Ruxolitinib reduces JAK2 p.V617F allele burden in patients with polycythemia vera enrolled in the RESPONSE study
In patients with polycythemia vera (PV), an elevated JAK2 p.V617F allele burden is associated with indicators of more severe disease (e.g., leukocytosis, splenomegaly, and increased thrombosis risk); however, correlations between allele burden reductions and clinical benefit in patients with PV have...
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| Veröffentlicht in: | Annals of hematology 2017-07, Vol.96 (7), p.1113-1120 |
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| creator | Vannucchi, Alessandro Maria Verstovsek, Srdan Guglielmelli, Paola Griesshammer, Martin Burn, Timothy C. Naim, Ahmad Paranagama, Dilan Marker, Mahtab Gadbaw, Brian Kiladjian, Jean-Jacques |
| description | In patients with polycythemia vera (PV), an elevated
JAK2
p.V617F allele burden is associated with indicators of more severe disease (e.g., leukocytosis, splenomegaly, and increased thrombosis risk); however, correlations between allele burden reductions and clinical benefit in patients with PV have not been extensively evaluated in a randomized trial. This exploratory analysis from the multicenter, open-label, phase 3 Randomized Study of Efficacy and Safety in Polycythemia Vera With JAK Inhibitor INCB018424 Versus Best Supportive Care trial evaluated the long-term effect of ruxolitinib treatment on
JAK2
p.V617F allele burden in patients with PV. Evaluable
JAK2
p.V617F-positive patients randomized to ruxolitinib (
n
= 107) or best available therapy (BAT) who crossed over to ruxolitinib at week 32 (
n
= 97) had consistent
JAK2
p.V617F allele burden reductions throughout the study. At all time points measured (up to weeks 208 [ruxolitinib-randomized] and 176 [ruxolitinib crossover]), mean changes from baseline over time in
JAK2
p.V617F allele burden ranged from −12.2 to −40.0% (ruxolitinib-randomized) and −6.3 to −17.8% (ruxolitinib crossover). Complete or partial molecular response was observed in 3 patients (ruxolitinib-randomized,
n
= 2; ruxolitinib crossover,
n
= 1) and 54 patients (ruxolitinib-randomized,
n
= 33; ruxolitinib crossover,
n
= 20; BAT,
n
= 1), respectively. Among patients treated with interferon as BAT (
n
= 13), the mean maximal reduction in allele burden from baseline was 25.6% after crossover to ruxolitinib versus 6.6% before crossover. Collectively, the data from this exploratory analysis suggest that ruxolitinib treatment for up to 4 years provides progressive reductions in
JAK2
p.V617F allele burden in patients with PV who are resistant to or intolerant of hydroxyurea. The relationship between allele burden changes and clinical outcomes in patients with PV remains unclear. |
| doi_str_mv | 10.1007/s00277-017-2994-x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5486779</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1904775248</sourcerecordid><originalsourceid>FETCH-LOGICAL-c470t-dc45214f21486a450f6948a7afc602c1d07c0eecf9a7655721db82a030a0d25b3</originalsourceid><addsrcrecordid>eNp1kVFvFCEQx4nR2Gv1A_hiSHzxZevAwbL7YtI0V2ttWtOqr4QFtkfDwQq79e7by-XappqUhEzC_OY_M_wRekfgkACITxmAClEBERVtW1atX6AZYXNaAW_YSzSDdt5WvJw9tJ_zLQChDaOv0V4JvG44maHhalpH70YXXIeTNZO2GZ8dfaN4OPxVE3GClffWW9xNydiAXcCDGp0NY8Z_3LjEQ_QbvRmXduUUvrNJYRtSLDVmy5Z3fLW4_n55cb3AeZzM5g161Suf7dv7eIB-nix-HJ9W55dfvh4fnVeaCRgroxmnhPXlNrViHPq6ZY0Sqtc1UE0MCA3W6r5VouZcUGK6hiqYgwJDeTc_QJ93usPUrazRZeKkvBySW6m0kVE5-W8muKW8iXeSl4ZCtEXg471Air8nm0e5cllb71WwccqSNOV3BVBKCvrhP_Q2TimU9SRpgQnBKWsKRXaUTjHnZPvHYQjIrZ9y56csfsqtn3Jdat4_3eKx4sHAAtAdkEsq3Nj0pPWzqn8BbTWryg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1904775248</pqid></control><display><type>article</type><title>Ruxolitinib reduces JAK2 p.V617F allele burden in patients with polycythemia vera enrolled in the RESPONSE study</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Vannucchi, Alessandro Maria ; Verstovsek, Srdan ; Guglielmelli, Paola ; Griesshammer, Martin ; Burn, Timothy C. ; Naim, Ahmad ; Paranagama, Dilan ; Marker, Mahtab ; Gadbaw, Brian ; Kiladjian, Jean-Jacques</creator><creatorcontrib>Vannucchi, Alessandro Maria ; Verstovsek, Srdan ; Guglielmelli, Paola ; Griesshammer, Martin ; Burn, Timothy C. ; Naim, Ahmad ; Paranagama, Dilan ; Marker, Mahtab ; Gadbaw, Brian ; Kiladjian, Jean-Jacques</creatorcontrib><description>In patients with polycythemia vera (PV), an elevated
JAK2
p.V617F allele burden is associated with indicators of more severe disease (e.g., leukocytosis, splenomegaly, and increased thrombosis risk); however, correlations between allele burden reductions and clinical benefit in patients with PV have not been extensively evaluated in a randomized trial. This exploratory analysis from the multicenter, open-label, phase 3 Randomized Study of Efficacy and Safety in Polycythemia Vera With JAK Inhibitor INCB018424 Versus Best Supportive Care trial evaluated the long-term effect of ruxolitinib treatment on
JAK2
p.V617F allele burden in patients with PV. Evaluable
JAK2
p.V617F-positive patients randomized to ruxolitinib (
n
= 107) or best available therapy (BAT) who crossed over to ruxolitinib at week 32 (
n
= 97) had consistent
JAK2
p.V617F allele burden reductions throughout the study. At all time points measured (up to weeks 208 [ruxolitinib-randomized] and 176 [ruxolitinib crossover]), mean changes from baseline over time in
JAK2
p.V617F allele burden ranged from −12.2 to −40.0% (ruxolitinib-randomized) and −6.3 to −17.8% (ruxolitinib crossover). Complete or partial molecular response was observed in 3 patients (ruxolitinib-randomized,
n
= 2; ruxolitinib crossover,
n
= 1) and 54 patients (ruxolitinib-randomized,
n
= 33; ruxolitinib crossover,
n
= 20; BAT,
n
= 1), respectively. Among patients treated with interferon as BAT (
n
= 13), the mean maximal reduction in allele burden from baseline was 25.6% after crossover to ruxolitinib versus 6.6% before crossover. Collectively, the data from this exploratory analysis suggest that ruxolitinib treatment for up to 4 years provides progressive reductions in
JAK2
p.V617F allele burden in patients with PV who are resistant to or intolerant of hydroxyurea. The relationship between allele burden changes and clinical outcomes in patients with PV remains unclear.</description><identifier>ISSN: 0939-5555</identifier><identifier>EISSN: 1432-0584</identifier><identifier>DOI: 10.1007/s00277-017-2994-x</identifier><identifier>PMID: 28456851</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Alleles ; Blood cancer ; Cross-Over Studies ; Female ; Gene Frequency ; Hematology ; Humans ; Inhibitor drugs ; Janus Kinase 2 - antagonists & inhibitors ; Janus Kinase 2 - genetics ; Janus Kinase 2 - metabolism ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Mutation, Missense ; Oncology ; Original ; Original Article ; Polycythemia Vera - drug therapy ; Polycythemia Vera - enzymology ; Polycythemia Vera - genetics ; Pyrazoles - therapeutic use ; Time Factors ; Treatment Outcome</subject><ispartof>Annals of hematology, 2017-07, Vol.96 (7), p.1113-1120</ispartof><rights>The Author(s) 2017</rights><rights>Annals of Hematology is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-dc45214f21486a450f6948a7afc602c1d07c0eecf9a7655721db82a030a0d25b3</citedby><cites>FETCH-LOGICAL-c470t-dc45214f21486a450f6948a7afc602c1d07c0eecf9a7655721db82a030a0d25b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00277-017-2994-x$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00277-017-2994-x$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28456851$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vannucchi, Alessandro Maria</creatorcontrib><creatorcontrib>Verstovsek, Srdan</creatorcontrib><creatorcontrib>Guglielmelli, Paola</creatorcontrib><creatorcontrib>Griesshammer, Martin</creatorcontrib><creatorcontrib>Burn, Timothy C.</creatorcontrib><creatorcontrib>Naim, Ahmad</creatorcontrib><creatorcontrib>Paranagama, Dilan</creatorcontrib><creatorcontrib>Marker, Mahtab</creatorcontrib><creatorcontrib>Gadbaw, Brian</creatorcontrib><creatorcontrib>Kiladjian, Jean-Jacques</creatorcontrib><title>Ruxolitinib reduces JAK2 p.V617F allele burden in patients with polycythemia vera enrolled in the RESPONSE study</title><title>Annals of hematology</title><addtitle>Ann Hematol</addtitle><addtitle>Ann Hematol</addtitle><description>In patients with polycythemia vera (PV), an elevated
JAK2
p.V617F allele burden is associated with indicators of more severe disease (e.g., leukocytosis, splenomegaly, and increased thrombosis risk); however, correlations between allele burden reductions and clinical benefit in patients with PV have not been extensively evaluated in a randomized trial. This exploratory analysis from the multicenter, open-label, phase 3 Randomized Study of Efficacy and Safety in Polycythemia Vera With JAK Inhibitor INCB018424 Versus Best Supportive Care trial evaluated the long-term effect of ruxolitinib treatment on
JAK2
p.V617F allele burden in patients with PV. Evaluable
JAK2
p.V617F-positive patients randomized to ruxolitinib (
n
= 107) or best available therapy (BAT) who crossed over to ruxolitinib at week 32 (
n
= 97) had consistent
JAK2
p.V617F allele burden reductions throughout the study. At all time points measured (up to weeks 208 [ruxolitinib-randomized] and 176 [ruxolitinib crossover]), mean changes from baseline over time in
JAK2
p.V617F allele burden ranged from −12.2 to −40.0% (ruxolitinib-randomized) and −6.3 to −17.8% (ruxolitinib crossover). Complete or partial molecular response was observed in 3 patients (ruxolitinib-randomized,
n
= 2; ruxolitinib crossover,
n
= 1) and 54 patients (ruxolitinib-randomized,
n
= 33; ruxolitinib crossover,
n
= 20; BAT,
n
= 1), respectively. Among patients treated with interferon as BAT (
n
= 13), the mean maximal reduction in allele burden from baseline was 25.6% after crossover to ruxolitinib versus 6.6% before crossover. Collectively, the data from this exploratory analysis suggest that ruxolitinib treatment for up to 4 years provides progressive reductions in
JAK2
p.V617F allele burden in patients with PV who are resistant to or intolerant of hydroxyurea. The relationship between allele burden changes and clinical outcomes in patients with PV remains unclear.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alleles</subject><subject>Blood cancer</subject><subject>Cross-Over Studies</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Hematology</subject><subject>Humans</subject><subject>Inhibitor drugs</subject><subject>Janus Kinase 2 - antagonists & inhibitors</subject><subject>Janus Kinase 2 - genetics</subject><subject>Janus Kinase 2 - metabolism</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Mutation, Missense</subject><subject>Oncology</subject><subject>Original</subject><subject>Original Article</subject><subject>Polycythemia Vera - drug therapy</subject><subject>Polycythemia Vera - enzymology</subject><subject>Polycythemia Vera - genetics</subject><subject>Pyrazoles - therapeutic use</subject><subject>Time Factors</subject><subject>Treatment Outcome</subject><issn>0939-5555</issn><issn>1432-0584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kVFvFCEQx4nR2Gv1A_hiSHzxZevAwbL7YtI0V2ttWtOqr4QFtkfDwQq79e7by-XappqUhEzC_OY_M_wRekfgkACITxmAClEBERVtW1atX6AZYXNaAW_YSzSDdt5WvJw9tJ_zLQChDaOv0V4JvG44maHhalpH70YXXIeTNZO2GZ8dfaN4OPxVE3GClffWW9xNydiAXcCDGp0NY8Z_3LjEQ_QbvRmXduUUvrNJYRtSLDVmy5Z3fLW4_n55cb3AeZzM5g161Suf7dv7eIB-nix-HJ9W55dfvh4fnVeaCRgroxmnhPXlNrViHPq6ZY0Sqtc1UE0MCA3W6r5VouZcUGK6hiqYgwJDeTc_QJ93usPUrazRZeKkvBySW6m0kVE5-W8muKW8iXeSl4ZCtEXg471Air8nm0e5cllb71WwccqSNOV3BVBKCvrhP_Q2TimU9SRpgQnBKWsKRXaUTjHnZPvHYQjIrZ9y56csfsqtn3Jdat4_3eKx4sHAAtAdkEsq3Nj0pPWzqn8BbTWryg</recordid><startdate>20170701</startdate><enddate>20170701</enddate><creator>Vannucchi, Alessandro Maria</creator><creator>Verstovsek, Srdan</creator><creator>Guglielmelli, Paola</creator><creator>Griesshammer, Martin</creator><creator>Burn, Timothy C.</creator><creator>Naim, Ahmad</creator><creator>Paranagama, Dilan</creator><creator>Marker, Mahtab</creator><creator>Gadbaw, Brian</creator><creator>Kiladjian, Jean-Jacques</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>C6C</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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170701</creationdate><title>Ruxolitinib reduces JAK2 p.V617F allele burden in patients with polycythemia vera enrolled in the RESPONSE study</title><author>Vannucchi, Alessandro Maria ; Verstovsek, Srdan ; Guglielmelli, Paola ; Griesshammer, Martin ; Burn, Timothy C. ; Naim, Ahmad ; Paranagama, Dilan ; Marker, Mahtab ; Gadbaw, Brian ; Kiladjian, Jean-Jacques</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-dc45214f21486a450f6948a7afc602c1d07c0eecf9a7655721db82a030a0d25b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alleles</topic><topic>Blood cancer</topic><topic>Cross-Over Studies</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Hematology</topic><topic>Humans</topic><topic>Inhibitor drugs</topic><topic>Janus Kinase 2 - antagonists & inhibitors</topic><topic>Janus Kinase 2 - genetics</topic><topic>Janus Kinase 2 - metabolism</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Mutation, Missense</topic><topic>Oncology</topic><topic>Original</topic><topic>Original Article</topic><topic>Polycythemia Vera - drug therapy</topic><topic>Polycythemia Vera - enzymology</topic><topic>Polycythemia Vera - genetics</topic><topic>Pyrazoles - therapeutic use</topic><topic>Time Factors</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vannucchi, Alessandro Maria</creatorcontrib><creatorcontrib>Verstovsek, Srdan</creatorcontrib><creatorcontrib>Guglielmelli, Paola</creatorcontrib><creatorcontrib>Griesshammer, Martin</creatorcontrib><creatorcontrib>Burn, Timothy C.</creatorcontrib><creatorcontrib>Naim, Ahmad</creatorcontrib><creatorcontrib>Paranagama, Dilan</creatorcontrib><creatorcontrib>Marker, Mahtab</creatorcontrib><creatorcontrib>Gadbaw, Brian</creatorcontrib><creatorcontrib>Kiladjian, Jean-Jacques</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Annals of hematology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vannucchi, Alessandro Maria</au><au>Verstovsek, Srdan</au><au>Guglielmelli, Paola</au><au>Griesshammer, Martin</au><au>Burn, Timothy C.</au><au>Naim, Ahmad</au><au>Paranagama, Dilan</au><au>Marker, Mahtab</au><au>Gadbaw, Brian</au><au>Kiladjian, Jean-Jacques</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ruxolitinib reduces JAK2 p.V617F allele burden in patients with polycythemia vera enrolled in the RESPONSE study</atitle><jtitle>Annals of hematology</jtitle><stitle>Ann Hematol</stitle><addtitle>Ann Hematol</addtitle><date>2017-07-01</date><risdate>2017</risdate><volume>96</volume><issue>7</issue><spage>1113</spage><epage>1120</epage><pages>1113-1120</pages><issn>0939-5555</issn><eissn>1432-0584</eissn><abstract>In patients with polycythemia vera (PV), an elevated
JAK2
p.V617F allele burden is associated with indicators of more severe disease (e.g., leukocytosis, splenomegaly, and increased thrombosis risk); however, correlations between allele burden reductions and clinical benefit in patients with PV have not been extensively evaluated in a randomized trial. This exploratory analysis from the multicenter, open-label, phase 3 Randomized Study of Efficacy and Safety in Polycythemia Vera With JAK Inhibitor INCB018424 Versus Best Supportive Care trial evaluated the long-term effect of ruxolitinib treatment on
JAK2
p.V617F allele burden in patients with PV. Evaluable
JAK2
p.V617F-positive patients randomized to ruxolitinib (
n
= 107) or best available therapy (BAT) who crossed over to ruxolitinib at week 32 (
n
= 97) had consistent
JAK2
p.V617F allele burden reductions throughout the study. At all time points measured (up to weeks 208 [ruxolitinib-randomized] and 176 [ruxolitinib crossover]), mean changes from baseline over time in
JAK2
p.V617F allele burden ranged from −12.2 to −40.0% (ruxolitinib-randomized) and −6.3 to −17.8% (ruxolitinib crossover). Complete or partial molecular response was observed in 3 patients (ruxolitinib-randomized,
n
= 2; ruxolitinib crossover,
n
= 1) and 54 patients (ruxolitinib-randomized,
n
= 33; ruxolitinib crossover,
n
= 20; BAT,
n
= 1), respectively. Among patients treated with interferon as BAT (
n
= 13), the mean maximal reduction in allele burden from baseline was 25.6% after crossover to ruxolitinib versus 6.6% before crossover. Collectively, the data from this exploratory analysis suggest that ruxolitinib treatment for up to 4 years provides progressive reductions in
JAK2
p.V617F allele burden in patients with PV who are resistant to or intolerant of hydroxyurea. The relationship between allele burden changes and clinical outcomes in patients with PV remains unclear.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>28456851</pmid><doi>10.1007/s00277-017-2994-x</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0939-5555 |
| ispartof | Annals of hematology, 2017-07, Vol.96 (7), p.1113-1120 |
| issn | 0939-5555 1432-0584 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5486779 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Adult Aged Aged, 80 and over Alleles Blood cancer Cross-Over Studies Female Gene Frequency Hematology Humans Inhibitor drugs Janus Kinase 2 - antagonists & inhibitors Janus Kinase 2 - genetics Janus Kinase 2 - metabolism Male Medicine Medicine & Public Health Middle Aged Mutation, Missense Oncology Original Original Article Polycythemia Vera - drug therapy Polycythemia Vera - enzymology Polycythemia Vera - genetics Pyrazoles - therapeutic use Time Factors Treatment Outcome |
| title | Ruxolitinib reduces JAK2 p.V617F allele burden in patients with polycythemia vera enrolled in the RESPONSE study |
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