<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cokic VP</submitter><funding>Intramural NIH HHS</funding><funding>National Institute of Diabetes and Digestive and Kidney Diseases</funding><funding>Serbian Ministry of Education, Science and Technological Development</funding><pagination>453020</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4602333</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>2015</volume><pubmed_abstract>The recent JAK1/2 inhibitor trial in myeloproliferative neoplasms (MPNs) showed that reducing inflammation can be more beneficial than targeting gene mutants. We evaluated the proinflammatory IL-6 cytokine and JAK-STAT signaling pathway related genes in circulating CD34(+) cells of MPNs. Regarding laboratory data, leukocytosis has been observed in polycythemia vera (PV) and JAK2V617F mutation positive versus negative primary myelofibrosis (PMF) patients. Moreover, thrombocytosis was reduced by JAK2V617F allele burden in essential thrombocythemia (ET) and PMF. 261 significantly changed genes have been detected in PV, 82 in ET, and 94 genes in PMF. The following JAK-STAT signaling pathway related genes had augmented expression in CD34(+) cells of MPNs: CCND3 and IL23A regardless of JAK2V617F</pubmed_abstract><journal>Mediators of inflammation</journal><pubmed_title>Proinflammatory Cytokine IL-6 and JAK-STAT Signaling Pathway in Myeloproliferative Neoplasms.</pubmed_title><pmcid>PMC4602333</pmcid><funding_grant_id>175053</funding_grant_id><pubmed_authors>Beleslin-Cokic BB</pubmed_authors><pubmed_authors>Kraguljac-Kurtovic N</pubmed_authors><pubmed_authors>Raj PK</pubmed_authors><pubmed_authors>Damjanovic S</pubmed_authors><pubmed_authors>Diklic M</pubmed_authors><pubmed_authors>Gotic M</pubmed_authors><pubmed_authors>Buac M</pubmed_authors><pubmed_authors>Markovic D</pubmed_authors><pubmed_authors>Milenkovic P</pubmed_authors><pubmed_authors>Cokic VP</pubmed_authors><pubmed_authors>Mitrovic-Ajtic O</pubmed_authors></additional><is_claimable>false</is_claimable><name>Proinflammatory Cytokine IL-6 and JAK-STAT Signaling Pathway in Myeloproliferative Neoplasms.</name><description>The recent JAK1/2 inhibitor trial in myeloproliferative neoplasms (MPNs) showed that reducing inflammation can be more beneficial than targeting gene mutants. We evaluated the proinflammatory IL-6 cytokine and JAK-STAT signaling pathway related genes in circulating CD34(+) cells of MPNs. Regarding laboratory data, leukocytosis has been observed in polycythemia vera (PV) and JAK2V617F mutation positive versus negative primary myelofibrosis (PMF) patients. Moreover, thrombocytosis was reduced by JAK2V617F allele burden in essential thrombocythemia (ET) and PMF. 261 significantly changed genes have been detected in PV, 82 in ET, and 94 genes in PMF. The following JAK-STAT signaling pathway related genes had augmented expression in CD34(+) cells of MPNs: CCND3 and IL23A regardless of JAK2V617F</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015</publication><modification>2026-05-04T14:38:45.034Z</modification><creation>2019-03-27T01:59:57Z</creation></dates><accession>S-EPMC4602333</accession><cross_references><pubmed>26491227</pubmed><doi>10.1155/2015/453020</doi></cross_references></HashMap>