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This unusual clinical study asks whether the best responders to imatinib therapy can discontinue taking the drug and maintain deep remissions.","journal-title":"Lancet Oncol."},{"key":"BFnrc3317_CR164","doi-asserted-by":"crossref","first-page":"603","DOI":"10.1182\/blood.V118.21.603.603","volume":"118","author":"F-X Mahon","year":"2011","unstructured":"Mahon, F.-X. et al. Discontinuation of imatinib in patients with Chronic Myeloid Leukemia who have maintained complete molecular response: update results of the STIM Study. Blood 118, 603 (2011).","journal-title":"Blood"},{"key":"BFnrc3317_CR165","doi-asserted-by":"crossref","first-page":"277","DOI":"10.1182\/blood.V118.21.3781.3781","volume":"118","author":"P Rousselot","year":"2011","unstructured":"Rousselot, P. et al. Discontinuation of dasatinib or nilotinib in chronic myeloid leukemia (CML) patients (pts) with stable undetectable Bcr-Abl transcripts: results from the French CML group (FILMC). 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