Skip to main content

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

 Â