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

Identifieur interne : 003084 ( PubMed/Curation ); précédent : 003083; suivant : 003085

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 [ 1528-0020 ] ; 2015.

RBID : pubmed:25370416

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

Without effective therapy, chronic-phase chronic myeloid leukemia (CP-CML) evolves into an acute leukemia (blast crisis [BC]) that displays either myeloid or B-lymphoid characteristics. This transition is often preceded by a clinically recognized, but biologically poorly characterized, accelerated phase (AP). Here, we report that IKAROS protein is absent or reduced in bone marrow blasts from most CML patients with advanced myeloid disease (AP or BC). This contrasts with primitive CP-CML cells and BCR-ABL1-negative acute myeloid leukemia blasts, which express readily detectable IKAROS. To investigate whether loss of IKAROS contributes to myeloid disease progression in CP-CML, we examined the effects of forced expression of a dominant-negative isoform of IKAROS (IK6) in CP-CML patients' CD34(+) cells. We confirmed that IK6 disrupts IKAROS activity in transduced CP-CML cells and showed that it confers on them features of AP-CML, including a prolonged increased output in vitro and in xenografted mice of primitive cells with an enhanced ability to differentiate into basophils. Expression of IK6 in CD34(+) CP-CML cells also led to activation of signal transducer and activator of transcription 5 and transcriptional repression of its negative regulators. These findings implicate loss of IKAROS as a frequent step and potential diagnostic harbinger of progressive myeloid disease in CML patients.

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

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<country xml:lang="fr">Canada</country>
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<author><name sortKey="Sloma, Ivan" sort="Sloma, Ivan" uniqKey="Sloma I" first="Ivan" last="Sloma">Ivan Sloma</name>
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<country xml:lang="fr">France</country>
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<country xml:lang="fr">Australie</country>
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</affiliation>
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<author><name sortKey="Babovic, Sonja" sort="Babovic, Sonja" uniqKey="Babovic S" first="Sonja" last="Babovic">Sonja Babovic</name>
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<country xml:lang="fr">Canada</country>
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</affiliation>
</author>
<author><name sortKey="Bulaeva, Elizabeth" sort="Bulaeva, Elizabeth" uniqKey="Bulaeva E" first="Elizabeth" last="Bulaeva">Elizabeth Bulaeva</name>
<affiliation wicri:level="1"><nlm:affiliation>Terry Fox Laboratory, British Columbia Cancer Agency and University of British Columbia, Vancouver, BC, Canada;</nlm:affiliation>
<country xml:lang="fr">Canada</country>
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</affiliation>
</author>
<author><name sortKey="Rabu, Gabrielle" sort="Rabu, Gabrielle" uniqKey="Rabu G" first="Gabrielle" last="Rabu">Gabrielle Rabu</name>
<affiliation wicri:level="1"><nlm:affiliation>Terry Fox Laboratory, British Columbia Cancer Agency and University of British Columbia, Vancouver, BC, Canada;</nlm:affiliation>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>Terry Fox Laboratory, British Columbia Cancer Agency and University of British Columbia, Vancouver, BC</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Terry, Jefferson" sort="Terry, Jefferson" uniqKey="Terry J" first="Jefferson" last="Terry">Jefferson Terry</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Molecular Medicine, McMaster University Medical Centre, Hamilton, ON, Canada;</nlm:affiliation>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>Department of Pathology and Molecular Medicine, McMaster University Medical Centre, Hamilton, ON</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Druker, Brian J" sort="Druker, Brian J" uniqKey="Druker B" first="Brian J" last="Druker">Brian J. Druker</name>
<affiliation wicri:level="4"><nlm:affiliation>Knight Cancer Institute, Oregon Health & Science University, Portland, OR; and.</nlm:affiliation>
<orgName type="university">Université des sciences et de la médecine de l'Oregon</orgName>
<country>États-Unis</country>
<placeName><settlement type="city">Portland</settlement>
<region type="state">Oregon</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Loriaux, Marc M" sort="Loriaux, Marc M" uniqKey="Loriaux M" first="Marc M" last="Loriaux">Marc M. Loriaux</name>
<affiliation wicri:level="4"><nlm:affiliation>Knight Cancer Institute, Oregon Health & Science University, Portland, OR; and.</nlm:affiliation>
<orgName type="university">Université des sciences et de la médecine de l'Oregon</orgName>
<country>États-Unis</country>
<placeName><settlement type="city">Portland</settlement>
<region type="state">Oregon</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Loeb, Keith R" sort="Loeb, Keith R" uniqKey="Loeb K" first="Keith R" last="Loeb">Keith R. Loeb</name>
<affiliation wicri:level="2"><nlm:affiliation>Fred Hutchinson Cancer Research Center, Seattle, WA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Washington (État)</region>
</placeName>
<wicri:cityArea>Fred Hutchinson Cancer Research Center, Seattle</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Radich, Jerald P" sort="Radich, Jerald P" uniqKey="Radich J" first="Jerald P" last="Radich">Jerald P. Radich</name>
<affiliation wicri:level="2"><nlm:affiliation>Fred Hutchinson Cancer Research Center, Seattle, WA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Washington (État)</region>
</placeName>
<wicri:cityArea>Fred Hutchinson Cancer Research Center, Seattle</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Erber, Wendy N" sort="Erber, Wendy N" uniqKey="Erber W" first="Wendy N" last="Erber">Wendy N. Erber</name>
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<country xml:lang="fr">Australie</country>
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</affiliation>
</author>
<author><name sortKey="Eaves, Connie J" sort="Eaves, Connie J" uniqKey="Eaves C" first="Connie J" last="Eaves">Connie J. Eaves</name>
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<country xml:lang="fr">Canada</country>
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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">Without effective therapy, chronic-phase chronic myeloid leukemia (CP-CML) evolves into an acute leukemia (blast crisis [BC]) that displays either myeloid or B-lymphoid characteristics. This transition is often preceded by a clinically recognized, but biologically poorly characterized, accelerated phase (AP). Here, we report that IKAROS protein is absent or reduced in bone marrow blasts from most CML patients with advanced myeloid disease (AP or BC). This contrasts with primitive CP-CML cells and BCR-ABL1-negative acute myeloid leukemia blasts, which express readily detectable IKAROS. To investigate whether loss of IKAROS contributes to myeloid disease progression in CP-CML, we examined the effects of forced expression of a dominant-negative isoform of IKAROS (IK6) in CP-CML patients' CD34(+) cells. We confirmed that IK6 disrupts IKAROS activity in transduced CP-CML cells and showed that it confers on them features of AP-CML, including a prolonged increased output in vitro and in xenografted mice of primitive cells with an enhanced ability to differentiate into basophils. Expression of IK6 in CD34(+) CP-CML cells also led to activation of signal transducer and activator of transcription 5 and transcriptional repression of its negative regulators. These findings implicate loss of IKAROS as a frequent step and potential diagnostic harbinger of progressive myeloid disease in CML patients.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25370416</PMID>
<DateCreated><Year>2015</Year>
<Month>01</Month>
<Day>16</Day>
</DateCreated>
<DateCompleted><Year>2015</Year>
<Month>03</Month>
<Day>12</Day>
</DateCompleted>
<DateRevised><Year>2016</Year>
<Month>10</Month>
<Day>19</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1528-0020</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>125</Volume>
<Issue>3</Issue>
<PubDate><Year>2015</Year>
<Month>Jan</Month>
<Day>15</Day>
</PubDate>
</JournalIssue>
<Title>Blood</Title>
<ISOAbbreviation>Blood</ISOAbbreviation>
</Journal>
<ArticleTitle>Disruption of IKAROS activity in primitive chronic-phase CML cells mimics myeloid disease progression.</ArticleTitle>
<Pagination><MedlinePgn>504-15</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1182/blood-2014-06-581173</ELocationID>
<Abstract><AbstractText>Without effective therapy, chronic-phase chronic myeloid leukemia (CP-CML) evolves into an acute leukemia (blast crisis [BC]) that displays either myeloid or B-lymphoid characteristics. This transition is often preceded by a clinically recognized, but biologically poorly characterized, accelerated phase (AP). Here, we report that IKAROS protein is absent or reduced in bone marrow blasts from most CML patients with advanced myeloid disease (AP or BC). This contrasts with primitive CP-CML cells and BCR-ABL1-negative acute myeloid leukemia blasts, which express readily detectable IKAROS. To investigate whether loss of IKAROS contributes to myeloid disease progression in CP-CML, we examined the effects of forced expression of a dominant-negative isoform of IKAROS (IK6) in CP-CML patients' CD34(+) cells. We confirmed that IK6 disrupts IKAROS activity in transduced CP-CML cells and showed that it confers on them features of AP-CML, including a prolonged increased output in vitro and in xenografted mice of primitive cells with an enhanced ability to differentiate into basophils. Expression of IK6 in CD34(+) CP-CML cells also led to activation of signal transducer and activator of transcription 5 and transcriptional repression of its negative regulators. These findings implicate loss of IKAROS as a frequent step and potential diagnostic harbinger of progressive myeloid disease in CML patients.</AbstractText>
<CopyrightInformation>© 2015 by The American Society of Hematology.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Beer</LastName>
<ForeName>Philip A</ForeName>
<Initials>PA</Initials>
<AffiliationInfo><Affiliation>Terry Fox Laboratory, British Columbia Cancer Agency and University of British Columbia, Vancouver, BC, Canada;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Knapp</LastName>
<ForeName>David J H F</ForeName>
<Initials>DJ</Initials>
<AffiliationInfo><Affiliation>Terry Fox Laboratory, British Columbia Cancer Agency and University of British Columbia, Vancouver, BC, Canada;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Miller</LastName>
<ForeName>Paul H</ForeName>
<Initials>PH</Initials>
<AffiliationInfo><Affiliation>Terry Fox Laboratory, British Columbia Cancer Agency and University of British Columbia, Vancouver, BC, Canada;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kannan</LastName>
<ForeName>Nagarajan</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Terry Fox Laboratory, British Columbia Cancer Agency and University of British Columbia, Vancouver, BC, Canada;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sloma</LastName>
<ForeName>Ivan</ForeName>
<Initials>I</Initials>
<AffiliationInfo><Affiliation>Laboratoire d'Hématologie, Hôpital Paul Brousse, Assistance Publique des Hôpitaux de Paris, INSERM U935, Villejuif, France;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Heel</LastName>
<ForeName>Kathy</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>School of Pathology and Laboratory Medicine, The University of Western Australia, Crawley WA, Australia;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Babovic</LastName>
<ForeName>Sonja</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Terry Fox Laboratory, British Columbia Cancer Agency and University of British Columbia, Vancouver, BC, Canada;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bulaeva</LastName>
<ForeName>Elizabeth</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Terry Fox Laboratory, British Columbia Cancer Agency and University of British Columbia, Vancouver, BC, Canada;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rabu</LastName>
<ForeName>Gabrielle</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Terry Fox Laboratory, British Columbia Cancer Agency and University of British Columbia, Vancouver, BC, Canada;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Terry</LastName>
<ForeName>Jefferson</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Pathology and Molecular Medicine, McMaster University Medical Centre, Hamilton, ON, Canada;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Druker</LastName>
<ForeName>Brian J</ForeName>
<Initials>BJ</Initials>
<AffiliationInfo><Affiliation>Knight Cancer Institute, Oregon Health & Science University, Portland, OR; and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Loriaux</LastName>
<ForeName>Marc M</ForeName>
<Initials>MM</Initials>
<AffiliationInfo><Affiliation>Knight Cancer Institute, Oregon Health & Science University, Portland, OR; and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Loeb</LastName>
<ForeName>Keith R</ForeName>
<Initials>KR</Initials>
<AffiliationInfo><Affiliation>Fred Hutchinson Cancer Research Center, Seattle, WA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Radich</LastName>
<ForeName>Jerald P</ForeName>
<Initials>JP</Initials>
<AffiliationInfo><Affiliation>Fred Hutchinson Cancer Research Center, Seattle, WA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Erber</LastName>
<ForeName>Wendy N</ForeName>
<Initials>WN</Initials>
<AffiliationInfo><Affiliation>School of Pathology and Laboratory Medicine, The University of Western Australia, Crawley WA, Australia;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Eaves</LastName>
<ForeName>Connie J</ForeName>
<Initials>CJ</Initials>
<AffiliationInfo><Affiliation>Terry Fox Laboratory, British Columbia Cancer Agency and University of British Columbia, Vancouver, BC, Canada;</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>P01 CA018029</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R37 CA065823</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><Agency>Canadian Institutes of Health Research</Agency>
<Country>Canada</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2014</Year>
<Month>11</Month>
<Day>04</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Blood</MedlineTA>
<NlmUniqueID>7603509</NlmUniqueID>
<ISSNLinking>0006-4971</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D018952">Antigens, CD34</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C586512">Ikaros 6 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D047428">Protein Kinase Inhibitors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D050799">STAT5 Transcription Factor</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>148971-36-2</RegistryNumber>
<NameOfSubstance UI="D051740">Ikaros Transcription Factor</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber>
<NameOfSubstance UI="D011505">Protein-Tyrosine Kinases</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>AIM</CitationSubset>
<CitationSubset>IM</CitationSubset>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018952" MajorTopicYN="N">Antigens, CD34</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001491" MajorTopicYN="N">Basophils</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015153" MajorTopicYN="N">Blotting, Western</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004804" MajorTopicYN="N">Eosinophils</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005434" MajorTopicYN="N">Flow Cytometry</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051740" MajorTopicYN="N">Ikaros Transcription Factor</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007124" MajorTopicYN="N">Immunoenzyme Techniques</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015466" MajorTopicYN="N">Leukemia, Myeloid, Chronic-Phase</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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   |texte=   Disruption of IKAROS activity in primitive chronic-phase CML cells mimics myeloid disease progression.
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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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