Heterogeneity of clonal development in chronic myeloproliferative disorders
Recent reports have suggested a previously unexpected variability in the expression of the dominant neoplastic clone in myeloproliferative disorders (MPD). We evaluated 49 female patients with MPD and informative at the X‐linked androgen receptor (AR) locus to establish the X chromosome inactivation...
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| Veröffentlicht in: | American journal of hematology 1999-02, Vol.60 (2), p.158-160 |
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| container_title | American journal of hematology |
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| creator | Ferraris, Anna Maria Mangerini, Rosa Racchi, Omar Rapezzi, Davide Rolfo, Michela Casciaro, Salvatore Gaetani, Gian Franco |
| description | Recent reports have suggested a previously unexpected variability in the expression of the dominant neoplastic clone in myeloproliferative disorders (MPD). We evaluated 49 female patients with MPD and informative at the X‐linked androgen receptor (AR) locus to establish the X chromosome inactivation pattern of hemopoietic cells. Whereas in chronic myelogenous leukemia (CML) the granulocytes (PMN) were uniformly of monoclonal origin, a striking heterogeneity of clonal development was found in PMN from patients with other MPD, with up to 50% of them expressing a polyclonal pattern of X inactivation. Am. J. Hematol. 60:158–160, 1999. © 1999 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/(SICI)1096-8652(199902)60:2<158::AID-AJH14>3.0.CO;2-9 |
| format | Article |
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We evaluated 49 female patients with MPD and informative at the X‐linked androgen receptor (AR) locus to establish the X chromosome inactivation pattern of hemopoietic cells. Whereas in chronic myelogenous leukemia (CML) the granulocytes (PMN) were uniformly of monoclonal origin, a striking heterogeneity of clonal development was found in PMN from patients with other MPD, with up to 50% of them expressing a polyclonal pattern of X inactivation. Am. J. 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Myelofibrosis ; Medical sciences ; Middle Aged ; myeloproliferative ; Myeloproliferative Disorders - genetics ; Myeloproliferative Disorders - pathology ; Neutrophils - pathology ; Polymerase Chain Reaction ; Receptors, Androgen - genetics ; T-Lymphocytes - pathology ; X inactivation</subject><ispartof>American journal of hematology, 1999-02, Vol.60 (2), p.158-160</ispartof><rights>Copyright © 1999 Wiley‐Liss, Inc.</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4694-3f4f3d4a23689a7c66e4fb8a23a6f88f7a67310acd77105bde5a89908c7ab7763</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2F%28SICI%291096-8652%28199902%2960%3A2%3C158%3A%3AAID-AJH14%3E3.0.CO%3B2-9$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2F%28SICI%291096-8652%28199902%2960%3A2%3C158%3A%3AAID-AJH14%3E3.0.CO%3B2-9$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,1433,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1650744$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9929111$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ferraris, Anna Maria</creatorcontrib><creatorcontrib>Mangerini, Rosa</creatorcontrib><creatorcontrib>Racchi, Omar</creatorcontrib><creatorcontrib>Rapezzi, Davide</creatorcontrib><creatorcontrib>Rolfo, Michela</creatorcontrib><creatorcontrib>Casciaro, Salvatore</creatorcontrib><creatorcontrib>Gaetani, Gian Franco</creatorcontrib><title>Heterogeneity of clonal development in chronic myeloproliferative disorders</title><title>American journal of hematology</title><addtitle>Am J Hematol</addtitle><description>Recent reports have suggested a previously unexpected variability in the expression of the dominant neoplastic clone in myeloproliferative disorders (MPD). We evaluated 49 female patients with MPD and informative at the X‐linked androgen receptor (AR) locus to establish the X chromosome inactivation pattern of hemopoietic cells. Whereas in chronic myelogenous leukemia (CML) the granulocytes (PMN) were uniformly of monoclonal origin, a striking heterogeneity of clonal development was found in PMN from patients with other MPD, with up to 50% of them expressing a polyclonal pattern of X inactivation. Am. J. Hematol. 60:158–160, 1999. © 1999 Wiley‐Liss, Inc.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>B-Lymphocytes - pathology</subject><subject>Biological and medical sciences</subject><subject>clonality</subject><subject>Clone Cells - pathology</subject><subject>Dosage Compensation, Genetic</subject><subject>Female</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>myeloproliferative</subject><subject>Myeloproliferative Disorders - genetics</subject><subject>Myeloproliferative Disorders - pathology</subject><subject>Neutrophils - pathology</subject><subject>Polymerase Chain Reaction</subject><subject>Receptors, Androgen - genetics</subject><subject>T-Lymphocytes - pathology</subject><subject>X inactivation</subject><issn>0361-8609</issn><issn>1096-8652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEuP0zAUhS0EGjoDPwEpC4RmFil2nPhRYKQqPFoYqQseW8t1rsHIiQc7HdR_j0OrsgCJla_PvT73-EPoFcFzgnH1_PLjul1fESxZKVhTXRIpJa6uGF5UL0kjFovl-nW5fL8i9TWd43m7eVGV8h6anV7cRzNMGck1lg_ReUrfMSakFvgMnUlZSULIDH1YwQgxfIUB3Lgvgi2MD4P2RQd34MNtD8NYuKEw32IYnCn6_aTG4J2FqEd3B0XnUogdxPQIPbDaJ3h8PC_Q57dvPrWr8mbzbt0ub0pTM1mX1NaWdrWuKBNSc8MY1HYr8l0zK4TlmnFKsDYd5wQ32w4aLfLfheF6yzmjF-jZwTfn-LGDNKreJQPe6wHCLikmG9YITugpgIkhpQhW3UbX67hXBKsJslITZDUhUxMydYCsGFa5boRSGbL6DVlRhVW7ybrMvk-OAXbbHrqT65Fq7j899nUy2tuoB-PSn-Wswbyu89iXw9hP52H_V7b_RPtXsoNAfwFScaR5</recordid><startdate>199902</startdate><enddate>199902</enddate><creator>Ferraris, Anna Maria</creator><creator>Mangerini, Rosa</creator><creator>Racchi, Omar</creator><creator>Rapezzi, Davide</creator><creator>Rolfo, Michela</creator><creator>Casciaro, Salvatore</creator><creator>Gaetani, Gian Franco</creator><general>John Wiley & Sons, Inc</general><general>Wiley-Liss</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>199902</creationdate><title>Heterogeneity of clonal development in chronic myeloproliferative disorders</title><author>Ferraris, Anna Maria ; Mangerini, Rosa ; Racchi, Omar ; Rapezzi, Davide ; Rolfo, Michela ; Casciaro, Salvatore ; Gaetani, Gian Franco</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4694-3f4f3d4a23689a7c66e4fb8a23a6f88f7a67310acd77105bde5a89908c7ab7763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>B-Lymphocytes - pathology</topic><topic>Biological and medical sciences</topic><topic>clonality</topic><topic>Clone Cells - pathology</topic><topic>Dosage Compensation, Genetic</topic><topic>Female</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>myeloproliferative</topic><topic>Myeloproliferative Disorders - genetics</topic><topic>Myeloproliferative Disorders - pathology</topic><topic>Neutrophils - pathology</topic><topic>Polymerase Chain Reaction</topic><topic>Receptors, Androgen - genetics</topic><topic>T-Lymphocytes - pathology</topic><topic>X inactivation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ferraris, Anna Maria</creatorcontrib><creatorcontrib>Mangerini, Rosa</creatorcontrib><creatorcontrib>Racchi, Omar</creatorcontrib><creatorcontrib>Rapezzi, Davide</creatorcontrib><creatorcontrib>Rolfo, Michela</creatorcontrib><creatorcontrib>Casciaro, Salvatore</creatorcontrib><creatorcontrib>Gaetani, Gian Franco</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of hematology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ferraris, Anna Maria</au><au>Mangerini, Rosa</au><au>Racchi, Omar</au><au>Rapezzi, Davide</au><au>Rolfo, Michela</au><au>Casciaro, Salvatore</au><au>Gaetani, Gian Franco</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Heterogeneity of clonal development in chronic myeloproliferative disorders</atitle><jtitle>American journal of hematology</jtitle><addtitle>Am J Hematol</addtitle><date>1999-02</date><risdate>1999</risdate><volume>60</volume><issue>2</issue><spage>158</spage><epage>160</epage><pages>158-160</pages><issn>0361-8609</issn><eissn>1096-8652</eissn><coden>AJHEDD</coden><abstract>Recent reports have suggested a previously unexpected variability in the expression of the dominant neoplastic clone in myeloproliferative disorders (MPD). We evaluated 49 female patients with MPD and informative at the X‐linked androgen receptor (AR) locus to establish the X chromosome inactivation pattern of hemopoietic cells. Whereas in chronic myelogenous leukemia (CML) the granulocytes (PMN) were uniformly of monoclonal origin, a striking heterogeneity of clonal development was found in PMN from patients with other MPD, with up to 50% of them expressing a polyclonal pattern of X inactivation. Am. J. Hematol. 60:158–160, 1999. © 1999 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>John Wiley & Sons, Inc</pub><pmid>9929111</pmid><doi>10.1002/(SICI)1096-8652(199902)60:2<158::AID-AJH14>3.0.CO;2-9</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Wiley Free Content; Wiley Online Library All Journals |
| subjects | Adult Aged Aged, 80 and over B-Lymphocytes - pathology Biological and medical sciences clonality Clone Cells - pathology Dosage Compensation, Genetic Female Hematologic and hematopoietic diseases Humans Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical sciences Middle Aged myeloproliferative Myeloproliferative Disorders - genetics Myeloproliferative Disorders - pathology Neutrophils - pathology Polymerase Chain Reaction Receptors, Androgen - genetics T-Lymphocytes - pathology X inactivation |
| title | Heterogeneity of clonal development in chronic myeloproliferative disorders |
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