The findings of a study, presented at the 12th International Congress on Myeloproliferative Neoplasms, suggest that ruxolitinib is more effective in JAK2 positive patients than JAK2 negative patients in terms of improving constitutional symptoms, reducing spleen size and, and enhancing quality of life.
To conduct this interventional study, which took place between 2014 and 2018, researchers enrolled 40 patients (42.5% JAK2 positive, 57.5% JAK2 negative) diagnosed with primary myelofibrosis (MF). They used PCR to detect JAK2 mutation and Sanger sequencing to perform a molecular mutational analysis for CALR and MPL. Patient response to treatment, which was evaluated in terms of hematological parameters, regression in spleen size, reduction in the transfusion requirements, constitutional symptoms and leukemic transformation, was assessed by IWG criteria.
Following analysis, the researchers observed a statistically significant reduction in spleen size in the JAK2 positive group (62.5%) juxtaposed to the JAK2 negative group (34.8%). Moreover, they noted that the frequency of red cell transfusion was diminished from 41% to 11.8% in JAK2 positive and 34.8% to 17.4% in JAK2 negative group, respectively. The results showed no statistical difference between the two groups in terms of symptoms like pruritis, fatigue and weight loss. Furthermore, the study found that leukemic transformation occurred in 6.25% and 8.7% of JAK2 positive and negative group. The overall survival in the JAK2 positive and negative groups was 82.6% and 88.2%, respectively.
“Ruxolitinib was more effective in JAK2 positive group of patients in terms of improvement in constitutional symptoms, reduction in spleen size and quality of life, but no survival advantage was noted between the two study groups,” the authors concluded.
Zaidi U, et al. Response of Ruxolitinib Treatment in JAK2 Positive Versus JAK2 Negative Primary Myelofibrosis Patients. Presented at the 12th International Congress on Myeloproliferative Neoplasms; October 24-25, 2019; New York, NY.