{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:00:53Z","timestamp":1791331253426,"version":"4.3.1"},"reference-count":43,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2013,7,9]],"date-time":"2013-07-09T00:00:00Z","timestamp":1373328000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancer Science"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:p>A number of <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> patients who achieve a sustained complete molecular response (<jats:styled-content style=\"fixed-case\">CMR<\/jats:styled-content>) for at least 2\u00a0years during imatinib (<jats:styled-content style=\"fixed-case\">IM<\/jats:styled-content>) therapy can discontinue <jats:styled-content style=\"fixed-case\">IM<\/jats:styled-content> without relapse. With the long\u2010term goal of developing immunological criteria for managing <jats:styled-content style=\"fixed-case\">IM<\/jats:styled-content> therapy in <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> patients, we compared the immunophenotypic profiles of three groups of <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> patients: those who received <jats:styled-content style=\"fixed-case\">IM<\/jats:styled-content> and had a <jats:styled-content style=\"fixed-case\">CMR<\/jats:styled-content> for more than two consecutive years (<jats:styled-content style=\"fixed-case\">CMR<\/jats:styled-content> group); patients who received <jats:styled-content style=\"fixed-case\">IM<\/jats:styled-content> and did not have a sustained <jats:styled-content style=\"fixed-case\">CMR<\/jats:styled-content> but maintained a major molecular response for more than 2\u00a0years (fluctuating <jats:styled-content style=\"fixed-case\">CMR<\/jats:styled-content> group); and patients with a sustained <jats:styled-content style=\"fixed-case\">CMR<\/jats:styled-content> for more than 6\u00a0months after <jats:styled-content style=\"fixed-case\">IM<\/jats:styled-content> discontinuation (<jats:styled-content style=\"fixed-case\">STOP<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">IM<\/jats:styled-content> group), together with healthy controls. The percentages of effector populations of natural killer (<jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content>) cells, such as interferon (<jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>)\u2010\u03b3<jats:sup>+<\/jats:sup>CD3<jats:sup>\u2212<\/jats:sup>CD56<jats:sup>+<\/jats:sup> cells, were significantly higher in the <jats:styled-content style=\"fixed-case\">STOP<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">IM<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">CMR<\/jats:styled-content> groups than in the fluctuating <jats:styled-content style=\"fixed-case\">CMR<\/jats:styled-content> and control groups. The elevated levels of these effector <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> cells were sustained for more than 3\u00a0years after <jats:styled-content style=\"fixed-case\">IM<\/jats:styled-content> discontinuation. In contrast, the percentages of effector memory CD8<jats:sup>+<\/jats:sup> T cells, such as IFN\u2010\u03b3<jats:sup>+<\/jats:sup> CCR7<jats:sup>\u2212<\/jats:sup>CD45RO<jats:sup>+<\/jats:sup>CD8<jats:sup>+<\/jats:sup> cells, were significantly higher in the <jats:styled-content style=\"fixed-case\">STOP<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">IM<\/jats:styled-content> and control groups than in the <jats:styled-content style=\"fixed-case\">CMR<\/jats:styled-content> and fluctuating <jats:styled-content style=\"fixed-case\">CMR<\/jats:styled-content> groups, possibly owing to <jats:styled-content style=\"fixed-case\">IM<\/jats:styled-content> intake. These results suggest that the immunological activation status of <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> cells contributes to <jats:styled-content style=\"fixed-case\">CMR<\/jats:styled-content> maintenance. Higher activation levels of effector <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> cells in <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> patients being treated with <jats:styled-content style=\"fixed-case\">IM<\/jats:styled-content> might reflect minimization of <jats:italic>BCR\u2010ABL1<\/jats:italic> transcript levels and therefore could be additive information for determining whether to stop <jats:styled-content style=\"fixed-case\">IM<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/cas.12216","type":"journal-article","created":{"date-parts":[[2013,6,12]],"date-time":"2013-06-12T13:27:12Z","timestamp":1371043632000},"page":"1146-1153","source":"Crossref","is-referenced-by-count":32,"title":["Sustained upregulation of effector natural killer cells in chronic myeloid leukemia after discontinuation of 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