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[Title] Selective KIT inhibitor KI-328 and HSP90 inhibitor show different potency against the type of KIT mutations recurrently identified in acute myeloid leukemia.

Activating mutations of KIT play an important role in the pathophysiology of several human malignancies, including acute myeloid leukemia.

Here we examined the potency of a novel KIT inhibitor KI-328 against different types of mutant KIT kinases recurrently identified in AML.

Furthermore, HSP90 inhibitors suppress the growth of D816V-KIT-expressing cells at the concentration at which the growth of other mutant-KIT-expressing cells is not affected.

[MeSH-major] Antineoplastic Agents / pharmacology. Carbamates / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Mutation. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-kit / antagonists & inhibitors. Proto-Oncogene Proteins c-kit / genetics. Pyrimidines / pharmacology

[MeSH-minor] Cell Line, Tumor. Humans. K562 Cells

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(PMID = 20890793.001).

[ISSN] 1865-3774

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

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

[Publication-country] Japan

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbamates; 0 / HSP90 Heat-Shock Proteins; 0 / KI 328; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit

   

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[Title] Myeloid sarcoma of the prostate revealed by urinary retention: a case report.

Myeloid sarcoma (MS) of the prostate is very uncommon with only 17 reported cases in the literature.

Here, a singular case of a MS of the prostate discovered through investigations for urinary retention and revealing an acute leukaemia classified as an acute myeloid leukaemia (AML) with inversion 16 (inv16) according to the World Health Organization (WHO) classification (AML-M4 with inv16 in the French-American-British (FAB) classification) in a 65-year-old man is presented.

None of the previously reported and reviewed cases of prostatic MS were of AML-M4 type.

Such a translocation was recently described in some acute myeloid processes.

Radiation therapy could be beneficial for the localised disease of the prostate.

Allogenic haematopoietic stem cell transplantation is also a promising therapy for MS.

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(PMID = 21686890.001).

[ISSN] 1757-790X

[Journal-full-title] BMJ case reports

[ISO-abbreviation] BMJ Case Rep

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC3029613

   

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[Title] beta-Tryptase up-regulates vascular endothelial growth factor expression via proteinase-activated receptor-2 and mitogen-activated protein kinase pathways in bone marrow stromal cells in acute myeloid leukemia.

Tryptases are predominantly mast cell-specific serine proteases with pleiotropic biological activities.

Recently, significant amounts of tryptases have been shown to be produced by myeloblasts in certain patients with acute myeloid leukemia (AML), but the function of secreted tryptases in pathological circumstances remains unknown.

In this study, we investigated whether beta-tryptase affects the expression of vascular endothelial growth factor (VEGF) in bone marrow stromal cells (BMSCs) in AML.

We detected the expression of proteinase-activated receptor-2 (PAR-2) on AML BMSCs and found that beta-tryptase significantly up-regulated VEGF mRNA and protein expression in a dose-dependent manner by real-time PCR, Western blot, and ELISA.

These results suggest that beta-tryptase up-regulates VEGF production in AML BMSCs via the PAR-2, ERK1/2, and p38MAPK signaling pathways.

[MeSH-major] Bone Marrow Cells / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukemia, Promyelocytic, Acute / metabolism. Mitogen-Activated Protein Kinases / metabolism. Receptor, PAR-2 / metabolism. Stromal Cells / metabolism. Tryptases / metabolism. Vascular Endothelial Growth Factor A / metabolism

[MeSH-minor] Blotting, Western. Cell Proliferation. Cells, Cultured. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Humans. Immunoenzyme Techniques. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Up-Regulation

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(PMID = 20578818.001).

[ISSN] 1029-2403

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptor, PAR-2; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.4.21.59 / Tryptases

   

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[Title] Aberrant CpG island methylation in acute myeloid leukemia is accentuated at relapse.

DNA methylation of CpG islands around gene transcription start sites results in gene silencing and plays a role in leukemia pathophysiology.

Its impact in leukemia progression is not fully understood.

We performed genomewide screening for methylated CpG islands and identified 8 genes frequently methylated in leukemia cell lines and in patients with acute myeloid leukemia (AML): NOR1, CDH13, p15, NPM2, OLIG2, PGR, HIN1, and SLC26A4.

We assessed the methylation status of these genes and of the repetitive element LINE-1 in 30 patients with AML, both at diagnosis and relapse.

Abnormal methylation was found in 23% to 83% of patients at diagnosis and in 47% to 93% at relapse, with CDH13 being the most frequently methylated.

We observed concordance in methylation of several genes, confirming the presence of a hypermethylator pathway in AML.

DNA methylation levels increased at relapse in 25 of 30 (83%) patients with AML.

These changes represent much larger epigenetic dysregulation, since methylation microarray analysis of 9008 autosomal genes in 4 patients showed hypermethylation ranging from 5.9% to 13.6% (median 8.3%) genes at diagnosis and 8.0% to 15.2% (median 10.6%) genes in relapse (P < .001).

Our data suggest that DNA methylation is involved in AML progression and provide a rationale for the use of epigenetic agents in remission maintenance.

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(PMID = 18523155.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P01 CA108631; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / 5P01CA108631-03; United States / NCI NIH HHS / CA / 5P50CA100632-05

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Other-IDs] NLM/ PMC2515110

   

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[Title] Evaluation of oxidative status and depression-like responses in Brown Norway rats with acute myeloid leukemia.

It has been proved that oxidative stress increases when leukemia is accompanied by depression.

The aim of this study was to determine whether the acute myeloid leukemia of Brown Norway rats, which is accompanied by oxidative stress, evoked behavioral and receptor changes resembling alterations characteristic of rat models of depression.

Leukemia was induced through intraperitoneal injection of 10(7) promyelocytic leukemia cells to the Brown Norway rats.

Radioligand binding assay was used to assess of the effect of leukemia on cortical receptors.

Leukemia influenced locomotory activity as well as forced swim test behavior in a 34-day series of experiments.

Signs of oxidative stress in leukemic rats were observed in each examined stage of leukemia development.

Upregulation of 5-HT(2A) receptors was observed in rat cortex after 30 days of leukemia development but not in 34-days series compared with the control.

It is concluded that disturbances in antioxidant system in brain cortex were accompanied by an activation of glycine sites of the NMDA receptor complex, regardless of stage of leukemia development, which are characteristic of model of depression.

Findings of our study demonstrate the link between glutamatergic activity, oxidative stress and leukemia.

[MeSH-major] Depression / etiology. Disease Models, Animal. Leukemia, Myeloid, Acute / complications. Oxidative Stress / physiology

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(PMID = 19268504.001).

[ISSN] 1878-4216

[Journal-full-title] Progress in neuro-psychopharmacology & biological psychiatry

[ISO-abbreviation] Prog. Neuropsychopharmacol. Biol. Psychiatry

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Receptors, Biogenic Amine; 9007-73-2 / Ferritins; EC 1.14.99.3 / Heme Oxygenase (Decyclizing); GAN16C9B8O / Glutathione; O9MIA842K9 / Biliverdine

   

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[Title] Comparison of cytogenetic clonal evolution patterns following allogeneic hematopoietic transplantation versus conventional treatment in patients at relapse of AML.

Relapse of acute myelogenous leukemia has been associated with clonal cytogenetic evolution, but no study focused specifically on relapse after allogeneic hematopoietic stem cell transplantation (HSCT).

We compared karyotypes in 160 patients at both diagnosis and relapse either after allo-HSCT (n = 26) or standard chemotherapy (n = 134) using chromosome banding analysis combined with fluorescein in situ hybridization.

At diagnosis, aberrant karyotypes were more frequent in the HSCT than in the chemotherapy cohort (16 of 26; 61.5% versus 63 of 134; 47.0%).

Differences in the karyotypes between diagnosis and relapse were more frequent in the allo-cohort (14 of 26; 53.8% versus 49 of 134; 36.6%) than in the conventional cohort (n.s.

The mean number of cytogenetic alterations per patient was increasing from 2.0 at diagnosis to 4.0 at relapse in the allo-cohort, in the conventionally treated patients from 0.9 to 1.3 (both P < .001).

Thus, higher frequencies of clonal evolution and increasing cytogenetic complexity were observed in the stem cell recipients probably related to the more unfavorable cytogenetic profiles already depicted at diagnosis.

[MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy

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[Copyright] Copyright © 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.

(PMID = 20558312.001).

[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

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Genetic parameter estimates of meat quality traits in Duroc pigs selected for average daily gain, longissimus muscle area, backfat thickness, and intramuscular fat content.

Using a multitrait animal model BLUP, selection was conducted over seven generations for growth rate (ADG), real-time ultrasound LM area (LMA), backfat thickness (BF), and intramuscular fat content (IMF) to develop a new line of purebred Duroc pigs with enhanced meat production and meat quality.

Genetic correlations of IMF with ADG and BF were low and positive, but low and negative with LMA.

Tenderness was correlated negatively with ADG (-0.44) and BF (-0.59), but positively correlated with LMA (0.32).

The genetic correlation between LMA and DL was positive and high (0.64).

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(PMID = 16100060.001).

[ISSN] 1525-3163

[Journal-full-title] Journal of animal science

[ISO-abbreviation] J. Anim. Sci.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 9007-34-5 / Collagen

   

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[Title] Safe and feasible outpatient treatment following induction and consolidation chemotherapy for patients with acute leukaemia.

Traditionally, patients with acute leukaemia are admitted to hospital during chemotherapy-induced pancytopenia, although a few recent reports have reported the feasibility and safety of outpatient treatment.

We have developed an outpatient treatment programme for patients with acute leukaemia incorporating comprehensive patient education for self-care management at home during pancytopenia and involvement of patients in care of their tunnelled central venous catheter (CVC).

Herein, we report the results of outpatient treatment of 60 patients with acute leukaemia (54 with acute myeloid leukaemia) followed prospectively in the period from March 2004 to 2007.

We conclude that outpatient treatment of patients with acute leukaemia is feasible and safe.

[MeSH-major] Ambulatory Care / methods. Anti-Infective Agents / administration & dosage. Leukemia / drug therapy. Neutropenia / drug therapy. Pancytopenia / drug therapy

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Prospective Studies

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(PMID = 20002732.001).

[ISSN] 1600-0609

[Journal-full-title] European journal of haematology

[ISO-abbreviation] Eur. J. Haematol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Anti-Infective Agents

   

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[Title] Molecular and chromosomal alterations: new therapies for relapsed acute myeloid leukemia.

Acute myeloid leukemia (AML) remains the most common form of leukemia and the most common cause of leukemia death.

Although conventional chemotherapy can cure between 25 and 45% of AML patients, the majority of patients die after relapse or of complications associated with treatment.

Thus, more specific and less toxic treatments for AML patients are needed, especially for elderly patients.

An indispensable prerequisite to investigate tailored approaches for AML is the recent progress in the understanding the molecular features that distinguish leukemia progenitors from normal hematopoietic counterparts and the identification of a variety of dysregulated molecular pathways.

In this review, we describe some of the signaling pathways that are aberrantly regulated in AML, with a specific focus on their pathogenetic and therapeutic significance, and we examine some recent therapies directed against these targets, used in clinical trial for relapsed patients or unfit for conventional chemotherapy.

[MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Signal Transduction / drug effects

[MeSH-minor] Antineoplastic Agents / pharmacology. Drug Design. Genetic Predisposition to Disease / genetics. Humans. Immunologic Factors / pharmacology. Remission Induction. Translocation, Genetic

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(PMID = 18534059.001).

[ISSN] 1607-8454

[Journal-full-title] Hematology (Amsterdam, Netherlands)

[ISO-abbreviation] Hematology

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunologic Factors; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases

[Number-of-references] 126

   

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[Title] Prognostic significance of FLT3 mutations in pediatric non-promyelocytic acute myeloid leukemia.

This is the first study of FLT3 mutations in pediatric non-promyelocytic AML patients that received the same treatment scheme in single institute.

Patients with FLT3/TKD remain alive after autologous stem cell transplantation.

The disease-free survival (DFS) of patients with FLT3/ITD (0%) was significantly lower than that of the others (52%).

New therapeutic scheme such as stem cell transplantation with more intensive conditioning just after complete remission could be applied in pediatric non-promyelocytic AML patients with the FLT3/ITD mutation.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics

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(PMID = 15863200.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

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[Title] Leukemia regression by vascular disruption and antiangiogenic therapy.

Acute myelogenous leukemias (AMLs) and endothelial cells depend on each other for survival and proliferation.

Monotherapy antivascular strategies such as targeting vascular endothelial growth factor (VEGF) has limited efficacy in treating AML.

Thus, in search of a multitarget antivascular treatment strategy for AML, we tested a novel vascular disrupting agent, OXi4503, alone and in combination with the anti-VEGF antibody, bevacizumab.

Using xenotransplant animal models, OXi4503 treatment of human AML chloromas led to vascular disruption in leukemia cores that displayed increased leukemia cell apoptosis.

However, viable rims of leukemia cells remained and were richly vascular with increased VEGF-A expression.

To target this peripheral reactive angiogenesis, bevacizumab was combined with OXi4503 and abrogated viable vascular rims, thereby leading to enhanced leukemia regression.

In a systemic model of primary human AML, OXi4503 regressed leukemia engraftment alone and in combination with bevacizumab.

Differences in blood vessel density alone could not account for the observed regression, suggesting that OXi4503 also exhibited direct cytotoxic effects on leukemia cells.

Together, these data show that OXi4503 alone is capable of regressing AML by a multitargeted mechanism and that the addition of bevacizumab mitigates reactive angiogenesis.

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[CommentIn] Blood. 2010 Sep 2;116(9):1389-90 [20813902.001]

(PMID = 20472832.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / K08 DK067359; United States / NCI NIH HHS / CA / CA084408; United States / NCI NIH HHS / CA / CA089655; United States / NCI NIH HHS / CA / R01 CA089655; United States / NHLBI NIH HHS / HL / R01 HL070738; United States / NCI NIH HHS / CA / R01 CA084408

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Diphosphates; 0 / Il2rg protein, mouse; 0 / Interleukin Receptor Common gamma Subunit; 0 / Oxi 4503; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Stilbenes; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 2S9ZZM9Q9V / Bevacizumab

[Other-IDs] NLM/ PMC2938842

   

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[Title] High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder.

Familial platelet disorder (FPD), a rare autosomal dominant disorder characterized by quantitative and qualitative platelet abnormalities, is considered as a model of genetic predisposition to acute myeloid leukemia (AML).

So far, monoallelic RUNX1 germline mutations have been found in 19 of 20 families with reported FPD, and the analysis of blast cells from only 5 patients at acute leukemia (AL) stage has shown no additional RUNX1 abnormality.

In addition to the germline RUNX1 mutation, we identified a second RUNX1 alteration in 6 AML cases (acquired point mutations in 4 cases and duplication of the altered RUNX1 allele associated with acquired trisomy 21 in 2 other cases).

Although haploinsufficiency of RUNX1 causes FPD, our findings suggest that a second genetic event involving RUNX1 is often associated with progression to AML.

[MeSH-major] Blood Platelet Disorders / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics

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(PMID = 19357396.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

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

[Publication-country] United States

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

   

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[Title] Pseudohypopyon: Extramedullary relapse of acute myelogenous leukemia with poor prognosis.

She was diagnosed with acute myelogenous leukemia.

[MeSH-major] Anterior Chamber / pathology. Eye Diseases / diagnosis. Leukemia, Myelomonocytic, Acute / diagnosis. Neoplasm Recurrence, Local / diagnosis

[MeSH-minor] Antimetabolites, Antineoplastic / therapeutic use. Cytarabine / therapeutic use. Female. Humans. Infant. Injections, Spinal. Prognosis. Suppuration / diagnosis

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[Copyright] (c) 2008 Wiley-Liss, Inc.

(PMID = 19090546.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine

   

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[Title] Acute myeloid leukaemia diagnosed by intra-oral myeloid sarcoma. A case report.

Myeloid sarcoma (MS) is a rare extramedullary malignant tumor composed of immature myeloid cells.

It is strongly associated with a well known or covert acute myeloid leukaemia, chronic myeloproliferative diseases or myelodysplastic syndromes.

An unusual case of acute myeloid leukaemia, which was diagnosed by mandibular MS that was developed in the alveolar socket after a dental extraction, is reported.

The histological examination (including immunohistochemical analysis) of a subsequent biopsy showed infiltration of the oral mucosa by neoplastic cells.

This lesion was therefore classified as acute myeloid leukaemia.

The patient was referred to oncologists that confirmed the initial diagnosis.

Forty days later, a relapse of the disease, which appeared as a great-ulcerated lesion, was developed in the hard palate.

Review of the literature shows no report of intraoral relapse and particularly multiple relapse of a MS that involves the oral cavity.

Even though MS is encountered infrequently in the oral cavity, it should be considered in the differential diagnosis of conditions (especially tumors) with a similar clinical appearance.

[MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Neoplasms, Multiple Primary / diagnosis. Sarcoma, Myeloid / diagnosis

[MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Biopsy. Diagnosis, Differential. Etoposide / therapeutic use. Fatal Outcome. Female. Humans. Mouth Mucosa / pathology. Mouth Neoplasms

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[Cites] J Oral Maxillofac Surg. 1990 Jul;48(7):748-52 [2193130.001]

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(PMID = 20512638.001).

[ISSN] 1936-0568

[Journal-full-title] Head and neck pathology

[ISO-abbreviation] Head Neck Pathol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 6PLQ3CP4P3 / Etoposide

[Other-IDs] NLM/ PMC2878628

   

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[Title] In vitro generation of tumor specific T cells that recognize a shared antigen of AML: molecular characterization of TCR genes.

We present data demonstrating in vitro induction of autologous acute myelogenous leukemia (AML)-specific CTL.

The specific T cell receptor has been identified and cloned.

The CTL demonstrated specific lysis to autologous tumor blasts, but not to autologous BLCL or the NK-sensitive target K562.

The clone secreted GM-CSF, TNFa, and IFNg when stimulated with AML blasts from 3 of 11 patients or cell lines tested, but not with K562 or autologous B-LCL.

These three AML samples share a single HLA Class I antigen, HLA-A24.

The T cell receptor genes identified by molecular methods are Vbeta7.9-J2.3-Cbeta2 and Valpha17-J49-Calpha.

[MeSH-major] Antigens, Neoplasm / immunology. HLA Antigens / immunology. Leukemia, Myeloid / immunology. Receptors, Antigen, T-Cell / genetics. T-Lymphocytes, Cytotoxic / immunology

[MeSH-minor] Acute Disease. Amino Acid Sequence. CD8-Positive T-Lymphocytes / immunology. Cell Line, Tumor. Humans. Molecular Sequence Data

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[CommentIn] Leuk Res. 2007 Feb;31(2):127-8 [17137625.001]

(PMID = 16750565.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / HLA Antigens; 0 / Receptors, Antigen, T-Cell

   

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[Title] Wilms tumor 1 gene mutations are associated with a higher risk of recurrence in young adults with acute myeloid leukemia: a study from the Acute Leukemia French Association.

BACKGROUND: Wilms tumor 1 (WT1) is a transcription factor that is overexpressed in most acute myeloid leukemias (AMLs).

Recently, 2 groups reported that WT1 mutations occur in approximately 10% of normal karyotype AMLs and are an independent predictor of poor outcome in this subgroup of patients with AML.

METHODS: The authors studied a cohort of 268 young adults (ages 15-50 years) with AML who were treated on the Acute Leukemia French Association 9802 trial.

Within the subgroup of patients who had normal karyotype AML (n = 106), WT1 mutation was identified as an independent adverse prognostic factor for the risk of recurrence.

CONCLUSIONS: The current results indicted that WT1 mutations represent an adverse prognostic factor in young adults with AML.

Prospective trials should confirm the clinical relevance of WT1 mutations in relation to other prognostic factors in patients with AML.

[MeSH-major] Genes, Wilms Tumor. Leukemia, Myeloid, Acute / genetics

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(PMID = 19536888.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

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

[Publication-country] United States

   

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[Title] Willow leaves' extracts contain anti-tumor agents effective against three cell types.

Many non-natural, synthetic drugs cause severe side effects that were not acceptable except as treatments of last resort for terminal diseases such as cancer.

In vitro the willow extract could kill the majority (75%-80%) of abnormal cells among primary cells harvested from seven patients with acute lymphoblastic leukemia (ALL) and 13 with AML (acute myeloid leukemia).

DNA fragmentation patterns within treated cells inferred targeted cell death by apoptosis had occurred.

The metabolites within the willow extract may act as tumor inhibitors that promote apoptosis, cause DNA damage, and affect cell membranes and/or denature proteins.

[MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Cell Line, Tumor / drug effects. Plant Extracts / pharmacology. Plant Leaves / chemistry. Salix

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(PMID = 17264881.001).

[ISSN] 1932-6203

[Journal-full-title] PloS one

[ISO-abbreviation] PLoS ONE

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Benzyl Alcohols; 0 / Glucosides; 0 / Plant Extracts; 4649620TBZ / salicin; FA1N0842KB / salicyl alcohol

[Other-IDs] NLM/ PMC1779808

[General-notes] NLM/ Original DateCompleted: 20070723

   

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[Title] Overexpression of CDX2 perturbs HOX gene expression in murine progenitors depending on its N-terminal domain and is closely correlated with deregulated HOX gene expression in human acute myeloid leukemia.

The mechanisms underlying deregulation of HOX gene expression in AML are poorly understood.

Deletion of the N-terminal domain of Cdx2 abrogated its ability to perturb Hox gene expression and to cause acute myeloid leukemia (AML) in mice.

In contrast inactivation of the putative Pbx interacting site of Cdx2 did not change the leukemogenic potential of the gene.

In an analysis of 115 patients with AML, expression levels of CDX2 were closely correlated with deregulated HOX gene expression.

All patients with AML with normal karyotype tested were negative for CDX1 and CDX4 expression.

They furthermore correlate the level of CDX2 expression with HOX gene expression in human AML and support a potential role of CDX2 in the development of human AML with aberrant Hox gene expression.

[MeSH-major] Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Transcription Factors / genetics

[MeSH-minor] Adult. Animals. Bone Marrow Cells / cytology. Bone Marrow Cells / physiology. Bone Marrow Transplantation. Cell Line, Tumor. Gene Expression Profiling. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / physiology. Humans. Karyotyping. Mice. Mutagenesis. NIH 3T3 Cells. Protein Structure, Tertiary. Translocation, Genetic. Up-Regulation / physiology

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(PMID = 17855634.001).

[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 / CDX2 protein, human; 0 / Cdx2 protein, mouse; 0 / Homeodomain Proteins; 0 / Transcription Factors

   

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[Title] [Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and acute myeloid leukemia and recurrent chromosome translocations].

OBJECTIVE: To investigate the impact of GSTM1, GSTT1 and NQO1 genotypes on susceptibility to acute myeloid leukemia (AML) and recurrent chromosome translocations of AML.

METHODS: GSTT1, GSTM1 and NQO1 genotypes were detected in 228 adult patients with de novo AML and 241 controls by PCR or PCR-RFLP.

RESULTS: The frequency of GSTM1 null genotype in the AML patients was 62.3%, significantly higher than that in the normal controls (52.7%, P = 0.036), however, no significant difference was found in the incidence of GSTT1 null genotype.

The frequencies of NQO1(C609T) C/T and T/T genotypes were 53.1% and 25.0% respectively among the total AML patients (53.1% and 25.0% respectively), 64.3% and 25.0% respectively among the AML patients with t (8;.

21) (q22; q22)/AML-ETO fusion gene, and 57.1% and 26.0% respectively among the AML patient with t (15;.

21) (q22; q22)/AML-ETO (+) AML was 4.487 (95% CI: 1.282-15.705) for the subjects with NQO1(C609T) C/T genotype, and was 6.293 (95% CI: 1.536-25.782) for the subjects with NQO1(C609T) T/T genotype.

17) (q22; q11)/PML-RARalpha (+) AML was 2.531 (95% CI: 1.286-4.981) for the subjects with NQO1(C609T) C/T genotype, and was 4.149 (95% CI: 1.856-9.275) for the subjects with NQO1(C609T) T/T genotype.

CONCLUSION: Determination of the NQO1(C609T) genotypes may be used as a stratification marker to predict high-risk individuals for AML, especially for AML with t (8;.

21) (q22; q22)/AML-ETO fusion gene and t (15;.

[MeSH-major] Chromosome Aberrations. Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics

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(PMID = 16321221.001).

[ISSN] 0376-2491

[Journal-full-title] Zhonghua yi xue za zhi

[ISO-abbreviation] Zhonghua Yi Xue Za Zhi

[Language] chi

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

[Publication-country] China

[Chemical-registry-number] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1

   

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Most of these patients are ventilated through endotracheal tubes (ETTs), others through laryngeal mask airways (LMAs).

The cuffs of both ETTs and LMAs inflate with increases in altitude as barometric pressure decreases (30 mbar/1000 feet).

METHODS: The change in dimensions of the inflated cuffs of a size 8 ETT and a size 5 LMA were measured with digital callipers at 1000 feet intervals in the unpressurised cabin of an Agusta 109 helicopter used by the Warwickshire and Northamptonshire Air Ambulance.

RESULTS: A linear expansion in cuff dimensions as a function of altitude increase was identified.

CONCLUSION: The data for LMA cuff expansion failed to show significant correlation with altitude change.

Further work is required to determine a similar rule of thumb for LMA cuff deflation.

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[CommentIn] Emerg Med J. 2007 Aug;24(8):605 [17652705.001]

(PMID = 17351218.001).

[ISSN] 1472-0213

[Journal-full-title] Emergency medicine journal : EMJ

[ISO-abbreviation] Emerg Med J

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2660019

   

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[Title] Spinal osteomyelitis due to Aspergillus flavus in a child: a rare complication after haematopoietic stem cell transplantation.

We report the case of a child affected by acute myeloid leukaemia who was treated with allogeneic haematopoietic stem cell transplantation and developed cervicothoracic spinal osteomyelitis due to Aspergillus flavus.

The diagnosis was difficult on a clinical basis, but made possible by conventional radiography and MRI.

[MeSH-major] Aspergillosis / complications. Hematopoietic Stem Cell Transplantation / adverse effects. Osteomyelitis / microbiology. Spinal Diseases / microbiology

[MeSH-minor] Aspergillus flavus / isolation & purification. Bronchoalveolar Lavage. Diagnosis, Differential. Fatal Outcome. Fever / etiology. Humans. Hydrocephalus / etiology. Infant. Leukemia, Myeloid, Acute / surgery. Magnetic Resonance Imaging. Male. Radiography. Rare Diseases. Recurrence. Spine / diagnostic imaging. Spine / pathology

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[Cites] Pediatr Radiol. 2003 Jul;33(7):453-60 [12739082.001]

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(PMID = 18392819.001).

[ISSN] 0301-0449

[Journal-full-title] Pediatric radiology

[ISO-abbreviation] Pediatr Radiol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

   

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[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

   

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[Title] Drug delivery in acute myeloid leukemia.

BACKGROUND: Acute myeloid leukemia was among the first malignancies to be cured by drug therapy alone, but overall survival rates remain unsatisfactory and have changed little over the past 20 years.

OBJECTIVE: We have chosen acute myeloid leukemia as a disease prototype to review established and novel targeted approaches in leukemia treatment.

CONCLUSION: While the toxicity profile of chemotherapeutics has been improved by liposomal formulations and antibody conjugation for leukemia-directed uptake, their efficacy has probably not changed significantly.

Further improvements may result from the characterization of novel acute myeloid leukemia (AML) cell surface receptors and of leukemic stem cells, as well as from the design of leukemia-targeted gene therapy vectors.

[MeSH-minor] Antibodies, Monoclonal / administration & dosage. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Drug Delivery Systems. Genetic Therapy. Humans. Integrin alpha4beta1 / antagonists & inhibitors. Leukemia, Myeloid, Acute / drug therapy. Liposomes. Neoplastic Stem Cells / drug effects. Sialic Acid Binding Ig-like Lectin 3

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(PMID = 18532921.001).

[ISSN] 1742-5247

[Journal-full-title] Expert opinion on drug delivery

[ISO-abbreviation] Expert Opin Drug Deliv

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Integrin alpha4beta1; 0 / Liposomes; 0 / Sialic Acid Binding Ig-like Lectin 3

[Number-of-references] 114

   

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[Title] Selective killing of leukemia and lymphoma cells ectopically expressing hCGbeta by a conjugate of curcumin with an antibody against hCGbeta subunit.

EXPERIMENTAL DESIGN: The study was carried out on MOLT-4 and U-937 cells expressing hCGbeta and on peripheral blood leukocytes of acute myeloid leukemia (AML) patients.

RESULTS: The antibody did not impair the growth of MOLT-4 and U-937 cells in culture.

Its conjugate with curcumin, however, was lethal to both cell lines.

The immunoconjugate killed tumor cells bearing the CD33 marker of an AML patient expressing hCGbeta but did not have a similar action on cells of another AML patient with the CD13 marker but who was negative for hCGbeta.

[MeSH-major] Chorionic Gonadotropin, beta Subunit, Human / metabolism. Curcumin / metabolism. Leukemia / drug therapy. Lymphoma / drug therapy

[MeSH-minor] Aged. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Cell Separation. Drug Design. Female. Humans. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Sialic Acid Binding Ig-like Lectin 3. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology. U937 Cells

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(PMID = 19127081.001).

[ISSN] 1423-0232

[Journal-full-title] Oncology

[ISO-abbreviation] Oncology

[Language] eng

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

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; IT942ZTH98 / Curcumin

   

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METHODS: We used modeling techniques to assess the cost-effectiveness of posaconazole versus FLU or ITRA in the prevention of IFIs among patients with acute myelogenous leukemia (AML) or myelodysplastic syndromes (MDS) and chemotherapy-induced neutropenia.

CONCLUSIONS: We conclude that posaconazole is very likely to be a cost-effective alternative to FLU or ITRA in the prevention of IFIs among neutropenic patients with AML and MDS, and may result in cost savings.

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(PMID = 19508661.001).

[ISSN] 1524-4733

[Journal-full-title] Value in health : the journal of the International Society for Pharmacoeconomics and Outcomes Research

[ISO-abbreviation] Value Health

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antifungal Agents; 304NUG5GF4 / Itraconazole; 8VZV102JFY / Fluconazole

   

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[Title] Achyrocline satureioides (LAM.) DC (Marcela): antimicrobial activity on Staphylococcus spp. and immunomodulating effects on human lymphocytes.

Achyrocline satureioides (LAM.

They were isolated from 18 patients with acne lesions and from 7 patients infected with Staphylococcus spp. (5 strains were taken from catheters and 2 from wounds).

On the other hand, cultures of lymphocytes were made from those patients who displayed infections caused by Staphylococcus spp. and from 12 control non-infected individuals.

The A. satureiodes decoction inhibited 95% of the isolated Staphylococcus spp. strains and stimulated the lymphocyte expansion, of which 40% were CD8+ T cells.

[MeSH-minor] Acne Vulgaris / microbiology. Adolescent. Adult. Bacteremia / microbiology. Catheterization. Cells, Cultured / drug effects. Drug Evaluation, Preclinical. Humans. Lymphocyte Activation / drug effects. Phytohemagglutinins / pharmacology. Plant Leaves / chemistry. Staphylococcal Infections / microbiology. Staphylococcal Skin Infections / microbiology. Wound Infection / microbiology

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(PMID = 18293658.001).

[ISSN] 0187-4640

[Journal-full-title] Revista latinoamericana de microbiología

[ISO-abbreviation] Rev. Latinoam. Microbiol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Mexico

[Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Anti-Bacterial Agents; 0 / Phytohemagglutinins; 0 / Plant Extracts

   

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[Title] Volatile components of Centaurea eryngiodes Lam. and Centaurea iberica Trev.var. hermonis Bois. Lam.,two Asteraceae growing wild in Lebanon.

The volatile components of the flowerheads of Centaurea eryngioides Lam. and Centaurea iberica Trev. var. hermonis Boiss. Lam. were obtained by hydrodistillation and identified by GC and GC-MS.

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(PMID = 16317829.001).

[ISSN] 1478-6419

[Journal-full-title] Natural product research

[ISO-abbreviation] Nat. Prod. Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Oils, Volatile; 0 / Plant Oils

   

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[Title] Nonleukemic granulocytic sarcoma in the bile duct: a case report.

Granulocytic sarcoma (GS) is an extramedullary tumor composed of immature myeloid cells, typically occurring during the course of acute myelogenous leukemia.

Non-leukemic GS, that is, GS with no evidence of overt leukemia and no previous history of leukemia, is very rare, and even more unusual is nonleukemic GS of the bile duct.

The patient was initially misdiagnosed as a bile duct carcinoma arising in the hilum of the liver (so-called Klatskin tumor), and received a right lobectomy of the liver.

Histological examination of the tumor yielded the diagnosis of GS, and the bone marrow biopsy did not show any evidence of leukemia.

Considering the risk of subsequent development of overt leukemia, the patient was treated with two cycles of combination chemotherapy as used in the cases of acute myelogenous leukemia.

To date, he has remained free of disease 15 months after treatment.

[MeSH-major] Bile Duct Neoplasms / chemically induced. Sarcoma, Myeloid / diagnosis

[MeSH-minor] Adult. Antigens, CD45 / analysis. Bile Ducts / chemistry. Bile Ducts / pathology. Diagnosis, Differential. Humans. Immunohistochemistry. Male. Peroxidase / analysis. Radiography, Abdominal. Tomography, X-Ray Computed / methods

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[Cites] Cancer. 2002 Mar 15;94(6):1739-46 [11920536.001]

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(PMID = 16891824.001).

[ISSN] 1011-8934

[Journal-full-title] Journal of Korean medical science

[ISO-abbreviation] J. Korean Med. Sci.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Korea (South)

[Chemical-registry-number] EC 1.11.1.7 / Peroxidase; EC 3.1.3.48 / Antigens, CD45

[Other-IDs] NLM/ PMC2729902

   

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[Title] Detailed analysis of FLT3 expression levels in acute myeloid leukemia.

BACKGROUND AND OBJECTIVES: FLT3 mutations are found in up to 30% of cases of acute myeloid leukemia (AML).

DESIGN AND METHODS: To further evaluate the role of FLT3 in AML we investigated FLT3 expression levels in 207 adult AML patients and 8 healthy donors by real-time polymerase chain reaction (PCR).

RESULTS: FLT3 expression levels were different in certain FAB types with increasing levels in the following order: M3<M3v<M6<M2<M4eo<M4<M0<M1<M5a<M5b.

Independent analysis of FLT3 expression in cytogenetic AML subgroups showed the lowest levels in t(15;17) and the highest in the t(11q23) positive AML.

On the molecular level, no differences in FLT3 expression levels were detected between AML with and without any FLT3 mutation as well as for FAB M5 with or without MLL abnormalities (p=0.495).

In patients with normal cytogenetics no impact or overall survival or event-free survival could be detected (p=0.128 and p=0.305, respectively) regardless of FLT3 muatation status, whereas investigating the group of patients with normal cytogenetics and wild-type FLT3, a clear tendency for a worse overall (p=0.059) and event free (p=0.087) survival was found.

[MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Myeloid / enzymology. Neoplasm Proteins / biosynthesis. fms-Like Tyrosine Kinase 3 / biosynthesis

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Antigens, CD34 / genetics. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Bone Marrow / pathology. Chromosome Aberrations. Disease-Free Survival. Enzyme Induction. Female. Gene Duplication. Humans. Karyotyping. Leukemia, Monocytic, Acute / genetics. Leukemia, Monocytic, Acute / pathology. Leukocyte Count. Life Tables. Male. Middle Aged. Polymerase Chain Reaction. Prognosis. Proportional Hazards Models. RNA, Messenger / biosynthesis. RNA, Messenger / metabolism. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / metabolism. Survival Analysis. Tandem Repeat Sequences

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[CommentIn] Haematologica. 2005 Dec;90(12):1586 [16330422.001]

(PMID = 16330434.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

[Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

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[Title] Spectral karyotyping and fluorescence in situ hybridization analyses identified a novel three-way translocation involving inversion 16 in therapy-related acute myeloid leukemia M4eo.

We report a novel three-way translocation involving inversion 16 and chromosome 12 at bands 16p13, 16q22, and 12q24 in a patient with therapy-related acute myeloid leukemia (AML)-M4eo.

Conventional G-banding of bone marrow cells at diagnosis was suggestive of inv(16)(p13q22) and a translocation of chromosomes 12 and 16.

Although we could not establish that this complex chromosomal aberration occurred either as a one-step, three-way event, or a sequential event with inv(16)(p13q22) followed by t(12;16)(q24;q22), SKY in combination with FISH and RT-PCR analyses successfully detected this complex chromosome abnormality in the patient.

[MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 16. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics. Spectral Karyotyping. Translocation, Genetic

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(PMID = 18617061.001).

[ISSN] 1873-4456

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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[Title] Notice of retraction. Alteration of p73 in acute myelogenous leukemia.

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[RetractionOf] Sahu GR, Mishra R, Nagpal JK, Das BR. Am J Hematol. 2005 May;79(1):1-7 [15849769.001]

(PMID = 18615454.001).

[ISSN] 1096-8652

[Journal-full-title] American journal of hematology

[ISO-abbreviation] Am. J. Hematol.

[Language] eng

[Publication-type] Retraction of Publication

[Publication-country] United States

   

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[Title] Peripheral blasts on day 21 of induction chemotherapy in a patient with core binding factor acute myeloid leukemia: more than meets the eye.

The combination of fludarabine, high-dose cytarabine, gemtuzumab ozogamicin, and granulocyte colony-stimulating factor (G-CSF), the FLAG-GO protocol, has resulted in excellent response rates and superior relapse-free survival as first-line therapy for patients with core binding factor acute myeloid leukemia (AML).

A side effect of administration of G-CSF is an increase in peripheral white blood cell count and blast cell percentage during the recovery phase of the bone marrow after induction chemotherapy.

A 60-year-old man with inversion 16 AML was admitted for induction chemotherapy with the FLAG-GO protocol at our institution.

Our case report underscores the importance of recognizing this phenomenon associated with the administration of G-CSF, and waiting for 5-7 days before administering re-induction therapy or classifying the disease as primary refractory AML.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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(PMID = 20709669.001).

[ISSN] 2152-2669

[Journal-full-title] Clinical lymphoma, myeloma & leukemia

[ISO-abbreviation] Clin Lymphoma Myeloma Leuk

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P30 CA016672

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Core Binding Factors; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; FLAG protocol

   

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With regard to hematological malignancies a stimulating effect of VEGF for proliferation, survival and migration of leukemia cells could be demonstrated.

Bone marrow of leukemia patients shows an increased microvessel density as well as VEGF expression.

Complete remissions in acute myeloid leukemia (AML) have been reported by targeting the receptor tyrosine kinase system of VEGF.

While the pathophysiology behind the contribution of VEGF to leukemia progression is not yet completely understood, VEGF and its receptors may provide promising targets not only in solid tumors but also hematological malignancies such as AML.

[MeSH-minor] Cell Proliferation. Cell Survival. Disease Progression. Humans

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(PMID = 17305503.001).

[ISSN] 1873-5592

[Journal-full-title] Current drug targets

[ISO-abbreviation] Curr Drug Targets

[Language] eng

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

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor

[Number-of-references] 226

   

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[Title] Successful treatment of disseminated mucormycosis with a combination of liposomal amphotericin B and posaconazole in a patient with acute myeloid leukaemia.

[MeSH-major] Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Leukemia, Myeloid, Acute / complications. Liposomes / therapeutic use. Mucormycosis / drug therapy. Rhizomucor / isolation & purification. Triazoles / therapeutic use

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(PMID = 16961579.001).

[ISSN] 0933-7407

[Journal-full-title] Mycoses

[ISO-abbreviation] Mycoses

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Antifungal Agents; 0 / Liposomes; 0 / Triazoles; 0 / liposomal amphotericin B; 6TK1G07BHZ / posaconazole; 7XU7A7DROE / Amphotericin B

   

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[Title] [Expression of mitosis checkpoint gene CHFR in acute leukemia].

OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with acute leukemia (AL) and its clinical significance.

METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with acute myelocytic leukemia (AML) and 22 with acute lymphocytic leukemia (ALL), 45 de novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.

The cell cycle was examined by flow cytometric analysis.

(1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent acute lymphoblastic leukemia (ALL) was 0.71, significantly higher than that of the de novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).

CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with acute leukemia.

Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of acute leukemia to chemotherapy.

[MeSH-major] Cell Cycle Proteins / biosynthesis. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Adolescent. Adult. Antineoplastic Agents / pharmacology. Cell Cycle. Child. Drug Resistance. Female. HL-60 Cells. Humans. Male. Middle Aged. Mitosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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(PMID = 16029562.001).

[ISSN] 0376-2491

[Journal-full-title] Zhonghua yi xue za zhi

[ISO-abbreviation] Zhonghua Yi Xue Za Zhi

[Language] chi

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

[Publication-country] China

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger

   

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[Title] Depletion of endogenous tumor-associated regulatory T cells improves the efficacy of adoptive cytotoxic T-cell immunotherapy in murine acute myeloid leukemia.

To elucidate host factors contributing to the poor response of adoptively transferred tumor-reactive cytotoxic T lymphocytes (CTLs), we used a systemic model of murine acute myeloid leukemia (AML).

AML progression resulted in a progressive regulatory T-cell (Treg) accumulation in disease sites.

The adoptive transfer of in vitro-generated, potently lytic anti-AML-reactive CTLs failed to reduce disease burden or extend survival.

Compared with non-AML-bearing hosts, transferred CTLs had reduced proliferation in AML sites of metastases.

Treg depletion by a brief course of interleukin-2 diphtheria toxin (IL-2DT) transiently reduced AML disease burden but did not permit long-term survival.

In contrast, IL-2DT prevented anti-AML CTL hypoproliferation, increased the number of transferred CTLs at AML disease sites, reduced AML tumor burden, and resulted in long-term survivors that sustained an anti-AML memory response.

These data demonstrated that Tregs present at AML disease sites suppress adoptively transferred CTL proliferation, limiting their in vivo expansion, and Treg depletion before CTL transfer can result in therapeutic efficacy in settings of substantial pre-existing tumor burden in which antitumor reactive CTL infusion alone has proven ineffective.

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(PMID = 19724059.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA120409-03; United States / NCI NIH HHS / CA / CA120409-03; United States / NCI NIH HHS / CA / R01 CA120409; United States / NCI NIH HHS / CA / R01 CA72669; United States / NHLBI NIH HHS / HL / R01 HL056067; United States / NCI NIH HHS / CA / R01 CA072669

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

[Publication-country] United States

[Chemical-registry-number] 0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins; 0 / interleukin 2-diphtheria toxin

[Other-IDs] NLM/ PMC2773484

   

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[Title] [The diagnosis of acute myeloid leukaemia enhanced by using DNA microarrays].

[Transliterated title] Diagnostiek van acute myeloïde leukemie in een stroomversnelling door toepassing van DNA-microarrays.

Recently, two studies have shown that the use ofgene-expression profiling using DNA microarrays or DNA chips may improve the classification of acute myeloid leukaemia (AML).

In both studies, cluster analyses based on the molecular signatures defined known subgroups as well as novel subgroups of AML.

Chromosomal lesions, mutations, and abnormal gene expression with prognostic value determined the clustering.

In fact, gene-expression profiling recognized leukaemias with certain chromosomal aberrations that had been missed by routine cytogenetics.

Thus, gene-expression profiling allows a comprehensive classification of AML that includes previously-identified genetically-defined as well as novel prognostically-relevant subgroups.

[MeSH-major] Chromosome Aberrations. Gene Expression Profiling / methods. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / genetics. Oligonucleotide Array Sequence Analysis

[MeSH-minor] Acute Disease. Cluster Analysis. Cytogenetic Analysis. Humans

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[CommentIn] Ned Tijdschr Geneeskd. 2005 Mar 19;149(12):618-22 [15813427.001]

(PMID = 15813428.001).

[ISSN] 0028-2162

[Journal-full-title] Nederlands tijdschrift voor geneeskunde

[ISO-abbreviation] Ned Tijdschr Geneeskd

[Language] dut

[Publication-type] English Abstract; Journal Article

[Publication-country] Netherlands

   

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[Title] Hematopoietic cell transplantation specific comorbidity index as an outcome predictor for patients with acute myeloid leukemia in first remission: combined FHCRC and MDACC experiences.

A new hematopoietic cell transplantation-specific comorbidity index (HCT-CI) was effective in predicting outcomes among patients with hematologic malignancies who underwent HCT at Fred Hutchinson Cancer Research Center (FHCRC).

Here, we compared the performance of the HCT-CI to 2 other indices and then tested its capacity to predict outcomes among 2 cohorts of patients diagnosed with a single disease entity, acute myeloid leukemia in first complete remission, who underwent transplantation at either FHCRC or M. D.

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(PMID = 17873123.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA18029; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / P30 CA015704; United States / NCI NIH HHS / CA / CA78902; United States / NHLBI NIH HHS / HL / R00 HL088021; United States / NCI NIH HHS / CA / CA15704; United States / NCI NIH HHS / CA / P01 CA078902; United States / NHLBI NIH HHS / HL / K99 HL088021; United States / NHLBI NIH HHS / HL / HL088021

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

[Publication-country] United States

[Other-IDs] NLM/ PMC2234788

   

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The International Prognostic Scoring System (IPSS) groups Low/Intermediate-1 (Low/Int-1) had longer response duration than Int-2/High (25 versus 7 months, P = .002).

The time until 25% developed acute myeloid leukemia (AML) was longer in the good and intermediate predictive groups for erythroid response compared with the poor predictive group (52 versus 13 months, P = .008).

Only 1 of 20 long-term responders developed AML.

There was no difference in survival (odds ratio [OR], 0.9; 95% confidence interval [CI], 0.7-1.2; P = .55) or risk of AML evolution (OR, 1.3; 95% CI, 0.7-2.2; P = .40) between treated and untreated patients.

Patients with high/intermediate probability of response and with IPSS Low/Int-1 show frequent and durable responses without adverse effects on outcome, while other patients should not be considered candidates for this treatment.

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Analysis of Variance. Cell Transformation, Neoplastic. Female. Humans. Leukemia, Myeloid / etiology. Male. Middle Aged. Predictive Value of Tests. Prognosis. Survival Analysis. Treatment Outcome

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(PMID = 15840690.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 11096-26-7 / Erythropoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor

   

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[Title] The FcgammaRIIa-polymorphic site as a potential target for acute graft-versus-host disease in allogeneic stem cell transplantation.

Graft-versus-host disease (GVHD) is a serious complication of allogeneic stem cell transplantation for hematologic diseases.

Polymorphisms are known for FcgammaRIIa, and this molecule is present on endothelial, dendritic, and Langerhans cells.

Donor cells reacting against the patient as GVHD can also react against the malignancy of the patient, and this is known as the graft-versus-leukemia (GVL) effect.

Because the FcgammaRIIa molecule is also present on acute myeloid leukemia (AML) cells, an FcgammaRIIa mismatch could be a target for both GVHD and GVL.

We retrospectively studied 73 AML patients and analyzed the differences in GVHD and relapse incidence between patients with and without a pro-GVHD/GVL FcgammaRIIa allotype mismatch.

Univariate and multivariate analyses demonstrated the pro-GVHD mismatch to be a significant risk factor for the development of acute GVHD.

The relapse incidence was not significantly different for patients with or without the pro-GVL mismatch, although there was a trend for fewer relapses in standard-risk AML patients with the pro-GVL mismatch.

We conclude that the polymorphism of the FcgammaRIIa receptor may be a candidate target for acute GVHD.

[MeSH-major] Antigens, CD / genetics. Graft vs Host Disease / genetics. Hematopoietic Stem Cell Transplantation / adverse effects. Polymorphism, Genetic. Receptors, IgG / genetics

[MeSH-minor] Acute Disease. Adult. Aged. Analysis of Variance. Cohort Studies. Female. Graft vs Leukemia Effect / genetics. Graft vs Leukemia Effect / immunology. Humans. Incidence. Leukemia, Myeloid / complications. Leukemia, Myeloid / therapy. Male. Middle Aged. Recurrence. Retrospective Studies. Transplantation Immunology. Transplantation, Homologous

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(PMID = 15744239.001).

[ISSN] 1083-8791

[Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation

[ISO-abbreviation] Biol. Blood Marrow Transplant.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Fc gamma receptor IIA; 0 / Receptors, IgG

   

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[Title] Clinical utility of a commercial LAM-ELISA assay for TB diagnosis in HIV-infected patients using urine and sputum samples.

BACKGROUND: The accurate diagnosis of TB in HIV-infected patients, particularly with advanced immunosuppression, is difficult.

Recent studies indicate that a lipoarabinomannan (LAM) assay (Clearview-TB(R)-ELISA) may have some utility for the diagnosis of TB in HIV-infected patients; however, the precise subgroup that may benefit from this technology requires clarification.

The utility of LAM in sputum samples has, hitherto, not been evaluated.

METHODS: LAM was measured in sputum and urine samples obtained from 500 consecutively recruited ambulant patients, with suspected TB, from 2 primary care clinics in South Africa.

Culture positivity for M. tuberculosis was used as the reference standard for TB diagnosis.

Urine-LAM positivity was associated with HIV positivity (p = 0.007) and test sensitivity, although low, was significantly higher in HIV-infected compared to uninfected patients (21% versus 6%; p<0.001), and also in HIV-infected participants with a CD4 <200 versus >200 cells/mm(3) (37% versus 0%; p = 0.003).

Urine-LAM remained highly specific in all 3 subgroups (95%-100%).

25% of smear-negative but culture-positive HIV-infected patients with a CD4 <200 cells/mm(3) were positive for urine-LAM.

Sputum-LAM had good sensitivity (86%) but poor specificity (15%) likely due to test cross-reactivity with several mouth-residing organisms including actinomycetes and nocardia species.

CONCLUSIONS: These preliminary data indicate that in a high burden primary care setting the diagnostic usefulness of urine-LAM is limited, as a rule-in test, to a specific patient subgroup i.e. smear-negative HIV-infected TB patients with a CD4 count <200 cells/mm(3), who would otherwise have required further investigation.

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(PMID = 20352098.001).

[ISSN] 1932-6203

[Journal-full-title] PloS one

[ISO-abbreviation] PLoS ONE

[Language] ENG

[Grant] None / None / / 89918; Canada / Canadian Institutes of Health Research / / 89918; Canada / Canadian Institutes of Health Research / / MOP-89918; United Kingdom / Medical Research Council / /

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

[Publication-country] United States

[Other-IDs] NLM/ PMC2844421

   

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[Title] Core binding factor acute myeloid leukemia.

Core binding factor (CBF) acute myeloid leukemia (AML) is cytogenetically defined by the presence of t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22), which are found in approximately 15% of all adult de novo AML cases.

Despite this molecular commonality, recent studies have demonstrated differences in genetic, clinical, and prognostic features between t(8;21) and inv(16)/t(16;16) AML, thereby supporting the notion that they represent two distinct biologic and clinical entities.

Furthermore, despite being considered as a more favorable AML risk group, only approximately half of the CBF AML patients are cured with current therapy, indicating the need for improved therapeutic approaches.

This review summarizes the most recent laboratory and clinical discoveries relevant to this subset of AML and how they are being applied for in an effort to improve the cure rate in patients with the disease.

[MeSH-major] Chromosome Inversion. Core Binding Factors / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Translocation, Genetic

[MeSH-minor] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Humans. Neoplasm, Residual / diagnosis. Prognosis

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(PMID = 18692691.001).

[ISSN] 0093-7754

[Journal-full-title] Seminars in oncology

[ISO-abbreviation] Semin. Oncol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Core Binding Factors

[Number-of-references] 76

   

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[Title] Therapy-related acute leukemia in breast cancer patients: twelve cases treated with a topoisomerase inhibitor.

BACKGROUND: Therapy-related myeloid neoplasm (t-MN) is a distinct class of acute myeloid leukemia (AML) in the World Health Organization (WHO) classification.

Both AML and acute lymphoblastic leukemia (ALL) may develop after treatment for primary cancer.

Topoisomerase inhibitors are commonly used to treat breast cancer patients and are well-known for their effect on leukemogenesis of therapy-related acute leukemias (t-AL).

METHODS: We retrospectively evaluated bone marrow test results, chromosomal findings, and clinical characteristics of 12 patients who received topoisomerase inhibitors for breast cancer treatment and later developed acute leukemia.

Among them, 9 patients (75%, 9/12) were diagnosed with therapy-related AML (t-AML) and 3 patients (25%, 3/12) with therapy-related ALL (t-ALL).

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(PMID = 21120206.001).

[ISSN] 2092-9129

[Journal-full-title] The Korean journal of hematology

[ISO-abbreviation] Korean J Hematol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Korea (South)

[Other-IDs] NLM/ PMC2983048

[Keywords] NOTNLM ; 11q23 / Breast cancer / Therapy-related acute myeloid leukemia / Topoisomerase inhibitors

   

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Body weight, 10th rib backfat (BF10), last rib backfat (LRF), and loin muscle area (LMA) were serially measured at 10, 13, 16, 19, 22, 24, and 26 wk of age.

At 26 wk of age, Duroc-sired progeny were heavier (143.4 vs. 132.7 kg, P < 0.001), had more BF10 (27.1 vs. 23.7 mm, P < 0.001) and LRF (21.2 vs. 19.2 mm, P < 0.001), but had similar LMA (46.4 vs. 47.1 cm2) compared with Pietrain-sired progeny.

Mean feed efficiency did not differ between breed of sire in any period of the study.

Random regression animal models with polynomial regression on week on-test were fitted to BW, BF10, LRF, LMA, FFTOLN, TOFAT, EBPRO, and EBLIPID from 10 to 26 wk of age.

Serial heritability estimates generally increased from 10 to 26 wk of age with ranges as follows: BW (0.05 to 0.39), BF10 (0.13 to 0.76), LRF (0.11 to 0.79), LMA (0.05 to 0.73), FFTOLN (0.07 to 0.16), TOFAT (0.19 to 0.45), EBPRO (0.02 to 0.55), and EBLIPID (0.12 to 0.60).

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(PMID = 16424252.001).

[ISSN] 1525-3163

[Journal-full-title] Journal of animal science

[ISO-abbreviation] J. Anim. Sci.

[Language] eng

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

[Publication-country] United States

   

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[Title] Aspergillus alliaceus and Aspergillus flavus co-infection in an acute myeloid leukemia patient.

We report a case of a pulmonary infection caused by Aspergillus flavus and Aspergillus alliaceus in an acute myeloid leukemia patient.

[MeSH-major] Aspergillosis / complications. Aspergillosis / microbiology. Aspergillus / isolation & purification. Aspergillus flavus / classification. Leukemia, Myeloid, Acute / complications. Lung Diseases, Fungal / complications. Lung Diseases, Fungal / microbiology

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(PMID = 20392148.001).

[ISSN] 1460-2709

[Journal-full-title] Medical mycology

[ISO-abbreviation] Med. Mycol.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / DNA, Intergenic; 0 / Fungal Proteins; 0 / Tubulin

   

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Intracellular NAD is essential for cell survival, and NAD depletion resulting from APO866 treatment elicits tumor cell death.

Here, we determine the in vitro and in vivo sensitivities of hematologic cancer cells to APO866 using a panel of cell lines (n = 45) and primary cells (n = 32).

Most cancer cells (acute myeloid leukemia [AML], acute lymphoblastic leukemia [ALL], mantle cell lymphoma [MCL], chronic lymphocytic leukemia [CLL], and T-cell lymphoma), but not normal hematopoietic progenitor cells, were sensitive to low concentrations of APO866 as measured in cytotoxicity and clonogenic assays.

The NAD depletion led to cell death.

At 96 hours, APO866-mediated cell death occurred in a caspase-independent mode, and was associated with mitochondrial dysfunction and autophagy.

Further, in vivo administration of APO866 as a single agent prevented and abrogated tumor growth in animal models of human AML, lymphoblastic lymphoma, and leukemia without significant toxicity to the animals.

[MeSH-minor] Animals. Cell Death / drug effects. Dose-Response Relationship, Drug. HL-60 Cells. Humans. Jurkat Cells. K562 Cells. Mice. Mice, Inbred BALB C. Mice, Nude. Tumor Cells, Cultured. U937 Cells. Xenograft Model Antitumor Assays

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[CommentIn] Blood. 2009 Jun 4;113(23):6035-7; author reply 6037-8 [19498032.001]

(PMID = 19196867.001).

[ISSN] 1528-0020

[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 / Acrylamides; 0 / Antineoplastic Agents; 0 / Cytokines; 0 / N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide; 0 / Piperidines; 0U46U6E8UK / NAD; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase; EC 2.4.2.12 / nicotinamide phosphoribosyltransferase, human

   

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[Title] Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia.

Translocations involving the Mixed Lineage Leukemia (MLL) gene at 11q23 are found in both acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML), but have different prognostic implications depending on the phenotype of the leukemia in de novo pediatric cases.

Rearrangements of the MLL gene are found in most cases of infant AML and regardless of age confer an intermediate risk.

The treatment of MLL-rearranged ALL in children involves increased intensification of chemotherapy, and infants with ALL are treated with an intensive regimen of ALL- and AML-like chemotherapy, with the proportion of MLL-rearranged cases being responsible for the poor outcome in this age group.

The use of DNA microarray analysis to distinguish a particular gene signature for MLL-rearranged leukemias is shedding light on the molecular mechanisms and potential therapeutic targets of these leukemias.

It may also prove to have a useful role in both diagnosis and prognosis.

[MeSH-major] Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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(PMID = 17905612.001).

[ISSN] 1079-9796

[Journal-full-title] Blood cells, molecules & diseases

[ISO-abbreviation] Blood Cells Mol. Dis.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein

[Number-of-references] 82

   

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[Title] Perspectives of proteomics in acute myeloid leukemia.

Acute myeloid leukemia (AML) is a frequent hematological malignancy.

Despite enormous therapeutic efforts that range from various cytotoxic agents to allogeneic stem cell transplantation, overall survival of patients with AML remains unsatisfying.

There is hope that elucidation of the AML-specific proteome will prompt the discovery of novel therapeutic targets and biomarkers in AML.

Modern mass-spectrometry instrumentation has achieved excellent performance in terms of sensitivity, resolution and mass accuracy; however, so far, the contribution of proteomics to the care of patients with AML is virtually zero.

Since mass-spectrometry instruments are very intricate devices, their successful operation will hinge on the willingness and ability of mass-spectrometry experts and clinical researchers to adopt new views, learn from each other and cooperate in order to ultimately benefit the patient suffering from AML.

This review highlights some clinical problems circumventing the treatment of patients with AML.

Furthermore, it provides a brief overview of the technical background of standard proteomics approaches and describes opportunities, challenges and pitfalls of proteomic studies with regards to AML.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Proteomics

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(PMID = 17134369.001).

[ISSN] 1744-8328

[Journal-full-title] Expert review of anticancer therapy

[ISO-abbreviation] Expert Rev Anticancer Ther

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins

[Number-of-references] 99