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[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

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[Copyright] Copyright 2006 International Society for Analytical Cytology.

(PMID = 16498671.001).

[ISSN] 1552-4949

[Journal-full-title] Cytometry. Part B, Clinical cytometry

[ISO-abbreviation] Cytometry B Clin Cytom

[Language] eng

[Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD3; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Benzenesulfonates; 0 / CD33 protein, human; 0 / Phenylurea Compounds; 0 / Pyridines; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / Stem Cell Factor; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.11.2 / Antigens, CD13; NI40JAQ945 / Tetradecanoylphorbol Acetate

   

[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.

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(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] GM-CSF and low-dose cytosine arabinoside in high-risk, elderly patients with AML or MDS.

In this study, we utilized these synergistic effects of granulocyte-macrophage colony-stimulating factor (GM-CSF, sargramostim [Leukine]), hydroxyurea, and low-dose cytosine arabinoside to treat elderly patients with acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS).

In a single-institution, retrospective study, we evaluated 94 treatments with concomitant hydroxyurea, cytosine arabinoside, and GM-CSF between the years of 1997 and 2003 in high-risk elderly patients with AML or MDS.

Overall, our study showed that low-dose cytosine arabinoside given by continuous infusion together with continuous infusion GM-CSF and hydroxyurea was well-tolerated and effective in treating elderly AML and MDS patients who were not eligible for standard induction therapy.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy

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(PMID = 15934494.001).

[ISSN] 0890-9091

[Journal-full-title] Oncology (Williston Park, N.Y.)

[ISO-abbreviation] Oncology (Williston Park, N.Y.)

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; X6Q56QN5QC / Hydroxyurea

   

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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Outcome of allo-SCT for women with MDS or AML occurring after breast cancer therapy.

Women with breast cancer who receive adjuvant therapy are at risk for developing therapy-related myelodysplastic syndrome (MDS) or AML (tMDS/AML).

Patients with tMDS/AML are often referred for consideration of allogeneic hematopoietic SCT (HSCT).

We report a retrospective study of all women who were treated with HSCT for MDS or AML at our institution between 1991 and 2008.

The cumulative incidences of tMDS/AML relapse and non-relapse mortality (NRM) were 38 and 17%, respectively.

A significant proportion of women with tAML/MDS after breast cancer treatment experience DFS after HSCT, similar to that of patients with de novo MDS or AML.

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[Cites] N Engl J Med. 1972 Nov 30;287(22):1119-22 [5082192.001]

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(PMID = 20154738.001).

[ISSN] 1476-5365

[Journal-full-title] Bone marrow transplantation

[ISO-abbreviation] Bone Marrow Transplant.

[Language] ENG

[Grant] United States / NIAID NIH HHS / AI / P01 AI 29350; United States / NIAID NIH HHS / AI / U19 AI029530-14; United States / NIAID NIH HHS / AI / AI029530-14; United States / NIAID NIH HHS / AI / U19 AI029530; United States / NCI NIH HHS / CA / P01 CA142106-06A1; United States / NCI NIH HHS / CA / P01 CA142106

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Other-IDs] NLM/ NIHMS180221; NLM/ PMC2889243

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Genetic variant of the human homologous recombination-associated gene RMI1 (S455N) impacts the risk of AML/MDS and malignant melanoma.

Mutations altering BLM function are associated with highly elevated cancer susceptibility (Bloom's syndrome).

We have analyzed the common polymorphism Ser455Asn in RMI1 and its association with cancer risk in acute myeloid leukemia (AML, N=93), myelodysplatic syndromes (MDS, N=74), and malignant melanoma (MM, N=166).

The results showed a consistent pattern, where carriers of the Asn variant had a significantly increased risk of AML/MDS.

The risk of AML/MDS for SerAsn+AsnAsn subjects was odds ratio (OR)=1.7, 95% confidence interval (CI) 1.1-2.5 or MM was OR=1.5, 95% CI 1.0-2.2.

[MeSH-major] Carrier Proteins / genetics. Genetic Variation. Leukemia, Myeloid, Acute / genetics. Melanoma / genetics. Myelodysplastic Syndromes / genetics. Nuclear Proteins / genetics. Recombination, Genetic. Skin Neoplasms / genetics

[MeSH-minor] Adenosine Triphosphatases / genetics. Adult. Aged. Aged, 80 and over. Bloom Syndrome / genetics. Case-Control Studies. DNA Helicases / genetics. Female. Genotype. Humans. Male. Middle Aged. Polymerase Chain Reaction. Polymorphism, Genetic. RecQ Helicases

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(PMID = 17900800.001).

[ISSN] 0304-3835

[Journal-full-title] Cancer letters

[ISO-abbreviation] Cancer Lett.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Ireland

[Chemical-registry-number] 0 / Carrier Proteins; 0 / Nuclear Proteins; 0 / RMI1 protein, human; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / Bloom syndrome protein; EC 3.6.4.- / DNA Helicases; EC 3.6.4.12 / RecQ Helicases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Fludarabine-melphalan conditioning for AML and MDS: alemtuzumab reduces acute and chronic GVHD without affecting long-term outcomes.

The purpose of this study was to determine the effect of alemtuzumab on treatment-related mortality (TRM), relapse, overall survival (OS), and disease-free survival (DSF) in patients with acute myelogenous leukemia (AML) and myelodysplastic syndromes (MDS) undergoing reduced intensity conditioning (RIC).

The incidence of acute graft-versus-host disease (aGVHD) grade II-IV (relative risk [RR] 5.5, P < .01) and chronic GVHD (cGVHD) (RR 6.6, P < .01) were significantly lower in patients receiving alemtuzumab.

The addition of alemtuzumab to an RIC regimen dramatically reduces the incidence of aGVHD and cGVHD in patients with AML and MDS undergoing allogeneic transplantation.

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(PMID = 19361753.001).

[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 / K24 CA116471; United States / NCI NIH HHS / CA / P01 CA055164; United States / NCI NIH HHS / CA / R21 CA101337; United States / NCI NIH HHS / CA / 1-R21 CA 101337-01

[Publication-type] Controlled Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 106XV160TZ / Vidarabine Phosphate; 1X9VK9O1SC / fludarabine phosphate; 3A189DH42V / alemtuzumab; Q41OR9510P / Melphalan

[Other-IDs] NLM/ NIHMS589065; NLM/ PMC4348112

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] AML/MDS with 11q/MLL amplification show characteristic gene expression signature and interplay of DNA copy number changes.

AML/MDS patients carrying 11q amplifications involving the mixed lineage leukemia gene (MLL) locus are characterized by a complex aberrant karyotype (CAK) frequently including deletions within 5q, 17p, and 7q, older age and fast progression of the disease with extremely poor prognosis.

In this study, we investigated 19 patients with AML/MDS and MLL gain/amplification.

Furthermore, we demonstrate that the gene expression signature can be used to discriminate AML/MDS with MLL amplification from several other types of AML.

[MeSH-major] Gene Dosage. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloid-Lymphoid Leukemia Protein / genetics

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(PMID = 19306356.001).

[ISSN] 1098-2264

[Journal-full-title] Genes, chromosomes & cancer

[ISO-abbreviation] Genes Chromosomes Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein

   

[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

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[CommentIn] Blood. 2008 Apr 15;111(8):3916-7 [18434965.001]

(PMID = 18192504.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Evi1 protein, mouse; 0 / Mutant Proteins; 0 / Transcription Factors

   

[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, chronic myelomonocytic leukaemia and acute myeloid leukaemia.

This paper presents a summary of the evidence review group (ERG) report into the clinical effectiveness and cost-effectiveness of azacitidine (aza) compared with conventional care regimes (CCR) for higher risk patients with myelodysplastic syndrome (MDS), chronic myelomonocytic leukaemia (CMML) and acute myeloid leukaemia (AML), based on the evidence submission from the manufacturer to the National Institute for Health and Clinical Excellence (NICE) as part of the single technology appraisal process.

The patient outcomes governing relative effectiveness and cost-effectiveness were defined as overall survival, time to progression (TTP) to AML, adverse events and health-related quality of life (HRQoL).

It compared aza with CCR in 358 patients with higher risk MDS, CMML and AML 20-30% blasts.

The outcomes reported in AZA-001 included overall survival, TTP to AML and adverse events.

The results showed that: the median overall survival was 24.5 months on aza, compared with 15.0 months in the CCR group (p = 0.0001); the response rates were low (complete remission 17% aza versus 8% CCR); the median time to transformation to AML was greater in the aza group (17.8 versus 11.5 months; p < 0.0001); and of patients who were red blood cell (RBC) transfusion-dependent at baseline, 45% of those on aza became RBC transfusion-independent during the treatment period, compared with 11.8% in the CCR group (p < 0.0001).

The AZA-001 study showed that, compared with CCR, those MDS patients receiving aza had prolonged median survival, had delayed progression to AML, had reduced dependence on transfusions and had a small improvement in response rate.

Given the general paucity of economic modelling work in MDS and the limitations of the submitted industry model there is an evident need for an independent cost-effectiveness analysis of aza in MDS.

At the time of writing, the guidance appraisal consultation document issued by NICE on 4 March 2010 states that azacitidine is not recommended as a treatment option for people not eligible for haemopoietic stem cell transplantation with the the following conditions: intermediate-2 and high-risk MDS according to the International Prognostic Scoring System, CMML with 10-29% marrow blasts without myeloproliferative disorder, or with AML with 20-30% blasts and multilineage dysplasia, according to World Health Organization classification.

[MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myelomonocytic, Chronic / drug therapy. Myelodysplastic Syndromes / drug therapy

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(PMID = 20507806.001).

[ISSN] 2046-4924

[Journal-full-title] Health technology assessment (Winchester, England)

[ISO-abbreviation] Health Technol Assess

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; M801H13NRU / Azacitidine

[Number-of-references] 2

   

[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

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[Copyright] Copyright 2010 S. Karger AG, Basel.

(PMID = 20197683.001).

[ISSN] 1423-0097

[Journal-full-title] International archives of allergy and immunology

[ISO-abbreviation] Int. Arch. Allergy Immunol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Glucocorticoids; X4W7ZR7023 / Methylprednisolone

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Efficacy of prophylactic transfusions using single donor apheresis platelets versus pooled platelet concentrates in AML/MDS patients receiving allogeneic hematopoietic stem cell transplantation.

We studied all transfusions administered to 33 patients with AML/MDS during the first 100 days after busulfan-based, myeloablative HSCT.

In the week following any given transfusion, the median number of new transfusions was similar (n=2), as well as the need of further transfusion (16 versus 24%, P=0.2).

[MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Platelet Transfusion / methods

[MeSH-minor] Acute Disease. Adult. Aged. Blood Platelets / cytology. Female. Hemorrhage / prevention & control. Humans. Male. Middle Aged. Platelet Count. Retrospective Studies. Transplantation, Homologous

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(PMID = 17589530.001).

[ISSN] 0268-3369

[Journal-full-title] Bone marrow transplantation

[ISO-abbreviation] Bone Marrow Transplant.

[Language] eng

[Publication-type] Comparative Study; Evaluation Studies; Journal Article

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Dendritic cells (DCs) can be successfully generated from leukemic blasts in individual patients with AML or MDS: an evaluation of different methods.

Myeloid-leukemic cells (AML, MDS, CML) can be differentiated to leukemia-derived dendritic cell [DC (DCleu)] potentially presenting the whole leukemic antigen repertoire without knowledge of distinct leukemia antigens and are regarded as promising candidates for a vaccination strategy.

We studied the capability of 6 serum-free DC culture methods, chosen according to different mechanisms, to induce DC differentiation in 137 cases of AML and 52 cases of MDS.

Comparing these methods on average 15% to 32% DC, depending on methods used, could be obtained from blast-containing mononuclear cells (MNC) in AML/MDS cases with a DC viability of more than 60%.

Average results of all culture methods tested were comparable, however not every given case of AML could be differentiated to DC with 1 selected method.

[MeSH-major] Cancer Vaccines. Cell Culture Techniques / methods. Dendritic Cells / pathology. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology

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(PMID = 20139775.001).

[ISSN] 1537-4513

[Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)

[ISO-abbreviation] J. Immunother.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Culture Media, Serum-Free; 0 / Cytokines; 24939-03-5 / Poly I-C; 39325-01-4 / Picibanil

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Efficiency of cyclosporin A therapy in patients with myelodysplastic syndrome].

AIM: To evaluate the efficacy of cyclosporin A (CsA) in patients with myelodysplastic syndromes (MDS) and to identify determinants of a response to this therapy.

SUBJECTS AND METHODS: The efficacy of CsA was evaluated in 52 patients (30 men and 22 women aged 16 to 74 years) with MDS.

Its efficacy was evaluated following 3, 6, and 12 months.

Baseline refractory anemia (RA) transformed to RA with excess blasts (RAEB) in 31% of cases; baseline RAEB did to acute myeloid leukemia in 34%.

CONCLUSION: CsA is the drug of choice in treating patients with MDS, including RA, RA with ringed sideroblasts, refractory cytopenia with multilineage dysplasia, with hypoplasia of hematopoiesis, with nodular polyclonal lymphoid infiltration in the BM, a normal karyotype or changes corresponding to a low or moderate IPSS risk.

[MeSH-major] Cyclosporine / therapeutic use. Immunosuppressive Agents / therapeutic use. Myelodysplastic Syndromes / drug therapy

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(PMID = 20873246.001).

[ISSN] 0040-3660

[Journal-full-title] Terapevticheskiĭ arkhiv

[ISO-abbreviation] Ter. Arkh.

[Language] rus

[Publication-type] Clinical Trial; English Abstract; Journal Article

[Publication-country] Russia (Federation)

[Chemical-registry-number] 0 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine

   

[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

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(PMID = 16498392.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Radiation-induced and therapy-related AML/MDS].

Radiation induced acute myeloid leukemia (AML) was recognized a century ago, soon after mankind found radiation.

Atomic bomb survivors developed de novo AML with relatively short latency with very high frequency.

By contrast, excess occurrence of myelodysplastic syndrome (MDS) as well as solid tumors was found decades late.

This difference may be due to etiology that many de novo AML patients harbor chimeric leukemogenic genes caused by chromosomal translocations, while MDS patients rarely carry chimeras.

Therapy related leukemia is mainly caused by topoisomerase II inhibitors that cause de novo AML with an 11q23 translocation or by alkyrating agents that induce MDS/AML with an AML1 point mutation and monosomy 7.

[MeSH-major] Leukemia, Myeloid, Acute / etiology. Leukemia, Radiation-Induced / etiology. Myelodysplastic Syndromes / etiology

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(PMID = 19860183.001).

[ISSN] 0047-1852

[Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine

[ISO-abbreviation] Nippon Rinsho

[Language] jpn

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Japan

[Chemical-registry-number] 0 / Alkylating Agents; 0 / Enzyme Inhibitors; 0 / Topoisomerase II Inhibitors

[Number-of-references] 7

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The pharmacokinetics of azacitidine following subcutaneous treatment in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML).

: 7087 Background: 5-azacitidine (AZA), through its effects on DNA metabolism, gene expression, and cell differentiation, has proven beneficial in treatment of MDS and AML and AZA therapy significantly increases survival in higher-risk MDS and AML compared to conventional care.

METHODS: Adult patients with MDS or AML and ECOG status 0-2 were treated with 7 consecutive daily SC doses of 75 mg/m² AZA during their first treatment cycle.

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(PMID = 27961481.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Phase I trial of laromustine in combination with infusional ara-C in elderly patients over age 60 with newly diagnosed AML or high-grade MDS.

: 7054 Background: Laromustine is a novel sulfonylhydrazine-alkylating agent with activity in acute myeloid leukemia (AML).

Laromustine in phase I and II trials shows activity in patients with relapsed/refractory leukemia (1) and elderly patients with new AML (2).

Based on this data, a phase I study to evaluate the safety and efficacy of combining escalating doses of laromustine with infusional ara-C in AML and MDS patients over 60.

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(PMID = 27961420.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Phase II study of vorinostat (V) in combination with idarubicin and high-dose cytarabine (IA) as front-line therapy in patients (pts) with high-risk myelodyplsatic syndrome (MDS) or acute myeloid leukemia (AML).

: 7004 Background: Standard induction therapy for pts with AML has not changed over the last 2 decades nor has the outcome of these pts.

We designed a phase II study of V with IA as front-line therapy for MDS/AML.

METHODS: Pts with untreated int-2/high-risk MDS or AML ages 15-65 with adequate liver and renal functions and PS, and EF ≥ 50% were eligible.

3 pts with relapsed/refractory AML were treated in the run-in phase.

Following these, 19 pts were enrolled on the phase 2 portion.

CONCLUSIONS: The combination of IA and V is safe and active in AML/MDS.

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(PMID = 27961376.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] MDS-associated cytogenetic abnormalities (MDS-CA) after total therapy (TT) regimens for newly diagnosed multiple myeloma (MM): Apparent surge after introduction of post-transplant consolidation chemotherapy (CONS) in TT2 and TT3.

: 8595 Background: We have previously reported on the variables associated with the development of MDS-CA in the context of autologous transplant-supported high-dose therapy regimens for MM (Barlogie et al, Blood 2008).

METHODS: Due to a perceived increase in MDS-CA frequency, our MM data base was reviewed again to determine the potential effect of CONS introduced in TT2 and retained in TT3 trials.

The frequency of MDS-CA post-transplant was determined, using Kaplan-Meier estimate plots, for 183 patients who received TT1, 554 enrolled in TT2 and 305 receiving TT3.

Persistence of MDS-CA implied their documentation on 3 successive occasions.

RESULTS: 3-year MDS-CA estimates were 2% for both TT1 and TT2 and 4% for TT3 (TT3 v TT2, p=0.04; TT3 v TT1, p=0.11); persistent MDS-CA were also more frequently observed in TT3 in comparison with TT2 and TT1 (2% v 0% v 0%, both p=0.01).

Multivariate analysis of features associated with transient and persistent MDS-CA revealed TT3 as an adverse feature (HR=2.84, p=0.043), along with incomplete platelet recovery of <165,000/uL 3mo after 1^st transplant.

CONCLUSIONS: Despite reduced induction chemotherapy prior to and CONS after tandem melphalan (200mg/m2)-based autotransplants from 4 in TT2 to 2 in TT3, overall and persistent MDS-CA increased significantly in TT3.

Clinical MDS and AML were rarely observed and a full account of hematopathologic findings will be presented.

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(PMID = 27962291.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A randomized phase II study of sapacitabine, an oral nucleoside analogue, in elderly patients with AML previously untreated or in first relapse or previously treated MDS.

It is orally administered and has demonstrated promising anti-leukemic activity against relapsed or refractory AML and MDS in a phase 1 trial.

METHODS: Eligible patients must be ≥70 years with AML previously untreated or in first relapse or ≥60 years with MDS previously treated with hypomethylating agents.

The planned sample size is 60 AML patients and 60 MDS patients.

RESULTS: As of December 2008, 60 AML and 13 MDS patients were enrolled and had ≥ 30 days of follow-up.

Preliminary efficacy data were available for the AML stratum.

Eight deaths of all causes occurred within 30 days of randomization and all were in the AML stratum (13%).

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(PMID = 27961383.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prevalence and therapeutic relationships of pericardial effusions in patients with leukemia.

: 7067 Background: Little is known regarding the prevalence and natural history of pericardial disease in patients with leukemia.

To study this issue, we retrospectively analyzed a large cohort of patients with leukemia, who were evaluated at MD Anderson Cancer Center (MDACC), to determine the prevalence, timing, and characteristics of PEf in leukemia.

METHODS: We reviewed 3,327 patients with acute myeloid leukemia (AML, N = 1,809, 54%), acute lymphocytic leukemia (ALL, N = 494, 15%), or myelodysplastic syndrome (MDS, N =1,024, 31%), who were seen at MDACC from August 2003 to July 2008.

RESULTS: The overall prevalence of PEf was 21.7%, 21.1%, and 19.9% (p = 0.72) in patients with AML, ALL, and MDS, respectively.

CONCLUSIONS: PEf are relatively common in patients with leukemia at initial presentation and are usually asymptomatic.

Their incidence increases with therapy administration although it appears that this is not a process related to specific classes of treatment or type of leukemia.

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(PMID = 27961462.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

: 7089 Background: Epigenetic therapy with hypomethylating agents (HA) is the standard of care in patients (pts) with myelodysplastic syndrome (MDS).

Moreover, there are no reports of use of these agents in pts with renal insufficiency (RI) commonly seen in pts with MDS.

METHODS: We investigated the outcomes of pts with RI and MDS, chronic myelomonocytic leukemia (CMML), or acute myeloid leukemia (AML) receiving therapy with HA.

RESULTS: Forty-two pts with sCr ≥ 1.5 mg/dL (including 17 with MDS, 16 with AML, and 9 with CMML) were treated with DAC or 5AZA alone or in combination with other agents (primarily histone deacetylase inhibitors).

CONCLUSIONS: The use of HA is well tolerated in pts with MDS and AML and RI who achieved comparable OR rates to those without RI.

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(PMID = 27961273.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The cumulative incidence of secondary MDS or AML was 8%.

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(PMID = 27960864.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Myelodysplastic syndromes developing after imatinib therapy for GIST.

Previously, we had detected clonal chromosomal abnormalities in the bone marrow of GIST pts. who developed a myelodysplastic syndrome during treatment with imatinib, so we performed a systematic study in a series of male and female GIST pts. during treatment with imatinib.

All pathologic material was reviewed to identify pts. with MDS or AML according to the WHO classification.

A trisomy 8 was detectable in seven pts. even if, curiously, in four of these pts. this come and went on repeated sampling without any apparent clinical effect, three pts. developed an MDS (two refractory cytopenias with multilineage dysplasia, and one refractory cytopenia with multilineage dysplasia and ringed sideroblast).

One patient developed a RAEB-1 with monosomy 7 which rapidly transformed into AML.

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(PMID = 27963910.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Identification by FISH of 4 novel partner loci of PRDM16 in myeloid malignancies.

It has been shown to be involved in the reciprocal translocation t(1;3)(p36;q21) and more rarely the t(1;21)(p36;q22) which both occur in myelodysplastic syndromes (MDS) and acute myeloid leukemias (AML).

This overexpression might play an important role in the pathogenesis of MDS and AML in blocking myeloid differentiation.

METHODS: We studied 35 myeloid malignancies, 12 lymphoid malignancies and 3 undifferentiated acute leukemias with 1p36 abnormalities by fluorescent in situ hybridization (FISH) with a bacterial artificial chromosomes (BAC) contig containing 50 BAC probes on 1p36.

RESULTS: In addition to the known t(1;3)(p36;q21) (11 cases) and t(1;21)(p36;q22) (1 case) involving RPN1 andAML1/RUNX1 respectively in myeloid malignancies, we specifically found PRDM16 to be rearranged in 4 additional translocations : a t(1;12)(p36;p13) in an AML-M4, a t(1;7)(p36;p12) in a MDS, an add(1)(p36) in an AML-M2 and a t(1;2)(p36;p12) in a relapsed AML-M4.

CONCLUSIONS: In our series of 50 cases of hematological malignancies with 1p36 abnormalities, PRDM16 was involved in about 45% of myeloid malignancies, and was never involved in lymphoid malignancies.

Interestingly, the shortest isoform of MDS/EVI-1, lacking the PR domain, is supposed to have an oncogenic effect due to its translocation-induced upregulation in AML.

Further characterization of these new partner genes and functional studies should give us more insight into the pathogenesis of AML and MDS mediated by PRDM16, and the role of its partner genes.

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(PMID = 27964015.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Midostaurin: Review of pharmacokinetics (PK) and PK/pharmacodynamic (PD) relationship in AML/MDS patients.

: e14540 Background: Midostaurin is a multi-tyrosine-kinases inhibitor targeting class III tyrosine-protein-kinases, including Fms-like tyrosine kinase-3 (FLT3), involved in hematopoiesis and leukemia.

METHODS: The two studies presented here involved patients with wild-type or FLT3-mutated de novo (phase Ib) or relapsed (phase II) AML or MDS.

Following multiple oral daily single-agent doses, midostaurin and CGP62221 concentrations accumulated significantly in the first 3-5 days then declined by 40- 80% prior to a new steady state 2-3 weeks post-dose.

These results support the ongoing phase III AML study in AML FLT3-mutated patients with midostaurin given in combination with chemotherapy.

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(PMID = 27963644.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute myeloid leukemia or myelodysplastic syndrome (AML/MDS) and overall mortality with chemotherapy (CT) and granulocyte colony-stimulating factor (G-CSF): A meta-analysis of randomized controlled trials (RCTs).

: 9524 Background: To evaluate the risk of AML/MDS and overall mortality in patients receiving CT ± G-CSF, a meta-analysis of RCTs were conducted.

Eligibility included RCTs of solid tumor or lymphoma patients randomized to CT ± primary G-CSF support, ≥2 years follow-up and reporting AML/MDS or all second malignancies.

Primary outcomes were AML/MDS and mortality.

RR for AML/MDS with CT+G-CSF compared to control was 1.92 [P=.006] with ARD increase of 0.4% [P=.008].

RR for AML/MDS in study categories to receive the same, dose-dense or dose-escalated CT+G-CSF were 1.95 [P=.346], 1.20 [P=.666] and 2.47 [P=.006], respectively.

No differences in estimates of AML/MDS or mortality were observed between industry and non-industry-funded studies.

CONCLUSIONS: Risk of AML/MDS is increased with dose escalated CT+G-CSF.

Dose-dense regimens are associated with the greatest RR reduction in mortality and lowest risk of AML/MDS.

Further research is needed to differentiate any impact of G-CSF on the risk of AML/MDS from that due to increased CT intensity.

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(PMID = 27964513.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Molecular pathways mediating MDS/AML with focus on AML1/RUNX1 point mutations.

AML1/RUNX1 point mutations have been identified in myelodysplastic syndrome (MDS) and MDS-related acute myeloid leukemia (AML), or MDS/AML, and are distributed throughout the full length of AML1/RUNX1.

Gene mutation is proposed to be one of the disease-defining genetic abnormalities of MDS/AML.

Most of the mutants lose trans-activation potential, which leads to a loss of normal function indicating that AML1/RUNX1 dysfunction is one of the major pathogenic mechanisms of MDS/AML.

Although biological analysis using a mouse bone marrow transplantation model transduced with Ni-type of D171N or Ct-type of S291fsX300 mutants has partially confirmed the oncogenic ability of AML1 mutants, it could not explain the mutant specific clinical features of MDS/AML.

Thus, AML1/RUNX1 mutants play a central role in the pathogenesis of MDS/AML.

Both AML1 mutants are initiating factors for MDS-genesis by inhibiting differentiation of hematopoietic stem cells, and Ni-type mutant requires acquisition of proliferation ability.

[MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Leukemic. Hematopoietic Stem Cells / metabolism. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Point Mutation

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(PMID = 19334039.001).

[ISSN] 1097-4652

[Journal-full-title] Journal of cellular physiology

[ISO-abbreviation] J. Cell. Physiol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD34; 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human

[Number-of-references] 27

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Dicentric chromosomes and 20q11.2 amplification in MDS/AML with apparent monosomy 20.

FISH analysis of 41 previously karyotyped cases of MDS and AML with apparent monosomy of chromosome 20 revealed a variety of dicentric abnormalities involving chromosome 20.

The retention and amplification of proximal 20q provides support for the hypothesis that there is an oncogene located in this region of 20q that is activated in cases of MDS/AML with del(20q).

Apparent monosomy 20 in MDS/AML should be treated as evidence of unidentified chromosome 20 abnormalities, and familiarity with the typical G-banded morphology of these derivatives can help with their identification.

The reported incidence of dicentric chromosomes is clearly an under-estimate but is increasing in myeloid disorders as more cases are studied with methods allowing their detection.

[MeSH-major] Chromosomes, Human, Pair 20 / genetics. Leukemia, Myeloid, Acute / genetics. Monosomy / genetics. Myelodysplastic Syndromes / genetics

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[Copyright] Copyright (c) 2008 S. Karger AG, Basel.

(PMID = 18253031.001).

[ISSN] 1424-859X

[Journal-full-title] Cytogenetic and genome research

[ISO-abbreviation] Cytogenet. Genome Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Switzerland

   

[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

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[Copyright] Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.

(PMID = 19874806.001).

[ISSN] 1872-7786

[Journal-full-title] Chemico-biological interactions

[ISO-abbreviation] Chem. Biol. Interact.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Ireland

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Redefining monosomy 5 by molecular cytogenetics in 23 patients with MDS/AML.

Deletion of the long arm of chromosome 5 [del(5q)] or loss of a whole chromosome 5 (-5) is a common finding, arising de novo in 10% of patients with myelodysplastic syndromes (MDS) or acute myeloid leukemia (AML) and in 40% of patients with therapy-related MDS or AML.

We investigated by molecular cytogenetics 23 MDS/AML patients for whom conventional cytogenetics detected a monosomy 5.

Sequential fluorescent in situ hybridization studies with whole chromosome paints and region-specific probes, used as a complement to conventional cytogenetic analysis, allow a better interpretation of karyotypes in MDS/AML patients.

[MeSH-major] Chromosomes, Human, Pair 5. Leukemia, Myeloid / genetics. Monosomy. Myelodysplastic Syndromes / genetics

[MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged

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(PMID = 17391336.001).

[ISSN] 0902-4441

[Journal-full-title] European journal of haematology

[ISO-abbreviation] Eur. J. Haematol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Denmark

   

[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

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(PMID = 19927982.001).

[ISSN] 1543-0790

[Journal-full-title] Clinical advances in hematology & oncology : H&O

[ISO-abbreviation] Clin Adv Hematol Oncol

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Non-intensive treatment with low-dose 5-aza-2'-deoxycytidine (DAC) prior to allogeneic blood SCT of older MDS/AML patients.

Novel, non-intensive treatment options in older MDS/AML patients planned for allografting, with the goal of down-staging the underlying disease and bridging time to transplantation, are presently being developed.

5-azacytidine and decitabine (DAC) are of particular interest, as they can be given repetitively, with very limited non-hematologic toxicity and result in responses both in MDS and AML even at low doses.

We describe 15 consecutive patients (median age 69 years, range 60-75 years) with MDS (n=10) or AML (n=5) who all received first-line treatment with DAC and subsequent allografting (from sibling donor in four patients, unrelated donor in 11) after reduced-intensity conditioning with the FBM regimen.

We conclude that allografting after low-dose DAC and subsequent conditioning with FBM is feasible, with no unexpected toxicities and appears as a valid alternative to standard chemotherapy ('InDACtion instead of induction') in elderly patients with MDS/AML.

[MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / analogs & derivatives. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy

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(PMID = 19363531.001).

[ISSN] 1476-5365

[Journal-full-title] Bone marrow transplantation

[ISO-abbreviation] Bone Marrow Transplant.

[Language] eng

[Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study

[Publication-country] England

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine

   

[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

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[Copyright] (c) 2006 Wiley-Liss, Inc.

(PMID = 16736498.001).

[ISSN] 1045-2257

[Journal-full-title] Genes, chromosomes & cancer

[ISO-abbreviation] Genes Chromosomes Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / GAB2 protein, human

   

[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.

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(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

   

[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: the role of dose intensity.

Allogeneic stem-cell transplantation (SCT) with both myeloablative and reduced-intensity conditioning (RIC) is an effective therapy in AML/MDS.

To define the role of dose intensity, we analyzed SCT outcomes of 112 consecutive patients with AML/MDS.

Myeloablative and RIC regimens had similar outcomes when leukemia was in remission at SCT; however, patients with active disease could only be salvaged by myeloablative conditioning.

[MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Myeloablative Agonists / therapeutic use. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. Retrospective Studies. Survival Analysis. Transplantation, Homologous. Treatment Outcome

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(PMID = 16307018.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Myeloablative Agonists

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Mutations of the PTPN11 gene in therapy-related MDS and AML with rare balanced chromosome translocations.

Activating mutations of the PTPN11 gene encoding the SHP2 tyrosine phosphatase is the most common genetic abnormality in juvenile myelomonocytic leukemia and is sporadically observed in myelodysplasia (MDS) and acute myeloid leukemia (AML).

An unselected series of 140 patients with therapy-related MDS or AML were investigated for mutations of PTPN11 in Exons 3, 4, 8, and 13.

[MeSH-major] Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Myelodysplastic Syndromes / genetics. Protein Tyrosine Phosphatases / genetics. Translocation, Genetic

[MeSH-minor] Acute Disease. Aged. Female. Humans. Male. Middle Aged. Molecular Sequence Data. Protein Tyrosine Phosphatase, Non-Receptor Type 11. Sequence Analysis, DNA

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[Copyright] (c) 2007 Wiley-Liss, Inc.

(PMID = 17330262.001).

[ISSN] 1045-2257

[Journal-full-title] Genes, chromosomes & cancer

[ISO-abbreviation] Genes Chromosomes Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Erlotinib exhibits antineoplastic off-target effects in AML and MDS: a preclinical study.

Erlotinib, an inhibitor of the epidermal growth factor receptor (EGFR), induces differentiation, cell-cycle arrest, and apoptosis of EGFR-negative myeloblasts of patients with myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), as well as in EGFR-negative cell lines representing these diseases (P39, KG-1, and HL 60).

In apoptosis-sensitive AML cells, erlotinib caused a rapid (within less than 1 hour) nucleocytoplasmic translocation of nucleophosmin-1 (NPM-1) and p14(ARF).

Moreover, erlotinib reduced the growth of xenografted human AML cells in vivo.

Erlotinib also killed CD34(+) bone marrow blasts from MDS and AML patients while sparing normal CD34(+) progenitors.

One patient afflicted with both MDS and non-small cell lung cancer manifested hematologic improvement in response to erlotinib.

In summary, we here provide novel evidence in vitro, ex vivo, and in vivo for the potential therapeutic efficacy of erlotinib in the treatment of high-risk MDS and AML.

[MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use

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(PMID = 17925489.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Comparative analysis of remission induction therapy for high-risk MDS and AML progressed from MDS in the MDS200 study of Japan Adult Leukemia Study Group.

A total of 120 patients with high-risk myelodysplastic syndrome (MDS) and AML progressed from MDS (MDS-AML) were registered in a randomized controlled study of the Japan Adult Leukemia Study Group (JALSG).

Untreated adult patients with high-risk MDS and MDS-AML were randomly assigned to receive either idarubicin and cytosine arabinoside (IDR/Ara-C) (Group A) or low-dose cytosine arabinoside and aclarubicin (CA) (Group B).

In conclusion, it is necessary to introduce the first line therapy excluding the chemotherapy that can prolong survival in patients with high-risk MDS and MDS-AML.

[MeSH-major] Aclarubicin / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cytarabine / administration & dosage. Idarubicin / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy

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(PMID = 20047095.001).

[ISSN] 1865-3774

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] Japan

[Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; 74KXF8I502 / Aclarubicin; ZRP63D75JW / Idarubicin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Genetic deletions in AML and MDS.

Chromosomal deletions are common molecular events in myeloid malignancies.

The most common karyotypic abnormality in myelodysplastic syndrome (MDS) is deletion of chromosome 5q.

A subset of patients with del(5q) as a sole cytogenetic abnormality has a consistent set of clinical features, termed the 5q- syndrome.

While no tumor suppressor genes have been identified on 5q that are homozygously inactivated, recent studies have highlighted several genes and micro RNAs (miRNAs) that cause the phenotype of the 5q- syndrome through allelic insufficiency.

For example, deletion of one allele of the RPS14 gene causes a severe defect in erythropoiesis, analogous to the congenital syndrome Diamond Blackfan anemia, which is itself caused by mutations that inactivate one allele of a ribosomal gene.

The functional approaches used to dissect the molecular basis of the 5q deletion in MDS have the potential to identify key genes and therapeutic targets within other chromosomal deletions in hematologic malignancies.

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[Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.

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(PMID = 21130407.001).

[ISSN] 1532-1924

[Journal-full-title] Best practice & research. Clinical haematology

[ISO-abbreviation] Best Pract Res Clin Haematol

[Language] ENG

[Grant] United States / NHLBI NIH HHS / HL / HL082945-06; United States / NHLBI NIH HHS / HL / R01 HL082945; United States / NHLBI NIH HHS / HL / R01 HL082945-06

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] Netherlands

[Chemical-registry-number] 0 / MIRN145 microRNA, human; 0 / MIRN146 microRNA, human; 0 / MicroRNAs; 0 / Neoplasm Proteins; 0 / RNA, Neoplasm; 0 / RPS14 protein, human; 0 / Ribosomal Proteins

[Other-IDs] NLM/ NIHMS251639; NLM/ PMC3032259

   

[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.

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[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Anthracyclines, mitoxantrone, radiotherapy, and granulocyte colony-stimulating factor: risk factors for leukemia and myelodysplastic syndrome after breast cancer.

PURPOSE: To determine the risk factors for acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) after breast cancer.

We included 182 AML and MDS patients and 534 matched controls.

RESULTS: The risk of AML/MDS was increased after topoisomerase-II inhibitor-based chemotherapy (P < 10-16) and was higher for mitoxantrone-based chemotherapy than for anthracycline-based chemotherapy (relative risk [RR] = 15.6; 95% CI, 7.1 to 34.2; and RR = 2.7; 95% CI, 1.7 to 4.5, respectively).

After adjustment for other treatment components, the risk of AML/MDS in patients who received radiotherapy was multiplied by 3.9 (95% CI, 1.4 to 10.8) but was not increased by alkylating agents.

Patients receiving granulocyte colony-stimulating factor (G-CSF) support had an increased risk of AML/MDS (RR = 6.3; 95% CI, 1.9 to 21), even when controlling for chemotherapy doses.

Similar results were obtained when AML and MDS were considered separately.

CONCLUSION: This large case-control study demonstrates that the risk of AML/MDS is much higher with mitoxantrone-based chemotherapy than with anthracyclines-based chemotherapy in a population of women recently treated for breast cancer.

The risk of AML/MDS associated with mitoxantrone must be kept in mind when using this drug to treat diseases other than breast cancer (eg, prostate cancer or multiple sclerosis).

[MeSH-major] Anthracyclines / adverse effects. Antineoplastic Agents / adverse effects. Breast Neoplasms / drug therapy. Breast Neoplasms / radiotherapy. Leukemia, Myeloid / chemically induced. Mitoxantrone / adverse effects. Myelodysplastic Syndromes / chemically induced. Neoplasms, Radiation-Induced

[MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Case-Control Studies. Female. France / epidemiology. Humans. Middle Aged. Risk Factors

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(PMID = 17159192.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Anthracyclines; 0 / Antineoplastic Agents; BZ114NVM5P / Mitoxantrone

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Exisulind induces apoptosis in advanced myelodysplastic syndrome (MDS) and acute myeloid leukaemia/MDS.

The influence of Exisulind on the viability and apoptosis of CD34(+) stem cells from patients with advanced myelodysplastic syndrome (MDS) and acute myeloid leukaemia (AML)/MDS was investigated.

Addition of a specific JNK-inhibitor to Exisulind-treated advanced MDS and AML/MDS cells partly abrogated apoptosis.

We propose that Exisulind is tested in clinical phase I/II trials for the treatment of advanced MDS and AML/MDS.

[MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Leukemia, Myeloid / physiopathology. Myelodysplastic Syndromes / physiopathology. Sulindac / analogs & derivatives

[MeSH-minor] Acute Disease. Antigens, CD34. Cell Survival / drug effects. Cells, Cultured. Enzyme Activation. Humans. JNK Mitogen-Activated Protein Kinases / antagonists & inhibitors. JNK Mitogen-Activated Protein Kinases / metabolism. Stem Cells / drug effects. Stem Cells / physiology

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(PMID = 16978222.001).

[ISSN] 0007-1048

[Journal-full-title] British journal of haematology

[ISO-abbreviation] Br. J. Haematol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents; 184SNS8VUH / Sulindac; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; K619IIG2R9 / sulindac sulfone

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute leukemia in polycythemia vera: an analysis of 1638 patients enrolled in a prospective observational study.

Progression to acute myeloid leukemia/myelodysplastic syndromes (AML/MDS) is a possible evolution of polycythemia vera (PV), but whether some patients are at increased natural risk for this complication and how much the contribution of pharmacologic cytoreduction can affect the natural course of the disease remain uncertain.

AML/MDS was diagnosed in 22 patients after a median of 2.5 years from recruitment in the study and a median of 8.4 years from the diagnosis of PV.

Variables associated with progression to AML/MDS were assessed using different models of multivariate analysis.

Exposure to P32, busulphan, and pipobroman (HR, 5.46; 95% CI, 1.84-16.25; P = .0023), but not to hydroxyurea (HU) alone (HR, 0.86; 95% CI, 0.26-2.88; P = .8021), had an independent role in producing an excess risk for progression to AML/MDS compared with treatment with phlebotomy or interferon.

[MeSH-major] Leukemia, Myeloid / epidemiology. Polycythemia Vera / epidemiology

[MeSH-minor] Acute Disease. Adult. Aged. Aspirin / therapeutic use. Databases, Factual. Disease Progression. Disease-Free Survival. Female. Humans. Male. Middle Aged. Multivariate Analysis. Platelet Aggregation Inhibitors / therapeutic use. Prospective Studies. Risk Factors

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[CommentIn] Curr Hematol Rep. 2005 May;4(3):211-2 [15865873.001]

(PMID = 15585653.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Platelet Aggregation Inhibitors; R16CO5Y76E / Aspirin

   

[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

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[Cites] J Clin Invest. 2008 Sep;118(9):3003-6 [18725993.001]

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(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Many are called MDS cell lines: one is chosen.

Myelodysplastic syndromes (MDS) comprise a heterogenous group of clonal disorders of hematopoietic progenitors, showing genetic instability and in many cases progression to acute myeloid leukemia (AML).

When MDS progress towards AML (AML/MDS), additional genetic lesions cause a block in differentiation and an accumulation of blast cells.

Hence, both pathophysiologically and clinically the MDS and AML/MDS phases are distinguishable.

Leukemia cell lines are key resources for modelling hematological malignancies.

Some 31 cell lines have been described in the literature purportedly established from patients with MDS.

However, a significant minority of these has proved false after DNA profiling which revealed their cross-contamination with older established leukemia cell lines.

Most remaining ("authentic") MDS cell lines were established during the leukemic phase of the disease progression rather than during the MDS phase.

Based on these data we have assigned the 31 candidate MDS cell lines to one of the three categories:.

(2) malignant cell lines established in the AML/MDS leukemic phase; and (3) apparently legitimate MDS cell lines established during the MDS phase.

While MDS and AML/MDS cell lines both provide singular resources for modelling pathology, mining oncogenically modified macromolecules, and testing druggability, we contend these groups should be considered separately.

[MeSH-major] Cell Line, Tumor. Hematopoietic Stem Cells. Myelodysplastic Syndromes

[MeSH-minor] Animals. Cell Transformation, Neoplastic. Genomic Instability. Humans. Leukemia, Myeloid, Acute. Models, Biological

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(PMID = 19344951.001).

[ISSN] 1873-5835

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Number-of-references] 45

   

[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

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(PMID = 18468682.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Evolution to myelofibrosis (MF), acute myeloid leukemia or myelodysplastic syndrome (AML/MDS) may occur over time in myeloproliferative neoplasms (MPN) patients most likely due to the acquisition of additional mutations.

The Groupe Francophone de cytogenetique hematologique (GFCH) has collected and reviewed 82 patients with transformation of MPN (66 AML/MDS and 16 MF).

Significantly more -7/del(7q) (P = 0.004) and -5/del(5q) (P = 0.03) were found in AML/MDS with a higher incidence of dup1q (P = 0.01) in MF.

In multivariate analysis, two factors were independently associated with an inferior overall survival (OS); AML/MDS transformation (P < 0.0001) and -5/del(5q) abnormality (P = 0.02).

Although both giving rise to loss of 7q, der(1;7) differed from other 7q deletions in terms of distribution (lower frequency of AML/MDS, P = 0.02), association with chromosomal abnormalities (absence of -5/del(5q), P = 0.003; increased del(20q), P = 0.05), and longer OS (P = 0.0007).

We detected 24/40 (60%) JAK2V617F and 8/25 (32%) TET2 mutations in samples following transformation, ranging from wild-type to mutated forms of both genes.

[MeSH-major] Cell Transformation, Neoplastic / genetics. Chromosome Aberrations. DNA-Binding Proteins / genetics. Janus Kinase 2 / genetics. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / genetics. Mutation / genetics. Proto-Oncogene Proteins / genetics

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(PMID = 20629097.001).

[ISSN] 1098-2264

[Journal-full-title] Genes, chromosomes & cancer

[ISO-abbreviation] Genes Chromosomes Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / TET2 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Progressive chromatin repression and promoter methylation of CTNNA1 associated with advanced myeloid malignancies.

Complete loss or deletion of the long arm of chromosome 5 is frequent in myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML).

This study is a comprehensive analysis of previously implicated and novel genes for epigenetic inactivation in AML and MDS.

In 146 AML cases, methylation of CTNNA1 was frequent, and more common in AML patients with 5q deletion (31%) than those without 5q deletion (14%), whereas no methylation of other 5q genes was observed.

In 31 MDS cases, CTNNA1 methylation was only found in high-risk MDS (>or=RAEB2), but not in low-risk MDS (<RAEB2), indicating that CTNNA1 methylation might be important in the transformation of MDS to AML.

CTNNA1 expression was lowest in AML/MDS patients with CTNNA1 methylation, although reduced expression was found in some patients without promoter methylation.

Repressive chromatin marks (H3K27me3) at the promoter were identified in CTNNA1-repressed AML cell lines and primary leukemias, with the most repressive state correlating with DNA methylation.

These results suggest progressive, acquired epigenetic inactivation at CTNNA1, including histone modifications and promoter CpG methylation, as a component of leukemia progression in patients with both 5q- and non-5q- myeloid malignancies.

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(PMID = 19826047.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA058184-090013; United States / NCI NIH HHS / CA / P50 CA058184; United States / NCI NIH HHS / CA / P50 CA058184-090013

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / CTNNA1 protein, human; 0 / Chromatin; 0 / RNA, Messenger; 0 / alpha Catenin; EC 1.13.12.- / Luciferases

[Other-IDs] NLM/ NIHMS142652; NLM/ PMC3081599

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Loss of the Y chromosome: an age-related or clonal phenomenon in acute myelogenous leukemia/myelodysplastic syndrome?

CONTEXT: The clinical association between loss of the Y chromosome and acute myelogenous leukemia and myelodysplastic syndrome (AML/MDS) has been debated because both phenomena are related to aging.

OBJECTIVE: To evaluate the relationship between loss of the Y chromosome and AML/MDS.

Of these, 16 patients demonstrated myeloid disease, with 2 cases of AML and 14 cases of MDS.

An increased incidence (P < .05) of AML/MDS was seen only in the group composed of 8 patients with complete loss of the Y chromosome in all karyotyped cells (1 case of AML and 7 cases of MDS).

However, in individuals in which all cells on cytogenetic analysis showed loss of the Y chromosome, there was a statistically significant increase in AML/MDS, suggesting that the absence of any normal-dividing cells in a bone marrow analysis may be indicative of AML/MDS.

[MeSH-major] Chromosome Deletion. Chromosomes, Human, Y. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics

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(PMID = 18684036.001).

[ISSN] 1543-2165

[Journal-full-title] Archives of pathology & laboratory medicine

[ISO-abbreviation] Arch. Pathol. Lab. Med.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Risk of acute myeloid leukemia and myelodysplastic syndrome in trials of adjuvant epirubicin for early breast cancer: correlation with doses of epirubicin and cyclophosphamide.

PURPOSE: We reviewed follow-up of patients treated in 19 randomized trials of adjuvant epirubicin in early breast cancer to determine incidence, risk, and risk factors for subsequent acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).

Cases of AML or MDS (AML/MDS) were reported, with disease characteristics.

RESULTS: In 7,110 patients treated with epirubicin-containing regimens (92% of whom also received cyclophosphamide), 8-year cumulative probability of AML/MDS was 0.55% (95% CI, 0.33% to 0.78%).

The risk of developing AML/MDS increased in relation to planned epirubicin dose per cycle, planned epirubicin dose-intensity, and administered cumulative doses of epirubicin and cyclophosphamide.

Patients with administered cumulative doses of both epirubicin and cyclophosphamide not exceeding those used in standard regimens (</= 720 mg/m(2) and </= 6,300 mg/m(2), respectively) had an 8-year cumulative probability of developing AML/MDS of 0.37% (95% CI, 0.13% to 0.61%) compared with 4.97% (95% CI, 2.06% to 7.87%) for patients administered higher cumulative doses of both epirubicin and cyclophosphamide.

CONCLUSION: Patients treated with standard cumulative doses of adjuvant epirubicin (</= 720 mg/m(2)) and cyclophosphamide (</= 6,300 mg/m(2)) for early breast cancer have a lower probability of secondary leukemia than patients treated with higher cumulative doses.

Increased risk of secondary leukemia must be considered when assessing the potential benefit to risk ratio of higher than standard doses.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Cyclophosphamide / adverse effects. Epirubicin / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced

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(PMID = 15961765.001).

[ISSN] 0732-183X

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Dexrazoxane-associated risk for acute myeloid leukemia/myelodysplastic syndrome and other secondary malignancies in pediatric Hodgkin's disease.

We evaluated incidence and risk factors of acute myeloid leukemia (AML)/myelodysplastic syndrome (MDS) and second malignant neoplasms (SMNs).

Six of eight patients developed AML/MDS, and both solid tumors (osteosarcoma and papillary thyroid carcinoma) occurred in recipients of DRZ.

With median 58 months' follow-up, 4-year cumulative incidence rate (CIR) for AML/MDS was 2.55% +/- 1.0% with DRZ versus 0.85% +/- 0.6% in the non-DRZ group (P = .160).

Among patients receiving DRZ, the standardized incidence rate (SIR) for AML/MDS was 613.6 compared with 202.4 for those not receiving DRZ (P = .0990).

Adding DRZ to ABVE and ABVE-PC may have increased the incidence of SMN and AML/MDS.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chelating Agents / adverse effects. Hodgkin Disease / drug therapy. Leukemia, Myeloid / chemically induced. Myelodysplastic Syndromes / chemically induced. Neoplasms, Second Primary / chemically induced. Razoxane / adverse effects

[MeSH-minor] Acute Disease. Adolescent. Cohort Studies. Enzyme Inhibitors / adverse effects. Female. Follow-Up Studies. Heart Diseases / chemically induced. Heart Diseases / prevention & control. Humans. Incidence. Lung Diseases / chemically induced. Lung Diseases / prevention & control. Male. Neoplasm Staging. Osteosarcoma / chemically induced. Risk Assessment. Risk Factors. Thyroid Neoplasms / chemically induced. Time Factors. Topoisomerase II Inhibitors

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[CommentIn] J Clin Oncol. 2007 Jul 20;25(21):3179; author reply 3180 [17634500.001]

[CommentIn] J Clin Oncol. 2007 Oct 10;25(29):4689-90; author reply 4690-1 [17925567.001]

(PMID = 17290056.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial

[Publication-country] United States

[Chemical-registry-number] 0 / Chelating Agents; 0 / Enzyme Inhibitors; 0 / Topoisomerase II Inhibitors; 5AR83PR647 / Razoxane

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute myeloid leukemia or myelodysplastic syndrome in randomized controlled clinical trials of cancer chemotherapy with granulocyte colony-stimulating factor: a systematic review.

PURPOSE: To evaluate the risk of acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) and overall mortality in patients receiving chemotherapy with or without granulocyte colony-stimulating factor (G-CSF), a systematic review of randomized controlled trials (RCTs) was conducted.

Eligibility included solid tumor or lymphoma patients randomly assigned to chemotherapy with or without G-CSF support, > or = 2 years of follow-up, and reporting AML/MDS or all second malignancies.

At mean and median follow-up across studies of 60 and 53 months, respectively, AML/MDS was reported in 22 control patients and 43 G-CSF-treated patients, with an estimated RR of 1.92 (95% CI, 1.19 to 3.07; P = .007) and AR increase of 0.41% (95% CI, 0.10% to 0.72%; P = .009).

CONCLUSION: Delivered chemotherapy dose-intensity and risk of AML/MDS are increased but all-cause mortality is decreased in patients receiving chemotherapy with G-CSF support.

[MeSH-major] Granulocyte Colony-Stimulating Factor / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy

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(PMID = 20385991.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor

[Number-of-references] 58

   

[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

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(PMID = 16687173.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Historical Article; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

   

[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

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[Copyright] (c) 2007 Wiley-Liss, Inc.

(PMID = 17551948.001).

[ISSN] 1045-2257

[Journal-full-title] Genes, chromosomes & cancer

[ISO-abbreviation] Genes Chromosomes Cancer

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / MAML2 protein, human; 0 / MLL protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The paradox of 20q11.21 amplification in a subset of cases of myeloid malignancy with chromosome 20 deletion.

Deletion of the long arm of one chromosome 20 (del(20q)) is a well-recognized abnormality in acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) and is presumed to cause loss of a tumor suppressor gene at 20q12.

In a previously published series of MDS and AML cases, which had lost this region via unbalanced translocation, around 40% of cases were shown to have additional copies of the chromosome 20 abnormalities, with resulting gain or amplification of the retained parts of chromosome 20, most often 20q11.2.

Localized and high level amplification of the common 250 kb region is evidence for activation of an oncogene in this region in these MDS and AML cases.

Cases with 20q11.21 amplification tended to have a high proportion of erythroblasts in the marrow, with two cases diagnosed as erythroleukemia (AML-M6).

Chromosome sub-band 20q11.21 amplification may therefore prove to be a marker of a specific subset of AML/MDS with a significant erythroid component.

[MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 20. Myelodysplastic Syndromes / genetics

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[Copyright] © 2010 Wiley-Liss, Inc.

(PMID = 20645416.001).

[ISSN] 1098-2264

[Journal-full-title] Genes, chromosomes & cancer

[ISO-abbreviation] Genes Chromosomes Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] DNA hypermethylation of myeloid cells, a novel therapeutic target in MDS and AML.

In vitro, inhibition of methylation using azanucleosides results in modest differentiation of transformed myeloid cell lines.

In vivo, low doses of these agents induce DNA demethylation of malignant myeloid cells.

Indeed, the first drug specifically approved for the treatment of myelodysplastic syndrome (MDS) was the azanucleoside 5-azacytidine (Vidaza).

FDA for treatment of MDS of all subtypes.

About 30 % of MDS patients with an abnormal karyotype have normalization of their karyotype after receiving the drug.

[MeSH-major] Amyotrophic Lateral Sclerosis / drug therapy. CpG Islands / drug effects. DNA Methylation / drug effects. Drug Delivery Systems / methods. Myelodysplastic Syndromes / drug therapy. Myeloid Cells / drug effects. Nucleosides / therapeutic use

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(PMID = 17076647.001).

[ISSN] 1873-4316

[Journal-full-title] Current pharmaceutical biotechnology

[ISO-abbreviation] Curr Pharm Biotechnol

[Language] eng

[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 / Antineoplastic Agents; 0 / Nucleosides

[Number-of-references] 49

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

A total of 21 out of 22 patients with AML/myelodysplastic syndrome (MDS) achieved remission after transplant (16 with relapsed/refractory AML).

Five out of the 12 patients (42%) with AML/MDS with <15% BM blasts survived long term as compared with none with more advanced disease (P=0.03).

HaploSCT with this fludarabine, melphalan and thiotepa and ATG RIC is an effective, well-tolerated conditioning regimen for patients with AML/MDS with low disease burden at the time of transplant and allowed a high rate of engraftment in patients without DSA.

[MeSH-minor] Adolescent. Adult. Antilymphocyte Serum / administration & dosage. Child. Female. Hematologic Neoplasms / therapy. Humans. Infection / etiology. Leukemia, Myeloid, Acute / therapy. Male. Melphalan / administration & dosage. Middle Aged. Myelodysplastic Syndromes / therapy. Survival Rate. T-Lymphocytes / immunology. Thiotepa / administration & dosage. Transplantation, Homologous. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Young Adult

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(PMID = 19668237.001).

[ISSN] 1476-5365

[Journal-full-title] Bone marrow transplantation

[ISO-abbreviation] Bone Marrow Transplant.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P01 CA055164

[Publication-type] Clinical Trial, Phase II; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Myeloablative Agonists; 905Z5W3GKH / Thiotepa; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan

[Other-IDs] NLM/ NIHMS598753; NLM/ PMC4080627

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Fluorescence in situ hybridization analysis of 110 hematopoietic disorders with chromosome 5 abnormalities: do de novo and therapy-related myelodysplastic syndrome-acute myeloid leukemia actually differ?

A retrospective cytogenetic study of acute myeloid leukemias (AML) and myelodysplastic syndromes (MDS) was conducted by the Groupe Francophone de Cytogénétique Hématologique (GFCH) to evaluate the structural abnormalities of chromosome 5 associated with other chromosomal abnormalities, in particular of chromosome 7, in these pathologies.

In all, 110 cases of AML/MDS were recruited based on the presence of chromosome 5 abnormalities under conventional cytogenetics and supplemented by a systematic fluorescence in situ hybridization study of chromosomes 5 and 7.

Among 82 patients with de novo AML/MDS, 63 were older than 60 years.

Systematic investigation of the exposure to mutagens and oncogenes is thus essential to specify the factors potentially involved in MDS/AML with 5q abnormalities.

[MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 5. Chromosomes, Human, Pair 7. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents / adverse effects. Chromosome Deletion. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasms, Radiation-Induced. Translocation, Genetic

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(PMID = 17574959.001).

[ISSN] 0165-4608

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents

   

[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.

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(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