Rabbit Anti-Human ABL1 polyclonal antibody

Achievement of MR4.5 (BCR-ABL1 <= 0.0032% on international scale) is an important goal of tyrosine kinase inhibitor (TKI) treatment for patients with chronic myeloid leukemia (CML). This study describes treatment patterns by region and assesses time to achieve MR4.5 in patients with CML - chronic phase (CP) treated with second-line nilotinib or dasatinib in 10 countries. A multivariate Cox proportional hazards model was used to assess time to MR4.5 for nilotinib versus dasatinib. The model accounted for the competing-risk event of TKI resistance, included random effects for country clustering, and was adjusted for baseline covariates. The study included 280 patients treated with either nilotinib (N = 135 [48%]) or dasatinib (N = 145 [52%]) as second-line TKI with median treatment durations of 19.1 and 18.7 months, respectively. Nilotinib was observed to be better in achieving MR4.5 than dasatinib (adjusted hazard ratio = 1.37, 95% CI [1.11, 1.69]) suggesting second-line nilotinib may perform better in achieving MR4.5 than dasatinib.

BACKGROUND The Janus kinase 2 (JAK2) V617F mutation is common in patients with breakpoint cluster region-Abelsonl (BCR-ABL1)-negative myeloproliferative neoplasms, including polycythemia vera, essential thrombocythemia and primary myelofibrosis, but is rarely detected in BCR-ABL1-positive chronic myeloid leukemia (CML) patients. Here, we report a CML patient with both a BCR-ABL1 rearrangement and JAK2 V617F mutation. CASE SUMMARY A 45-year-old Chinese woman was admitted to our department with a history of significant thrombocytosis for 20 d. Color Doppler ultrasound examination showed mild splenomegaly. Bone marrow aspiration revealed a karyotype of 46, XX, t(9;22)(q34;q11.2) in 20/20 metaphases by cytogenetic analysis, rearrangement of BCR-ABL1 (32.31%) by fluorescent polymerase chain reaction (PCR) and mutation of JAK2 V617F (10%) by PCR and Sanger DNA sequencing. The patient was diagnosed with CML and JAK2 V617F mutation. Following treatment with imatinib for 3 mo, the patient had an optimal response and BCR-ABL1 (IS) was 0.143%, while the mutation rate of JAK2 V617F rose to 15%. CONCLUSION Emphasis should be placed on the detection of JAK2 mutation when CML is diagnosed to distinguish JAK2 mutation-positive CML and formulate treatment strategies.