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Published on: March 25, 2016
Clinical and cytologic characteristics of blastic phase in Ph-positive chronic myeloid leukemia treated with
G Alimena1, M Lazzarino, E Morra
1Department of Human Biopathology, University La Sapienza, Rome, Italy.
Insights
This study found that some chronic myeloid leukemia patients on alpha-interferon may develop blastic crises, particularly those with low risk and good response, who are prone to lymphoid blastic crises.
Area of Science:
- Hematology
- Oncology
- Internal Medicine
Background:
- Alpha-interferon (IFN) is a treatment for Philadelphia chromosome-positive chronic myeloid leukemia (Ph+ CML).
- Blastic crisis (BC) is a late-stage complication of CML.
Purpose of the Study:
- To investigate the incidence and characteristics of blastic crises (BC) in Ph+ CML patients treated with IFN.
- To identify patient subsets at higher risk for developing BC.
Main Methods:
- Retrospective analysis of 238 Ph+ CML patients treated with IFN in chronic phase (CP).
- Patients were stratified by Sokal's risk score (low, intermediate, high) and CP treatment groups.
- Analysis of BC type (myeloid vs. lymphoid) and correlation with risk group and treatment.
Main Results:
- 72 blastic crises (BC) occurred in 238 patients over a median of 51 months.
- BC incidence was similar across treatment groups but higher in high-risk patients.
- Lymphoid BC was more frequent in low-risk patients and those who responded well to IFN.
Conclusions:
- A subset of low-risk CML patients, particularly those responding well to IFN, may be prone to lymphoid BC.
- Further research is needed to define the role of IFN in BC development.
Abstract:
We report 72 blastic crises (BC), occurring in 238 Ph+ chronic myeloid leukemia (CML) patients treated in chronic phase (CP) with alpha-interferon (IFN) for a median time of 51 months (range 7-96). The 238 patients were grouped by Sokal's risk at diagnosis in low- (LR), intermediate- (IR) and high-risk (HR), and by CP treatment. Group 1: 160 patients (57% LR, 31% IR, 12% HR) given IFN alone in early CP. Group 2: 31 patients (65% LR, 32% IR, 3% HR) given IFN alone in late CP. Group 3: 23 patients (78% LR, 22% IR) given IFN before and after autologous stem cell transplantation (ASCT). Group 4: 24 patients (83% LR, 17% IR) given IFN after ASCT. Of the 72 BC, 52 (72%) were myeloid (My), and 20 (28%) lymphoid (Ly). Overall BC incidence was similar in all CP treatment groups, although with a prevalence of Ly BC in groups 3 + 4 vs groups 1 + 2, (p = NS); the incidence of BC was higher in HR patients (P = NS), but on the whole it was lower than expected on the basis of historical controls. Lymphoid BC was more frequent in LR than in IR + HR patients (P < 0.05), and was more frequent in responders to IFN, than in non-responders (P < 0.05). In conclusion, a subset of patients with low risk at diagnosis, better response to IFN and proneness to evolve into Ly BC can be identified. The role played by IFN in this context remains to be defined.
