Intensive chemotherapy induction followed by interferon-alpha maintenance in patients with Philadelphia chromosome-positive chronic myelogenous leukemia

✍ Scribed by Hagop M. Kantarjian; Moshe Talpaz; Michael J. Keating; Elihu H. Estey; Susan O'brien; Miloslav Beran; Kenneth B. McCredie; Jordan Gutterman; Emil J Freireich

• Publisher: John Wiley and Sons
• Year: 1991
• Tongue: English
• Weight: 585 KB
• Volume: 68
• Category: Article
• ISSN: 0008-543X
• DOI: 10.1002/1097-0142(19910915)68:6<1201::aid-cncr2820680604>3.0.co;2-1

✦ Synopsis

In a pilot study, 32 patients with Philadelphia chromosome-positive chronic myelogenous leukemia were treated with intensive chemotherapy induction followed by interferon-alpha (IFN-A) maintenance. Intensive chemotherapy consisted of three cycles of daunorubicin 120 mg/mz on day 1, cytarabine 80 mg/m2 daily for 10 days, vincristine 2 mg on day 1, and prednisone 100 mg daily for 5 days (DOAP). Maintenance therapy with IFN-A at a doses of 3 X lo6 to 5 X lo6 units/m2 daily was adjusted according to counts and toxicity. The outcome of patients was compared with a matched historic population of 64 patients treated with IFN-A alone. Overall, 60% of patients had a cytogenetic response (partial or complete) with induction chemotherapy, but only eight (25%) had a sustained cytogenetic response with IFN-A maintenance. After a median follow-up of 67 months, the 6year survival rate of the 32 patients was 58'3'0, compared with 36% for the matched historic group (P = 0.084). The incidence of lymphoid blastic transformation in the two groups was 25% and 48%, respectively (P = 0.10) and durable cytogenetic responses, 25% and 19%, respectively (P = 0.48). In summary, the addition of intensive chemotherapy induction to IFN-A maintenance does not improve the survival rate, incidence of lymphoid blastic transformation, or incidence of durable cytogenetic response compared with the results achieved with IFN-A therapy alone. Cancer 68:1201-1207,1991, HRONIC MYELOGENOUS LEUKEMIA (CML) is char-C acterized by the presence in the leukemic cells of a balanced chromosomal translocation between the long arms of chromosomes 9 and 22 [t(9;22) (q34;ql l)], the so-called Philadelphia chromosome (Ph').] This genetic abnormality is associated with abnormal molecular events at the DNA, RNA, and protein levels.*,' These may be From the