Secondary acute lymphoblastic leukaemia is constitutional and probably not related to prior therapy. (30th March 2015)

• Record Type: Journal Article
• Authors: Ganzel, Chezi; Devlin, Sean; Douer, Dan; Rowe, Jacob M.; Stein, Eytan M.; Tallman, Martin S.
• Is Part Of: British journal of haematology. Volume 170:Number 1(2015:Jul.)
• Page Start: 50
• Page End: 55
• Publication Date: 2015-03-30
• Subjects: Hematology -- Periodicals; Blood -- Diseases -- Periodicals; 616.15
• DOI: 10.1111/bjh.13386
• Languages: English
• ISSNs: 0007-1048

Abstract

<abstract abstract-type="main" id="bjh13386-abs-0001"> <title>Summary</title> <p>Very little is known about secondary acute lymphoblastic leukaemia (s‐ALL). This retrospective analysis studied a cohort of s‐ALL patients treated at a single centre between 1994 and 2013, while comparing therapy‐associated ALL (t‐ALL) and antecedent malignancy ALL (am‐ALL) patients. Thirty‐two patients with s‐ALL were identified. The overall incidence was 9·4% among ALL adults while T‐cell s‐ALL was rare (12% of s‐ALLs). The median time interval between two malignant diagnoses was 5·3 years (range: 0·1–28). In contrast to previous reports, most of the s‐ALLs were CD10 + and without <italic>KMT2A</italic> (<italic>MLL</italic>) abnormalities. The overall survival (OS) rates of the entire cohort at 12 and 24 months from ALL diagnosis was 49% and 25%, respectively. Most patients (<italic>n</italic> = 23, 72%) received prior chemo‐/radio‐therapy for their first malignancy (t‐ALL) and only 9 (28%) did not (am‐ALL). No significant difference was found in the incidence of B‐/T‐ lineage ALL, extramedullary disease, blood count, and the rate of Philadelphia‐positive ALL, nor in the rates of complete remission (<italic>P</italic> = 0·55) and OS (<italic>P</italic> = 0·97). This similarity, together with high incidence of family malignancy in both groups, raise the possibility that s‐ALL patients may have an inherent predisposition to malignancies and a history of previous therapy may be of lesser importance in the pathogenesis of s‐ALL.</p> </abstract>