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1. Díaz-Beyá M, Brunet S, Nomdedéu J, Pratcorona M, Cordeiro A, Gallardo D, Escoda L, Tormo M, Heras I, Ribera JM, Duarte R, de Llano MP, Bargay J, Sampol A, Nomdedeu M, Risueño RM, Hoyos M, Sierra J, Monzo M, Navarro A, Esteve J, Cooperative AML group CETLAM: The lincRNA HOTAIRM1, located in the HOXA genomic region, is expressed in acute myeloid leukemia, impacts prognosis in patients in the intermediate-risk cytogenetic category, and is associated with a distinctive microRNA signature. Oncotarget; 2015 Oct 13;6(31):31613-27
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  • [Title] The lincRNA HOTAIRM1, located in the HOXA genomic region, is expressed in acute myeloid leukemia, impacts prognosis in patients in the intermediate-risk cytogenetic category, and is associated with a distinctive microRNA signature.
  • Long non-coding RNAs (lncRNAs) are deregulated in several tumors, although their role in acute myeloid leukemia (AML) is mostly unknown.We have examined the expression of the lncRNA HOX antisense intergenic RNA myeloid 1 (HOTAIRM1) in 241 AML patients.
  • We have also analyzed the prognostic value of HOTAIRM1 expression in 215 intermediate-risk AML (IR-AML) patients.The lowest expression level was observed in acute promyelocytic leukemia (P < 0.001) and the highest in t(6;9) AML (P = 0.005).
  • In 215 IR-AML patients, high HOTAIRM1 expression was independently associated with shorter overall survival (OR:2.04;P = 0.001), shorter leukemia-free survival (OR:2.56; P < 0.001) and a higher cumulative incidence of relapse (OR:1.67; P = 0.046).
  • [MeSH-major] Biomarkers, Tumor / genetics. Cytogenetic Analysis. Gene Expression Profiling. Homeodomain Proteins / genetics. Leukemia, Myeloid, Acute / genetics. MicroRNAs / genetics. RNA, Long Noncoding / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Chi-Square Distribution. Disease Progression. Disease-Free Survival. Female. Gene Expression Regulation, Neoplastic. Genetic Predisposition to Disease. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Multivariate Analysis. Mutation. Nuclear Proteins / genetics. Odds Ratio. Phenotype. Predictive Value of Tests. Proportional Hazards Models. Risk Assessment. Risk Factors. Time Factors. Treatment Outcome. Young Adult

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  • (PMID = 26436590.001).
  • [ISSN] 1949-2553
  • [Journal-full-title] Oncotarget
  • [ISO-abbreviation] Oncotarget
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Homeodomain Proteins; 0 / MIRN196 microRNA, human; 0 / MicroRNAs; 0 / Nuclear Proteins; 0 / RNA, Long Noncoding; 0 / long non-coding RNA HOTAIRM1, human; 117896-08-9 / nucleophosmin; 157907-48-7 / HoxA protein
  • [Other-IDs] NLM/ PMC4741628
  • [Keywords] NOTNLM ; AML / HOTAIRM / HOX / lincRNA / lncRNA
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2. Yang YJ, Yun GW, Song IC, Baek SW, Lee KS, Ryu HW, Lee MW, Lee HJ, Yun HJ, Kim S, Jo DY: Clinical implications of elevated antiphospholipid antibodies in adult patients with primary immune thrombocytopenia. Korean J Intern Med; 2011 Dec;26(4):449-54
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  • [Title] Clinical implications of elevated antiphospholipid antibodies in adult patients with primary immune thrombocytopenia.
  • BACKGROUND/AIMS: Antiphospholipid antibodies (aPL) have been detected in various proportions of patients with primary immune thrombocytopenia (ITP), but the clinical significance of this is debatable.
  • The present study aimed to determine the frequency and clinical implications of elevated aPL in adult patients with ITP.
  • METHODS: We prospectively studied newly diagnosed adult patients with ITP who were enrolled between January 2003 and December 2008 at Chungnam National University Hospital.
  • Twenty patients (28.5%) were positive for aPL at the time of diagnosis: aCL alone in 15 (75%), aCL and LA in two (10%), and LA alone in three (15%).
  • No difference was found between the aPL-positive and -negative groups regarding gender, initial platelet count, and response to the therapy.
  • After a median follow-up of 20 months (range, 2 to 68), two of 20 patients who were aPL-positive (10%) developed thrombosis, whereas no thrombotic event was found among those who were aPL-negative.
  • CONCLUSIONS: Our data suggest that aPL levels should be determined at the initial presentation of ITP and that patients found to be aPL-positive should receive closer follow-up for thrombotic events.
  • [MeSH-minor] Adolescent. Adult. Aged. Antibodies, Antiphospholipid / blood. Chi-Square Distribution. Female. Glucocorticoids / therapeutic use. Humans. Male. Middle Aged. Prednisolone / therapeutic use. Prospective Studies. Thrombosis. Young Adult

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  • (PMID = 22205846.001).
  • [ISSN] 2005-6648
  • [Journal-full-title] The Korean journal of internal medicine
  • [ISO-abbreviation] Korean J. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Antiphospholipid; 0 / Glucocorticoids; 0 / Lupus Coagulation Inhibitor; 9PHQ9Y1OLM / Prednisolone
  • [Other-IDs] NLM/ PMC3245394
  • [Keywords] NOTNLM ; Antibodies, anticardiolipin / Antiphospholipid syndrome / Lupus coagulation inhibitor / Purpura, thrombocytopenic, idiopathic / Thrombosis
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3. Dinmohamed AG, Visser O, van Norden Y, Blijlevens NM, Cornelissen JJ, Huls GA, Huijgens PC, Sonneveld P, van de Loosdrecht AA, Ossenkoppele GJ, Löwenberg B, Jongen-Lavrencic M: Treatment, trial participation and survival in adult acute myeloid leukemia: a population-based study in the Netherlands, 1989-2012. Leukemia; 2016 Jan;30(1):24-31
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  • [Title] Treatment, trial participation and survival in adult acute myeloid leukemia: a population-based study in the Netherlands, 1989-2012.
  • Large, comprehensive population-based studies in acute myeloid leukemia (AML) are scarce.
  • We conducted a nationwide population-based study on treatment, trial participation and survival among all adult patients diagnosed with AML (n=12,032) and acute promyelocytic leukemia (APL; n=585) in the Netherlands between 1989-2012.
  • For APL patients, the use of chemotherapy increased across all age groups.
  • When a clinical trial was open for accrual in the Netherlands, the inclusion rates were 68%, 57%, 30% and 12% for AML patients in the four age groups, respectively (data for APL unavailable).
  • Relative survival improved over time among AML (up to age 70 years) and APL patients.
  • In the period 2007-2012, 5-year relative survival rates were 54%, 38%, 14% and 2% for AML patients and 84%, 75%, 54% and 37% for APL patients in the four age groups, respectively.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Patient Participation
  • [MeSH-minor] Adolescent. Adult. Aged. Clinical Trials as Topic. Female. Hematopoietic Stem Cell Transplantation. Humans. Male. Middle Aged. Netherlands. Time Factors. Tretinoin / therapeutic use. Young Adult


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4. Chen SJ, Zhou GB, Zhang XW, Mao JH, de Thé H, Chen Z: From an old remedy to a magic bullet: molecular mechanisms underlying the therapeutic effects of arsenic in fighting leukemia. Blood; 2011 Jun 16;117(24):6425-37
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  • [Title] From an old remedy to a magic bullet: molecular mechanisms underlying the therapeutic effects of arsenic in fighting leukemia.
  • In the past 3 decades, arsenic was revived and shown to be able to induce complete remission and to achieve, when combined with all-trans retinoic acid and chemotherapy, a 5-year overall survival of 90% in patients with acute promyelocytic leukemia driven by the t(15;17) translocation-generated promyelocytic leukemia-retinoic acid receptor α (PML-RARα) fusion.
  • Interestingly, arsenic directly binds the C3HC4 zinc finger motif in the RBCC domain of PML and PML-RARα, induces their homodimerization and multimerization, and enhances their interaction with the SUMO E2 conjugase Ubc9, facilitating subsequent sumoylation/ubiquitination and proteasomal degradation.
  • Arsenic-caused intermolecular disulfide formation in PML also contributes to PML-multimerization.
  • All-trans retinoic acid, which targets PML-RARα for degradation through its RARα moiety, synergizes with arsenic in eliminating leukemia-initiating cells.
  • Arsenic perturbs a number of proteins involved in other hematologic malignancies, including chronic myeloid leukemia and adult T-cell leukemia/lymphoma, whereby it may bring new therapeutic benefits.
  • The successful revival of arsenic in acute promyelocytic leukemia, together with modern mechanistic studies, has thus allowed a new paradigm to emerge in translational medicine.
  • [MeSH-major] Arsenic / therapeutic use. Leukemia / drug therapy. Leukemia / genetics. Medicine, Traditional / methods. Signal Transduction / drug effects. Signal Transduction / genetics
  • [MeSH-minor] Adult. Animals. Humans. Magic. Models, Biological. Models, Molecular. Treatment Outcome

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  • (PMID = 21422471.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] N712M78A8G / Arsenic
  • [Other-IDs] NLM/ PMC3123014
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5. Hills RK, Castaigne S, Appelbaum FR, Delaunay J, Petersdorf S, Othus M, Estey EH, Dombret H, Chevret S, Ifrah N, Cahn JY, Récher C, Chilton L, Moorman AV, Burnett AK: Addition of gemtuzumab ozogamicin to induction chemotherapy in adult patients with acute myeloid leukaemia: a meta-analysis of individual patient data from randomised controlled trials. Lancet Oncol; 2014 Aug;15(9):986-96
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  • [Title] Addition of gemtuzumab ozogamicin to induction chemotherapy in adult patients with acute myeloid leukaemia: a meta-analysis of individual patient data from randomised controlled trials.
  • BACKGROUND: Gemtuzumab ozogamicin was the first example of antibody-directed chemotherapy in cancer, and was developed for acute myeloid leukaemia.
  • We did a meta-analysis of individual patient data to assess the efficacy of adding gemtuzumab ozogamicin to induction chemotherapy in adult patients with acute myeloid leukaemia.
  • METHODS: We searched PubMed for reports of randomised controlled trials published in any language up to May 1, 2013, that included an assessment of gemtuzumab ozogamicin given to adults (aged 15 years and older) in conjunction with the first course of intensive induction chemotherapy for acute myeloid leukaemia (excluding acute promyelocytic leukaemia) compared with chemotherapy alone.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal, Humanized / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / mortality
  • [MeSH-minor] Adult. Confidence Intervals. Cytarabine / therapeutic use. Daunorubicin / therapeutic use. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Infusions, Intravenous. Male. Middle Aged. Odds Ratio. Prognosis. Randomized Controlled Trials as Topic. Remission Induction / methods. Risk Assessment. Survival Rate. Treatment Outcome

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  • [Copyright] Copyright © 2014 Elsevier Ltd. All rights reserved.
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  • [CommentIn] Lancet Oncol. 2014 Aug;15(9):913-4 [25008259.001]
  • (PMID = 25008258.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA015704; United States / NCI NIH HHS / CA / U10 CA032102; United States / NCI NIH HHS / CA / U10 CA038926; United States / NCI NIH HHS / CA / U10 CA180819; United States / NCI NIH HHS / CA / U10 CA180888
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal, Humanized; 0 / gemtuzumab; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS619853; NLM/ PMC4137593
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6. Folgiero V, Goffredo BM, Filippini P, Masetti R, Bonanno G, Caruso R, Bertaina V, Mastronuzzi A, Gaspari S, Zecca M, Torelli GF, Testi AM, Pession A, Locatelli F, Rutella S: Indoleamine 2,3-dioxygenase 1 (IDO1) activity in leukemia blasts correlates with poor outcome in childhood acute myeloid leukemia. Oncotarget; 2014 Apr 30;5(8):2052-64
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  • [Title] Indoleamine 2,3-dioxygenase 1 (IDO1) activity in leukemia blasts correlates with poor outcome in childhood acute myeloid leukemia.
  • Microenvironmental factors contribute to the immune dysfunction characterizing acute myeloid leukemia (AML).
  • We investigated IDO1 expression and function in 37 children with newly diagnosed AML other than acute promyelocytic leukemia.
  • These data indicate that IDO1 expression by leukemia blasts negatively affects the prognosis of childhood AML.
  • [MeSH-major] Biomarkers, Tumor / analysis. Indoleamine-Pyrrole 2,3,-Dioxygenase / metabolism. Leukemia, Myeloid, Acute / enzymology
  • [MeSH-minor] Adolescent. Blotting, Western. Child. Child, Preschool. Disease-Free Survival. Enzyme-Linked Immunosorbent Assay. Female. Fluorescent Antibody Technique. Humans. Immunoprecipitation. Infant. Kaplan-Meier Estimate. Male. Real-Time Polymerase Chain Reaction. Young Adult


7. Zhu X, Zhang H, Qian M, Zhao X, Yang W, Wang P, Zhang J, Wang K: The significance of low PU.1 expression in patients with acute promyelocytic leukemia. J Hematol Oncol; 2012;5:22
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  • [Title] The significance of low PU.1 expression in patients with acute promyelocytic leukemia.
  • BACKGROUND: Although the importance of the hematopoietic transcription factor PU.1 in acute myeloid leukemia (AML) has been demonstrated, the expression of PU.1 in acute promyelocytic leukemia (APL) patient samples awaits further investigation.
  • The current study used APL patient samples to assess the expression pattern of PU.1 in the initiation and progression of APL.
  • FINDINGS: We used real-time RT-PCR to compare PU.1 expression between de novo APL patient samples and normal blood specimens, and the results indicated that PU.1 expression was significantly lower in newly diagnosed APL patient samples as compared to normal hematopoietic cells.
  • Further evidence showed a significant inverse correlation between the expression level of PML-RARα and that of PU.1.
  • In addition, we analyzed the correlation between PML-RARα and PU.1 expression in a large population of AML patients retrieved from the expression profiles.
  • The results showed that PU.1 expression was lower in patients with APL than other AML subtypes and there was also a trend towards increasing PU.1 expression from AML-M0 to AML-M5, with the exception of AML-M3 (APL).
  • These observations suggested that PU.1 expression was reduced by PML-RARα in APL patients.
  • Furthermore, we measured PU.1 expression in APL-initiating cells isolated from de novo APL patients by side population cell analysis and found that suppression of PU.1 expression occurred concurrently with PML-RARα expression, indicating the pivotal role of PU.1 in APL initiation.
  • CONCLUSION: Our findings provide evidence that low PU.1 expression in APL patients is required for disease initiation and progression.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / pathology. Proto-Oncogene Proteins / genetics. Trans-Activators / genetics
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Disease Progression. Female. Fetal Blood / cytology. Fetal Blood / metabolism. Gene Expression Profiling. Humans. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Oncogene Proteins, Fusion / genetics. Prognosis. RNA, Messenger / genetics. Real-Time Polymerase Chain Reaction. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • (PMID = 22569057.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Trans-Activators; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 0 / proto-oncogene protein Spi-1
  • [Other-IDs] NLM/ PMC3407792
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8. Xu L, Zhong H, Wan H, Chen FY, Zhong J, Xiao F, Liu J, Shen L: miR-146a expression level as a novel putative prognostic marker for acute promyelocytic leukemia. Dis Markers; 2014;2014:150604
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  • [Title] miR-146a expression level as a novel putative prognostic marker for acute promyelocytic leukemia.
  • BACKGROUND: Although the curative rate for acute promyelocytic leukemia (APL) has been improved over decades, long-term prognosis is still poor.
  • The genetic pathways that regulated cell lineage fate during the development of APL remain unclear.
  • We also analyzed their expression in clinical samples from APL patients.
  • RESULTS: miR-146a influenced apoptosis and proliferation in NB4 cells. miR-146a influenced endogenous Smad4 protein levels in APL cells. miR-146a expression levels were positively correlated with white cell counts and PML/RARα fusion protein expression. miR-146a expression levels were negatively correlated with Smad4 protein and the helper T cell (Th)/the suppressor T cell (Ts) ratio in these patients.
  • CONCLUSIONS: These findings indicated that miR-146a played an important role in the development of APL in part through the repression on Smad4 protein expression. miR-146a functioned as an oncogene and may be a novel prognostic biomarker in APL.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Leukemia, Promyelocytic, Acute / metabolism. MicroRNAs / metabolism
  • [MeSH-minor] Adult. Apoptosis. Cell Line, Tumor. Cell Proliferation. Female. Humans. Male. Middle Aged. Prognosis. Smad4 Protein / genetics. Smad4 Protein / metabolism. T-Lymphocytes, Helper-Inducer / metabolism. T-Lymphocytes, Helper-Inducer / physiology

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  • (PMID = 25161335.001).
  • [ISSN] 1875-8630
  • [Journal-full-title] Disease markers
  • [ISO-abbreviation] Dis. Markers
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MIRN146 microRNA, human; 0 / MicroRNAs; 0 / SMAD4 protein, human; 0 / Smad4 Protein
  • [Other-IDs] NLM/ PMC4138935
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9. Constantinides MG, Picard D, Savage AK, Bendelac A: A naive-like population of human CD1d-restricted T cells expressing intermediate levels of promyelocytic leukemia zinc finger. J Immunol; 2011 Jul 01;187(1):309-15
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  • [Title] A naive-like population of human CD1d-restricted T cells expressing intermediate levels of promyelocytic leukemia zinc finger.
  • Notably, these cells expressed the NKT lineage-specific transcription promyelocytic leukemia zinc finger (PLZF), indicating a developmental relationship with NKT cells and ruling out the possibility that they were conventional MHC-restricted T cells cross-reacting against CD1d-α-galactosylceramide.
  • [MeSH-minor] Adult. Animals. Cell Line, Transformed. Clone Cells. Gene Expression Regulation / immunology. Humans. Leukemia, Promyelocytic, Acute / immunology. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Mice. Mice, Inbred C57BL. Mice, Transgenic. Middle Aged. Thymus Gland / cytology. Thymus Gland / immunology. Thymus Gland / metabolism. Young Adult. Zinc Fingers

  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
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  • (PMID = 21632718.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE28726
  • [Grant] United States / NIAID NIH HHS / AI / AI053725; United States / NIAID NIH HHS / AI / AI038339; United States / NIAID NIH HHS / AI / P01 AI053725-10; United States / Howard Hughes Medical Institute / / ; United States / NIAID NIH HHS / AI / P01 AI053725; United States / NIAID NIH HHS / AI / R01 AI038339; United States / NIAID NIH HHS / AI / R01 AI038339-05
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD1d; 0 / Kruppel-Like Transcription Factors; 147855-37-6 / ZBTB16 protein, human
  • [Other-IDs] NLM/ NIHMS293218; NLM/ PMC3119760
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10. Liu Y, Wen Q, Chen XL, Yang SJ, Gao L, Gao L, Zhang C, Li JL, Xiang XX, Wan K, Chen XH, Zhang X, Zhong JF: All-trans retinoic acid arrests cell cycle in leukemic bone marrow stromal cells by increasing intercellular communication through connexin 43-mediated gap junction. J Hematol Oncol; 2015;8:110
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Connexin 43 (Cx43) is the major gap junction (GJ) protein; our previous study revealed that Cx43 expression and GJIC were decreased in acute leukemic BMSCs.
  • All-trans retinoic acid (ATRA) increases GJIC in a variety of cancer cells and has been used to treat acute promyelocytic leukemia, but the effects of ATRA on leukemic BMSCs is unknown.
  • METHODS: Human BMSCs obtained from 25 patients with primary acute leukemia, and 10 normal healthy donors were cultured.
  • [MeSH-minor] Acute Disease. Adult. Amphotericin B / pharmacology. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Apoptosis / genetics. Blotting, Western. Cell Proliferation / drug effects. Cell Proliferation / genetics. Cells, Cultured. Female. Fluorescence Recovery After Photobleaching. Gene Expression / drug effects. Humans. Leukemia, Myeloid / genetics. Leukemia, Myeloid / metabolism. Leukemia, Myeloid / pathology. Male. Microscopy, Confocal. Reverse Transcriptase Polymerase Chain Reaction

  • Hazardous Substances Data Bank. AMPHOTERICIN B .
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
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  • (PMID = 26446715.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Connexin 43; 0 / GJA1 protein, human; 5688UTC01R / Tretinoin; 7XU7A7DROE / Amphotericin B
  • [Other-IDs] NLM/ PMC4597383
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