{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T15:49:01Z","timestamp":1792511341569,"version":"4.5.0"},"reference-count":89,"publisher":"MDPI AG","issue":"9","license":[{"start":{"date-parts":[[2015,9,21]],"date-time":"2015-09-21T00:00:00Z","timestamp":1442793600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Chronic myeloid leukemia was the first haematological neoplasia that benefited from a targeted therapy with imatinib nearly 15 years ago. Since then, several studies have investigated the role of genes, their variants (i.e., polymorphisms) and their encoded proteins in the pharmacokinetics and pharmacodynamics of BCR-ABL1 tyrosine kinase activity inhibitors (TKIs). Transmembrane transporters seem to influence in a significant manner  the disposition of TKIs, especially that of imatinib at both cellular and systemic levels. In particular, members of the ATP-binding cassette (ABC) family (namely ABCB1 and ABCG2) together with solute carrier (SLC) transporters (i.e., SLC22A1) are responsible for the differences in drug pharmacokinetics. In the case of the newer TKIs, such as nilotinib and dasatinib, the substrate affinity of these drugs for transporters is variable but lower than that measured for imatinib. In this scenario, the investigation of genetic variants as possible predictive markers has led to some discordant results. With the partial exception of imatinib, these discrepancies seem to limit the application of discovered biomarkers in the clinical settings. In order to overcome these issues, larger prospective confirmative trials are needed.<\/jats:p>","DOI":"10.3390\/ijms160922811","type":"journal-article","created":{"date-parts":[[2015,9,21]],"date-time":"2015-09-21T10:17:32Z","timestamp":1442830652000},"page":"22811-22829","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":35,"title":["Pharmacogenetics of BCR\/ABL Inhibitors in Chronic  Myeloid Leukemia"],"prefix":"10.3390","volume":"16","author":[{"given":"Marialuisa","family":"Polillo","sequence":"first","affiliation":[{"name":"Department of Clinical and Experimental Medicine, Section of Pharmacology, University of Pisa,  Via Roma 55, 56126 Pisa, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sara","family":"Galimberti","sequence":"additional","affiliation":[{"name":"Department of Clinical and Experimental Medicine, Section of Hematology, University of Pisa,  Via Roma 57, 56126 Pisa, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudia","family":"Barat\u00e8","sequence":"additional","affiliation":[{"name":"Department of Clinical and Experimental Medicine, Section of Hematology, University of Pisa,  Via Roma 57, 56126 Pisa, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mario","family":"Petrini","sequence":"additional","affiliation":[{"name":"Department of Clinical and Experimental Medicine, Section of Hematology, University of Pisa,  Via Roma 57, 56126 Pisa, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4414-8934","authenticated-orcid":false,"given":"Romano","family":"Danesi","sequence":"additional","affiliation":[{"name":"Department of Clinical and Experimental Medicine, Section of Pharmacology, University of Pisa,  Via Roma 55, 56126 Pisa, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antonello","family":"Di Paolo","sequence":"additional","affiliation":[{"name":"Department of Clinical and Experimental Medicine, Section of Pharmacology, University of Pisa,  Via Roma 55, 56126 Pisa, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2015,9,21]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"601","DOI":"10.1358\/dot.2002.38.9.696536","article-title":"Imatinib mesylate (Gleevec, Glivec): A new therapy for chronic myeloid leukemia and other malignancies","volume":"38","author":"Cervantes","year":"2002","journal-title":"Drugs Today"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"156","DOI":"10.1002\/ajh.23887","article-title":"How I treat newly diagnosed chronic myeloid leukemia in 2015","volume":"90","author":"Piazza","year":"2015","journal-title":"Am. 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