Premium
Incidence of secondary acute myelogenous leukemia after treatment of childhood acute lymphoblastic leukemia
Author(s) -
Kreissman Susan G.,
Gelber Richard D.,
Cohen Harvey J.,
Clavell Luis A.,
Leavitt Pearl,
Sallan Stephen E.
Publication year - 1992
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19921015)70:8<2208::aid-cncr2820700832>3.0.co;2-p
Subject(s) - medicine , leukemia , incidence (geometry) , confidence interval , pediatrics , lymphoblastic leukemia , population , physics , environmental health , optics
Background . Recent reports of secondary acute myelogenous leukemia (AML) occuring in children previously treated for acute lymphoblastic leukemia (ALL) prompted a review of patients with ALL treated at the Dana Farber Cancer Institute consortium (DFCI) between 1973 and 1987. Seven hundred fifty‐two of 779 children treated for ALL entered complete remission. The mean follow‐up time for the 752 patients was 4.4 years. Two children had AML develop 12 and 13 months after the diagnosis of ALL, respectively. Methods . The estimated overall risk of secondary AML was calculated for the patient population as instances per 1000 patient‐years of follow‐up. This was compared with recent reported cases from another institution. Results . The estimated overall risk of secondary AML was 0.61 instances per 1000 patient‐years of follow‐up (95% confidence interval: 0.15, 4.4). The difference between the risk of 0.61 among DFCL patients versus previously reported risk of 5.8 among a differently treated group of patients with ALL was statistically significant (P= 0.0008). No epipodophyllotoxin was used in the patients in the DFCI consortium. In contrast, an epipodophyllotoxin was used in 12 of 13 previously reported patients who had secondary AML develop. Conclusions . The authors concluded that the use of epipodophyllotoxins may be associated with an increased risk of having secondary AML develop in patients with ALL.