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In our study, we analyzed the telomeric complex expression and function in the molecular pathogenesis of CML.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>We employed CD34+\u2009primary leukemic cells, comprising both leukemic stem and progenitor cell populations, isolated from peripheral blood or bone marrow of CML patients in chronic and blastic phase to analyze the telomere length and telomeric-associated proteins.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>The reduction in telomere length during disease progression was correlated with increased expression of <jats:italic>BCR::ABL1<\/jats:italic> transcript and the dynamic changes were neither associated with the enzymatic activity of telomerase nor with gene copy number and expression of telomerase subunits. Increased expression of <jats:italic>BCR::ABL1<\/jats:italic> was positively correlated with expression of <jats:italic>TRF2<\/jats:italic>, <jats:italic>RAP1<\/jats:italic>, <jats:italic>TPP1<\/jats:italic>, <jats:italic>DKC1<\/jats:italic>, <jats:italic>TNKS1<\/jats:italic>, and <jats:italic>TNKS2<\/jats:italic> genes.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>The dynamics of telomere length changes in CD34+\u2009CML cells is dependent on the expression level of <jats:italic>BCR::ABL<\/jats:italic>, which promotes the expression of certain shelterins including <jats:italic>RAP1<\/jats:italic> and <jats:italic>TRF2<\/jats:italic>, as well as <jats:italic>TNKS<\/jats:italic>, and <jats:italic>TNKS2<\/jats:italic>, and results in telomere shortening regardless of telomerase activity. Our results may allow better understanding of the mechanisms responsible for the genomic instability of leukemic cells and CML progression.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1007\/s00432-023-04662-w","type":"journal-article","created":{"date-parts":[[2023,3,5]],"date-time":"2023-03-05T03:02:31Z","timestamp":1677985351000},"page":"7103-7112","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["The interplay between telomeric complex members and BCR::ABL1 oncogenic tyrosine kinase in the maintenance of telomere length in chronic myeloid leukemia"],"prefix":"10.1007","volume":"149","author":[{"given":"Anna","family":"Der\u0119gowska","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Monika","family":"P\u0119pek","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Iwona","family":"Solarska","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marcin M.","family":"Machnicki","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katarzyna","family":"Pruszczyk","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marek","family":"Dudzi\u0144ski","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joanna","family":"Niesiob\u0119dzka-Kr\u0119\u017cel","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ilona","family":"Sefery\u0144ska","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Waldemar","family":"Sawicki","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maciej","family":"Wnuk","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomasz","family":"Stok\u0142osa","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2023,3,5]]},"reference":[{"key":"4662_CR1","doi-asserted-by":"publisher","first-page":"35218","DOI":"10.1038\/srep35218","volume":"6","author":"GA Andriani","year":"2016","unstructured":"Andriani GA, Almeida VP, Faggioli F et al (2016) Whole chromosome instability induces senescence and promotes SASP. 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