Effect of retinoic acid and interferon alpha on granulocyte-macrophage colony forming cells in chronic myeloid leukemia: Increased inhibition by all- trans - and 13- cis -retinoic acids in advanced stage disease
Identifieur interne : 000873 ( Istex/Corpus ); précédent : 000872; suivant : 000874Effect of retinoic acid and interferon alpha on granulocyte-macrophage colony forming cells in chronic myeloid leukemia: Increased inhibition by all- trans - and 13- cis -retinoic acids in advanced stage disease
Auteurs : Grace E. Sagayadan ; Peter H. Wiernik ; Nancy Sun ; Greg Ahearn ; Deborah Thompson ; Steven J. Hallam ; Xiao-Ping Hu ; Janice P. Dutcher ; Robert E. GallagherSource :
- Leukemia Research [ 0145-2126 ] ; 1994.
English descriptors
- Teeft :
- Acute promyelocytic leukemia, Albert einstein cancer center, Annealing temperature, Antisense primer, Assay, Blast cells, Blastic, Blastic crisis, Bone marrow, Cfc, Chain reaction, Chronic myeloid leukemia, Chronic phase, Clonal growth, Clonogenic, Clonogenic assays, Cmlcp cases, Colony formation, Colony morphology, Colony size, Current study, Differentiation therapy, Fetal calf serum, Individual points, Inftr, Inhibition, Inhibition curves, Interferon, Leukemia, Mrna, Myelogenous leukemia, Myeloid, Myeloproliferative disease, None none, Peripheral blood, Primer, Primer pair, Promyelocytic, Propositus case, Recombinant, Recombinant interferon, Retinoic, Retinoic acid, Retinoic acids, Sense primer, Single agent, Strong inhibition, Titration curves, Total clones, Various concentrations.
Abstract
Abstract: Granulocyte-macrophage colony forming units (CFU-GM) from patients with advanced stage chronic myelogenous leukemia (CML), i.e. in blastic crisis (BC) or accelerated phase (AP), were inhibited by all-trans-retinoic acid (tRA) approximately 1000-fold more potently than those from chronic phase (CP) CML patients (median ic50 = 10−9 M tRA for six CML-AP/BC cases vs > 10−6 M tRA for seven CML-CP cases). A similar activity pattern was observed for the stereoisomer 13-cis-RA (cRA). There was no apparent correlation of CFU-GM retinoid sensitivity with cloning efficiency or other colony characteristics. Interferon alpha-2a (INFα) alone strongly inhibited CFU-GM growth in all four CML-AP/BC cases (ic50 ⩽ 250 IU/ml) and three out of seven CML-CP cases (ic50 ⩽ 500 IU/ml), but there was little or no interactive effect between various concentrations of tRA and INFα (50 IU/ml) on CFU-GM from either CML-AP/BC or CML-CP cases. These results suggest that CML-AP/BC CFU-GM have some intrinsic molecular alteration(s) which markedly enhances their responsiveness to tRA and cRA, which may be clinically exploitable.
Url:
DOI: 10.1016/0145-2126(94)90055-8
Links to Exploration step
ISTEX:C5B9A77C81EB4B3891F7309A3235793023D7D6F6Le document en format XML
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Wiernik</name><affiliation><mods:affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Sun, Nancy" sort="Sun, Nancy" uniqKey="Sun N" first="Nancy" last="Sun">Nancy Sun</name><affiliation><mods:affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Ahearn, Greg" sort="Ahearn, Greg" uniqKey="Ahearn G" first="Greg" last="Ahearn">Greg Ahearn</name><affiliation><mods:affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Thompson, Deborah" sort="Thompson, Deborah" uniqKey="Thompson D" first="Deborah" last="Thompson">Deborah Thompson</name><affiliation><mods:affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Hallam, Steven J" sort="Hallam, Steven J" uniqKey="Hallam S" first="Steven J." last="Hallam">Steven J. 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Sagayadan</name><affiliation><mods:affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Wiernik, Peter H" sort="Wiernik, Peter H" uniqKey="Wiernik P" first="Peter H." last="Wiernik">Peter H. Wiernik</name><affiliation><mods:affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Sun, Nancy" sort="Sun, Nancy" uniqKey="Sun N" first="Nancy" last="Sun">Nancy Sun</name><affiliation><mods:affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Ahearn, Greg" sort="Ahearn, Greg" uniqKey="Ahearn G" first="Greg" last="Ahearn">Greg Ahearn</name><affiliation><mods:affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Thompson, Deborah" sort="Thompson, Deborah" uniqKey="Thompson D" first="Deborah" last="Thompson">Deborah Thompson</name><affiliation><mods:affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Hallam, Steven J" sort="Hallam, Steven J" uniqKey="Hallam S" first="Steven J." last="Hallam">Steven J. Hallam</name><affiliation><mods:affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Hu, Xiao Ping" sort="Hu, Xiao Ping" uniqKey="Hu X" first="Xiao-Ping" last="Hu">Xiao-Ping Hu</name><affiliation><mods:affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Dutcher, Janice P" sort="Dutcher, Janice P" uniqKey="Dutcher J" first="Janice P." last="Dutcher">Janice P. Dutcher</name><affiliation><mods:affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Gallagher, Robert E" sort="Gallagher, Robert E" uniqKey="Gallagher R" first="Robert E." last="Gallagher">Robert E. Gallagher</name><affiliation><mods:affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Leukemia Research</title><title level="j" type="abbrev">LR</title><idno type="ISSN">0145-2126</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1994">1994</date><biblScope unit="volume">18</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="741">741</biblScope><biblScope unit="page" to="748">748</biblScope></imprint><idno type="ISSN">0145-2126</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0145-2126</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acute promyelocytic leukemia</term><term>Albert einstein cancer center</term><term>Annealing temperature</term><term>Antisense primer</term><term>Assay</term><term>Blast cells</term><term>Blastic</term><term>Blastic crisis</term><term>Bone marrow</term><term>Cfc</term><term>Chain reaction</term><term>Chronic myeloid leukemia</term><term>Chronic phase</term><term>Clonal growth</term><term>Clonogenic</term><term>Clonogenic assays</term><term>Cmlcp cases</term><term>Colony formation</term><term>Colony morphology</term><term>Colony size</term><term>Current study</term><term>Differentiation therapy</term><term>Fetal calf serum</term><term>Individual points</term><term>Inftr</term><term>Inhibition</term><term>Inhibition curves</term><term>Interferon</term><term>Leukemia</term><term>Mrna</term><term>Myelogenous leukemia</term><term>Myeloid</term><term>Myeloproliferative disease</term><term>None none</term><term>Peripheral blood</term><term>Primer</term><term>Primer pair</term><term>Promyelocytic</term><term>Propositus case</term><term>Recombinant</term><term>Recombinant interferon</term><term>Retinoic</term><term>Retinoic acid</term><term>Retinoic acids</term><term>Sense primer</term><term>Single agent</term><term>Strong inhibition</term><term>Titration curves</term><term>Total clones</term><term>Various concentrations</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Granulocyte-macrophage colony forming units (CFU-GM) from patients with advanced stage chronic myelogenous leukemia (CML), i.e. in blastic crisis (BC) or accelerated phase (AP), were inhibited by all-trans-retinoic acid (tRA) approximately 1000-fold more potently than those from chronic phase (CP) CML patients (median ic50 = 10−9 M tRA for six CML-AP/BC cases vs > 10−6 M tRA for seven CML-CP cases). A similar activity pattern was observed for the stereoisomer 13-cis-RA (cRA). There was no apparent correlation of CFU-GM retinoid sensitivity with cloning efficiency or other colony characteristics. Interferon alpha-2a (INFα) alone strongly inhibited CFU-GM growth in all four CML-AP/BC cases (ic50 ⩽ 250 IU/ml) and three out of seven CML-CP cases (ic50 ⩽ 500 IU/ml), but there was little or no interactive effect between various concentrations of tRA and INFα (50 IU/ml) on CFU-GM from either CML-AP/BC or CML-CP cases. These results suggest that CML-AP/BC CFU-GM have some intrinsic molecular alteration(s) which markedly enhances their responsiveness to tRA and cRA, which may be clinically exploitable.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>retinoic</json:string><json:string>promyelocytic</json:string><json:string>myeloid</json:string><json:string>retinoic acid</json:string><json:string>blastic</json:string><json:string>interferon</json:string><json:string>inftr</json:string><json:string>primer</json:string><json:string>recombinant</json:string><json:string>clonogenic</json:string><json:string>acute promyelocytic leukemia</json:string><json:string>cfc</json:string><json:string>leukemia</json:string><json:string>mrna</json:string><json:string>assay</json:string><json:string>clonogenic assays</json:string><json:string>chronic myeloid leukemia</json:string><json:string>propositus case</json:string><json:string>blastic crisis</json:string><json:string>chronic phase</json:string><json:string>myeloproliferative disease</json:string><json:string>current study</json:string><json:string>retinoic acids</json:string><json:string>bone marrow</json:string><json:string>annealing temperature</json:string><json:string>peripheral blood</json:string><json:string>none none</json:string><json:string>clonal growth</json:string><json:string>cmlcp cases</json:string><json:string>antisense primer</json:string><json:string>myelogenous leukemia</json:string><json:string>albert einstein cancer center</json:string><json:string>colony morphology</json:string><json:string>strong inhibition</json:string><json:string>recombinant interferon</json:string><json:string>sense primer</json:string><json:string>fetal calf serum</json:string><json:string>primer pair</json:string><json:string>individual points</json:string><json:string>titration curves</json:string><json:string>blast cells</json:string><json:string>colony formation</json:string><json:string>inhibition curves</json:string><json:string>chain reaction</json:string><json:string>total clones</json:string><json:string>single agent</json:string><json:string>colony size</json:string><json:string>various concentrations</json:string><json:string>differentiation therapy</json:string><json:string>inhibition</json:string></teeft></keywords><author><json:item><name>Grace E. Sagayadan</name><affiliations><json:string>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</json:string></affiliations></json:item><json:item><name>Peter H. Wiernik</name><affiliations><json:string>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</json:string></affiliations></json:item><json:item><name>Nancy Sun</name><affiliations><json:string>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</json:string></affiliations></json:item><json:item><name>Greg Ahearn</name><affiliations><json:string>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</json:string></affiliations></json:item><json:item><name>Deborah Thompson</name><affiliations><json:string>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</json:string></affiliations></json:item><json:item><name>Steven J. Hallam</name><affiliations><json:string>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</json:string></affiliations></json:item><json:item><name>Xiao-Ping Hu</name><affiliations><json:string>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</json:string></affiliations></json:item><json:item><name>Janice P. Dutcher</name><affiliations><json:string>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</json:string></affiliations></json:item><json:item><name>Robert E. Gallagher</name><affiliations><json:string>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Chronic myelogenous leukemia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CFU-GM</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>retinoic acid</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>interferon</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>reverse transcriptase-polymerase chain reaction</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>BCR-ABL</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PML-RARα</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>tRA : all- trans -retinoic acid</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cRA : 13- cis -retinoic acid</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>INFα : recombinant interferon alpha-2a</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CML : chronic myelogenous leukemia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>BC : blastic crisis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>AP : accelerated phase</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CP : chronic phase</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MPD : myeloproliferative disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>APL : acute promyelocytic leukemia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>AML : acute myelogenous leukemia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CFU-GM : colony forming unit-granulocyte-macrophage</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CFC : colony forming cells</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ic50 : 50% inhibitory concentration</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PB : peripheral blood</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>BM : bone marrow</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>FCS : fetal calf serum</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MC : methylcellulose</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PHALy : phytohemagglutinin-stimulated lymphocyte</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CM : conditioned medium</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>RT : reverse transcriptase</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PCR : polymerase chain reaction</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>G3PDH : glyceraldehyde-3-phosphate dehydrogenase</value></json:item></subject><arkIstex>ark:/67375/6H6-DZS2XL68-P</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Granulocyte-macrophage colony forming units (CFU-GM) from patients with advanced stage chronic myelogenous leukemia (CML), i.e. in blastic crisis (BC) or accelerated phase (AP), were inhibited by all-trans-retinoic acid (tRA) approximately 1000-fold more potently than those from chronic phase (CP) CML patients (median ic50 = 10−9 M tRA for six CML-AP/BC cases vs > 10−6 M tRA for seven CML-CP cases). A similar activity pattern was observed for the stereoisomer 13-cis-RA (cRA). There was no apparent correlation of CFU-GM retinoid sensitivity with cloning efficiency or other colony characteristics. Interferon alpha-2a (INFα) alone strongly inhibited CFU-GM growth in all four CML-AP/BC cases (ic50 ⩽ 250 IU/ml) and three out of seven CML-CP cases (ic50 ⩽ 500 IU/ml), but there was little or no interactive effect between various concentrations of tRA and INFα (50 IU/ml) on CFU-GM from either CML-AP/BC or CML-CP cases. These results suggest that CML-AP/BC CFU-GM have some intrinsic molecular alteration(s) which markedly enhances their responsiveness to tRA and cRA, which may be clinically exploitable.</abstract><qualityIndicators><refBibsNative>true</refBibsNative><abstractWordCount>166</abstractWordCount><abstractCharCount>1120</abstractCharCount><keywordCount>29</keywordCount><score>8.992</score><pdfWordCount>5068</pdfWordCount><pdfCharCount>28472</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>8</pdfPageCount><pdfPageSize>576 x 792 pts</pdfPageSize></qualityIndicators><title>Effect of retinoic acid and interferon alpha on granulocyte-macrophage colony forming cells in chronic myeloid leukemia: Increased inhibition by all- trans - and 13- cis -retinoic acids in advanced stage disease</title><pmid><json:string>7934131</json:string></pmid><pii><json:string>0145-2126(94)90055-8</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Proc. Am. Ass. Cancer Res.</title><language><json:string>unknown</json:string></language><volume>33</volume><pages><first>74</first></pages></serie><host><title>Leukemia Research</title><language><json:string>unknown</json:string></language><publicationDate>1994</publicationDate><issn><json:string>0145-2126</json:string></issn><pii><json:string>S0145-2126(00)X0178-6</json:string></pii><volume>18</volume><issue>10</issue><pages><first>741</first><last>748</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1994</json:string><json:string>10-7-10</json:string></date><geogName></geogName><orgName><json:string>Department of Oncology, Montefiore Medical Center</json:string><json:string>National Biosciences, Inc</json:string><json:string>GALLAGHER Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY</json:string><json:string>National Cancer Institute</json:string><json:string>Department of Oncology, Albert Einstein Cancer Center</json:string><json:string>American Medical Association Education and Research Foundation, the National Leukemia Association</json:string><json:string>Elsevier Science Ltd</json:string><json:string>Florence Carter Grant</json:string></orgName><orgName_funder><json:string>Florence Carter Grant</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Elisabeth Paietta</json:string><json:string>R. Stanley</json:string><json:string>La Roche</json:string><json:string>Fox Labs</json:string></persName><placeName><json:string>Plymouth</json:string><json:string>MN</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>[36, 37]</json:string><json:string>[34]</json:string><json:string>[29]</json:string><json:string>[2-4]</json:string><json:string>[22]</json:string><json:string>[8]</json:string><json:string>[28]</json:string><json:string>[1]</json:string><json:string>[22-24]</json:string><json:string>[32]</json:string><json:string>[38]</json:string><json:string>[20, 22]</json:string><json:string>[5, 6]</json:string><json:string>[26]</json:string><json:string>[30]</json:string><json:string>[7]</json:string><json:string>[25]</json:string><json:string>[20, 21]</json:string><json:string>[13]</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-DZS2XL68-P</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - oncology</json:string><json:string>2 - hematology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - immunology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Cancer Research</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Oncology</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Hematology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>1994</publicationDate><copyrightDate>1994</copyrightDate><doi><json:string>10.1016/0145-2126(94)90055-8</json:string></doi><id>C5B9A77C81EB4B3891F7309A3235793023D7D6F6</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/C5B9A77C81EB4B3891F7309A3235793023D7D6F6/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/C5B9A77C81EB4B3891F7309A3235793023D7D6F6/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/C5B9A77C81EB4B3891F7309A3235793023D7D6F6/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Effect of retinoic acid and interferon alpha on granulocyte-macrophage colony forming cells in chronic myeloid leukemia: Increased inhibition by all- trans - and 13- cis -retinoic acids in advanced stage disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>1994</date></publicationStmt><notesStmt><note type="content">Section title: Original article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Effect of retinoic acid and interferon alpha on granulocyte-macrophage colony forming cells in chronic myeloid leukemia: Increased inhibition by all- trans - and 13- cis -retinoic acids in advanced stage disease</title><author xml:id="author-0000"><persName><forename type="first">Grace E.</forename><surname>Sagayadan</surname></persName><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Peter H.</forename><surname>Wiernik</surname></persName><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Nancy</forename><surname>Sun</surname></persName><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Greg</forename><surname>Ahearn</surname></persName><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Deborah</forename><surname>Thompson</surname></persName><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Steven J.</forename><surname>Hallam</surname></persName><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation></author><author xml:id="author-0006"><persName><forename type="first">Xiao-Ping</forename><surname>Hu</surname></persName><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation></author><author xml:id="author-0007"><persName><forename type="first">Janice P.</forename><surname>Dutcher</surname></persName><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation></author><author xml:id="author-0008"><persName><forename type="first">Robert E.</forename><surname>Gallagher</surname></persName><note type="correspondence"><p>Correspondence to: R. E. Gallagher, Department of Oncology, Montefiore Medical Center, 111 East 210th Street, Bronx, NY 10467, U.S.A.</p></note><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation></author><idno type="istex">C5B9A77C81EB4B3891F7309A3235793023D7D6F6</idno><idno type="DOI">10.1016/0145-2126(94)90055-8</idno><idno type="PII">0145-2126(94)90055-8</idno></analytic><monogr><title level="j">Leukemia Research</title><title level="j" type="abbrev">LR</title><idno type="pISSN">0145-2126</idno><idno type="PII">S0145-2126(00)X0178-6</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1994"></date><biblScope unit="volume">18</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="741">741</biblScope><biblScope unit="page" to="748">748</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1994</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Granulocyte-macrophage colony forming units (CFU-GM) from patients with advanced stage chronic myelogenous leukemia (CML), i.e. in blastic crisis (BC) or accelerated phase (AP), were inhibited by all-trans-retinoic acid (tRA) approximately 1000-fold more potently than those from chronic phase (CP) CML patients (median ic50 = 10−9 M tRA for six CML-AP/BC cases vs > 10−6 M tRA for seven CML-CP cases). A similar activity pattern was observed for the stereoisomer 13-cis-RA (cRA). There was no apparent correlation of CFU-GM retinoid sensitivity with cloning efficiency or other colony characteristics. Interferon alpha-2a (INFα) alone strongly inhibited CFU-GM growth in all four CML-AP/BC cases (ic50 ⩽ 250 IU/ml) and three out of seven CML-CP cases (ic50 ⩽ 500 IU/ml), but there was little or no interactive effect between various concentrations of tRA and INFα (50 IU/ml) on CFU-GM from either CML-AP/BC or CML-CP cases. These results suggest that CML-AP/BC CFU-GM have some intrinsic molecular alteration(s) which markedly enhances their responsiveness to tRA and cRA, which may be clinically exploitable.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Chronic myelogenous leukemia</term></item><item><term>CFU-GM</term></item><item><term>retinoic acid</term></item><item><term>interferon</term></item><item><term>reverse transcriptase-polymerase chain reaction</term></item><item><term>BCR-ABL</term></item><item><term>PML-RARα</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>Abbreviations</head><item><term>tRA</term><term>all- trans -retinoic acid</term></item><item><term>cRA</term><term>13- cis -retinoic acid</term></item><item><term>INFα</term><term>recombinant interferon alpha-2a</term></item><item><term>CML</term><term>chronic myelogenous leukemia</term></item><item><term>BC</term><term>blastic crisis</term></item><item><term>AP</term><term>accelerated phase</term></item><item><term>CP</term><term>chronic phase</term></item><item><term>MPD</term><term>myeloproliferative disease</term></item><item><term>APL</term><term>acute promyelocytic leukemia</term></item><item><term>AML</term><term>acute myelogenous leukemia</term></item><item><term>CFU-GM</term><term>colony forming unit-granulocyte-macrophage</term></item><item><term>CFC</term><term>colony forming cells</term></item><item><term>ic50</term><term>50% inhibitory concentration</term></item><item><term>PB</term><term>peripheral blood</term></item><item><term>BM</term><term>bone marrow</term></item><item><term>FCS</term><term>fetal calf serum</term></item><item><term>MC</term><term>methylcellulose</term></item><item><term>PHALy</term><term>phytohemagglutinin-stimulated lymphocyte</term></item><item><term>CM</term><term>conditioned medium</term></item><item><term>RT</term><term>reverse transcriptase</term></item><item><term>PCR</term><term>polymerase chain reaction</term></item><item><term>G3PDH</term><term>glyceraldehyde-3-phosphate dehydrogenase</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1994">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/C5B9A77C81EB4B3891F7309A3235793023D7D6F6/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>LR</jid><aid>94900558</aid><ce:pii>0145-2126(94)90055-8</ce:pii><ce:doi>10.1016/0145-2126(94)90055-8</ce:doi><ce:copyright type="unknown" year="1994"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Original article</ce:textfn></ce:dochead><ce:title>Effect of retinoic acid and interferon alpha on granulocyte-macrophage colony forming cells in chronic myeloid leukemia: Increased inhibition by all-<ce:italic>trans</ce:italic>- and 13-<ce:italic>cis</ce:italic>-retinoic acids in advanced stage disease</ce:title><ce:author-group><ce:author><ce:given-name>Grace E.</ce:given-name><ce:surname>Sagayadan</ce:surname></ce:author><ce:author><ce:given-name>Peter H.</ce:given-name><ce:surname>Wiernik</ce:surname></ce:author><ce:author><ce:given-name>Nancy</ce:given-name><ce:surname>Sun</ce:surname></ce:author><ce:author><ce:given-name>Greg</ce:given-name><ce:surname>Ahearn</ce:surname></ce:author><ce:author><ce:given-name>Deborah</ce:given-name><ce:surname>Thompson</ce:surname></ce:author><ce:author><ce:given-name>Steven J.</ce:given-name><ce:surname>Hallam</ce:surname></ce:author><ce:author><ce:given-name>Xiao-Ping</ce:given-name><ce:surname>Hu</ce:surname></ce:author><ce:author><ce:given-name>Janice P.</ce:given-name><ce:surname>Dutcher</ce:surname></ce:author><ce:author><ce:given-name>Robert E.</ce:given-name><ce:surname>Gallagher</ce:surname><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:affiliation><ce:textfn>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Correspondence to: R. E. Gallagher, Department of Oncology, Montefiore Medical Center, 111 East 210th Street, Bronx, NY 10467, U.S.A.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="11" month="3" year="1994"></ce:date-received><ce:date-accepted day="22" month="5" year="1994"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Granulocyte-macrophage colony forming units (CFU-GM) from patients with advanced stage chronic myelogenous leukemia (CML), i.e. in blastic crisis (BC) or accelerated phase (AP), were inhibited by all-<ce:italic>trans</ce:italic>-retinoic acid (tRA) approximately 1000-fold more potently than those from chronic phase (CP) CML patients (median <ce:small-caps>ic</ce:small-caps><ce:inf>50</ce:inf> = 10<ce:sup>−9</ce:sup> M tRA for six CML-AP/BC cases vs > 10<ce:sup>−6</ce:sup> M tRA for seven CML-CP cases). A similar activity pattern was observed for the stereoisomer 13-<ce:italic>cis</ce:italic>-RA (cRA). There was no apparent correlation of CFU-GM retinoid sensitivity with cloning efficiency or other colony characteristics. Interferon alpha-2a (INFα) alone strongly inhibited CFU-GM growth in all four CML-AP/BC cases (<ce:small-caps>ic</ce:small-caps><ce:inf>50</ce:inf> ⩽ 250 IU/ml) and three out of seven CML-CP cases (<ce:small-caps>ic</ce:small-caps><ce:inf>50</ce:inf> ⩽ 500 IU/ml), but there was little or no interactive effect between various concentrations of tRA and INFα (50 IU/ml) on CFU-GM from either CML-AP/BC or CML-CP cases. These results suggest that CML-AP/BC CFU-GM have some intrinsic molecular alteration(s) which markedly enhances their responsiveness to tRA and cRA, which may be clinically exploitable.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Chronic myelogenous leukemia</ce:text></ce:keyword><ce:keyword><ce:text>CFU-GM</ce:text></ce:keyword><ce:keyword><ce:text>retinoic acid</ce:text></ce:keyword><ce:keyword><ce:text>interferon</ce:text></ce:keyword><ce:keyword><ce:text>reverse transcriptase-polymerase chain reaction</ce:text></ce:keyword><ce:keyword><ce:text>BCR-ABL</ce:text></ce:keyword><ce:keyword><ce:text>PML-RARα</ce:text></ce:keyword></ce:keywords><ce:keywords class="abr"><ce:section-title>Abbreviations</ce:section-title><ce:keyword><ce:text><ce:italic>tRA</ce:italic></ce:text><ce:keyword><ce:text>all-<ce:italic>trans</ce:italic>-retinoic acid</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>cRA</ce:italic></ce:text><ce:keyword><ce:text>13-<ce:italic>cis</ce:italic>-retinoic acid</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>INFα</ce:italic></ce:text><ce:keyword><ce:text>recombinant interferon alpha-2a</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>CML</ce:italic></ce:text><ce:keyword><ce:text>chronic myelogenous leukemia</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>BC</ce:italic></ce:text><ce:keyword><ce:text>blastic crisis</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>AP</ce:italic></ce:text><ce:keyword><ce:text>accelerated phase</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>CP</ce:italic></ce:text><ce:keyword><ce:text>chronic phase</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>MPD</ce:italic></ce:text><ce:keyword><ce:text>myeloproliferative disease</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>APL</ce:italic></ce:text><ce:keyword><ce:text>acute promyelocytic leukemia</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>AML</ce:italic></ce:text><ce:keyword><ce:text>acute myelogenous leukemia</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>CFU-GM</ce:italic></ce:text><ce:keyword><ce:text>colony forming unit-granulocyte-macrophage</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>CFC</ce:italic></ce:text><ce:keyword><ce:text>colony forming cells</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:small-caps>ic</ce:small-caps><ce:inf>50</ce:inf></ce:text><ce:keyword><ce:text>50% inhibitory concentration</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>PB</ce:italic></ce:text><ce:keyword><ce:text>peripheral blood</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>BM</ce:italic></ce:text><ce:keyword><ce:text>bone marrow</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>FCS</ce:italic></ce:text><ce:keyword><ce:text>fetal calf serum</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>MC</ce:italic></ce:text><ce:keyword><ce:text>methylcellulose</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>PHALy</ce:italic></ce:text><ce:keyword><ce:text>phytohemagglutinin-stimulated lymphocyte</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>CM</ce:italic></ce:text><ce:keyword><ce:text>conditioned medium</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>RT</ce:italic></ce:text><ce:keyword><ce:text>reverse transcriptase</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>PCR</ce:italic></ce:text><ce:keyword><ce:text>polymerase chain reaction</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text><ce:italic>G3PDH</ce:italic></ce:text><ce:keyword><ce:text>glyceraldehyde-3-phosphate dehydrogenase</ce:text></ce:keyword></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Effect of retinoic acid and interferon alpha on granulocyte-macrophage colony forming cells in chronic myeloid leukemia: Increased inhibition by all- trans - and 13- cis -retinoic acids in advanced stage disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Effect of retinoic acid and interferon alpha on granulocyte-macrophage colony forming cells in chronic myeloid leukemia: Increased inhibition by all-</title></titleInfo><name type="personal"><namePart type="given">Grace E.</namePart><namePart type="family">Sagayadan</namePart><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter H.</namePart><namePart type="family">Wiernik</namePart><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nancy</namePart><namePart type="family">Sun</namePart><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Greg</namePart><namePart type="family">Ahearn</namePart><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Deborah</namePart><namePart type="family">Thompson</namePart><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Steven J.</namePart><namePart type="family">Hallam</namePart><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Xiao-Ping</namePart><namePart type="family">Hu</namePart><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Janice P.</namePart><namePart type="family">Dutcher</namePart><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robert E.</namePart><namePart type="family">Gallagher</namePart><affiliation>Department of Oncology, Montefiore Medical Center, Albert Einstein Cancer Center, Bronx, NY 10467, U.S.A.</affiliation><description>Correspondence to: R. E. Gallagher, Department of Oncology, Montefiore Medical Center, 111 East 210th Street, Bronx, NY 10467, U.S.A.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1994</dateIssued><copyrightDate encoding="w3cdtf">1994</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Granulocyte-macrophage colony forming units (CFU-GM) from patients with advanced stage chronic myelogenous leukemia (CML), i.e. in blastic crisis (BC) or accelerated phase (AP), were inhibited by all-trans-retinoic acid (tRA) approximately 1000-fold more potently than those from chronic phase (CP) CML patients (median ic50 = 10−9 M tRA for six CML-AP/BC cases vs > 10−6 M tRA for seven CML-CP cases). A similar activity pattern was observed for the stereoisomer 13-cis-RA (cRA). There was no apparent correlation of CFU-GM retinoid sensitivity with cloning efficiency or other colony characteristics. Interferon alpha-2a (INFα) alone strongly inhibited CFU-GM growth in all four CML-AP/BC cases (ic50 ⩽ 250 IU/ml) and three out of seven CML-CP cases (ic50 ⩽ 500 IU/ml), but there was little or no interactive effect between various concentrations of tRA and INFα (50 IU/ml) on CFU-GM from either CML-AP/BC or CML-CP cases. These results suggest that CML-AP/BC CFU-GM have some intrinsic molecular alteration(s) which markedly enhances their responsiveness to tRA and cRA, which may be clinically exploitable.</abstract><note type="content">Section title: Original article</note><subject><genre>Keywords</genre><topic>Chronic myelogenous leukemia</topic><topic>CFU-GM</topic><topic>retinoic acid</topic><topic>interferon</topic><topic>reverse transcriptase-polymerase chain reaction</topic><topic>BCR-ABL</topic><topic>PML-RARα</topic></subject><subject><genre>Abbreviations</genre><topic>tRA : all- trans -retinoic acid</topic><topic>cRA : 13- cis -retinoic acid</topic><topic>INFα : recombinant interferon alpha-2a</topic><topic>CML : chronic myelogenous leukemia</topic><topic>BC : blastic crisis</topic><topic>AP : accelerated phase</topic><topic>CP : chronic phase</topic><topic>MPD : myeloproliferative disease</topic><topic>APL : acute promyelocytic leukemia</topic><topic>AML : acute myelogenous leukemia</topic><topic>CFU-GM : colony forming unit-granulocyte-macrophage</topic><topic>CFC : colony forming cells</topic><topic>ic50 : 50% inhibitory concentration</topic><topic>PB : peripheral blood</topic><topic>BM : bone marrow</topic><topic>FCS : fetal calf serum</topic><topic>MC : methylcellulose</topic><topic>PHALy : phytohemagglutinin-stimulated lymphocyte</topic><topic>CM : conditioned medium</topic><topic>RT : reverse transcriptase</topic><topic>PCR : polymerase chain reaction</topic><topic>G3PDH : glyceraldehyde-3-phosphate dehydrogenase</topic></subject><relatedItem type="host"><titleInfo><title>Leukemia Research</title></titleInfo><titleInfo type="abbreviated"><title>LR</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">199410</dateIssued></originInfo><identifier type="ISSN">0145-2126</identifier><identifier type="PII">S0145-2126(00)X0178-6</identifier><part><date>199410</date><detail type="volume"><number>18</number><caption>vol.</caption></detail><detail type="issue"><number>10</number><caption>no.</caption></detail><extent unit="issue-pages"><start>725</start><end>795</end></extent><extent unit="pages"><start>741</start><end>748</end></extent></part></relatedItem><identifier type="istex">C5B9A77C81EB4B3891F7309A3235793023D7D6F6</identifier><identifier type="ark">ark:/67375/6H6-DZS2XL68-P</identifier><identifier type="DOI">10.1016/0145-2126(94)90055-8</identifier><identifier type="PII">0145-2126(94)90055-8</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/C5B9A77C81EB4B3891F7309A3235793023D7D6F6/metadata/json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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