Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis
Polycythemia vera (PV), essential thrombocythemia (ET), and myeloid metaplasia with myelofibrosis (MMM) are clonal disorders arising from hematopoietic progenitors. An internet-based protocol was used to collect clinical information and biological specimens from patients with these diseases. High-th...
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| Veröffentlicht in: | Cancer cell 2005-04, Vol.7 (4), p.387-397 |
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| creator | Levine, Ross L. Wadleigh, Martha Cools, Jan Ebert, Benjamin L. Wernig, Gerlinde Huntly, Brian J.P. Boggon, Titus J. Wlodarska, Iwona Clark, Jennifer J. Moore, Sandra Adelsperger, Jennifer Koo, Sumin Lee, Jeffrey C. Gabriel, Stacey Mercher, Thomas D’Andrea, Alan Fröhling, Stefan Döhner, Konstanze Marynen, Peter Vandenberghe, Peter Mesa, Ruben A. Tefferi, Ayalew Griffin, James D. Eck, Michael J. Sellers, William R. Meyerson, Matthew Golub, Todd R. Lee, Stephanie J. Gilliland, D. Gary |
| description | Polycythemia vera (PV), essential thrombocythemia (ET), and myeloid metaplasia with myelofibrosis (MMM) are clonal disorders arising from hematopoietic progenitors. An internet-based protocol was used to collect clinical information and biological specimens from patients with these diseases. High-throughput DNA resequencing identified a recurrent somatic missense mutation
JAK2V617F in granulocyte DNA samples of 121 of 164 PV patients, of which 41 had homozygous and 80 had heterozygous mutations. Molecular and cytogenetic analyses demonstrated that homozygous mutations were due to duplication of the mutant allele.
JAK2V617F was also identified in granulocyte DNA samples from 37 of 115 ET and 16 of 46 MMM patients, but was not observed in 269 normal individuals. In vitro analysis demonstrated that JAK2V617F is a constitutively active tyrosine kinase. |
| doi_str_mv | 10.1016/j.ccr.2005.03.023 |
| format | Article |
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JAK2V617F in granulocyte DNA samples of 121 of 164 PV patients, of which 41 had homozygous and 80 had heterozygous mutations. Molecular and cytogenetic analyses demonstrated that homozygous mutations were due to duplication of the mutant allele.
JAK2V617F was also identified in granulocyte DNA samples from 37 of 115 ET and 16 of 46 MMM patients, but was not observed in 269 normal individuals. In vitro analysis demonstrated that JAK2V617F is a constitutively active tyrosine kinase.</description><identifier>ISSN: 1535-6108</identifier><identifier>EISSN: 1878-3686</identifier><identifier>DOI: 10.1016/j.ccr.2005.03.023</identifier><identifier>PMID: 15837627</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Cell Line, Tumor ; Enzyme Activation - genetics ; Female ; Genotype ; Granulocytes - metabolism ; Heterozygote ; Homozygote ; Humans ; Janus Kinase 2 ; Male ; Middle Aged ; Mitosis - genetics ; Models, Molecular ; Mouth Mucosa - metabolism ; Mutation, Missense - genetics ; Phosphorylation ; Polycythemia Vera - genetics ; Primary Myelofibrosis - complications ; Primary Myelofibrosis - genetics ; Protein-Tyrosine Kinases - genetics ; Protein-Tyrosine Kinases - metabolism ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - metabolism ; Recombination, Genetic - genetics ; Thrombocythemia, Essential - genetics ; Transfection</subject><ispartof>Cancer cell, 2005-04, Vol.7 (4), p.387-397</ispartof><rights>2005 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c425t-aeb412f4aa731bd640d94b1184ffc9c978b65a3b11211444806142fd2c31652e3</citedby><cites>FETCH-LOGICAL-c425t-aeb412f4aa731bd640d94b1184ffc9c978b65a3b11211444806142fd2c31652e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ccr.2005.03.023$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>315,782,786,3554,27933,27934,46004</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15837627$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Levine, Ross L.</creatorcontrib><creatorcontrib>Wadleigh, Martha</creatorcontrib><creatorcontrib>Cools, Jan</creatorcontrib><creatorcontrib>Ebert, Benjamin L.</creatorcontrib><creatorcontrib>Wernig, Gerlinde</creatorcontrib><creatorcontrib>Huntly, Brian J.P.</creatorcontrib><creatorcontrib>Boggon, Titus J.</creatorcontrib><creatorcontrib>Wlodarska, Iwona</creatorcontrib><creatorcontrib>Clark, Jennifer J.</creatorcontrib><creatorcontrib>Moore, Sandra</creatorcontrib><creatorcontrib>Adelsperger, Jennifer</creatorcontrib><creatorcontrib>Koo, Sumin</creatorcontrib><creatorcontrib>Lee, Jeffrey C.</creatorcontrib><creatorcontrib>Gabriel, Stacey</creatorcontrib><creatorcontrib>Mercher, Thomas</creatorcontrib><creatorcontrib>D’Andrea, Alan</creatorcontrib><creatorcontrib>Fröhling, Stefan</creatorcontrib><creatorcontrib>Döhner, Konstanze</creatorcontrib><creatorcontrib>Marynen, Peter</creatorcontrib><creatorcontrib>Vandenberghe, Peter</creatorcontrib><creatorcontrib>Mesa, Ruben A.</creatorcontrib><creatorcontrib>Tefferi, Ayalew</creatorcontrib><creatorcontrib>Griffin, James D.</creatorcontrib><creatorcontrib>Eck, Michael J.</creatorcontrib><creatorcontrib>Sellers, William R.</creatorcontrib><creatorcontrib>Meyerson, Matthew</creatorcontrib><creatorcontrib>Golub, Todd R.</creatorcontrib><creatorcontrib>Lee, Stephanie J.</creatorcontrib><creatorcontrib>Gilliland, D. Gary</creatorcontrib><title>Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis</title><title>Cancer cell</title><addtitle>Cancer Cell</addtitle><description>Polycythemia vera (PV), essential thrombocythemia (ET), and myeloid metaplasia with myelofibrosis (MMM) are clonal disorders arising from hematopoietic progenitors. An internet-based protocol was used to collect clinical information and biological specimens from patients with these diseases. High-throughput DNA resequencing identified a recurrent somatic missense mutation
JAK2V617F in granulocyte DNA samples of 121 of 164 PV patients, of which 41 had homozygous and 80 had heterozygous mutations. Molecular and cytogenetic analyses demonstrated that homozygous mutations were due to duplication of the mutant allele.
JAK2V617F was also identified in granulocyte DNA samples from 37 of 115 ET and 16 of 46 MMM patients, but was not observed in 269 normal individuals. In vitro analysis demonstrated that JAK2V617F is a constitutively active tyrosine kinase.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Cell Line, Tumor</subject><subject>Enzyme Activation - genetics</subject><subject>Female</subject><subject>Genotype</subject><subject>Granulocytes - metabolism</subject><subject>Heterozygote</subject><subject>Homozygote</subject><subject>Humans</subject><subject>Janus Kinase 2</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Mitosis - genetics</subject><subject>Models, Molecular</subject><subject>Mouth Mucosa - metabolism</subject><subject>Mutation, Missense - genetics</subject><subject>Phosphorylation</subject><subject>Polycythemia Vera - genetics</subject><subject>Primary Myelofibrosis - complications</subject><subject>Primary Myelofibrosis - genetics</subject><subject>Protein-Tyrosine Kinases - genetics</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Recombination, Genetic - genetics</subject><subject>Thrombocythemia, Essential - genetics</subject><subject>Transfection</subject><issn>1535-6108</issn><issn>1878-3686</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcuO1DAQRSMEYh7wAWyQV6wmwWU7diJWrREMj5HYwNpynArjJrEb290ov8BX41Y3YgerKlWde0v2raoXQBugIF9vG2tjwyhtG8obyvij6hI61dVcdvJx6Vve1hJod1FdpbSlRQOqf1pdQNtxJZm6rH5tbHYHk53_RpZ9Lk3wxHmSH5DkNYbkPJLvzpuE5OPmEzvudmFe7VqIxRlywGhuCKaEPjszF2EMyxD-7G-I8SNZVpyDKxWz2c0mFd1Plx9O88kNxzvpWfVkMnPC5-d6XX199_bL7fv6_vPdh9vNfW0Fa3NtcBDAJmGM4jCMUtCxFwNAJ6bJ9rZX3SBbw8uEAQghOipBsGlkloNsGfLr6tXJdxfDjz2mrBeXLM6z8Rj2SUulWqpY_18QJKNcSlZAOIG2PCRFnPQuusXEVQPVx6T0Vpek9DEpTbkuSRXNy7P5flhw_Ks4R1OANycAy18cHEadrENvcXQRbdZjcP-w_w1xi6YI</recordid><startdate>20050401</startdate><enddate>20050401</enddate><creator>Levine, Ross L.</creator><creator>Wadleigh, Martha</creator><creator>Cools, Jan</creator><creator>Ebert, Benjamin L.</creator><creator>Wernig, Gerlinde</creator><creator>Huntly, Brian J.P.</creator><creator>Boggon, Titus J.</creator><creator>Wlodarska, Iwona</creator><creator>Clark, Jennifer J.</creator><creator>Moore, Sandra</creator><creator>Adelsperger, Jennifer</creator><creator>Koo, Sumin</creator><creator>Lee, Jeffrey C.</creator><creator>Gabriel, Stacey</creator><creator>Mercher, Thomas</creator><creator>D’Andrea, Alan</creator><creator>Fröhling, Stefan</creator><creator>Döhner, Konstanze</creator><creator>Marynen, Peter</creator><creator>Vandenberghe, Peter</creator><creator>Mesa, Ruben A.</creator><creator>Tefferi, Ayalew</creator><creator>Griffin, James D.</creator><creator>Eck, Michael J.</creator><creator>Sellers, William R.</creator><creator>Meyerson, Matthew</creator><creator>Golub, Todd R.</creator><creator>Lee, Stephanie J.</creator><creator>Gilliland, D. 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Gary</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Levine, Ross L.</au><au>Wadleigh, Martha</au><au>Cools, Jan</au><au>Ebert, Benjamin L.</au><au>Wernig, Gerlinde</au><au>Huntly, Brian J.P.</au><au>Boggon, Titus J.</au><au>Wlodarska, Iwona</au><au>Clark, Jennifer J.</au><au>Moore, Sandra</au><au>Adelsperger, Jennifer</au><au>Koo, Sumin</au><au>Lee, Jeffrey C.</au><au>Gabriel, Stacey</au><au>Mercher, Thomas</au><au>D’Andrea, Alan</au><au>Fröhling, Stefan</au><au>Döhner, Konstanze</au><au>Marynen, Peter</au><au>Vandenberghe, Peter</au><au>Mesa, Ruben A.</au><au>Tefferi, Ayalew</au><au>Griffin, James D.</au><au>Eck, Michael J.</au><au>Sellers, William R.</au><au>Meyerson, Matthew</au><au>Golub, Todd R.</au><au>Lee, Stephanie J.</au><au>Gilliland, D. Gary</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis</atitle><jtitle>Cancer cell</jtitle><addtitle>Cancer Cell</addtitle><date>2005-04-01</date><risdate>2005</risdate><volume>7</volume><issue>4</issue><spage>387</spage><epage>397</epage><pages>387-397</pages><issn>1535-6108</issn><eissn>1878-3686</eissn><abstract>Polycythemia vera (PV), essential thrombocythemia (ET), and myeloid metaplasia with myelofibrosis (MMM) are clonal disorders arising from hematopoietic progenitors. An internet-based protocol was used to collect clinical information and biological specimens from patients with these diseases. High-throughput DNA resequencing identified a recurrent somatic missense mutation
JAK2V617F in granulocyte DNA samples of 121 of 164 PV patients, of which 41 had homozygous and 80 had heterozygous mutations. Molecular and cytogenetic analyses demonstrated that homozygous mutations were due to duplication of the mutant allele.
JAK2V617F was also identified in granulocyte DNA samples from 37 of 115 ET and 16 of 46 MMM patients, but was not observed in 269 normal individuals. In vitro analysis demonstrated that JAK2V617F is a constitutively active tyrosine kinase.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15837627</pmid><doi>10.1016/j.ccr.2005.03.023</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Cell Press Free Archives; Access via ScienceDirect (Elsevier); EZB-FREE-00999 freely available EZB journals |
| subjects | Adult Aged Aged, 80 and over Cell Line, Tumor Enzyme Activation - genetics Female Genotype Granulocytes - metabolism Heterozygote Homozygote Humans Janus Kinase 2 Male Middle Aged Mitosis - genetics Models, Molecular Mouth Mucosa - metabolism Mutation, Missense - genetics Phosphorylation Polycythemia Vera - genetics Primary Myelofibrosis - complications Primary Myelofibrosis - genetics Protein-Tyrosine Kinases - genetics Protein-Tyrosine Kinases - metabolism Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Recombination, Genetic - genetics Thrombocythemia, Essential - genetics Transfection |
| title | Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis |
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