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Therefore, we studied the development of second malignancies in 868 patients diagnosed with <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> between 2002 and 2011 using the Swedish <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> register, cross\u2010linked to the Swedish Cancer register. With a median follow\u2010up of 3\u00b77 (range 0\u20139\u00b79)\u00a0years, 65 (7\u00b75%) patients developed 75 second malignancies (non\u2010haematological), 52 of which were of the invasive type. Compared to expected rates in the background population, the risk of second malignancies was higher in the <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> cohort, with a standardized incidence ratio (<jats:styled-content style=\"fixed-case\">SIR<\/jats:styled-content>) of 1\u00b752 (95% CI 1\u00b713\u20131\u00b799). The <jats:styled-content style=\"fixed-case\">SIR<\/jats:styled-content> before and after the second year following diagnosis of <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> was 1\u00b758 and 1\u00b747, respectively. Among specific cancer types, gastrointestinal and nose and throat cancer were significantly increased. Founded on a population\u2010based material, our results indicate that <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> patients treated in the <jats:styled-content style=\"fixed-case\">TKI<\/jats:styled-content> era are at an increased risk of developing a second malignancy, with indications that this risk may more likely be linked to <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> itself rather than to the <jats:styled-content style=\"fixed-case\">TKI<\/jats:styled-content> treatment.<\/jats:p>","DOI":"10.1111\/bjh.13346","type":"journal-article","created":{"date-parts":[[2015,3,27]],"date-time":"2015-03-27T22:13:59Z","timestamp":1427494439000},"page":"683-688","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":52,"title":["Second malignancies following treatment of chronic myeloid leukaemia in the tyrosine kinase inhibitor era"],"prefix":"10.1111","volume":"169","author":[{"given":"Niklas","family":"Gunnarsson","sequence":"first","affiliation":[{"name":"Department of Public Health and Clinical Medicine Ume\u00e5 University Ume\u00e5 Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Leif","family":"Stenke","sequence":"additional","affiliation":[{"name":"Department of Haematology Karolinska University Hospital Stockholm Sweden"},{"name":"Department of Medicine Karolinska Institutet Stockholm Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martin","family":"H\u00f6glund","sequence":"additional","affiliation":[{"name":"Department of Medical Science and Division of Haematology University Hospital Uppsala Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fredrik","family":"Sandin","sequence":"additional","affiliation":[{"name":"Regional Cancer Centre Uppsala\u2010\u00d6rebro 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