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The aim of study was to evaluate the <jats:italic>PDL1<\/jats:italic> mRNA and <jats:italic>JAK2<\/jats:italic> mRNA level in molecularly defined essential thrombocythaemia (ET) patients (pts) during disease progression to post-ET- myelofibrosis (post-ET-MF). The study group consisted of 162 ET pts, including 30 pts diagnosed with post-ET-MF. The <jats:italic>JAK2<\/jats:italic>V617F, <jats:italic>CALR<\/jats:italic>, and <jats:italic>MPL<\/jats:italic> mutations were found in 59.3%, 19.1%, and 1.2% of pts, respectively. No copy-number alternations of the <jats:italic>JAK2<\/jats:italic>, <jats:italic>PDL1<\/jats:italic>, and <jats:italic>PDCDL1G2<\/jats:italic> (<jats:italic>PDL2<\/jats:italic>) genes were found. The level of PD-L1 was significantly higher in the <jats:italic>JAK2<\/jats:italic>V617F than in the <jats:italic>JAK2<\/jats:italic>WT, <jats:italic>CALR<\/jats:italic> mutation-positive, and triple-negative pts. The PD-L1 mRNA level was weakly correlated with both the <jats:italic>JAK2<\/jats:italic>V617F variant allele frequency (VAF), and with the JAK2V617F allele mRNA level. The total <jats:italic>JAK2<\/jats:italic> level in post-ET-MF pts was lower than in ET pts, despite the lack of differences in the <jats:italic>JAK2<\/jats:italic>V617F VAF. In addition, the PD-L1 level was lower in post-ET-MF. A detailed analysis has shown that the decrease in <jats:italic>JAK2<\/jats:italic> and <jats:italic>PDL1<\/jats:italic> mRNA levels depended on the bone marrow fibrosis grade. The <jats:italic>PDL1<\/jats:italic> expression showed no differences in relation to the genotype of the <jats:italic>JAK2<\/jats:italic> haplotype<jats:sup>GGCC_46\/1<\/jats:sup>, hemoglobin concentration, hematocrit value, leukocyte, and platelet counts. The observed drop of the total <jats:italic>JAK2<\/jats:italic> and <jats:italic>PDL1<\/jats:italic> levels during the ET progression to the post-ET-MF may reflect the changes in the <jats:italic>JAK2<\/jats:italic>V617F positive clone proliferative potential and the PD-L1 level\u2013related immunosuppressive effect. The above-mentioned hypothesis is supported by The Cancer Genome Atlas (TCGA) data, confirming a strong positive association between <jats:italic>CD274<\/jats:italic> (encoding PD-L1), <jats:italic>CXCR3<\/jats:italic> (encoding CXCR3), and <jats:italic>CSF1<\/jats:italic> (encoding M-CSF) expression levels, and recently published results documenting a drop in the CXCR3 level and circulating M-CSF in patients with post-ET-MF.\n<\/jats:p>","DOI":"10.1007\/s00277-022-05001-8","type":"journal-article","created":{"date-parts":[[2022,10,21]],"date-time":"2022-10-21T02:03:27Z","timestamp":1666317807000},"page":"2665-2677","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Essential thrombocythaemia progression to the fibrotic phase is associated with a decrease in JAK2 and PDL1 levels"],"prefix":"10.1007","volume":"101","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0992-2020","authenticated-orcid":false,"given":"Krzysztof","family":"Lewandowski","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3734-271X","authenticated-orcid":false,"given":"Zuzanna","family":"Kandu\u0142a","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7535-3316","authenticated-orcid":false,"given":"Micha\u0142","family":"Gniot","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7052-9741","authenticated-orcid":false,"given":"Edyta","family":"Paczkowska","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7879-2261","authenticated-orcid":false,"given":"Paulina Maria","family":"Nawrocka","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8979-2723","authenticated-orcid":false,"given":"Marzena","family":"Wojtaszewska","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4656-9318","authenticated-orcid":false,"given":"Micha\u0142","family":"Janowski","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Magdalena","family":"Mariak","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Luiza","family":"Handschuh","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3770-7715","authenticated-orcid":false,"given":"Piotr","family":"Kozlowski","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2022,10,21]]},"reference":[{"key":"5001_CR1","doi-asserted-by":"crossref","unstructured":"Vainchenker W, Kralovics R (2017) Genetic basis and molecular pathophysiology of classical myeloproliferative neoplasms. 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