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Impact of CALR mutations in patients with MF treated with ruxolitinib
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The JAKi ruxolitinib is commonly used for the management of MF-related splenomegaly and symptoms, regardless of MPN driver mutation.1 However, its mechanism of action does not specifically target CALR mutations.1 Given the development of novel CALR-targeted therapies, a subanalysis of the retrospective observational RUX-MF (NCT06516406) study (N = 1,055) evaluated how CALR mutations impact treatment and survival outcomes in patients with CALR mutations and MF receiving ruxolitinib treatment (n = 135) outside of clinical trials in 25 hematology centers.1 Findings were published by Palandri et al.1 in Annals of Hematology. |
| Key learnings |
| At treatment initiation, patients with CALR-mutations had a more severe disease burden, with higher rates of anemia, fibrosis, and high-risk mutations, along with lower hemoglobin levels and higher peripheral blast counts vs those with JAK2 mutations. |
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At 6 months, spleen response rates were similar at 21.4% in CALR-mutated patients vs 25.7% in JAK2-mutated patients. However, symptom response was lower with CALR at 56.1% vs 66.7% (p = 0.04), and anemia was more frequent at 60.3% vs 50.3% (p = 0.04). |
| 5-year survival rates were comparable between CALR and JAK2-mutations, at 63.7% and 69.1%, respectively. However, ruxolitinib discontinuation rates were higher with CALR mutations at 24.0% per year vs 16.1% in JAK2-mutated patients. |
| Despite the initial benefits of ruxolitinib therapy, patients with CALR mutations may require novel therapeutic interventions to achieve optimal outcomes. Early intervention and personalized treatment strategies are essential, and further research is needed to evaluate CALR-targeted therapies. |
Abbreviations: CALR, calreticulin; JAK, Janus kinase; JAKi, JAK inhibitor; MF, myelofibrosis; MPN, myeloproliferative neoplasms.
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