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Table 1 Treatment strategy. The patient had difficulty tolerating TKIs due to hematologic toxicity (thrombocytopenia). Additionally, identification of three genetic variants triggered three treatment changes: imatinib and nilotinib-resistant BCR-ABL1 E255V, ponatinib-sensitive BCR-ABL1 T315I, ruxolitinib-sensitive CSF3R mutations. Dates initiated and discontinued are the number of weeks post-diagnosis of CML

From: Outgrowth of a CSF3R-mutant clone drives a second myeloproliferative neoplasm in a chronic myeloid leukemia patient: a case report

Inhibitor Molecular Target Initiated Discontinued Reason Discontinued
Nilotinib BCR-ABL1 0w 28w Thrombocytopenia
Imatinib BCR-ABL1 33w 78w BCR-ABL1 p.E255V
Dasatinib BCR-ABL1 79w 118w BCR-ABL1 p.T315I
Ponatinib BCR-ABL1 128w   
Ruxolitinib CSF3R 252w