Sustained Response to Ruxolitinib of Eosinophilia-Associated Myeloproliferative Neoplasm with Translocation t(8;9)(p21;p24)

The translocation t(8;9) produces the fusion gene PCM1-JAK2, resulting in the continuous activation of the JAK2 tyrosine kinase. Myelodysplastic/myeloproliferative neoplasms are the most common disease with t(8;9)/PCM1-JAK2. Individuals with this abnormality have similar features, and JAK2 kinase inhibitor (ruxolitinib) is an effective treatment of the condition. The long-term remission results of ruxolitinib are varied. It is important to determine the response to ruxolitinib. Here, we describe a patient who has been diagnosed with eosinophilia-associated myeloproliferative neoplasm with t(8;9)(p21;p24). This patient has achieved sustained response for >1 year since the administration of ruxolitinib.

Automated summary

The translocation t(8;9) generates the fusion gene PCM1-JAK2, leading to continuous activation of JAK2 tyrosine kinase. t(8;9)/PCM1-JAK2 is the most common myelodysplastic/myeloproliferative neoplasm. Patients with this abnormality have similar features and JAK2 kinase inhibitor (ruxolitinib) is an effective treatment. However, the long-term remission results of ruxolitinib are varied, so it is important to determine the response to ruxolitinib. This study describes a patient with eosinophilia-associated myeloproliferative neoplasm with t(8;9)(p21;p24), who has achieved sustained response for >1 year since the administration of ruxolitinib.