AustralieFrV1, Main, Exploration, bibRecord, 007740

Micro-RNA response to imatinib mesylate in patients with chronic myeloid leukemia

Identifieur interne : 007740 ( Main/Exploration ); précédent : 007739; suivant : 007741

Micro-RNA response to imatinib mesylate in patients with chronic myeloid leukemia

Auteurs : Stéphane Flamant [Australie, Canada] ; William Ritchie [Australie] ; Joëlle Guilhot [France] ; Jeff Holst [Australie] ; Marie-Laure Bonnet [France] ; Jean-Claude Chomel [France] ; François Guilhot [France] ; Ali G. Turhan [France] ; John E. J. Rasko [Australie]

Source :

Haematologica : (Roma) [ 0390-6078 ] ; 2010.

RBID : Pascal:10-0445793

Descripteurs français

Pascal (Inist)
- Imatinib, Micro ARN, Homme, Leucémie myéloïde chronique, Gène hybride, Translocation chromosomique, Chromosome C9 anormal, Chromosome G22 anormal, Chromosome Ph1, Non-specific serine/threonine protein kinase, Gène onc cellulaire, Interférence ARN, Hématologie, Anticancéreux, STI 571, Gène abl, Gène bcr.
Wicri :
- topic : Homme.

English descriptors

KwdEn :
- Abnormal chromosome C9, Abnormal chromosome G22, Antineoplastic agent, C-Onc gene, Chromosome translocation, Chronic myelogenous leukemia, Hematology, Human, Hybrid gene, Imatinib, Micro RNA, Non-specific serine/threonine protein kinase, Philadelphia chromosome, RNA interference, bcr gene.

Abstract

Background Micro-RNAs (miRNAs) control gene expression by destabilizing targeted transcripts and inhibiting their translation. Aberrant expression of miRNAs has been described in many human cancers, including chronic myeloid leukemia. Current first-line therapy for newly diagnosed chronic myeloid leukemia is imatinib mesylate, which typically produces a rapid hematologic response. However the effect of imatinib on miRNA expression in vivo has not been thoroughly examined. Design and Methods Using a TaqMan Low-Density Array system, we analyzed miRNA expression in blood samples from newly diagnosed chronic myeloid leukemia patients before and within the first two weeks of imatinib therapy. Quantitative real-time PCR was used to validate imatinib-modulated miRNAs in sequential primary chronic myeloid leukemia samples (n=11, plus 12 additional validation patients). Bioinformatic target gene prediction analysis was performed based on changes in miRNA expression. Results We observed increased expression of miR-150 and miR-146a, and reduced expression of miR-142-3p and miR-199b-5p (3-fold median change) after two weeks of imatinib therapy. A significant correlation (P<0.05) between the Sokal score and pre-treatment miR-142-3p levels was noted. Expression changes in the same miRNAs were consistently found in an additional cohort of chronic myeloid leukemia patients, as compared to healthy subjects. Peripheral blood cells from chronic phase and blast crisis patients displayed a 30-fold lower expression of miR-150 compared to normal samples, which is of particular interest since c-Myb, a known target of miR-150, was recently shown to be necessary for Bcr-Abl-mediated transformation. Conclusions We found that imatinib treatment of chronic myeloid leukemia patients rapidly normalizes the characteristic miRNA expression profile, suggesting that miRNAs may serve as a novel clinically useful biomarker in this disease.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913081

Affiliations:

Le document en format XML

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<orgName type="university">Université de Poitiers</orgName>
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<affiliation wicri:level="1"><inist:fA14 i1="05"><s1>Service d'Hématologie et Oncologie Biologique, CHU de Poitiers</s1>
<s3>FRA</s3>
<sZ>6 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
<country>France</country>
<wicri:noRegion>CHU de Poitiers</wicri:noRegion>
<wicri:noRegion>Service d'Hématologie et Oncologie Biologique, CHU de Poitiers</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Rasko, John E J" sort="Rasko, John E J" uniqKey="Rasko J" first="John E. J." last="Rasko">John E. J. Rasko</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Gene & Stem Cell Therapy Program, Centenary Institute</s1>
<s2>Newtown</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
<country>Australie</country>
<wicri:noRegion>Newtown</wicri:noRegion>
</affiliation>
<affiliation wicri:level="4"><inist:fA14 i1="07"><s1>Faculty of Medicine, University of Sydney</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>9 aut.</sZ>
</inist:fA14>
<country>Australie</country>
<placeName><settlement type="city">Sydney</settlement>
<region type="état">Nouvelle-Galles du Sud</region>
<settlement type="city">Sydney</settlement>
</placeName>
<orgName type="university">Université de Sydney</orgName>
</affiliation>
<affiliation wicri:level="1"><inist:fA14 i1="08"><s1>Cell and Molecular Therapies, Sydney Cancer Centre, Royal Prince Alfred Hospital</s1>
<s2>Camperdown</s2>
<s3>AUS</s3>
<sZ>9 aut.</sZ>
</inist:fA14>
<country>Australie</country>
<wicri:noRegion>Camperdown</wicri:noRegion>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Haematologica : (Roma)</title>
<title level="j" type="abbreviated">Haematologica : (Roma)</title>
<idno type="ISSN">0390-6078</idno>
<imprint><date when="2010">2010</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Haematologica : (Roma)</title>
<title level="j" type="abbreviated">Haematologica : (Roma)</title>
<idno type="ISSN">0390-6078</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Abnormal chromosome C9</term>
<term>Abnormal chromosome G22</term>
<term>Antineoplastic agent</term>
<term>C-Onc gene</term>
<term>Chromosome translocation</term>
<term>Chronic myelogenous leukemia</term>
<term>Hematology</term>
<term>Human</term>
<term>Hybrid gene</term>
<term>Imatinib</term>
<term>Micro RNA</term>
<term>Non-specific serine/threonine protein kinase</term>
<term>Philadelphia chromosome</term>
<term>RNA interference</term>
<term>bcr gene</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Imatinib</term>
<term>Micro ARN</term>
<term>Homme</term>
<term>Leucémie myéloïde chronique</term>
<term>Gène hybride</term>
<term>Translocation chromosomique</term>
<term>Chromosome C9 anormal</term>
<term>Chromosome G22 anormal</term>
<term>Chromosome Ph1</term>
<term>Non-specific serine/threonine protein kinase</term>
<term>Gène onc cellulaire</term>
<term>Interférence ARN</term>
<term>Hématologie</term>
<term>Anticancéreux</term>
<term>STI 571</term>
<term>Gène abl</term>
<term>Gène bcr</term>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Background Micro-RNAs (miRNAs) control gene expression by destabilizing targeted transcripts and inhibiting their translation. Aberrant expression of miRNAs has been described in many human cancers, including chronic myeloid leukemia. Current first-line therapy for newly diagnosed chronic myeloid leukemia is imatinib mesylate, which typically produces a rapid hematologic response. However the effect of imatinib on miRNA expression in vivo has not been thoroughly examined. Design and Methods Using a TaqMan Low-Density Array system, we analyzed miRNA expression in blood samples from newly diagnosed chronic myeloid leukemia patients before and within the first two weeks of imatinib therapy. Quantitative real-time PCR was used to validate imatinib-modulated miRNAs in sequential primary chronic myeloid leukemia samples (n=11, plus 12 additional validation patients). Bioinformatic target gene prediction analysis was performed based on changes in miRNA expression. Results We observed increased expression of miR-150 and miR-146a, and reduced expression of miR-142-3p and miR-199b-5p (3-fold median change) after two weeks of imatinib therapy. A significant correlation (P<0.05) between the Sokal score and pre-treatment miR-142-3p levels was noted. Expression changes in the same miRNAs were consistently found in an additional cohort of chronic myeloid leukemia patients, as compared to healthy subjects. Peripheral blood cells from chronic phase and blast crisis patients displayed a 30-fold lower expression of miR-150 compared to normal samples, which is of particular interest since c-Myb, a known target of miR-150, was recently shown to be necessary for Bcr-Abl-mediated transformation. Conclusions We found that imatinib treatment of chronic myeloid leukemia patients rapidly normalizes the characteristic miRNA expression profile, suggesting that miRNAs may serve as a novel clinically useful biomarker in this disease.</div>
</front>
</TEI>
<affiliations><list><country><li>Australie</li>
<li>Canada</li>
<li>France</li>
</country>
<region><li>Nouvelle-Galles du Sud</li>
<li>Poitou-Charentes</li>
</region>
<settlement><li>Poitiers</li>
<li>Sydney</li>
</settlement>
<orgName><li>Université de Poitiers</li>
<li>Université de Sydney</li>
</orgName>
</list>
<tree><country name="Australie"><noRegion><name sortKey="Flamant, Stephane" sort="Flamant, Stephane" uniqKey="Flamant S" first="Stéphane" last="Flamant">Stéphane Flamant</name>
</noRegion>
<name sortKey="Holst, Jeff" sort="Holst, Jeff" uniqKey="Holst J" first="Jeff" last="Holst">Jeff Holst</name>
<name sortKey="Rasko, John E J" sort="Rasko, John E J" uniqKey="Rasko J" first="John E. J." last="Rasko">John E. J. Rasko</name>
<name sortKey="Rasko, John E J" sort="Rasko, John E J" uniqKey="Rasko J" first="John E. J." last="Rasko">John E. J. Rasko</name>
<name sortKey="Rasko, John E J" sort="Rasko, John E J" uniqKey="Rasko J" first="John E. J." last="Rasko">John E. J. Rasko</name>
<name sortKey="Ritchie, William" sort="Ritchie, William" uniqKey="Ritchie W" first="William" last="Ritchie">William Ritchie</name>
</country>
<country name="Canada"><noRegion><name sortKey="Flamant, Stephane" sort="Flamant, Stephane" uniqKey="Flamant S" first="Stéphane" last="Flamant">Stéphane Flamant</name>
</noRegion>
</country>
<country name="France"><noRegion><name sortKey="Guilhot, Joelle" sort="Guilhot, Joelle" uniqKey="Guilhot J" first="Joëlle" last="Guilhot">Joëlle Guilhot</name>
</noRegion>
<name sortKey="Bonnet, Marie Laure" sort="Bonnet, Marie Laure" uniqKey="Bonnet M" first="Marie-Laure" last="Bonnet">Marie-Laure Bonnet</name>
<name sortKey="Chomel, Jean Claude" sort="Chomel, Jean Claude" uniqKey="Chomel J" first="Jean-Claude" last="Chomel">Jean-Claude Chomel</name>
<name sortKey="Chomel, Jean Claude" sort="Chomel, Jean Claude" uniqKey="Chomel J" first="Jean-Claude" last="Chomel">Jean-Claude Chomel</name>
<name sortKey="Guilhot, Francois" sort="Guilhot, Francois" uniqKey="Guilhot F" first="François" last="Guilhot">François Guilhot</name>
<name sortKey="Guilhot, Francois" sort="Guilhot, Francois" uniqKey="Guilhot F" first="François" last="Guilhot">François Guilhot</name>
<name sortKey="Guilhot, Francois" sort="Guilhot, Francois" uniqKey="Guilhot F" first="François" last="Guilhot">François Guilhot</name>
<name sortKey="Guilhot, Joelle" sort="Guilhot, Joelle" uniqKey="Guilhot J" first="Joëlle" last="Guilhot">Joëlle Guilhot</name>
<name sortKey="Turhan, Ali G" sort="Turhan, Ali G" uniqKey="Turhan A" first="Ali G." last="Turhan">Ali G. Turhan</name>
<name sortKey="Turhan, Ali G" sort="Turhan, Ali G" uniqKey="Turhan A" first="Ali G." last="Turhan">Ali G. Turhan</name>
</country>
</tree>
</affiliations>
</record>

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Micro-RNA response to imatinib mesylate in patients with chronic myeloid leukemia

Micro-RNA response to imatinib mesylate in patients with chronic myeloid leukemia

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