AustralieFrV1, Ncbi, Curation, bibRecord, 001F59

Disruption of IKAROS activity in primitive chronic-phase CML cells mimics myeloid disease progression

Identifieur interne : 001F59 ( Ncbi/Curation ); précédent : 001F58; suivant : 001F60

Disruption of IKAROS activity in primitive chronic-phase CML cells mimics myeloid disease progression

Auteurs : Philip A. Beer [Canada] ; David J. H. F. Knapp [Canada] ; Paul H. Miller [Canada] ; Nagarajan Kannan [Canada] ; Ivan Sloma [France] ; Kathy Heel [Australie] ; Sonja Babovic [Canada] ; Elizabeth Bulaeva [Canada] ; Gabrielle Rabu [Canada] ; Jefferson Terry [Canada] ; Brian J. Druker [États-Unis] ; Marc M. Loriaux [États-Unis] ; Keith R. Loeb [États-Unis] ; Jerald P. Radich [États-Unis] ; Wendy N. Erber [Australie] ; Connie J. Eaves [Canada]

Source :

Blood [ 0006-4971 ] ; 2015.

RBID : PMC:4300391

Descripteurs français

English descriptors

KwdEn :
- Animals, Antigens, CD34 (metabolism), Apoptosis (drug effects), Basophils (drug effects), Basophils (metabolism), Basophils (pathology), Blotting, Western, Cell Differentiation (drug effects), Cell Proliferation (drug effects), Cells, Cultured, Disease Progression, Eosinophils (drug effects), Eosinophils (metabolism), Eosinophils (pathology), Flow Cytometry, Humans, Ikaros Transcription Factor (antagonists & inhibitors), Ikaros Transcription Factor (genetics), Ikaros Transcription Factor (metabolism), Immunoenzyme Techniques, Leukemia, Myeloid, Chronic-Phase (genetics), Leukemia, Myeloid, Chronic-Phase (metabolism), Leukemia, Myeloid, Chronic-Phase (pathology), Mice, Mice, Inbred NOD, Mice, SCID, Protein Kinase Inhibitors (pharmacology), Protein-Tyrosine Kinases (antagonists & inhibitors), RNA, Messenger (genetics), Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, STAT5 Transcription Factor (genetics), STAT5 Transcription Factor (metabolism).
MESH :
- chemical , antagonists & inhibitors : Ikaros Transcription Factor, Protein-Tyrosine Kinases.
- chemical , genetics : Ikaros Transcription Factor, RNA, Messenger, STAT5 Transcription Factor.
- chemical , metabolism : Antigens, CD34, Ikaros Transcription Factor, STAT5 Transcription Factor.
- drug effects : Apoptosis, Basophils, Cell Differentiation, Cell Proliferation, Eosinophils.
- genetics : Leukemia, Myeloid, Chronic-Phase.
- metabolism : Basophils, Eosinophils, Leukemia, Myeloid, Chronic-Phase.
- pathology : Basophils, Eosinophils, Leukemia, Myeloid, Chronic-Phase.
- chemical , pharmacology : Protein Kinase Inhibitors.
- Animals, Blotting, Western, Cells, Cultured, Disease Progression, Flow Cytometry, Humans, Immunoenzyme Techniques, Mice, Mice, Inbred NOD, Mice, SCID, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction.

Abstract

Key Points

CML patients with advanced-phase myeloid disease frequently show decreased IKAROS protein in primitive cells.

Expression of a dominant-negative IKAROS isoform expands primitive human CML cells and enhances their differentiation into basophils.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4300391

DOI: 10.1182/blood-2014-06-581173
PubMed: 25370416
PubMed Central: 4300391

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PMC:4300391

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Antigens, CD34 (metabolism)</term>
<term>Apoptosis (drug effects)</term>
<term>Basophils (drug effects)</term>
<term>Basophils (metabolism)</term>
<term>Basophils (pathology)</term>
<term>Blotting, Western</term>
<term>Cell Differentiation (drug effects)</term>
<term>Cell Proliferation (drug effects)</term>
<term>Cells, Cultured</term>
<term>Disease Progression</term>
<term>Eosinophils (drug effects)</term>
<term>Eosinophils (metabolism)</term>
<term>Eosinophils (pathology)</term>
<term>Flow Cytometry</term>
<term>Humans</term>
<term>Ikaros Transcription Factor (antagonists & inhibitors)</term>
<term>Ikaros Transcription Factor (genetics)</term>
<term>Ikaros Transcription Factor (metabolism)</term>
<term>Immunoenzyme Techniques</term>
<term>Leukemia, Myeloid, Chronic-Phase (genetics)</term>
<term>Leukemia, Myeloid, Chronic-Phase (metabolism)</term>
<term>Leukemia, Myeloid, Chronic-Phase (pathology)</term>
<term>Mice</term>
<term>Mice, Inbred NOD</term>
<term>Mice, SCID</term>
<term>Protein Kinase Inhibitors (pharmacology)</term>
<term>Protein-Tyrosine Kinases (antagonists & inhibitors)</term>
<term>RNA, Messenger (genetics)</term>
<term>Real-Time Polymerase Chain Reaction</term>
<term>Reverse Transcriptase Polymerase Chain Reaction</term>
<term>STAT5 Transcription Factor (genetics)</term>
<term>STAT5 Transcription Factor (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (génétique)</term>
<term>Animaux</term>
<term>Antigènes CD34 (métabolisme)</term>
<term>Apoptose ()</term>
<term>Cellules cultivées</term>
<term>Cytométrie en flux</term>
<term>Différenciation cellulaire ()</term>
<term>Facteur de transcription Ikaros (antagonistes et inhibiteurs)</term>
<term>Facteur de transcription Ikaros (génétique)</term>
<term>Facteur de transcription Ikaros (métabolisme)</term>
<term>Facteur de transcription STAT-5 (génétique)</term>
<term>Facteur de transcription STAT-5 (métabolisme)</term>
<term>Granulocytes basophiles ()</term>
<term>Granulocytes basophiles (anatomopathologie)</term>
<term>Granulocytes basophiles (métabolisme)</term>
<term>Granulocytes éosinophiles ()</term>
<term>Granulocytes éosinophiles (anatomopathologie)</term>
<term>Granulocytes éosinophiles (métabolisme)</term>
<term>Humains</term>
<term>Inhibiteurs de protéines kinases (pharmacologie)</term>
<term>Leucémie myéloïde en phase chronique (anatomopathologie)</term>
<term>Leucémie myéloïde en phase chronique (génétique)</term>
<term>Leucémie myéloïde en phase chronique (métabolisme)</term>
<term>Prolifération cellulaire ()</term>
<term>Protein-tyrosine kinases (antagonistes et inhibiteurs)</term>
<term>RT-PCR</term>
<term>Réaction de polymérisation en chaine en temps réel</term>
<term>Souris</term>
<term>Souris SCID</term>
<term>Souris de lignée NOD</term>
<term>Technique de Western</term>
<term>Techniques immunoenzymatiques</term>
<term>Évolution de la maladie</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Ikaros Transcription Factor</term>
<term>Protein-Tyrosine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Ikaros Transcription Factor</term>
<term>RNA, Messenger</term>
<term>STAT5 Transcription Factor</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antigens, CD34</term>
<term>Ikaros Transcription Factor</term>
<term>STAT5 Transcription Factor</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Granulocytes basophiles</term>
<term>Granulocytes éosinophiles</term>
<term>Leucémie myéloïde en phase chronique</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Facteur de transcription Ikaros</term>
<term>Protein-tyrosine kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term>
<term>Basophils</term>
<term>Cell Differentiation</term>
<term>Cell Proliferation</term>
<term>Eosinophils</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Leukemia, Myeloid, Chronic-Phase</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term>
<term>Facteur de transcription Ikaros</term>
<term>Facteur de transcription STAT-5</term>
<term>Leucémie myéloïde en phase chronique</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Basophils</term>
<term>Eosinophils</term>
<term>Leukemia, Myeloid, Chronic-Phase</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antigènes CD34</term>
<term>Facteur de transcription Ikaros</term>
<term>Facteur de transcription STAT-5</term>
<term>Granulocytes basophiles</term>
<term>Granulocytes éosinophiles</term>
<term>Leucémie myéloïde en phase chronique</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basophils</term>
<term>Eosinophils</term>
<term>Leukemia, Myeloid, Chronic-Phase</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Inhibiteurs de protéines kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Protein Kinase Inhibitors</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Blotting, Western</term>
<term>Cells, Cultured</term>
<term>Disease Progression</term>
<term>Flow Cytometry</term>
<term>Humans</term>
<term>Immunoenzyme Techniques</term>
<term>Mice</term>
<term>Mice, Inbred NOD</term>
<term>Mice, SCID</term>
<term>Real-Time Polymerase Chain Reaction</term>
<term>Reverse Transcriptase Polymerase Chain Reaction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Apoptose</term>
<term>Cellules cultivées</term>
<term>Cytométrie en flux</term>
<term>Différenciation cellulaire</term>
<term>Granulocytes basophiles</term>
<term>Granulocytes éosinophiles</term>
<term>Humains</term>
<term>Prolifération cellulaire</term>
<term>RT-PCR</term>
<term>Réaction de polymérisation en chaine en temps réel</term>
<term>Souris</term>
<term>Souris SCID</term>
<term>Souris de lignée NOD</term>
<term>Technique de Western</term>
<term>Techniques immunoenzymatiques</term>
<term>Évolution de la maladie</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><title>Key Points</title>
<p><list list-type="bullet"><list-item><p>CML patients with advanced-phase myeloid disease frequently show decreased IKAROS protein in primitive cells.</p>
</list-item>
<list-item><p>Expression of a dominant-negative IKAROS isoform expands primitive human CML cells and enhances their differentiation into basophils.</p>
</list-item>
</list>
</p>
</div>
</front>
</TEI>
</record>

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Disruption of IKAROS activity in primitive chronic-phase CML cells mimics myeloid disease progression

Disruption of IKAROS activity in primitive chronic-phase CML cells mimics myeloid disease progression

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