of the long arm of chromosome 5, or del(5q), is a frequent clonal chromosomal abnormality in human myelodysplastic syndrome (MDS, a preleukemic disorder) and acute myeloid leukemia (AML), and is thought to contribute to the pathogenesis of these diseases by deleting one or more tumor-suppressor genes.
  • We focused our analysis of gene expression on RNA from primitive leukemia-initiating cells, which harbor 5q deletions, and analyzed 12 genes within the CDR that are expressed by normal hematopoietic stem cells.
  • Here we show that the gene encoding alpha-catenin (CTNNA1) is expressed at a much lower level in leukemia-initiating stem cells from individuals with AML or MDS with a 5q deletion than in individuals with MDS or AML lacking a 5q deletion or in normal hematopoietic stem cells.
  • Analysis of HL-60 cells, a myeloid leukemia line with deletion of the 5q31 region, showed that the CTNNA1 promoter of the retained allele is suppressed by both methylation and histone deacetylation.
  • Thus, loss of expression of the alpha-catenin tumor suppressor in hematopoietic stem cells may provide a growth advantage that contributes to human MDS or AML with del(5q).
  • [MeSH-major] Cell Transformation, Neoplastic. Chromosome Deletion. Chromosomes, Human, Pair 5 / genetics. Myeloid Progenitor Cells / pathology. alpha Catenin / genetics
  • [MeSH-minor] Acute Disease. Blotting, Western. Cell Line. Cell Line, Tumor. DNA Methylation / drug effects. Flow Cytometry. Gene Expression Regulation, Neoplastic / drug effects. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. HL-60 Cells. Humans. Hydroxamic Acids / pharmacology. In Situ Hybridization, Fluorescence / methods. K562 Cells. Leukemia, Myeloid / blood. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Mutation. Myelodysplastic Syndromes / blood. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Reverse Transcriptase Polymerase Chain Reaction. Transfection. U937 Cells



32. Chen BA, Gao C, Ding J, Ding JH, Sun YY, Zhao G, Cheng J, Wang J, Bao W, Song HH, Xia GH, Ma JL, Wu LL: [Analysis on laboratory and clinical characteristics in 65 cases of myelodysplastic syndrome]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Dec;17(6):1472-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Analysis on laboratory and clinical characteristics in 65 cases of myelodysplastic syndrome].
  • The aim of this study was to gain more insight into the understanding of myelodysplastic syndrome in the clinical and laboratory features.
  • The clinical data of 65 patients with MDS were reviewed and analysed.
  • The median age of them was 66 years old (range 19-89 years), and 6 patients had a history of toxic exposure (secondary MDS).
  • The results showed that dysplasia was found in 64 patients examined with bone marrow smears (98.5%), among them trilineage dysplasia in 21 patients (32.3%), bilineage dysplasia in 33 patients (50.8%), only erythroid dysplasia in 8 cases (12.3%) and 2 patients (3.1%) only with myeloid dysplasia.
  • The abnormal chromosome was the major cytogenetic abnormality, which occurred more often in secondary MDS and the patients with RAEB or RAEB-T.
  • Among the 49 patients who had received cytogenetic examination, 15 patients transformed into AML with the incidence of 30.61%, but only 3 out of 20 patients in the group of normal chromosome transformed into AML (15%), while 12 out of 29 patients in the group of abnormal karyotypes transformed into AML (41.4%).
  • The median time of following up was 35 months (range 2 - 106 months).
  • In conclusion, the incidence of MDS in our country is younger than that in Western countries, the rate of abnormal chromosome in high risk MDS is higher than that in low risk MDS.
  • Meanwhile, those who have the change of chromosome are related to the transformation of MDS into AML and have shorter survival time than those MDS patients with normal karyotypes.



33. Andersson BS, de Lima M, Thall PF, Wang X, Couriel D, Korbling M, Roberson S, Giralt S, Pierre B, Russell JA, Shpall EJ, Jones RB, Champlin RE: Once daily i.v. busulfan and fludarabine (i.v. Bu-Flu) compares favorably with i.v. busulfan and cyclophosphamide (i.v. BuCy2) as pretransplant conditioning therapy in AML/MDS. Biol Blood Marrow Transplant; 2008 Jun;14(6):672-84
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Once daily i.v. busulfan and fludarabine (i.v. Bu-Flu) compares favorably with i.v. busulfan and cyclophosphamide (i.v. BuCy2) as pretransplant conditioning therapy in AML/MDS.
  • To account for improved supportive care and other unidentified factors that may affect outcome ("period" effects), 78 acute myelogenous leukemia (AML) patients receiving Melphalan-Flu (MF), treated in parallel during this time (1997-2004) were used to estimate the period effect.
  • These results support replacing BuCy +/- ATG with Bu-Flu +/- rabbit-antithymocyte globulin (ATG), and warrant a prospective comparison between allogeneic HSCT and conventional induction/consolidation chemotherapy for AML in CR1.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. MELPHALAN .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. BUSULFAN .
  • Hazardous Substances Data Bank. VIDARABINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18489993.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 2P01 CA55164; United States / NCI NIH HHS / CA / P01 CA055164-160020; United States / NCI NIH HHS / CA / 2P30CA16672-26; United States / NCI NIH HHS / CA / P01 CA055164
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Antineoplastic Agents; 0 / Myeloablative Agonists; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
  • [Other-IDs] NLM/ NIHMS52878; NLM/ PMC4230823
  •  go-up   go-down



34. Yagasaki H, Mugishima H: [Hereditary diseases with propensity to myeloid malignancy]. Nihon Rinsho; 2009 Oct;67(10):1884-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Hereditary diseases with propensity to myeloid malignancy].
  • Hematological malignancy is known to be associated with Down syndrome (DS), neurofibromatosis type 1 (NF1) and congenital bone marrow failure syndromes (CBMFS).
  • Although many responsible germ-cell mutations have been identified, the secondary mutations that are responsible for the development of myelodysplastic syndrome and acute myelogenous leukemia (MDS/AML) have not been determined.
  • Additional chromosomal abnormalities such as monosomy 7 and trisomy 21 are often observed in the progression to MDS/AML, and the critical genes for monosomy 7 have recently been reported.
  • In this review, we briefly present recent findings regarding DS, NF1 and CBMFS with a tendency for malignant transformation; Fanconi anemia, familial platelet disorder with propensity to myeloid malignancy and congenital severe neutropenia.
  • [MeSH-major] Blood Platelet Disorders / genetics. Down Syndrome / genetics. Fanconi Anemia / genetics. Leukemia, Myeloid / genetics. Neurofibromatosis 1 / genetics. Neutropenia / genetics



35. Montoto S, Canals C, Rohatiner AZ, Taghipour G, Sureda A, Schmitz N, Gisselbrecht C, Fouillard L, Milpied N, Haioun C, Slavin S, Conde E, Fruchart C, Ferrant A, Leblond V, Tilly H, Lister TA, Goldstone AH, EBMT Lymphoma Working Party: Long-term follow-up of high-dose treatment with autologous haematopoietic progenitor cell support in 693 patients with follicular lymphoma: an EBMT registry study. Leukemia; 2007 Nov;21(11):2324-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Thirty-nine patients developed secondary myelodysplastic syndrome/acute myeloid leukaemia (MDS/AML), in 34 cases having received TBI as the conditioning regimen.



36. Wilking N, Lidbrink E, Wiklund T, Erikstein B, Lindman H, Malmström P, Kellokumpu-Lehtinen P, Bengtsson NO, Söderlund G, Anker G, Wist E, Ottosson S, Salminen E, Ljungman P, Holte H, Nilsson J, Blomqvist C, Bergh J: Long-term follow-up of the SBG 9401 study comparing tailored FEC-based therapy versus marrow-supported high-dose therapy. Ann Oncol; 2007 Apr;18(4):694-700
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Ten patients in the tailored FEC regimen developed acute myeloid leukaemia (AML)/myelodysplasia (MDS).
  • CONCLUSION: The update of this study shows an improved outcome linked to the tailored FEC treatment in relation to breast cancer relapse, but also an increased incidence of AML/MDS.

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CARBOPLATIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • Hazardous Substances Data Bank. THIO-TEPA .
  • Hazardous Substances Data Bank. EPIRUBICIN .
  • 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 = 17301072.001).
  • [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] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor; 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; 905Z5W3GKH / Thiotepa; BG3F62OND5 / Carboplatin; U3P01618RT / Fluorouracil
  •  go-up   go-down



37. Tanvetyanon T, Stiff PJ: Recurrent steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations. Leuk Lymphoma; 2005 Jan;46(1):151-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations.
  • Several paraneoplastic inflammatory conditions, particularly autoimmune diseases, have been described in association with myelodysplastic syndromes (MDS).
  • However, to date, recurrent acute pancreatitis has never been described in association with MDS.
  • Aortitis and pericarditis were diagnosed simultaneously with MDS, refractory anemia with excess blast type 2.
  • The vasculitic syndrome responded rapidly to corticosteroids, but soon after tapering of corticosteroids, acute pancreatitis developed.
  • Finally, his MDS transformed into acute myeloid leukemia (AML); severe acute pancreatitis closely accompanied.
  • A subsequent pancreatitis attack with pseudocyst formation occurred, but again was controlled with corticosteroids, although this was followed closely by another relapse of AML.
  • All etiologies for recurrent acute pancreatitis were ruled out.
  • The dramatic response of his pancreatitis attacks to immunosuppression suggested its autoimmune origin, while the close relationship in both the timing and severity of acute pancreatitis and MDS/AML suggested that the autoimmune pancreatitis was a paraneoplastic phenomenon related to MDS.
  • [MeSH-major] Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / pathology. Pancreatitis / drug therapy. Pancreatitis / pathology. Steroids / therapeutic use



38. Shimoni A, Hardan I, Shem-Tov N, Yerushalmi R, Nagler A: Allogeneic hematopoietic stem-cell transplantation in AML and MDS using myeloablative versus reduced-intensity conditioning: long-term follow-up. Leukemia; 2010 May;24(5):1050-2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic hematopoietic stem-cell transplantation in AML and MDS using myeloablative versus reduced-intensity conditioning: long-term follow-up.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Myeloablative Agonists / therapeutic use. Myelodysplastic Syndromes / therapy. Transplantation Conditioning



39. Carvalho G, Fabre C, Braun T, Grosjean J, Ades L, Agou F, Tasdemir E, Boehrer S, Israel A, Véron M, Fenaux P, Kroemer G: Inhibition of NEMO, the regulatory subunit of the IKK complex, induces apoptosis in high-risk myelodysplastic syndrome and acute myeloid leukemia. Oncogene; 2007 Apr 5;26(16):2299-307
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of NEMO, the regulatory subunit of the IKK complex, induces apoptosis in high-risk myelodysplastic syndrome and acute myeloid leukemia.
  • In high-risk myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML), blasts constitutively activate the antiapoptotic transcription factor nuclear factor-kappaB (NF-kappaB).
  • A cell-permeable peptide that mimics the leucine zipper subdomain of IKKgamma, thus preventing its oligomerization, inhibited the constitutive NF-kappaB activation and induced apoptotic cell death in a panel of human MDS and AML cell lines (P39, MOLM13, THP1 and MV4-11).
  • Primary bone marrow CD34(+) cells from high-risk MDS and AML patients also succumbed to the IKKgamma/NEMO-antagonistic peptide, but not to a mutated control peptide.
  • Altogether, these data indicate that malignant cells in high-risk MDS and AML cells critically depend on IKKgamma/NEMO to survive.
  • [MeSH-major] I-kappa B Kinase / antagonists & inhibitors. Leukemia, Myeloid / pathology. Myelodysplastic Syndromes / pathology
  • [MeSH-minor] Acute Disease. Amino Acid Sequence. Apoptosis. Cell Line, Tumor. Humans. Molecular Sequence Data. NF-kappa B / physiology. Peptide Fragments / chemistry. Protein Subunits. RNA, Small Interfering / genetics. Transfection



40. Niimi H, Harada H, Harada Y, Ding Y, Imagawa J, Inaba T, Kyo T, Kimura A: Hyperactivation of the RAS signaling pathway in myelodysplastic syndrome with AML1/RUNX1 point mutations. Leukemia; 2006 Apr;20(4):635-44
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hyperactivation of the RAS signaling pathway in myelodysplastic syndrome with AML1/RUNX1 point mutations.
  • AML1/RUNX1 mutations have been reported frequently in myelodysplastic syndrome (MDS) patients, especially those diagnosed with refractory anemia with excess blast (RAEB), RAEB in transformation (RAEBt), or AML following MDS (these categories are defined as MDS/AML).
  • Although AML1 mutations are suspected to play a pivotal role in the development of MDS/AML, acquisition of additional genetic alterations is also necessary.
  • We analyzed gene alterations in MDS/AML patients with AML1 mutations, comparing them to alterations in those without an AML1 mutation.
  • AML1 mutations were significantly associated with -7/7q-, whereas MDS/AML patients without AML1 mutations showed a high frequency of -5/5q- and a complex karyotype.
  • Patients with AML1 mutations showed more mutations of their FLT3, N-RAS, PTPN11, and NF1 genes, resulting in a significantly higher mutation frequency for receptor tyrosine kinase (RTK)-RAS signaling pathways in AML1-mutated MDS/AML patients compared to AML1-wild-type MDS/AML patients (38% versus 6.3%, P < 0.0001).
  • Furthermore, blast cells of the AML1-mutated patients expressing surface c-KIT, and SHP-2 mutants contributed to prolonged and enhanced extracellular signal-regulated kinase activation following stem cell factor stimulation.
  • Our results suggest that MDS/AML arising from AML1/RUNX1 mutations has a significant association with -7/7q- alteration, and frequently involves RTK-RAS signaling pathway activation.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Genes, ras. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / metabolism. Point Mutation. Signal Transduction



41. Alter BP, Giri N, Savage SA, Peters JA, Loud JT, Leathwood L, Carr AG, Greene MH, Rosenberg PS: Malignancies and survival patterns in the National Cancer Institute inherited bone marrow failure syndromes cohort study. Br J Haematol; 2010 Jul;150(2):179-88
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Fanconi anaemia (FA), dyskeratosis congenita (DC), Diamond-Blackfan anaemia (DBA), and Shwachman-Diamond syndrome (SDS) comprise major inherited bone marrow failure syndromes (IBMFS).
  • Adverse events include severe bone marrow failure (BMF), myelodysplastic syndrome (MDS), acute myeloid leukaemia (AML), and solid tumours (ST).
  • Most patients in each syndrome survived to young adulthood.
  • While FA and DC patients had markedly increased risks of cancer, AML and MDS, there were no cases of leukaemia in DBA or SDS patients.
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Anemia, Diamond-Blackfan / complications. Anemia, Diamond-Blackfan / genetics. Child. Child, Preschool. Dyskeratosis Congenita / complications. Dyskeratosis Congenita / genetics. Epidemiologic Methods. Fanconi Anemia / complications. Fanconi Anemia / genetics. Female. Genetic Predisposition to Disease. Genotype. Humans. Male. Middle Aged. Prognosis. Syndrome. Young Adult



42. Warlick ED, O'Donnell PV, Borowitz M, Grupka N, Decloe L, Garrett-Mayer E, Borrello I, Brodsky R, Fuchs E, Huff CA, Luznik L, Matsui W, Ambinder R, Jones RJ, Smith BD: Myeloablative allogeneic bone marrow transplant using T cell depleted allografts followed by post-transplant GM-CSF in high-risk myelodysplastic syndromes. Leuk Res; 2008 Sep;32(9):1439-47
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myeloablative allogeneic bone marrow transplant using T cell depleted allografts followed by post-transplant GM-CSF in high-risk myelodysplastic syndromes.
  • Allogeneic blood and marrow transplantation (alloBMT) remains the only curative treatment for patients with myelodysplastic syndromes (MDS), but its application has been limited by the older age range of patients with this disease.
  • Myeloid growth factors have been used to speed engraftment following alloBMT, but data suggest that they may also have anti-tumor properties.
  • We treated 43 patients (median age 56) with MDS/AML with high-risk features using a myeloablative T cell depleted alloBMT followed by prolonged systemic GM-CSF.
  • These results suggest that it is possible to maintain treatment intensity while minimizing toxicity in older, high-risk MDS patients.



43. Andersen MK, Christiansen DH, Pedersen-Bjergaard J: Amplification or duplication of chromosome band 21q22 with multiple copies of the AML1 gene and mutation of the TP53 gene in therapy-related MDS and AML. Leukemia; 2005 Feb;19(2):197-200
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Amplification or duplication of chromosome band 21q22 with multiple copies of the AML1 gene and mutation of the TP53 gene in therapy-related MDS and AML.
  • Amplification or duplication of the AML1 gene at chromosome band 21q22 was detected by FISH using a locus-specific probe in three out of 171 unselected patients with therapy-related myelodysplasia (t-MDS) or t-AML (1.7%).
  • The results support a pivotal role of impaired TP53 function in the development of gene amplification or duplication in t-MDS and t-AML.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. DNA-Binding Proteins / genetics. Gene Amplification / genetics. Gene Duplication. Genes, p53. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics



44. Corey SJ, Minden MD, Barber DL, Kantarjian H, Wang JC, Schimmer AD: Myelodysplastic syndromes: the complexity of stem-cell diseases. Nat Rev Cancer; 2007 Feb;7(2):118-29
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myelodysplastic syndromes: the complexity of stem-cell diseases.
  • The prevalence of patients with myelodysplastic syndromes (MDS) is increasing owing to an ageing population and increased awareness of these diseases.
  • MDS represent many different conditions, not just a single disease, that are grouped together by several clinical characteristics.
  • A striking feature of MDS is genetic instability, and a large proportion of cases result in acute myeloid leukaemia (AML).
  • We Review three emerging principles of MDS biology: stem-cell dysfunction and the overlap with AML, genetic instability and the deregulation of apoptosis, in the context of inherited bone marrow-failure syndromes, and treatment-related MDS and AML.
  • [MeSH-major] Myelodysplastic Syndromes / pathology. Stem Cells / pathology



45. Gupta G, Singh R, Kotasthane DS, Kotasthane VD: Myelodysplastic syndromes/neoplasms: recent classification system based on World Health Organization Classification of Tumors - International Agency for Research on Cancer for Hematopoietic and Lymphoid Tissues. J Blood Med; 2010;1:171-82
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myelodysplastic syndromes/neoplasms: recent classification system based on World Health Organization Classification of Tumors - International Agency for Research on Cancer for Hematopoietic and Lymphoid Tissues.
  • The myelodysplastic Syndromes (MDS) are a group of clonal hematopoietic stem cell diseases characterized by cytopenia(s), dysplasia in one or more of the major myeloid cell lines, ineffective hematopoiesis, and increased risk of development of acute myeloid leukemia.
  • The myelodysplastic syndromes are now classified into the following categories - refractory cytopenia with unilineage dysplasia, refractory anemia with ring sideroblasts, refractory cytopenia with multilineage dysplasia, refractory anemia with excess blasts, myelodysplastic syndrome associated with isolated del (5q), myelodysplastic syndrome - unclassifiable, and childhood myelodysplastic syndrome.

  • 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 = 22282696.001).
  • [ISSN] 1179-2736
  • [Journal-full-title] Journal of blood medicine
  • [ISO-abbreviation] J Blood Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC3262332
  • [Keywords] NOTNLM ; leukemia / myelodysplastic syndromes
  •  go-up   go-down



46. Voso MT, D'Alò F, Greco M, Fabiani E, Criscuolo M, Migliara G, Pagano L, Fianchi L, Guidi F, Hohaus S, Leone G: Epigenetic changes in therapy-related MDS/AML. Chem Biol Interact; 2010 Mar 19;184(1-2):46-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epigenetic changes in therapy-related MDS/AML.
  • Therapy-related Myelodysplastic Syndromes/Acute Myeloid Leukemias (t-MDS/AML) are one of the most compelling long term adverse events occurring in cancer survivors treated with chemo-radiotherapy regimes.
  • Gene promoter methylation is a common finding in t-MDS/AML and has been associated to a shorter latency period from the treatment of the primary tumor.
  • We found frequent methylation of DAPK in the t-MDS/AML group, especially in patients with a previous lymphoproliferative disease.
  • In patients studied for concurrent methylation of several promoters, t-MDS/AML were significantly more frequently hypermethylated in 2 or more promoter regions than de novo MDS or AML suggesting that promoter hypermethylation of genes involved in cell cycle control, apoptosis and DNA repair pathways is a frequent finding in t-MDS/AML and may contribute to secondary leukemogenesis.
  • [MeSH-major] Epigenesis, Genetic. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics



47. Pulliam-Leath AC, Ciccone SL, Nalepa G, Li X, Si Y, Miravalle L, Smith D, Yuan J, Li J, Anur P, Orazi A, Vance GH, Yang FC, Hanenberg H, Bagby GC, Clapp DW: Genetic disruption of both Fancc and Fancg in mice recapitulates the hematopoietic manifestations of Fanconi anemia. Blood; 2010 Oct 21;116(16):2915-20
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Fanconi anemia (FA) is an inherited chromosomal instability syndrome characterized by bone marrow failure, myelodysplasia (MDS), and acute myeloid leukemia (AML).
  • Here we show that double-mutant Fancc(-/-);Fancg(-/-) mice develop spontaneous hematologic sequelae including bone marrow failure, AML, MDS and complex random chromosomal abnormalities that the single-mutant mice do not.
  • Importantly, this model closely recapitulates the phenotypes found in FA patients and may be useful as a preclinical platform to evaluate the molecular pathogenesis of spontaneous bone marrow failure, MDS and AML in FA.



48. Pagel JM, Gooley TA, Rajendran J, Fisher DR, Wilson WA, Sandmaier BM, Matthews DC, Deeg HJ, Gopal AK, Martin PJ, Storb RF, Press OW, Appelbaum FR: Allogeneic hematopoietic cell transplantation after conditioning with 131I-anti-CD45 antibody plus fludarabine and low-dose total body irradiation for elderly patients with advanced acute myeloid leukemia or high-risk myelodysplastic syndrome. Blood; 2009 Dec 24;114(27):5444-53
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic hematopoietic cell transplantation after conditioning with 131I-anti-CD45 antibody plus fludarabine and low-dose total body irradiation for elderly patients with advanced acute myeloid leukemia or high-risk myelodysplastic syndrome.
  • Fifty-eight patients older than 50 years with advanced acute myeloid leukemia (AML) or high-risk myelodysplastic syndrome (MDS) were treated with (131)I-BC8 Ab and fludarabine plus 2 Gy total body irradiation.
  • Eighty-six percent of patients had AML or MDS with greater than 5% marrow blasts at the time of transplantation.
  • These results show that CD45-targeted radiotherapy can be safely combined with a reduced-intensity conditioning regimen to yield encouraging overall survival for older, high-risk patients with AML or MDS.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Acute Disease. Aged. Antibodies / administration & dosage. Antibodies / immunology. Antigens, CD45 / immunology. Combined Modality Therapy. Female. Humans. Iodine Radioisotopes / pharmacokinetics. Male. Middle Aged. Risk Factors. Survival Analysis. Survival Rate. Tissue Distribution. Transplantation, Homologous. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Whole-Body Irradiation



49. Park CH, Kimler BF, Yi SY, Park SH, Kim K, Jung CW, Kim SH, Lee ER, Rha M, Kim S, Park MH, Lee SJ, Park HK, Lee MH, Yoon SS, Min YH, Kim BS, Kim JA, Kim WS: Depletion of L-ascorbic acid alternating with its supplementation in the treatment of patients with acute myeloid leukemia or myelodysplastic syndromes. Eur J Haematol; 2009 Aug;83(2):108-18
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Depletion of L-ascorbic acid alternating with its supplementation in the treatment of patients with acute myeloid leukemia or myelodysplastic syndromes.
  • PURPOSE: L-ascorbic acid (LAA) modifies the in vitro growth of leukemic cells from approximately 50% of patients with acute myeloid leukemia (AML) or myelodysplastic syndromes (MDS).
  • Experimental results: During depletion phase, patients with refractory AML or MDS were placed on a diet deficient in LAA; during supplementation phase, patients received daily intravenous administration of LAA.
  • [MeSH-major] Ascorbic Acid / metabolism. Ascorbic Acid / therapeutic use. Leukemia, Myeloid, Acute / diet therapy. Myelodysplastic Syndromes / diet therapy



50. Rudd E, Göransdotter Ericson K, Zheng C, Uysal Z, Ozkan A, Gürgey A, Fadeel B, Nordenskjöld M, Henter JI: Spectrum and clinical implications of syntaxin 11 gene mutations in familial haemophagocytic lymphohistiocytosis: association with disease-free remissions and haematopoietic malignancies. J Med Genet; 2006 Apr;43(4):e14
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Two of the six patients harbouring STX11 gene defects developed myelodysplastic syndrome (MDS) or acute myelogenous leukaemia (AML).
  • These results suggest that STX11 gene mutations may be associated with secondary malignancies (MDS/AML), and that there is segregation of specific clinical features in FHL patients with an underlying genotype.
  • [MeSH-major] Leukemia, Myeloid / genetics. Lymphohistiocytosis, Hemophagocytic / diagnosis. Lymphohistiocytosis, Hemophagocytic / genetics. Mutation. Myelodysplastic Syndromes / genetics. Qa-SNARE Proteins / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged, 80 and over. Child. Child, Preschool. DNA Mutational Analysis. Female. Genotype. Humans. Infant. Male. Pedigree. Phenotype. Psychomotor Disorders / complications. Psychomotor Disorders / genetics. Remission, Spontaneous



51. Bacher U, Haferlach T, Kern W, Haferlach C, Schnittger S: A comparative study of molecular mutations in 381 patients with myelodysplastic syndrome and in 4130 patients with acute myeloid leukemia. Haematologica; 2007 Jun;92(6):744-52
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A comparative study of molecular mutations in 381 patients with myelodysplastic syndrome and in 4130 patients with acute myeloid leukemia.
  • BACKGROUND AND OBJECTIVES: The precise relationship between myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) is unclear and the role of molecular mutations in leukemic transformation in MDS is controversial.
  • The aim of this study was to clarify the relationship between AML and MDS by comparing the frequency of molecular mutations in the two conditions.
  • DESIGN AND METHODS: We compared the frequency of FLT3-length mutations (FLT3-LM), FLT3-TKD, MLL-partial tandem duplications (MLL-PTD), NRAS, and KITD816 in 381 patients with MDS refractory anemia with excess blasts [RAEB] n=49; with ringed sideroblasts [RARS] n=310; chronic monomyelocytic leukemia [CMML] n=22) and in 4130 patients with AML (de novo: n=3139; secondary AML [s-AML] following MDS: n=397; therapy-related [t-AML]: n=233; relapsed: n=361).
  • RESULTS: All mutations were more frequent in s-AML than in MDS and all but the FLT3-TKD were more frequent in RAEB than in RA/RARS.
  • The higher incidences in s-AML were significant for FLT3-TKD (p=0.032), MLL-PTD (p=0.034), and FLT3-LM (RA/RARS: 0/45; RAEB: 8/293; 2.7%; s-AML: 45/389; 11.6%; p<0.0001).
  • The incidence of NRAS-mutations increased from 17/272 (6.3%) in MDS to 41/343 in s-AML (12.0%) and that of KITD816-mutations from 2/290 (0.7%) to 5/341 (1.5%) (p=n.s.).
  • FLT3-LM-acquisition occurred in 3/22 cases (13.6%) during MDS transformation; NRAS-acquisition occurred in 1/24 (4.2%).
  • FLT3-LM and MLL-PTD were more frequent in AML relapse than in de novo AML or s-AML (p<0.0001).
  • INTERPRETATION AND CONCLUSIONS: The increase of molecular mutations from low- to high-risk MDS, to s-AML, and to relapsed AML emphasizes the value of these mutations as markers of progressing disease.
  • Finally, we found a low rate of 5q- in the molecularly mutated cases in MDS which might explain the stability of this subtype.
  • [MeSH-major] Leukemia, Myeloid / genetics. Mutation. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Disease Progression. Gene Frequency. Histone-Lysine N-Methyltransferase. Humans. Molecular Epidemiology. Myeloid-Lymphoid Leukemia Protein / genetics. Proto-Oncogene Proteins c-kit / genetics. fms-Like Tyrosine Kinase 3 / genetics. ras Proteins / genetics



52. McVey M, Cserti-Gazdewich CM: Platelet transfusion refractoriness responding preferentially to single donor aphaeresis platelets compatible for both ABO and HLA. Transfus Med; 2010 Oct;20(5):346-53
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Patient 1, age 59 years, group O, with myelodysplastic syndrome/acute myelogenous leukemia (MDS/AML), was unresponsive to either fresh ABO-m or HLA-m platelets.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2010 The Authors. Transfusion Medicine © 2010 British Blood Transfusion Society.
  • (PMID = 20492602.001).
  • [ISSN] 1365-3148
  • [Journal-full-title] Transfusion medicine (Oxford, England)
  • [ISO-abbreviation] Transfus Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABO Blood-Group System; 0 / HLA Antigens
  •  go-up   go-down



53. Li X, Wu LY, Ying SX, Chang CK, He Q, Song LQ, Pu Q: [Preliminary study of biological characteristics of myelodysplastic syndromes clonal cells]. Zhonghua Xue Ye Xue Za Zhi; 2007 Jul;28(7):478-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Preliminary study of biological characteristics of myelodysplastic syndromes clonal cells].
  • OBJECTIVE: To investigate the biological difference of clonal cells between myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML).
  • METHOD: Bone marrow (BM) clonal cells (which had cytogenetic markers detected by FISH assay) and blasts were quantitatively analysed in 51 MDS and 11 AML patients.
  • The biological functions for phagocytosis and oxidation of MDS peripheral blood (PB) neutrophils were compared with that of normal controls.
  • RESULTS: Almost all MDS patients BM had a higher clonal cell percentage (mean 48.2%) than blasts percentage (mean 6.7%) (P < 0.01), but with the subtype of MDS advancing this percentage gap was closing up, and in 11 AML patients no such gap was observed.
  • This gap in MDS patients with + 8 abnormality was smaller than in those with 5q -.
  • In MDS BM, clonal cells were detected in segmented granulocytes (mean 45.9%), orthochromatic normoblasts (mean 46.0%) and mature megakaryocytes (mean 38.0%).
  • In Addition, an approximate amount of clonal cells with the same karyotype abnormality in BM were detected in MDS PB (mean 37.3% in blood vs 48.6% in marrow).
  • Functional analysis showed that the neutrophils in MDS PB could exert nearly normal physiological functions (P > 0.05), but those from AML could not as compared to healthy donors (P < 0.01).
  • CONCLUSION: There is a significant difference in the biological features between MDS and AML clonal cells.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology



54. Iwai M, Kiyoi H, Ozeki K, Kinoshita T, Emi N, Ohno R, Naoe T: Expression and methylation status of the FHIT gene in acute myeloid leukemia and myelodysplastic syndrome. Leukemia; 2005 Aug;19(8):1367-75
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and methylation status of the FHIT gene in acute myeloid leukemia and myelodysplastic syndrome.
  • To clarify the role of fragile histidine triad (FHIT) in hematological malignancies, we examined the methylation status and the expression level of the FHIT gene in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) cells in comparison with the methylation of the p15(INK4B) gene.
  • The FHIT methylation was found in 13 of 94 (13.8%) AML and 22 of 40 (55.0%) MDS cases, but not in normal mononuclear cells (MNCs).
  • Both the frequency and density of methylation increased in the advanced-stages MDS and the relapsed AML cases.
  • Although FHIT and p15(INK4B) methylations were not correlated in MDS and AML, increased FHIT methylation at the relapse in AML was associated with p15(INK4B) methylation.
  • The median expression level in AML was significantly higher than in normal MNCs, although the median expression level in those with methylation was significantly lower than in those without methylation.
  • Furthermore, the methylation level at relapse was significantly higher than at diagnosis in AML.
  • These results suggested that FHIT methylation was accumulated through the disease progression of MDS and AML, and the role of the FHIT gene as a tumor suppressor seemed different in AML and MDS.
  • [MeSH-major] Acid Anhydride Hydrolases / genetics. DNA Methylation. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Neoplasm Proteins / genetics
  • [MeSH-minor] Acute Disease. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Bone Marrow / pathology. Cell Cycle Proteins / genetics. Cyclin-Dependent Kinase Inhibitor p15. Genes, Tumor Suppressor. Humans. RNA, Messenger / analysis. Recurrence. Tumor Suppressor Proteins / genetics

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Leukemia (2005) 19, 1367-1375.
  • (PMID = 15902282.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; 0 / fragile histidine triad protein; 776B62CQ27 / decitabine; EC 3.6.- / Acid Anhydride Hydrolases; M801H13NRU / Azacitidine
  •  go-up   go-down



55. Reindl C, Quentmeier H, Petropoulos K, Greif PA, Benthaus T, Argiropoulos B, Mellert G, Vempati S, Duyster J, Buske C, Bohlander SK, Humphries KR, Hiddemann W, Spiekermann K: CBL exon 8/9 mutants activate the FLT3 pathway and cluster in core binding factor/11q deletion acute myeloid leukemia/myelodysplastic syndrome subtypes. Clin Cancer Res; 2009 Apr 1;15(7):2238-47
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CBL exon 8/9 mutants activate the FLT3 pathway and cluster in core binding factor/11q deletion acute myeloid leukemia/myelodysplastic syndrome subtypes.
  • In this study, we determined the frequency of CBL mutations in acute leukemias and evaluated the oncogenic potential of mutant CBL.
  • EXPERIMENTAL DESIGN: The cDNA of 300 acute myeloid leukemia (AML)/myelodysplastic syndrome (MDS) and acute lymphoblastic leukemia (ALL) patients and 82 human leukemic cell lines was screened for aberrations in the linker and RING finger domain of CBL.
  • RESULTS: We identified 3 of 279 AML/MDS patients expressing CBL exon 8/9 deletion mutants.
  • One of 116 sequenced AML/MDS cases carried a R420G missense mutation.
  • All AML/MDS patients with identified CBL mutants belonged to the core binding factor and 11q deletion AML subtypes.
  • CONCLUSION: CBL exon8/9 mutants occur in genetically defined AML/MDS subtypes and transform hematopoietic cells by constitutively activating the FLT3 pathway.
  • This phenotype resembles the one of mutated RTKs and suggests that CBL mutant AML patients might benefit from treatment with FLT3 PTK inhibitors.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins c-cbl / genetics. fms-Like Tyrosine Kinase 3 / metabolism



56. Cashen AF, Shah AK, Todt L, Fisher N, DiPersio J: Pharmacokinetics of decitabine administered as a 3-h infusion to patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS). Cancer Chemother Pharmacol; 2008 Apr;61(5):759-66
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacokinetics of decitabine administered as a 3-h infusion to patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
  • PURPOSE: In this study, pharmacokinetics (PK) of decitabine administered as a 3-h intravenous infusion of 15 mg/m2 every 8 h for 3 days (cycles repeated every 6 weeks) was evaluated in patients with MDS or AML.
  • METHODS: The PK of this dosing regimen was evaluated in sixteen patients with MDS or AML.
  • CONCLUSIONS: Decitabine dosed at 15 mg/m2 iv every 8 h for 3 days resulted in a predictable and manageable toxicity profile in patients with MDS/AML.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacokinetics. Azacitidine / analogs & derivatives. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy



57. Epling-Burnette PK, Loughran TP Jr: Suppression of farnesyltransferase activity in acute myeloid leukemia and myelodysplastic syndrome: current understanding and recommended use of tipifarnib. Expert Opin Investig Drugs; 2010 May;19(5):689-98
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Suppression of farnesyltransferase activity in acute myeloid leukemia and myelodysplastic syndrome: current understanding and recommended use of tipifarnib.
  • IMPORTANCE OF THE FIELD: Acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) incidence in the United States increases with age.
  • There is an acute need for therapeutic developments because of the poor prognosis of these diseases.
  • Since the knowledge of molecular genetics in AML and MDS has expanded recently, targeted therapeutics should offer an exciting new frontier for advancement.
  • AREAS COVERED IN THIS REVIEW: Described in this review are the molecular targets of tipifarnib, safety and tolerability of the drug, chemistry, and clinical efficacy in AML.
  • WHAT THE READER WILL GAIN: The reader will gain a thorough understanding of tipifarnib as it relates to the current and future use of the drug in AML.
  • TAKE HOME MESSAGE: The future of tipifarnib, along with other molecularly-targeted drugs, lies in achieving a better understanding of leukemia biology and harnessing the activity of this agent using predictive biomarkers for improved patient selection.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Quinolones / therapeutic use



58. Pan F, Peng S, Fleurence R, Linnehan JE, Knopf K, Kim E: Economic analysis of decitabine versus best supportive care in the treatment of intermediate- and high-risk myelodysplastic syndromes from a US payer perspective. Clin Ther; 2010 Dec;32(14):2444-56
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Economic analysis of decitabine versus best supportive care in the treatment of intermediate- and high-risk myelodysplastic syndromes from a US payer perspective.
  • BACKGROUND: Myelodysplastic syndromes (MDS) are blood and bone marrow disorders that occur primarily in the elderly population, with 30% of all cases progressing to acute myeloid leukemia (AML).
  • Red blood cell transfusions--a conventional treatment of MDS--have been associated with high costs and decreased quality of life compared with transfusion independence.
  • Phase III clinical trial data suggest that decitabine may offer an improved AML-free survival versus best supportive care (BSC), which consists of red blood cell transfusions, deferoxamine, erythropoiesis-stimulating agents, platelet transfusions, and colony-stimulating factors.
  • OBJECTIVE: The aim of this study was to assess the cost-effectiveness of 5-day dosing of decitabine versus BSC in US patients with intermediate- and high-risk MDS from a US payer perspective.
  • METHODS: A Markov model with 3 health states (MDS, AML, and death) was constructed to simulate natural disease progression.
  • Drug and AML costs were obtained from published sources.
  • RESULTS: In the base-case model, decitabine yielded 0.276 additional year of AML-free survival and 0.052 more quality-adjusted life-year (QALY) compared with BSC.
  • CONCLUSION: In this study, decitabine administered on a 5-day dosing schedule was likely a cost-effective treatment option in patients with intermediate- and high-risk MDS from a US payer perspective.
  • [MeSH-major] Antimetabolites, Antineoplastic / economics. Azacitidine / analogs & derivatives. Drug Costs. Models, Economic. Myelodysplastic Syndromes / drug therapy. Patient Care / economics
  • [MeSH-minor] Clinical Trials, Phase III as Topic. Cost-Benefit Analysis. Disease-Free Survival. Drug Administration Schedule. Humans. Leukemia, Myeloid, Acute / economics. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / prevention & control. Markov Chains. Randomized Controlled Trials as Topic. Risk. United States



59. Hasserjian RP, Zuo Z, Garcia C, Tang G, Kasyan A, Luthra R, Abruzzo LV, Kantarjian HM, Medeiros LJ, Wang SA: Acute erythroid leukemia: a reassessment using criteria refined in the 2008 WHO classification. Blood; 2010 Mar 11;115(10):1985-92
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute erythroid leukemia: a reassessment using criteria refined in the 2008 WHO classification.
  • Acute erythroid leukemia (AEL) is a rare type of acute myeloid leukemia (AML) for which diagnostic criteria have been refined in the 2008 World Health Organization (WHO) classification of AML.
  • The relationship of AEL to myelodysplastic syndromes (MDSs) and to AML with myelodysplasia-related changes (AML-MRC) is not clearly defined.
  • We conducted a retrospective, multi-institutional study of patients with AEL and compared them with patients with MDS or AML-MRC with erythroid hyperplasia (> or = 50% erythroid cells).
  • Among a total of 124 patients with AEL, 32% had a history of MDS or chronic cytopenia, 32% had therapy-related disease, and 35% had de novo disease.
  • Sixty-four percent of patients had unfavorable AML risk-group karyotypes.
  • The median overall survival (OS) of all AEL patients was 8 months, comparable with that of patients with MDS or AML-MRC with erythroid hyperplasia.
  • The OS was related to cytogenetic risk group, but not blast count or morphologic dysplasia.
  • Our findings suggest that AEL is in the continuum of MDS and AML with erythroid hyperplasia, where karyotype rather than an arbitrary blast cutoff represents the most important prognostic factor.
  • [MeSH-major] Classification / methods. Leukemia, Erythroblastic, Acute / classification. World Health Organization

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 2002 Aug;16(8):1399-401 [12145675.001]
  • [Cites] Leukemia. 2009 Dec;23(12):2275-80 [19741728.001]
  • [Cites] Leuk Res. 2003 May;27(5):397-404 [12620291.001]
  • [Cites] Blood. 2003 Apr 1;101(7):2895-6 [12642345.001]
  • [Cites] Ann Intern Med. 1985 Oct;103(4):620-5 [3862359.001]
  • [Cites] Blood. 1992 Dec 1;80(11):2873-82 [1450412.001]
  • [Cites] Blood. 1997 Mar 15;89(6):2079-88 [9058730.001]
  • [Cites] Leuk Res. 1997 May;21(5):415-25 [9225069.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1567-72 [16049515.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Dec;163(2):113-22 [16337853.001]
  • [Cites] Br J Haematol. 2006 Jan;132(2):162-7 [16398650.001]
  • [Cites] Am J Clin Pathol. 2006 Oct;126(4):530-3 [16938665.001]
  • [Cites] Am J Clin Pathol. 2007 Feb;127(2):197-205 [17210514.001]
  • [Cites] Blood. 2007 Dec 15;110(13):4385-95 [17726160.001]
  • [Cites] Blood. 2008 Feb 15;111(4):1855-61 [18056840.001]
  • [Cites] J Clin Oncol. 2008 Oct 10;26(29):4791-7 [18695255.001]
  • [Cites] Mod Pathol. 2008 Nov;21(11):1394-402 [18839018.001]
  • [Cites] Blood. 2009 Feb 26;113(9):1906-8 [19131546.001]
  • [Cites] Mod Pathol. 2009 Aug;22(8):1023-31 [19430420.001]
  • [Cites] Blood. 2002 Nov 1;100(9):3135-40 [12384410.001]
  • (PMID = 20040759.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / UL1 RR024153
  • [Publication-type] Evaluation Studies; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2942006
  •  go-up   go-down



60. Greiner RA, Meier Y, Papadopoulos G, O'Sullivan AK, Imhof A: Cost-effectiveness of posaconazole compared with standard azole therapy for prevention of invasive fungal infections in patients at high risk in Switzerland. Oncology; 2010;78(3-4):172-80
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Decision tree models based on the results of two registration trials and subsequent Markov models over patient lifetimes were developed for patients with acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS) with neutropenia and for hematopoietic stem cell transplant recipients with graft-versus-host disease (GVHD).
  • RESULTS: By reducing IFIs in AML/MDS patients with posaconazole prophylaxis, the contained IFI-related treatment costs more than compensated for the incremental cost of posaconazole, resulting in savings of CHF 1,118 per patient.
  • [MeSH-minor] Cost-Benefit Analysis. Decision Support Techniques. Graft vs Host Disease / therapy. Hematopoietic Stem Cell Transplantation. Humans. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Markov Chains. Models, Theoretical. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / drug therapy. Neutropenia / complications. Neutropenia / drug therapy. Risk. Switzerland. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Fungal Infections.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20414005.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Triazoles; 6TK1G07BHZ / posaconazole
  •  go-up   go-down



61. Grant S: New agents for AML and MDS. Best Pract Res Clin Haematol; 2009 Dec;22(4):501-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New agents for AML and MDS.
  • The heterogeneity of acute myeloid leukaemia (AML) and myelodysplastic syndromes (MDS) has led to a multiplicity of treatments, from cytotoxic agents to signal transduction modulators, cell-cycle inhibitors and epigenetic therapies.
  • While some have shown promising initial results, the outlook for AML patients, particularly older and relapsed patients, as well as patients whose cells exhibit certain adverse chromosomal abnormalities or mutant oncoproteins, continues to be grim.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Invest. 2008 Sep;118(9):3003-6 [18725993.001]
  • [Cites] Blood. 2008 Sep 1;112(5):1638-45 [18565853.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4603-9 [18559876.001]
  • [Cites] Leukemia. 2008 Nov;22(11):2091-6 [18685609.001]
  • [Cites] Cancer Cell. 2008 Dec 9;14(6):485-93 [19061839.001]
  • [Cites] Clin Cancer Res. 2008 Dec 15;14(24):8102-11 [19088025.001]
  • [Cites] Ann Hematol. 2009 Mar;88(3):213-9 [18696067.001]
  • [Cites] Lancet Oncol. 2009 Mar;10(3):223-32 [19230772.001]
  • [Cites] Cancer Res. 2009 Apr 1;69(7):3032-41 [19318574.001]
  • [Cites] Blood. 2009 Apr 23;113(17):3938-46 [19029442.001]
  • [Cites] Expert Opin Investig Drugs. 2007 Jul;16(7):1111-20 [17594194.001]
  • [Cites] Cancer Res. 2007 Jul 15;67(14):6916-24 [17638903.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2302-8 [17596541.001]
  • [Cites] Chem Biol. 2007 Oct;14(10):1186-97 [17961830.001]
  • [Cites] Blood. 2007 Dec 15;110(13):4427-35 [17804695.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1060-6 [17962510.001]
  • [Cites] Leuk Res. 2008 May;32(5):771-80 [18031811.001]
  • [Cites] Cell. 2003 Dec 12;115(6):727-38 [14675537.001]
  • [Cites] Invest New Drugs. 2005 Jan;23(1):31-7 [15528978.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4163-9 [15687234.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4261-8 [16150937.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6361-9 [16778214.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1254-60 [16642049.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3271-9 [16882711.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2006;:178-84 [17124058.001]
  • [Cites] J Clin Oncol. 2007 Jan 1;25(1):25-31 [17146105.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1387-94 [17082323.001]
  • [Cites] Cell. 2007 Feb 23;128(4):683-92 [17320506.001]
  • [Cites] Clin Cancer Res. 2008 May 15;14(10):3077-82 [18483374.001]
  • [Cites] Blood. 2008 Aug 15;112(4):981-9 [18495956.001]
  • [Cites] Cancer Control. 2008 Oct;15 Suppl:40-9 [18813208.001]
  • (PMID = 19959100.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R21 CA115260-01; United States / NCI NIH HHS / CA / P50 CA130805-02; United States / NCI NIH HHS / CA / CA63753; United States / NCI NIH HHS / CA / RC2 CA148431-01; United States / NCI NIH HHS / CA / R01 CA063753-13; United States / NCI NIH HHS / CA / R01 CA100866; United States / NCI NIH HHS / CA / R01 CA063753; United States / NCI NIH HHS / CA / R01 CA100866-04; United States / NCI NIH HHS / CA / P50CA130805; United States / NCI NIH HHS / CA / R01 CA093738; United States / CCR NIH HHS / RC / RC2 CA148431-01; United States / NCI NIH HHS / CA / CA100866; United States / NCI NIH HHS / CA / P50 CA130805; United States / NCI NIH HHS / CA / RC2 CA148431; United States / NCI NIH HHS / CA / R01 CA093738-05A2; United States / NCI NIH HHS / CA / CA93738; United States / NCI NIH HHS / CA / R21 CA115260
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytotoxins; 0 / Protein Kinase Inhibitors
  • [Number-of-references] 38
  • [Other-IDs] NLM/ NIHMS157911; NLM/ PMC2793080
  •  go-up   go-down



62. Graubert T: AML1 and Evi1: coconspirators in MDS/AML? Blood; 2008 Apr 15;111(8):3916-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AML1 and Evi1: coconspirators in MDS/AML?
  • In this issue of Blood, Watanabe-Okochi and colleagues use a mouse bone marrow transplantation model to demonstrate that mutant alleles of AML1 (RUNX1) can initiate a myelodysplastic syndrome (MDS) that progresses to acute myelogenous leukemia (AML) in association with overexpression of Evi1.

  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • 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
  • [CommentOn] Blood. 2008 Apr 15;111(8):4297-308 [18192504.001]
  • (PMID = 18434965.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  •  go-up   go-down



63. Park MJ, Park YH, Ahn HJ, Choi W, Paik KH, Kim JM, Chang YH, Ryoo BY, Yang SH: Secondary hematological malignancies after breast cancer chemotherapy. Leuk Lymphoma; 2005 Aug;46(8):1183-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • According to several reports, the 10 year incidence of secondary acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS) after systemic chemotherapy is approximately 1.5%.
  • We detected 2 cases of secondary AML and 1 case of MDS, 19, 52 and 12 months, respectively, after systemic chemotherapy for breast cancer.
  • Published data on the occurrence of secondary hematological malignancies other than AML or MDS in this setting are scarce.



64. Balleisen S, Kuendgen A, Hildebrandt B, Haas R, Germing U: Prognostic relevance of achieving cytogenetic remission in patients with acute myelogenous leukemia or high-risk myelodysplastic syndrome following induction chemotherapy. Leuk Res; 2009 Sep;33(9):1189-93
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic relevance of achieving cytogenetic remission in patients with acute myelogenous leukemia or high-risk myelodysplastic syndrome following induction chemotherapy.
  • Cytogenetic findings at diagnosis have influence on prognosis in patients with acute myelogenous leukaemia (AML) or MDS who undergo induction chemotherapy.
  • Median survival (excluding patients with AML M3) of the CCR group was 37 months, as compared to 11 months in patients with persistence of abnormal karyotype (p < 0.0001).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Remission Induction



65. Harada H, Harada Y, Kimura A: Implications of somatic mutations in the AML1/RUNX1 gene in myelodysplastic syndrome (MDS): future molecular therapeutic directions for MDS. Curr Cancer Drug Targets; 2006 Sep;6(6):553-65
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Implications of somatic mutations in the AML1/RUNX1 gene in myelodysplastic syndrome (MDS): future molecular therapeutic directions for MDS.
  • Myelodysplastic syndrome (MDS) is a clonal disorder of hematopoietic stem cells characterized by ineffective and inadequate hematopoiesis.
  • MDS is also a susceptibility to acute myeloid leukemia (AML) and shown to be extremely resistant to current therapeutic strategies.
  • MDS in a subset of 10-20% of patients arise after previous chemotherapy or radiation exposure for other malignancies.
  • Because MDS is a heterogeneous disorder, specific gene abnormalities playing a role in the myelodysplastic process have been difficult to identify.
  • Cytogenetic abnormalities are seen in half of MDS patients, and generally consist of partial or complete chromosome deletion or addition, whereas balanced translocations are rare.
  • Genes more frequently implicated in the pathogenesis of MDS remain unknown.
  • Although point mutations of critical genes have been demonstrated to contribute to the development MDS, there was no strong correlation between these mutations and clinical features.
  • Recently, we reported the high incidence of somatic mutations in the AML1/RUNX1 gene, which is a critical regulator of definitive hematopoiesis and the most frequent target for translocation of AML, in MDS, especially refractory anemia with excess blasts (RAEB), RAEB in transformation (RAEBt) and AML following MDS (defined here as MDS/AML).
  • The MDS/AML patients with AML1 mutations had a significantly worse prognosis than those without AML1 mutations.
  • Most of AML1/RUNX1 mutants lose trans-activation potential, which leads to a loss of AML1 function indicating that AML1/RUNX1 dysfunction is one of the major pathogenesis of MDS/AML.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Genetic Therapy / trends. Mutation. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / therapy



66. Wang XL, Shao ZH, Yao C, He GS, Liu H, Shi J, Bai J, Cao YR, Tu MF, Wang HQ, Xing LM, Sun J, Jia HR, Yang CL: [Study of Th cell subsets in bone marrow of myelodysplastic syndromes patients]. Zhonghua Xue Ye Xue Za Zhi; 2005 Dec;26(12):743-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Study of Th cell subsets in bone marrow of myelodysplastic syndromes patients].
  • OBJECTIVE: To study the quantity and ratio of Th1, Th2 cells in the bone marrow of myelodysplastic syndromes (MDS) patients, and to evaluate the correlation between the ratio of the blast cells and the number of the Th1 cells in the bone marrow of MDS patients.
  • METHODS: By FACS, the quantity and ratio of IFN-gamma producing CD4(+) T cell (Th1) and IL-4 producing CD4(+) T cell (Th2) cells in the bone marrow were detected in 21 MDS patients, 18 normal controls and 13 severe aplastic anemia (SAA) patients respectively.
  • The karyotypes of 18 MDS patients and 15 normal controls were assayed.
  • The correlation between the ratio of the blast cells in the bone marrow and the number of the Th1 cells in the MDS patients were analyzed.
  • RESULTS: The percentages of Th1 cells, Th2 cells and ratio of Th1/Th2 in the bone marrow of normal controls were (0.48 +/- 0.10)%, (0.24 +/- 0.19)% and 2.31 +/- 0.76 respectively, while those of the MDS patients were (0.36 +/- 0.11)%, (0.76 +/- 0.35)% and 0.51 +/- 0.13.
  • The percentage of Th1 cells of patients with MDS was reduced and the Th1/Th2 ratio was significantly lower than that of normal controls (P < 0.01).
  • In all of the 15 normal controls the karyotypes were normal, but that of MDS patients was (50.00 +/- 0.10)%.
  • The lower ratio of the Th1 cells in the bone marrow of the patients with MDS and the AML which progressed from MDS was negatively correlated with the higher percentage of the blast cells (r = -0.563, P < 0.01). CONCLUSIONS:.
  • (1) The immune function of T lymphocytes in MDS is abnormal: the balance between Th1 and Th2 cells is broken. (2) With descending of the number of Th1 cells in the bone marrow of the MDS patients, the disease is progressing to leukemia.
  • [MeSH-major] Bone Marrow / immunology. Myelodysplastic Syndromes / immunology. T-Lymphocytes, Helper-Inducer / immunology



67. Andersson BS, de Lima M, Thall PF, Madden T, Russell JA, Champlin RE: Reduced-toxicity conditioning therapy with allogeneic stem cell transplantation for acute leukemia. Curr Opin Oncol; 2009 Jun;21 Suppl 1:S11-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reduced-toxicity conditioning therapy with allogeneic stem cell transplantation for acute leukemia.
  • We hypothesized that standardized systemic drug delivery would improve treatment safety and provide better leukemia control.
  • We used a Bayesian method to compare the outcomes of 67 acute myeloid leukemia (AML)/myelodysplastic syndrome (MDS) patients who received intravenous busulfan-cyclophosphamide (BuCy2) with 148 subsequent AML/MDS patients who received busulfan-fludarabine (Bu-Flu).
  • Overall, the data support replacing BuCy2 with or without antithymocyte globulin (ATG) with Bu-Flu with or without rabbit-ATG for AML or MDS.
  • The extremely low one-year treatment-related mortality as well as high overall and event-free survival of patients in the Bu-Flu group indicate that it is time to revisit the value of alloSCT compared with conventional maintenance chemotherapy for patients in first complete remission of AML/MDS.

  • 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 .
  • Hazardous Substances Data Bank. VIDARABINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Transplant Proc. 1996 Dec;28(6):3101 [8962201.001]
  • [Cites] Bone Marrow Transplant. 2000 May;25(9):915-24 [10800057.001]
  • [Cites] Bone Marrow Transplant. 1998 Sep;22(5):439-43 [9733266.001]
  • [Cites] J Clin Oncol. 2005 Apr 1;23(10):2208-14 [15753460.001]
  • [Cites] J Clin Oncol. 2000 Jan;18(2):348-57 [10637249.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Jun;14(6):672-84 [18489993.001]
  • [Cites] Blood. 2001 Feb 1;97(3):631-7 [11157478.001]
  • [Cites] Cancer Chemother Pharmacol. 2001 Aug;48 Suppl 1:S53-8 [11587368.001]
  • [Cites] Blood. 2001 Dec 15;98(13):3569-74 [11739158.001]
  • [Cites] Clin Pharmacokinet. 2002;41(2):93-103 [11888330.001]
  • [Cites] Biol Blood Marrow Transplant. 2002;8(3):145-54 [11939604.001]
  • [Cites] Br J Haematol. 2002 Aug;118(2):385-400 [12139722.001]
  • [Cites] Biol Blood Marrow Transplant. 2002;8(9):477-85 [12374452.001]
  • [Cites] Blood. 2003 Mar 1;101(5):2043-8 [12406916.001]
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1352-8 [12663726.001]
  • [Cites] Bone Marrow Transplant. 2004 Jun;33(12):1191-9 [15122310.001]
  • [Cites] Blood. 2004 Aug 1;104(3):857-64 [15073038.001]
  • [Cites] N Engl J Med. 1983 Dec 1;309(22):1347-53 [6355849.001]
  • [Cites] Blood. 1987 Nov;70(5):1382-8 [3311203.001]
  • [Cites] Blood. 1993 Apr 15;81(8):2187-93 [8471778.001]
  • [Cites] Cancer Chemother Pharmacol. 1996;37(5):401-8 [8599861.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Feb;14(2):220-8 [18215782.001]
  • [Cites] N Engl J Med. 1997 Mar 27;336(13):897-904 [9070469.001]
  • (PMID = 19561406.001).
  • [ISSN] 1531-703X
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA055164; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 2P01 CA55164; United States / NCI NIH HHS / CA / 2P30CA16672-26
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ NIHMS588342; NLM/ PMC4037323
  •  go-up   go-down



68. Babicka L, Ransdorfova S, Brezinova J, Zemanova Z, Sindelarova L, Siskova M, Maaloufova J, Cermak J, Michalova K: Analysis of complex chromosomal rearrangements in adult patients with MDS and AML by multicolor FISH. Leuk Res; 2007 Jan;31(1):39-47
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of complex chromosomal rearrangements in adult patients with MDS and AML by multicolor FISH.
  • We analyzed complex chromosomal aberrations in 37 adult patients with myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) using classical cytogenetic method, FISH with locus-specific probes, multicolor FISH (mFISH) and multicolor banding (mBAND).
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human / genetics. Gene Rearrangement / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics



69. Bernasconi P, Klersy C, Boni M, Cavigliano PM, Giardini I, Rocca B, Zappatore R, Dambruoso I, Calvello C, Caresana M, Lazzarino M: Does cytogenetic evolution have any prognostic relevance in myelodysplastic syndromes? A study on 153 patients from a single institution. Ann Hematol; 2010 Jun;89(6):545-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does cytogenetic evolution have any prognostic relevance in myelodysplastic syndromes? A study on 153 patients from a single institution.
  • The present study was designed to establish the incidence of cytogenetic evolution (CE), defined as the acquisition of chromosomal defects during the course of MDS, in order to correlate it with the WHO classification and IPSS score, and to assess its impact on overall survival (OS) and risk of MDS/AML evolution (progression-free interval, PFI) by means of Cox models for time-dependent covariates.
  • The study was carried out in 153 MDS patients who were followed for a median period of 45.2 months.
  • Our study shows that (1) CE was more common in advanced than in early MDS, and advanced MDS presented secondary chromosomal defects distinct from those of early MDS;.
  • [MeSH-major] Myelodysplastic Syndromes / diagnosis. Myelodysplastic Syndromes / genetics



70. Teng Y, Liu Q, Ma J, Liu F, Han Z, Wang Y, Wang W: Cloning, expression and characterization of a novel human CAP10-like gene hCLP46 from CD34(+) stem/progenitor cells. Gene; 2006 Apr 12;371(1):7-15
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A novel human gene, named as human CAP10-like protein 46 kDa (hCLP46), was isolated and identified from human acute myeloid leukemia transformed from myelodysplastic syndrome (MDS-AML) CD34(+) cells. hCLP46 (3q13.33) contains 11 exons encoding a putative protein of 392 amino acids, with a highly conserved CAP10 domain, a hydrophobic signal peptide at its N-terminus, and an endoplasmic reticulum (ER) retention signal motif KTEL at the C-terminus.
  • [MeSH-major] Antigens, CD34. Chromosomes, Human, Pair 3 / genetics. Gene Expression Regulation, Leukemic / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / genetics. Neoplastic Stem Cells. Proteins / genetics
  • [MeSH-minor] Amino Acid Sequence. Endoplasmic Reticulum / genetics. Glucosyltransferases. Humans. Molecular Sequence Data. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / metabolism. Myelodysplastic Syndromes / pathology. Organ Specificity / genetics. Protein Structure, Tertiary / genetics. Sequence Homology, Amino Acid. U937 Cells



71. Buchmann I, Meyer RG, Herr W, Helisch A, Bartenstein P: [Radioimmunotherapy for treatment of acute myeloid leukaemia and myelodysplastic syndrome: conceptual chances]. Nuklearmedizin; 2005;44(3):107-17; quiz N21-2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Radioimmunotherapy for treatment of acute myeloid leukaemia and myelodysplastic syndrome: conceptual chances].
  • The prognosis of patients with acute myeloid leukaemia (AML) has improved considerably by introduction of aggressive consolidation chemotherapy and haematopoietic stem cell transplantation (SCT).
  • Nevertheless, only 20-30% of patients with AML achieve long-term disease-free survival after SCT.
  • Including radioimmunotherapies in the treatment of AML and myelodyplastic syndrome (MDS) allows for the achievement of a pronounced antileukaemic effect for the reduction of relapse rates on the one hand.
  • On the other hand, no increase of acute toxicity and later complications should be induced.
  • This paper provides a systematic and critical review of the currently used radionuclides and immunoconjugates for the treatment of AML and MDS and summarizes the literature on primary tumour cell reductive radioimmunotherapies on the one hand and conditioning radioimmunotherapies before SCT on the other hand.
  • [MeSH-major] Leukemia, Myeloid, Acute / radiotherapy. Myelodysplastic Syndromes / radiotherapy. Radioimmunotherapy



72. Liu YC, Miyazawa K, Sashida G, Kodama A, Ohyashiki K: Deletion (20q) as the sole abnormality in Waldenström macroglobulinemia suggests distinct pathogenesis of 20q11 anomaly. Cancer Genet Cytogenet; 2006 Aug;169(1):69-72
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The deletion of the long arm of chromosome 20, or del(20q), is a common cytogenetic abnormality in various myeloid disorders but is less commonly seen in lymphoid neoplasms.
  • Reviewing all 11 reported cases of plasma cell dyscrasia possessing sole del(20q), including our case, none of 4 cases with del(20q) as an initial anomaly developed myelodysplastic syndrome-acute myeloid leukemia (MDS/AML), but at least 3 cases with del(20q) appearing after chemotherapy developed MDS/AML at or after the time of del(20q).
  • We propose that the del(20q) may have different clinical significance in plasma cell dyscrasia: one is when del(20q) appears at diagnosis and may involve the initial event of oncogenesis, and the other is when del(20q) appears after treatment and is associated with therapy-related and potential MDS/AML risk.



73. Mihara K, Chowdhury M, Nakaju N, Hidani S, Ihara A, Hyodo H, Yasunaga S, Takihara Y, Kimura A: Bmi-1 is useful as a novel molecular marker for predicting progression of myelodysplastic syndrome and patient prognosis. Blood; 2006 Jan 1;107(1):305-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bmi-1 is useful as a novel molecular marker for predicting progression of myelodysplastic syndrome and patient prognosis.
  • The International Prognostic Scoring System (IPSS) has been widely used to predict the prognosis of patients with myelodysplastic syndrome (MDS).
  • Here, we analyzed the expression of Bmi-1, which is required to regulate the self-renewal in CD34+ cells from 51 patients with cases of MDS and acute myeloid leukemia preceded by MDS (MDS-AML).
  • Higher positivity rate of Bmi-1 was preferentially seen in refractory anemia with excess blasts (RAEB), RAEB in transformation (RAEB-T), and MDS-AML compared with refractory anemia (RA) and RA with ringed sideroblasts (RARS).
  • Here, we propose Bmi-1 as a novel molecular marker to predict the progression and prognosis of MDS.
  • [MeSH-major] Myelodysplastic Syndromes / diagnosis. Nuclear Proteins / analysis. Proto-Oncogene Proteins / analysis. Repressor Proteins / analysis
  • [MeSH-minor] Aged. Aged, 80 and over. Anemia, Refractory / diagnosis. Antigens, CD34. Biomarkers / analysis. Bone Marrow / chemistry. Bone Marrow / pathology. Case-Control Studies. Cell Proliferation. Disease Progression. Female. Humans. Leukemia, Myeloid. Male. Middle Aged. Polycomb Repressive Complex 1. Prognosis

  • Genetic Alliance. consumer health - Myelodysplastic syndromes.
  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16160010.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / BMI1 protein, human; 0 / Biomarkers; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; EC 6.3.2.19 / Polycomb Repressive Complex 1
  •  go-up   go-down



74. Sun Y, Cook JR: Fluorescence in situ hybridization for del(5q) in myelodysplasia/acute myeloid leukemia: comparison of EGR1 vs. CSF1R probes and diagnostic yield over metaphase cytogenetics alone. Leuk Res; 2010 Mar;34(3):340-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fluorescence in situ hybridization for del(5q) in myelodysplasia/acute myeloid leukemia: comparison of EGR1 vs. CSF1R probes and diagnostic yield over metaphase cytogenetics alone.
  • To determine the clinical utility of FISH for del(5q) in MDS/AML, we first compared FISH for 5q31 (EGR1) and 5q33 (CSF1R) in 51 myeloid neoplasms containing del(5q) by metaphase cytogenetics.
  • Next, EGR1 FISH was compared to metaphase cytogenetics alone in 269 cases of known or suspected MDS/AML.
  • EGR1 FISH detects del(5q) in a broad variety of myeloid neoplasms, including at least most cases of 5q- syndrome, while studies for CSF1R add little to the diagnostic yield.
  • [MeSH-major] Cytogenetics / methods. In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Receptors, Colony-Stimulating Factor / genetics



76. Ma W, Kantarjian H, Bekele B, Donahue AC, Zhang X, Zhang ZJ, O'Brien S, Estey E, Estrov Z, Cortes J, Keating M, Giles F, Albitar M: Proteasome enzymatic activities in plasma as risk stratification of patients with acute myeloid leukemia and advanced-stage myelodysplastic syndrome. Clin Cancer Res; 2009 Jun 1;15(11):3820-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Proteasome enzymatic activities in plasma as risk stratification of patients with acute myeloid leukemia and advanced-stage myelodysplastic syndrome.
  • PURPOSE: Cytogenetic abnormalities are currently the most important predictors of response and clinical outcome for patients with acute myeloid leukemia (AML) or advanced-stage myelodysplastic syndrome (MDS).
  • EXPERIMENTAL DESIGN: We assessed the utility of measuring pretreatment proteasome chymotrypsin-like, caspase-like, and trypsin-like activities in plasma to predict response and survival of patients with AML (n = 174) or advanced-stage MDS (n = 52).
  • RESULTS: All three enzymatic activities were significantly (P < 0.001) increased in the plasma of patients with AML and MDS compared with normal controls.
  • CONCLUSIONS: Measuring plasma chymotrypsin-like activity may provide a powerful biomarker for risk stratification in patients with AML and advanced-stage MDS, including those with normal karyotype.
  • [MeSH-major] Leukemia, Myeloid / blood. Myelodysplastic Syndromes / blood. Proteasome Endopeptidase Complex / blood
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Caspases / blood. Caspases / metabolism. Chymotrypsin / blood. Chymotrypsin / metabolism. Female. Humans. Male. Middle Aged. Multivariate Analysis. Neoplasm Staging. Prognosis. Risk Factors. Survival Analysis. Trypsin / blood. Trypsin / metabolism. Young Adult



77. Ebihara Y, Manabe A, Tsuruta T, Ishikawa K, Hasegawa D, Ohtsuka Y, Kawasaki H, Ogami K, Wada Y, Kanda T, Tsuji K: The effect of donor leukocyte infusion on refractory pure red blood cell aplasia after allogeneic stem cell transplantation in a patient with myelodysplastic syndrome developing from Kostmann syndrome. Int J Hematol; 2007 Dec;86(5):446-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effect of donor leukocyte infusion on refractory pure red blood cell aplasia after allogeneic stem cell transplantation in a patient with myelodysplastic syndrome developing from Kostmann syndrome.
  • We describe the clinical course of a patient who experienced refractory pure red cell aplasia (PRCA) after undergoing HLA-matched allogeneic peripheral blood stem cell transplantation (allo-PBSCT) for refractory anemia with an excess of blasts in transformation that had evolved from Kostmann syndrome.
  • The treatment for patients with myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML) developing from Kostmann syndrome has not been standardized.
  • Myeloid and platelet recoveries were achieved rapidly.
  • The results indicate that the conditioning regimen we describe seems safe and effective for those who have MDS/AML and that DLI might be a valuable approach for refractory PRCA after ABO-incompatible SCT.
  • [MeSH-major] Leukocyte Transfusion. Living Donors. Myelodysplastic Syndromes / therapy. Myelopoiesis. Peripheral Blood Stem Cell Transplantation. Red-Cell Aplasia, Pure / therapy
  • [MeSH-minor] Child. Cyclophosphamide / administration & dosage. Graft Survival. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Immunosuppressive Agents / administration & dosage. Infant. Male. Myeloablative Agonists / administration & dosage. Recombinant Proteins. Remission Induction. Syndrome. Transplantation, Homologous. Whole-Body Irradiation



78. Stone R, Sekeres M, Garcia-Manero G: Evolving strategies in the treatment of MDS and AML. Clin Adv Hematol Oncol; 2009 Aug;7(8):1-14; quiz 2 p following 14
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evolving strategies in the treatment of MDS and AML.
  • Myelodysplastic syndrome (MDS) is a clonal hematopoietic disorder characterized by a hyperproliferative bone marrow, cellular dysplasia, and ineffective hematopoiesis.
  • The treatment of MDS involves improving patient survival and quality of life while decreasing the likelihood of progression to acute myelogenous leukemia (AML).
  • In addition to supportive care with transfusions and hematopoietic growth factors as well as stem cell transplantation, three chemotherapeutic agents have been approved to treat MDS--lenalidomide, azacitidine, and decitabine.
  • In addition, multiple agents and novel combinations are currently in development to treat both MDS AML.
  • Several clinical studies which have investigated these therapeutic approaches, as well as the incorporation of new tools used in the diagnosis of MDS, have been published since the 2008 American Society of Hematology (ASH) Annual Meeting and Exposition, and are discussed here.
  • [MeSH-major] Education, Medical, Continuing. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy



79. Kuendgen A, Knipp S, Fox F, Strupp C, Hildebrandt B, Steidl C, Germing U, Haas R, Gattermann N: Results of a phase 2 study of valproic acid alone or in combination with all-trans retinoic acid in 75 patients with myelodysplastic syndrome and relapsed or refractory acute myeloid leukemia. Ann Hematol; 2005 Dec;84 Suppl 1:61-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Results of a phase 2 study of valproic acid alone or in combination with all-trans retinoic acid in 75 patients with myelodysplastic syndrome and relapsed or refractory acute myeloid leukemia.
  • Valproic acid (VPA) inhibits histone deacetylase activity and induces differentiation of acute myeloid leukemia (AML) blasts in vitro.
  • We observed clinical responses to VPA in patients with myelodysplastic syndrome (MDS) and AML.
  • Hematological improvement, according to international working group criteria for MDS, was observed in 18 patients (24%).
  • We found a response rate of 52% in MDS patients with a normal blast count (refractory sideroblastic anemia, refractory cytopenia with multilineage dysplasia, and refractory sideroblastic cytopenia with multilineage dysplasia).
  • The response rate was 6% in refractory anemia with excess blasts (I + II), 16% in AML, and 0% in chronic myelomonocytic leukemia.
  • We conclude that VPA is clinically useful in low-risk MDS.
  • For patients with high-risk MDS, VPA may be combined with chemotherapy or demethylating drugs.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Histone Deacetylase Inhibitors. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. Valproic Acid / therapeutic use
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Cell Differentiation / drug effects. Female. Histone Deacetylases / drug effects. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Remission Induction. Treatment Outcome. Tretinoin / administration & dosage



80. Tabata R, Tabata C, Omori K, Nagai T: Disappearing myelodysplastic syndrome-associated hemolytic anemia in leukemic transformation. Int Arch Allergy Immunol; 2010;152(4):407-12
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disappearing myelodysplastic syndrome-associated hemolytic anemia in leukemic transformation.
  • BACKGROUND: Here we report 2 rare cases of acute myeloid leukemia (AML) complicated with hemolytic anemia limited to the myelodysplastic syndrome (MDS) stage, and disappearing in leukemic transformation.
  • METHODS/RESULTS: A 66-year-old man with MDS-RAEB-2 was admitted to hospital for severe anemia with increased reticulocyte counts.
  • In another case, a 68-year-old man was admitted to hospital when laboratory findings showed a white blood cell count of 24,800/microl with increased myeloblasts (62.5%), leading to the diagnosis of AML with multilineage dysplasia.
  • Following a decrease in blasts due to anti-cancer drugs, supporting the MDS-RAEB-2 status, severe anemia with increased reticulocytes and positive direct antiglobulin test was diagnosed, suggesting the existence of autoimmune hemolytic anemia, which was then ameliorated by steroid therapy.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Myelodysplastic Syndromes / diagnosis



81. Li LJ, Fu R, Shao ZH, Wang HQ, Yue LZ, Ruan EB, Liu H, Wang J, Wang HL: [Abnormalities of CD34+ cells differentiation and bone marrow cell cycle in myelodysplastic syndrome]. Zhonghua Nei Ke Za Zhi; 2010 Nov;49(11):963-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Abnormalities of CD34+ cells differentiation and bone marrow cell cycle in myelodysplastic syndrome].
  • OBJECTIVES: To detect the abnormalities of CD(34)(+) cells differentiation and bone marrow cell cycle in myelodysplastic syndrome (MDS).
  • METHODS: Fifty newly diagnosed MDS (17 in low risk and 33 in high risk), 8 acute myeloid leukemia preceded by MDS (MDS-AML) and 25 normal controls were enrolled into this study.
  • RESULTS: The mean percentages of CD(34)(+) cells in bone marrow karyocyte of high risk [(2.29 ± 2.17)%] and MDS-AML groups [(18.69 ± 17.47)%] were significantly higher than that of control group [(0.36 ± 0.49)%, P < 0.05].
  • The mean percentages of CD(34)(+)CD(38)(+) cells were significantly lower in low risk, high risk and MDS-AML groups [(86.09 ± 7.79)%, (81.68 ± 11.82)% and (82.88 ± 2.60)%, respectively] than that in control group [(92.21 ± 3.85)%, P < 0.05], thus the percentages of CD(34)(+)CD(38)(-) cells were significantly higher in either MDS (low risk and high risk) or MDS-AML groups [(13.91 ± 7.79)%, (18.32 ± 11.82)% or (17.13 ± 2.60)%, respectively] than that in control group [(7.79 ± 3.85)%, P < 0.05].
  • The percentages of CD(34)(+)CD(38)(-) cells of MDS cases correlated directly with their International Prognostic Scoring System (IPSS) (r = 0.493, P = 0.001) and WHO Adapted Prognostic Scoring System (WPSS) (r = 0.586, P = 0.000) scores.
  • The percentages of bone marrow mononuclear cells (BMMNCs) in G(0)/G(1) phase of in low risk, high risk and MDS-AML groups [(94.52 ± 4.32)%, (96.07 ± 3.88)% and (94.65 ± 4.55)%, respectively] were significantly higher than that in control group [(88.94 ± 7.30)%, P < 0.01], thus the percentages of BMMNCs in S and G(2)/M phase were significantly lower in either MDS (low risk and high risk) or MDS-AML groups than that in control group (P < 0.05).
  • MDS patients with low percentages of CD(34)(+)CD(38)(-) cells presented higher therapeutic efficacy than those with high percentages of CD(34)(+)CD(38)(-) cells, while without significant differences (P > 0.05).
  • CONCLUSIONS: There are abnormalities of differentiation of CD(34)(+) bone marrow cells and high proportion of G(0)/G(1) cells which indicates a G(1) phase arrest in MDS that might be involved in the pathogenesis of MDS.
  • So the examination of CD(34)(+) bone marrow cells and cell cycle might be helpful for MDS diagnosis and assessment of prognosis and therapeutic effects.
  • [MeSH-major] Bone Marrow Cells / cytology. Cell Cycle. Myelodysplastic Syndromes / diagnosis



82. Nand S, Godwin J, Smith S, Barton K, Michaelis L, Alkan S, Veerappan R, Rychlik K, Germano E, Stiff P: Hydroxyurea, azacitidine and gemtuzumab ozogamicin therapy in patients with previously untreated non-M3 acute myeloid leukemia and high-risk myelodysplastic syndromes in the elderly: results from a pilot trial. Leuk Lymphoma; 2008 Nov;49(11):2141-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hydroxyurea, azacitidine and gemtuzumab ozogamicin therapy in patients with previously untreated non-M3 acute myeloid leukemia and high-risk myelodysplastic syndromes in the elderly: results from a pilot trial.
  • Elderly patients with acute myeloid leukemia (AML) and high-risk myelodysplastic syndromes (MDS) have a poor prognosis due to low response rates (26-46%) to standard chemotherapy and high treatment-related mortality (11-31%).
  • Twenty patients with non-M3 AML and MDS were treated with this regimen.
  • The combination of HU, azacitdine and GO appears to be a safe and effective regimen in the treatment of AML and high risk MDS in the elderly.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy



83. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • MEASUREMENTS AND MAIN RESULTS: The effects of the following covariates on average (Cav) and maximum (Cmax) posaconazole plasma concentrations at steady state were explored: age, sex, and race-ethnicity; proven or probable IFI; baseline body weight and body surface area; and baseline (on or before day 7) increases in liver enzyme levels, mucositis, neutropenia, diarrhea, vomiting, or use of an H2-receptor antagonist or proton pump inhibitor.
  • [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



84. Bhatia R, Van Heijzen K, Palmer A, Komiya A, Slovak ML, Chang KL, Fung H, Krishnan A, Molina A, Nademanee A, O'Donnell M, Popplewell L, Rodriguez R, Forman SJ, Bhatia S: Longitudinal assessment of hematopoietic abnormalities after autologous hematopoietic cell transplantation for lymphoma. J Clin Oncol; 2005 Sep 20;23(27):6699-711
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: Autologous hematopoietic cell transplantation (HCT) is being increasingly used as an effective treatment strategy for patients with relapsed or refractory Hodgkin's lymphoma (HL) or non-Hodgkin's lymphoma (NHL) but is associated with therapy-related myelodysplasia and acute myeloid leukemia (t-MDS/AML) as a major cause of nonrelapse mortality.
  • The phenomenon of hematopoietic reconstitution after autologous HCT and the role of proliferative stress in the pathogenesis of t-MDS/AML are poorly understood.
  • Patients within this cohort who developed t-MDS/AML had reduced recovery of committed progenitors and poorer telomere recovery, possibly indicating a functional defect in primitive hematopoietic cells.
  • Increased proliferative stress on stem cells bearing genotoxic damage could contribute to the pathogenesis of t-MDS/AML.
  • Extended follow-up of a larger number of patients is required to confirm whether alterations in progenitor and telomere recovery predict for increased risk of t-MDS/AML.

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Hodgkin Disease.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • 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 = 16170178.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 5M01 RR00043; United States / NCI NIH HHS / CA / P01 CA30206
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  •  go-up   go-down



85. La Starza R, Aventin A, Matteucci C, Crescenzi B, Romoli S, Testoni N, Pierini V, Ciolli S, Sambani C, Locasciulli A, Di Bona E, Lafage-Pochitaloff M, Martelli MF, Marynen P, Mecucci C: Genomic gain at 6p21: a new cryptic molecular rearrangement in secondary myelodysplastic syndrome and acute myeloid leukemia. Leukemia; 2006 Jun;20(6):958-64
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic gain at 6p21: a new cryptic molecular rearrangement in secondary myelodysplastic syndrome and acute myeloid leukemia.
  • Fluorescence in situ hybridization and comparative genomic hybridization characterized 6p rearrangements in eight primary and in 10 secondary myeloid disorders (including one patient with Fanconi anemia) and found different molecular lesions in each group.
  • In the 10 patients with secondary acute myeloid leukemia/myelodysplastic syndrome (AML/MDS), the short arm of chromosome 6 was involved in unbalanced translocations in 7.
  • Consequently, in secondary AML/MDS, we hypothesize that 6p gains are major pathogenetic events arising from acquired and/or congenital genomic instability.
  • [MeSH-major] Chromosomes, Human, Pair 6 / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Neoplasms, Second Primary / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Cytogenetic Analysis. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Sensitivity and Specificity



86. Chakraborty S, Sun CL, Francisco L, Sabado M, Li L, Chang KL, Forman S, Bhatia S, Bhatia R: Accelerated telomere shortening precedes development of therapy-related myelodysplasia or acute myelogenous leukemia after autologous transplantation for lymphoma. J Clin Oncol; 2009 Feb 10;27(5):791-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Accelerated telomere shortening precedes development of therapy-related myelodysplasia or acute myelogenous leukemia after autologous transplantation for lymphoma.
  • PURPOSE: Therapy-related myelodysplasia or acute myelogenous leukemia (t-MDS/AML) is a lethal complication of autologous hematopoietic stem-cell transplantation (aHCT) for Hodgkin's lymphoma (HL) and non-Hodgkin's lymphoma (NHL).
  • Here, we investigated the hypothesis that accelerated telomere shortening after aHCT could contribute to the development of t-MDS/AML.
  • PATIENTS AND METHODS: A prospective longitudinal cohort was constructed to investigate the sequence of cellular and molecular abnormalities leading to development of t-MDS/AML after aHCT for HL/NHL.
  • This cohort formed the sampling frame for a nested case-control study to compare changes in telomere length in serial blood samples from patients who developed t-MDS/AML with matched controls who did not develop t-MDS/AML.
  • RESULTS: An initial increase in telomere length at day 100 after aHCT was followed by an accelerated telomere shortening in t-MDS/AML patients when compared with controls.
  • These telomere alterations preceded the onset of t-MDS and were independent of other known risk factors associated with development of t-MDS/AML on multivariate analysis.
  • Additionally, we observed reduced generation of committed progenitors in patients who developed t-MDS/AML, indicating that these telomere alterations were associated with reduced regenerative capacity of hematopoietic stem cells.
  • CONCLUSION: The development of t-MDS/AML after aHCT is associated with and preceded by markedly altered telomere dynamics in hematopoietic cells.
  • Accelerated telomere loss in patients developing t-MDS/AML may reflect increased clonal proliferation and/or altered telomere regulation in premalignant cells.
  • Genetic instability associated with shortened telomeres may contribute to leukemic transformation in t-MDS/AML.



87. Trobaugh-Lotrario AD, Kletzel M, Quinones RR, McGavran L, Proytcheva MA, Hunger SP, Malcolm J, Schissel D, Hild E, Giller RH: Monosomy 7 associated with pediatric acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS): successful management by allogeneic hematopoietic stem cell transplant (HSCT). Bone Marrow Transplant; 2005 Jan;35(2):143-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monosomy 7 associated with pediatric acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS): successful management by allogeneic hematopoietic stem cell transplant (HSCT).
  • Pediatric acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) with monosomy 7 is associated with poor disease-free survival when treated by conventional chemotherapy, immunosuppression or supportive measures.
  • To better understand the curative potential of HSCT in these patients, all cases of AML and MDS with monosomy 7 treated by two transplant programs (1992 to present) were reviewed.
  • Primary diagnoses were MDS (N = 5), therapy-related MDS (N = 3), AML (N = 5) and therapy-related AML (N = 3).
  • Toxicity caused deaths of the five nonsurviving patients, four of whom were transplanted with active leukemia.
  • Allogeneic HSCT is effective therapy for childhood AML and MDS associated with monosomy 7, particularly for patients with AML in complete remission and MDS.
  • [MeSH-major] Chromosomes, Human, Pair 7. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Monosomy. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Cause of Death. Child. Child, Preschool. Disease Management. Female. Humans. Male. Neoplasms, Second Primary / mortality. Neoplasms, Second Primary / therapy. Remission Induction. Retrospective Studies. Survival Rate. Transplantation, Homologous. Treatment Outcome



88. Joslin JM, Fernald AA, Tennant TR, Davis EM, Kogan SC, Anastasi J, Crispino JD, Le Beau MM: Haploinsufficiency of EGR1, a candidate gene in the del(5q), leads to the development of myeloid disorders. Blood; 2007 Jul 15;110(2):719-26
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Haploinsufficiency of EGR1, a candidate gene in the del(5q), leads to the development of myeloid disorders.
  • Loss of a whole chromosome 5 or a deletion of the long arm, del(5q), is a recurring abnormality in myelodysplastic syndromes (MDSs) and acute myeloid leukemia (AML).
  • To identify a leukemia-related gene on chromosome 5, we previously delineated a 970-kb segment of 5q31 that is deleted in all patients examined, and prepared a transcript map of this region.
  • To test the hypothesis that loss of function of Egr1 is an initiating event in the pathogenesis of AML/MDS, Egr1-deficient mice were treated with a potent DNA alkylating agent, N-ethyl-nitrosourea (ENU), to induce secondary cooperating mutations.
  • Our data suggest that haploinsufficiency for Egr1 plays a role in murine leukemogenesis, and in the development of AML/MDS characterized by abnormalities of chromosome 5.

  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • Jackson Laboratory JAX®Mice Database. culture/stock collections - B6N;129-Egr1<tm1Jmi>/J (subscription/membership/fee required).
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood Cells Mol Dis. 1996;22(3):271-80 [9075579.001]
  • [Cites] Int J Cancer. 1988 May 15;41(5):738-43 [3130314.001]
  • [Cites] Cancer Gene Ther. 1998 Jan-Feb;5(1):3-28 [9476963.001]
  • [Cites] J Biol Chem. 1999 Feb 12;274(7):4400-11 [9933644.001]
  • [Cites] Oncogene. 1999 Jul 1;18(26):3870-7 [10445850.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):144-6 [10508507.001]
  • [Cites] EMBO J. 2005 Jan 26;24(2):368-81 [15635450.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1921-6 [15774784.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):5133-43 [15958557.001]
  • [Cites] Cancer. 2005 Sep 1;104(5):925-30 [15999367.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2232-40 [16281072.001]
  • [Cites] Cancer Gene Ther. 2006 Feb;13(2):115-24 [16138117.001]
  • [Cites] EMBO J. 2006 Mar 8;25(5):1093-103 [16456537.001]
  • [Cites] Cancer Res. 2006 May 15;66(10):5029-38 [16707424.001]
  • [Cites] Cell. 2006 Aug 25;126(4):755-66 [16923394.001]
  • [Cites] Genomics. 2001 Jan 15;71(2):235-45 [11161817.001]
  • [Cites] J Clin Oncol. 2001 Mar 1;19(5):1405-13 [11230485.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10398-403 [11526243.001]
  • [Cites] Blood. 2002 Apr 15;99(8):2985-91 [11929790.001]
  • [Cites] Blood. 2002 Jul 1;100(1):238-45 [12070033.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):63-74 [12086889.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Mar 18;100(6):3233-8 [12629205.001]
  • [Cites] Blood. 2003 Jul 1;102(1):43-52 [12623843.001]
  • [Cites] Blood. 2003 Aug 1;102(3):1072-4 [12689927.001]
  • [Cites] Int J Radiat Biol. 2003 Jun;79(6):423-30 [12963544.001]
  • [Cites] Mamm Genome. 2004 Aug;15(8):585-91 [15457338.001]
  • [Cites] J Biol Chem. 1995 Apr 28;270(17):9971-7 [7730380.001]
  • [Cites] J Cell Biol. 1996 Apr;133(1):211-20 [8601609.001]
  • [Cites] Hematol Oncol Clin North Am. 1996 Apr;10(2):293-320 [8707757.001]
  • [Cites] Science. 1987 Nov 6;238(4828):797-9 [3672127.001]
  • [Cites] Cell. 1988 Apr 8;53(1):37-43 [3127059.001]
  • [Cites] Genes Chromosomes Cancer. 1997 Nov;20(3):282-91 [9365836.001]
  • (PMID = 17420284.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / CA84221; United States / NCI NIH HHS / CA / R01 CA101774; United States / NCI NIH HHS / CA / R01 CA101774-06; United States / NCI NIH HHS / CA / CA101774-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EGR1 protein, human; 0 / Early Growth Response Protein 1; 0 / Egr1 protein, mouse
  • [Other-IDs] NLM/ PMC1924479
  •  go-up   go-down



89. Galván AB, Mallo M, Arenillas L, Salido M, Espinet B, Pedro C, Florensa L, Serrano S, Solé F: Does monosomy 5 really exist in myelodysplastic syndromes and acute myeloid leukemia? Leuk Res; 2010 Sep;34(9):1242-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does monosomy 5 really exist in myelodysplastic syndromes and acute myeloid leukemia?
  • Abnormalities of chromosome 5 are common aberrations in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML), being del(5q) the most frequent.
  • The aim of this study was to analyze, by FISH for 5q31 (EGR1), a series of 28 MDS and AML cases with monosomy 5 detected by G-banding.
  • [MeSH-major] Chromosomes, Human, Pair 5. Leukemia, Myeloid, Acute / genetics. Monosomy. Myelodysplastic Syndromes / genetics



90. Raza A, Mehdi M, Mumtaz M, Ali F, Lascher S, Galili N: Combination of 5-azacytidine and thalidomide for the treatment of myelodysplastic syndromes and acute myeloid leukemia. Cancer; 2008 Oct 1;113(7):1596-604
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combination of 5-azacytidine and thalidomide for the treatment of myelodysplastic syndromes and acute myeloid leukemia.
  • BACKGROUND: The treatment of myelodysplastic syndromes (MDS) remains a challenge to the clinician despite recent advances.
  • Eventually, 30% of patients with MDS will progress and develop acute myeloid leukemia (AML).
  • METHODS: 5-Azacytidine (AZA) and thalidomide were administered to 40 patients with MDS or AML.
  • Six patients had refractory anemia (RA), 2 patients had RA with ringed sideroblasts, 10 patients had RA with excess blasts (RAEB), 1 patient had RAEB in transformation, 4 patients had chronic myelomonocytic leukemia, 1 patient had chronic idiopathic myelofibrosis, and 16 patients had AML.
  • It was noteworthy that 9 of 14 patients with AML had a history of prior MDS, 2 of 9 patients achieved a CR, 4 of 9 patients had HI (HI-E and bilineage HI), and 1 patient had stable disease and was continuing treatment.
  • CONCLUSIONS: The current findings indicated that a combination of low-dose AZA and thalidomide was well tolerated and was effective therapy for the treatment of patients with MDS and AML arising from prior MDS.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Azacitidine / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Thalidomide / administration & dosage



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

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