Publication Only: Acute myeloid leukemia - Clinical
AML is a heterogenous disease with multiple established prognostic factors including molecular genetic markers, and also many genetic changes with yet little or unknown role. Mutation of JAK2 tyrosine kinase has been detected in myeloproliferative disorder that can evolve into AML, but yet its prognostic role in AML not established.
to study JAK-II gene expression pattern in AML patients and its relation with other established prognostic variables and outcome parameters
Prospective study on 175 AML patients treated at medical oncology department. Jak2 gene expression was evaluated by quantitative real time PCR using taqman primer probe assay. All patients received current standard of care treatment for AML at NCI, Cairo University, Egypt.
the median age was 31 year with male to female ratio of 53.1/46.9. The most common FAB subtypes were M2 followed by M4. The median OS of the whole group is 4 months, and significantly higher for APL than AML (29.8 v 2.8 month, p = 0.005), for favorable risk cytogenetic patients than other patients (29.8 v 1.8 month, p < 0.001), and lower for poor risk group than other groups (1.2 v 4.2 month, p = 0.019). Patients with JAK-II expression fold change ≤0.5 had better OS than those with >0.5 (median 17.5 v2.4 month, p = 0.011). The median DFS for patients who achieved complete remission (CR) was 11.8 months. APL patients had better DFS than AML (median 28.8 v 8.7 month, p = 0.007). DFS according to risk grouping, low risk group had significantly better DFS than either intermediate or poor risk (p = 0.019 and p = 0.029). On multivariate analysis, combined (cytogenetic and molecular genetic)risk status (low v high) and cytogenetic catgorization were independent factors for survival (p = 0.048 & 0.005 respectively), JAK-II expression fold change remained an independent factor for OS.
JAK-II gene expression is associated with decreased overall survival and disease free survival in AML patients